Male Reproductive 3352: Penile Fracture � Presentation: sudden onset, mild to

severe pain in penis; ??cracking?? sound with loss of erection, swelling/bruising

of penis at site of fracture o Urethrogram indicated with blood at penile meatus,
hematuria, dysuria, or urinary retention as these indicated urethral injury o
Frequently injury occurs during sexual intercourse * Pathophysiology: typically,
from rupture of the corpus cavernosum due to tear in tunica albuginea * Dx:
clinical * Tx: emergent urologic repair o Suprapubic catheter may be needed post-
surgically while urethra repairs 4525: Varicocele � Presentation: soft scrotal mass
(??bag of worms??) that decreases supine and increases with standing/Valsalva
maneuver. Scrotum does NOT illuminate with light application.o Testicular atrophy
(poor bloodflow), and poor fertility (increased scrotal temp from increased blood
pooling)o Morecommonlyonleftside(??
nutcrackersyndrome??)duetoleftrenalveincompressionasit passes between the SMA &
abdominal aortao Right sided varicocele is likely due to malignant compression
(renal cell carcinoma) or thrombosis of the IVC or the right gonadal artery (as it
drains directly into the IVC) * Imaging: ultrasound (torturous tubules next to
testis, retrograde venous flow, & dilation of the pampiniform plexus) * Dx: clnical
presentation with ultrasound findings * Tx: o Boys/Youngmen:gonadalveinligation o
Oldermen:scrotalsupportandNSAIDs * Other things presenting like Varicoele o
Spermatocele�swellingofspermaticcordwithpainlessmassatthesuperiorpoleofthetestis;
distinct from testis, sometimes will transilluminate o
Hydrocele�fluidaccumulationbetweenparietal/viscerallayersofthetunicavaginalis,often
due to patent processus vaginalis. May increase with Valsalva/standing (peritoneal
communication) or not. Fluid is easily trans-illuminated with light application.
Often resolve within the 1st year of life Infectious Disease9111: Prosthetic Joint
Infection * Early Infection (<3 mo post-op)o
Presentation:drainagefromprosthesissite,erythema/swelling/fever/elevatedWBC o
Micro:S.auerus,gram(-)bugs,anaerobeso Dx:synovialjointaspiration/cultureo
Tx:implantremoval/exchangeORdebridement/retention+Abx * Late Infection (>3 mo post-
op)o Presentation: persistent joint pain, loosening of prosthesis, sinus tract
formation/drainage o
Micro:Coag(-)Staph(S.epidermitisiscommon),Propionibacteriumspp.,Enerococcio
Dx:synovialjointaspiration/cultureo Tx:implantremoval/exchange+Abx 4544: Acute
Bacterial Parotitis * Presentation: unilateral pain/swelling/tenderness at angle of
jaw that??s aggravated by chewing, fever/leukocytosis, purulent saliva expression
from parotid duct, may occur post-operatively * Micro: S.aureus * Dx: clinical
presentation + purulent fluid culture * Prevention: adequate fluid hydration and
oral therapy are extremely effective! * Tx: expression of purulent saliva + Abx
2749: Necrotizing Fasciitis * Presentation: fever, hypotension,
fever/swelling/edema/extreme pain overlying skin (most commonly on perineum or
extremities) ?? rapid discoloration, bullae, purulent discharge ?? necrosis of area
o Classically area of pain looks OK on exam (??pain out of proportion??)o
Oftenpthashistoryofsomeminortrauma(cut/scrape)toareanowaffectedo
Oftenwillmoveacrossmultiplemusclegroups(differentiatesfrompyomyositis) o
C.perfringens classically will cause crepitus & bubbles to form on imaging *
Pathogenesis: minor bacterial invasion gets to the fascial layer and rapidly spread
throughout fascial planes causing major necrosis * Micro: Strep. pyogenes (GAS),
S.aureus, C.perfringens, polymicrobial * Imaging: CT scan with ??bubbles?? or air
on in the deep tissue * Dx: clinical presentation * Tx: broad spectrum Abx +
aggressive surgical debridement or amputation o
Shouldnotbedelayedifdiagnosisisstronglysuspected;startTx,thengetimaging 4102:
Necrotizing Surgical Site Infection * Presentation: pain/edema/erythema of surgical
site, systemic signs (fever, tachycardia, hypotension), Paresthesia or anesthesia
at edges of surgical wound, ??Dishwater drainage?? (purulent/grey) from surgical
site, Crepitus or release of gas from surgical site o
Thesemayspreadtofascialplanecausingnecrotizingfasciitis o More common in diabetic
patients (blunted immune response) * Micro: most commonly polymicrobial * Dx:
clinical presentation * Tx: aggressive surgical debridement + broad-spectrum abx +
supportive care (hydration, control of co- morbid conditions)o Note that negative
pressure wound therapy (Wound-Vac) is reserved for only healthy, granulating
surgical wounds; NOT infected ones! 3464/4526: Post-Operative Fever * The 5 Ws:
Wind (pneumonia, aspiration, PE), Wound (surgical site infection), Water (UTI),
Walking (DVT), Wonder drugs (drug fever, blood product reaction, catheter site
infection) * Immediate (within 1 day) � prior trauma/infection, blood production
reaction, malignant hyperthermia o
Mostcommonbloodproductionreactionisanonhemolytictransfusionreaction(cytokines built
up in stored blood illicit inflammatory response); occurs within 1-6hr post-
transfusion) * Acute (within 1 week) � SSI (GAS or C.perfringens), nosocomial
infection, DVT/PE, MIo Most common nosocomial infection is S.epidermitis (local
skin flora) at a catheter site * Subacute (within 1 month) � SSI (not
GAS/C.perfringens), catheter infection, C.diff, drug fever, PE/DVT * Delayed (past
1 month) � SSI (fastidious organisms), viral infection (possibly from blood
products! Endocrine/Diabetes/Metabolism 8876/8882: Hypoparathyroidism �
Presentation: asymptomatic ?? fatigue/anxiety/depression ?? perioral
tingling/numbness, Chvostik??s sign, Trousseau??s sign, QT-
prolongation/arrhythmias, seizure o Most commonly occurs after thyroidectomy or
31�2 removal parathyroidectomyo
Othercauses:autoimmune>DiGeorgesyndrome>defectiveCa-SRreceptor>non- autoimmune
destruction (hemochromatosis, Wilson??s Disease, neck irradiation) o
Labs:lowCa2+/highphos/normalrenalfunctiontests � Dx:o Lowmagnesium?
DrugsthatcausehypoCa?RecentBloodtransfusion???correctitifyes. o
Ifno,measurePTHlevel * ?? �Low/normal PTH � surgical damage to parathyroids,
autoimmune destruction of parathyroids, or some infiltrative disease (Wilson??s,
hemochromatosis, etc.) * ?? �High PTH � Vit D deficiency (check 25-Vit D levels),
CKD, sepsis, tumor lysis syndrome � Tx: Aim at underlying cause; Vit. D
supplementation???, Ca2+ supplementation??? 4077: Acute Adrenal Insufficiency
(Adrenal Crisis) * Presentation: severe/refractory hypotension (loss of
mineralocorticoids), vomiting, abdominal pain, fever, * Pathophysiology: adrenal
hemorrhage/infarction, illness/injury/surgery in pt with chronic glucocorticoid use
(may have Cushing??s Disease features) or adrenal insufficiency (Addison??s
Disease) o As little as >3wk of prednisone 20mg/day can lead to HPA axis
suppression * Labs: hyponatremia, hyperkalemia * Dx: clinical presentation with
history * Tx: hydrocortisone or dexamethasone + aggressive fluid hydration 2174:
Addison�s Disease (Adrenal Insufficiency) * Presentation: constitutional (fatigue,
weight loss, weakness), GI (N/V, diarrhea, decreased appetite), aldosterone
deficiency (volume depletion, hyperkalemia, hyponatremia, hypotension/syncope,
increased ADH), skin (vitiligo or hyperpigmentation) * Dx: 8AM serum cortisol +
plasma ACTH or ACTH stimulation test (250mcg cosyntropin) o Low cort + high ACTH or
poor response = primary adrenal adrenal insufficiencyo Low cort + low ACTH or poor
response = secondary or tertiary adrenal insufficiencyo Low cort + Normal ACTH or
normal response = likely something else, keep investigating * Tx: depends on
underlying cause 2592/4721/4419: Cushing�s Syndrome * Presentation: central
obesity, buffalo hump, moon facies, skin atrophy with purple striae, proximal
muscle weakness, hypertension (mineralocorticoids), glucose intolerance, skin
hyperpigmentation, eccymoses/easy bruising, women may have hirsutism/menstrual
irregularities o Labs:hyperglycemia,hypokalemia * Etiology: exogenous
corticosteroid administration (most common), ACTH-producing tumor (Cushing??s
disease), ectopic ACTH-production (small-cell lung cancer), or primary adrenal
disease * Dx: o Establishhypercortisolismwithsalivarycortisolassay,24-
hrfreeurinecortisol,andlow-dose dexamethasone suppression test (2/3 must be
positive) o If hypercorticolism present ?? ACTH level measurement (see if process
is ACTH dependent or independent) o IfACTHiselevated??high-
dosedexamethasonesuppressiontesttodetermineifsourceof ACTH is pituitary (will be
suppressed) or ectopic (won??t be suppressed, likely lung cancer) � Tx: aimed at
underlying cause GI/Nutrition3877/4098: Ischemic Colitis * Risk Factors: age >60,
chronic renal disease/dialysis, atherosclerotic disease, recent vascular procedure
(classic is AAA repair), hx of myocardial infarction * Presentation: mild/localized
abdominal pain & tenderness, bright red bloody diarrhea, lactic acidosis,
leukocytosis * Pathophysiology: poor bloodflow via mesenteric arteries causes end
organ damage of the bowel, leading to dysfunction/breakdown/bleeding. o Most common
areas to be affected are watershed areas * ?? �Splenic flexure (SMA & IMA
watershed) * ?? �Rectosigmoid junction (sigmoid artery & superior rectal artery) o
AAA surgery may have as post-op complication (disruption of collaterals, clamping
of aorta, manipulation, etc.) o Acute hypotension may result in enough lack of
bloodflow to precipitate this � Imaging: o
CTscan:Localizedthickeningofcolon,pneumatosiscoli(airinbowelwall),doublehalosign
(inner and outer ??rings?? of density from inflamed bowel) o
Colonoscopy/Flexiblesigmoidoscopy:mucosalpallor,petechiae/ulceration/bleedinginloca
l site (bowel above and below are NORMAL!) * Dx: clinical signs + imaging (CT
for emergency; colonoscopy for non-emergency) * Tx: supportive care (IV
fluids/bowel rest), IV Abx o Colon resection if clinical deterioration or necrotic
bowel 2921: Management of non-symptomatic Esophageal Varicies � Non-selective beta-
blockers (propranolol/nadolol/others) are recommended as the unopposed a-
adrenergic activity causes constriction of the splanchnic veins ?? shrinking of
varices/slowed progression and decreased risk of bleeding; Ligation of esophageal
varices is also a good option 2922/4386: Emergent Treatment of Pt with Gastric
Variceal Hemorrhage * First Step in anyone with upper GI hemorrhage: place 2 large-
bore IV catheters & start fluids * Next step due to variceal hemorrhage: IV PPI
(decrease acid secretion) + make pt NPO + IV octreotide (splanchnic
vasoconstriction to shrink varices) + Abx (any pt with cirrhosis) + continue
monitoring ABCs * After stabilization: urgent upper endoscopy to assess varices o
Bleeding Stopped: B-blocker + endoscopic banding/ligation in 1-2wk o
ActiveBleeding:balloontamponade(temp.)??TIPSproceduretorelieveporto-systemicHTN *
Early Re-bleeding: endoscopic evaluation again...same approach as above 2904: Acute
Cholecystitis � Presentation: RUQ pain after a fatty meal, referred pain to the
shoulder, Murphey??s sign (halt of inspiration with palpation under right ribcage),
fever, nausea/vomiting, leukocytosiso
90%arecausedbygallstoneimpactioninthecysticduct??uncomplicated,causesmild
elevations of LFTs/bilirubino Ifgallstonegoesintothecommonbileduct??
complicated,icterus&veryhighAlk.phos o
Gangrene,perforation,abscess,orperitonitismaybecomplications * Dx: presentation
with confirmatory imaging * Tx: Supportive care OR laparoscopic cholecystectomy if
complications arise 4655/2930: Gallstone Management * Gallstones without
symptoms ?? no treatment necessary, simply monitor * Gallstones with biliary
colic ?? elective laparoscopic cholecystectomy or ursodeoxycholic acid *
Complicated gallstones (acute cholecystitis, choledocolithiasis, or gallstone
pancreatits) ?? cholecystectomy within 72 hrs (lower rates of complication compared
to delayed 7 days) 4086: Diverticulosis * Outpouchings of the colon due to weakened
areas encountering pressure, thus bulging out. They??re typically asymptomatic and
increase incidence with age, but can cause complications.o Associated with
constipation and oddly enough, may worsen existing constipation! * Complications:
diverticular hemorrhage, diverticulitis, perforation, abscess formationo
Adequatefruit/vegetablefiberinthedietandphysicalactivitylowerriskofcomplications o
Meat,aspirin/NSAIDs,obesity,andsmokingincreaseriskofcomplications * While these
often pose no problem, it??s important to take steps to limit the risk of
complication in those with diverticulitis with lifestyle changes 2204/3182: Acute
Diverticulitis * Presentation: LLQ abdominal pain, fever, nausea, vomiting,
ileus/urinary urgency and frequency (due to peritoneal irritation in sigmoid colon
affecting the bladder)o Labs:leukocytosis,o
Mayresultinobstruction,fistula,perforation,orabcessformation * Dx: Abdominal CT
w/oral & IV contrast (pericolic fat inflammation, diverticula, bowel wall
thickening, soft tissue masses, abscesses) o Sigmoid/colonoscopy are
contraindicated due to concern of perforation * Tx: o
Uncomplicated:hospitalization,bowelrest,IVAbx,closewatcho Complicated (abscess,
perforation, obstruction, or fistula: treatment based on severity * ?? �Abscess
<3cm diameter � IV abx, bowel rest, close observation * ?? �Abscess >3cm diameter �
CT-guided percutaneous drainage * ?? �Free fluids/feces or failure to improve by
day 5 � surgical drainage, washout, and debridement with possible bowel resection *
?? �Pts who cannot tolerate surgery should be treated as ??uncomplicated??
4292/4930/4500: Acute Management of Blunt Abdominal Trauma * Presentation: hx of
trauma, ??seatbelt sign?? (abdominal ecchymosis), abdominal guarding/distention,
rebound tenderness, hypotension, associated fractures * First Step: 2 large-bore
IVs with fluids wide-open * Hemodynamically stable: FAST exam (focused assessment
with sonography for trauma) to evaluate the abdomen/pericardium for free fluido
FAST(-):serialabdominalexamstotrackclinicalcourse+/-CTabdomeno
FAST(+):CTabdomentofindsourceofinjury??exploratorylaparotomyo
EquivocalFAST:diagnosticperitoneallavage??exploratorylaparotomyif(+) *
Hemodynamically unstable: FAST examo FAST(-)??CTabdomen??
monitorif(-)/exploratorylaparotomyif(+) o FAST(+)??exploratorylaparotomy 4555:
Bowel Perforation from Blunt Abdominal Trauma.� Often this is due to damage to
mesenteric blood supply, subsequent necrosis, then perforation. Classically seen as
worsening bowel pain and free air in the peritoneum on imaging. Perforation most
often occurs in the jejunum in this situation. Pt needs exploratory laparotomy for
washout and repair. 4498: Hepatic Laceration from Blunt Abdominal Trauma *
Presentation: post-abdominal trauma RUQ pain, referred right shoulder pain, ??
seatbelt sign??, hypotension/tachycardia, free abdominal fluid, concomitant
fractures o Classically fractured 8th/9th ribs can cause these lacerations * First
step: FAST exam with trauma evaluation ?? treat like any other trauma patient
2372/4292: Splenic Laceration from Blunt Abdominal trauma * Presentation: post-
abdominal trauma LUQ pain, left chest wall pain, referred left shoulder pain,
hypotension/tachycardia, anemia, free abdominal fluid, concomitant fractureso
ClassicallyinyoungerpatientswithHxofviralinfectionsymptomssuggestiveofmononucleosis
* First step: FAST exam with trauma evaluation ?? treat like any other trauma
patient * If spleen can be repaired, then repair is preferred, especially in
children/teens * If splenectomy is needed, post-op immunization against
encapsulated organisms is manadatory 3420: Penetrating Abdominal Trauma * First
Step: FAST exam + quick history + quick physical exam * Next Step o
Hemodynamicallyunstable/signsofperitonitis/evisceration/bloodfromnasogastrictubeoro
n rectal exam ?? exploratory laparotomy o Ifnoneoftheabovearepresent??
localexplorationofwound+eFAST+CTscan(extended FAST checks for pneumothorax,
hemothorax, and peritoneal injury) ?? Diagnostic peritoneal lavage may be used if
ultrasound/CT are unavailable 3851: Duodenal Hematoma * Presentation: o
Initially:abdominalwalltrauma;mayhonestlyseemfineandbedischarged o 24-
36hrlater:epigastricpain,nausea,vomiting,failuretopassgastriccontents *
Pathophysiology: classically a complication of BAT of children (thinner abdominal
wall, less fat, more pliable ribs) when duodenum clashes against the vertebral
column.o
Delayedpresentationduetotimeittakesforbloodtoresultinobstructionoftheduodenum *
Imaging: CT abdomen showing hematoma/obstruction * Dx: clinical presentation with
imaging * Tx: resolution within 1-2wk of nasogastric suction/parenteral nutrition o
Surgical or percutaneous drainage can be considered with clinical deterioration or
failure to resolve 3358: Blunt Genitourinary Trauma * Rarely life-threatening, the
biggest concerns here are kidney contusions/lacerations and damage to the
vasculature of the kidneys * First Step: focused genitourinary exam + urinalysis +
standard trauma evaluation o Hematuria + hemodynamically stable = CT scan
w/contrast of abdomen & pelvis o Ifhemodynamicallyunstable=IVpyelogramen-
routetosurgery � Note that catheter insertion is avoided until a urethrogram is
done. This is to rule out urethral damage which may be exacerbated by catheter
insertion 2476: Umbilical Hernia * Risk Factors: African American race, premature
birth, developmental syndromes (Beckwith- Wiedemann or Ehler??s Danlos), or
hypothyroidism (cretinism) * Presentation: soft, non-tender, skin-covered bulge at
site of umbilicus which protrudes with crying, straining, or coughing. May contain
omentum or portions of small intestine * Dx: clinical presentation * Tx: o
<5yroldmanualreductionthroughumbilicalring(oftenspontaneouslyresolvesviaconcentric
fibrosis/scarring; more likely in smaller hernias) o
>5yroldwarrantssurgicalclosure(morelikelyinlargehernias>1.5cm)4601: Remember that
any patient with therapeutic anti-coagulation with Warfarin (Coumadin) must be
anti- coagulated before surgical intervention. This is most quickly achieved with
Fresh-Frozen Plasma (FFP) 2933/2982/4434/2965/2929: Acute Pancreatitis�
Presentation: severe abdominal pain, nausea/vomiting, elevated serum lipase,
sometimes xanthomas o
Alcohol(40%),gallstones(40%),hypertriglyceridemia(classically>1000)arecommono
Drugs(azathioprine,valproicacid,thiazidediuretics),infections,oriatrogeniccauses(cl
assically cholesterol emboli from cardiac catheterization) can also be causes � Dx:
two of the following o Acuteepigastricabdominalpainradiatingtothebacko
Increasedamylaseandlipasex3thenormallimit??typicallythefirststepinworkupo
Diffusepancreaticenlargementwithcontrastenhancement(CT)orhyperechoicity(ultrasound)
and sometimes with fat-stranding; Ultrasound is preferred in patients suspected
with gallstones as underlying cause (fat/40/fertile/female = gallstone)� Tx:
supportive care (pain control/fluids) as most cases are self-limited (4-7 days) o
If caused by something that can be treated (drug, infection, etc) then treat thato
Ifgallstonessuspected/found,earlycholecystectomyshouldbedoneoncesymtpomsresolve
4603: Severe Acute Pancreatitis * Pancreatitis + evidence of organ failure due to
release of pancreatic enzymes into the vasculature. This causes increased vascular
permeability in/around the pancreas, causing shock! * Presentation: pancreatitis
symptoms with additional ones o
Organdysfunctionduetofluidoverload(dyspnea,tachypnea,abdominalditention,etc.) o
Cullensign:periumbilicalblue-ishcolorationindicatinghemoperitoneumo Grey-Turner
sign:
red-brown coloration around the flanks indicating retroperitoneal bleed * Risk
factors: >75yrs, obesity, alcoholism, pulmonary infiltration on X-ray o
Labsat48hrs??CRP>150mg/dL,RisingBUNandCreatinine * Tx: aggressive IV fluid
resuscitation to replace lost volume 2143/2822: Acute Mesenteric Ischemia * Risk
Factors: atherosclerosis, hypercoagulable state, heart vegetations, mural thrombus,
etc. * Presentation: acute/severe/poorly-localized peri-umbilical pain (out of
proportion to exam!), N/V o
BowelInfarctionmayoccur(localabdominalpain,peritonealsigns,rectalbleeding,sepsis) o
Labs:leukocytosis,metabolicacidosis(lactate),elevatedamylase,elevatedphosphate,&
elevated Hb (hemoconcentration) * Pathophysiology: atherosclerosis or embolic
disease lodging somewhere within mesenteric arteries * Imaging: CTa or MRa to show
area of infarct; mesenteric angiography if other scans unclear * Dx: presentation
with imaging showing ischemia/infarct * Tx: endovascular thrombolysis or open
embolectomy with vascular bypass o Removal of infarcted bowel may be necessaryo
Post-opAbx(worryofrupture)andanti-coagulation(ifappropriate) 4486: Gastric Outlet
Obstruction * Presentation: post-prandial pain, early satiety, vomiting, abdominal
succession splash (splashing sound on upper abdominal auscultation while rocking pt
back and forth; retained gastric contents >3hr) * Pathophysiology: anything that
can obstruct the pyloric sphincter can cause this (gastric cancer, PUD, Crohn??s
disease, stricture secondary to caustic ingestion, gastric bezoars)o Caustic
ingestion causes fibrosis at the pylorus 6-12wk following injury resolution *
Imaging: upper endoscopy (visualize the problem!) * Dx: presentation with
confirmation on imaging * Tx: surgical resolution of obstruction 2903: Gallstone
Ileus * Presentation: evidence of gallstones (biliary colic, Hx of passage, etc.),
colicky nausea/vomiting, abdominal distension, constipation/lack of flatus,
pneumobilia, hyperactive bowel sounds, dilated loops of bowel, hypovolemia
(tachycardia, hypotension) * Pathophysiology: gallstone ??tumbles?? down the small
intestine causing an intermittent mechanical obstruction. At times it??s relieved,
giving a colicky flavor. o Most common site to lodge is the ileum at the ileocecal
valveo Often gallstones capable of this are too large to pass through the
hepatobiliary tree. The gallbladder will actually be weighed down and form an
adhesion tract for the gallstone to pass into the small bowel for this to occur *
Imaging: CT C/A/P showing gall bladder thickening, pneumobilia, bowel air-fluid
levels, and obstruction by the stone * Dx: clinical presentation with imaging * Tx:
surgical removal of stone with early cholecystectomy (best if done at same time!)
4062: Dumping Syndrome * Presentation: post-gastrectomy complication causing
abdominal pain, diarrhea, nausea, hypotension, tachycardia, dizziness/confusion,
fatigue, and diaphoresis o Occurs15-30minsafterameal * Pathophysiology: post-
gastrectomy (50%), loss of the pyloric sphincter can result in rapid emptying of
hypertonic gastric contents directly into small intestine o Hypertonic fluid pulls
fluid from blood into the gut/intestinal wall resulting in symptoms o Loss of
volume releases vasoactive peptides, resulting in full spectrum of symptoms *
Imaging: upper GI series or gastric emptying study may be useful if diagnosis is
unclear * Dx: clinical presentation * Tx: small, frequent meals post-gastrectomy;
consumption of complex carbs > simple sugars, high-fiber, and protein rich diet
until return of normal bowel functioning, drink fluid between (not with) meals o
Refractory symptoms (rare) = octreotide (decrease vasoactive response to chyme) or
reconstructive surgery 2245/2946: Acalculous Cholecystitis * Acute inflammation of
the gallbladder WITHOUT gallstones typically in critically ill, hospitalized pts
resulting in cholestasis/ischemia of gallbladder ?? 2o infection of gallbladder ??
distention/necrosis * Predisposing factors: recent surgery, severe trauma,
extensive burns, sepsis/shock, prolonged fasting/TPN, mechanical intubation *
Presentation: unexplained fever, leukocytosis, RUQ abdominal pain/mass, jaundice,
abnormal LFTs o
Gallbladderinflammationmaycausegangrene,perforation,oremphysematouscholecystitis
(infection with gas-producing bacteria causing gas in the gallbladder) o Note that
gaseuous distention of the bowel WITHOUT air-fluid levels suggests distention
without obstruction (like with inflammation) o
Highindexofsuspicionshouldbeheldforcriticallyillpatients * Dx: Abdominal ultrasound
is preferred (gallbladder wall thickening, pericholic fluid); CT abdomen or
cholescintigraphy are more sensitive/specific and can be used in unclear ultrasound
* Tx: can be managed medically (abx/anti-inflammatory) or surgically (percutaneous
cholecystectomy with drainage of abscesses) 2940: Emphysematous Cholecystitis *
Presentation: fever, N/V. RUQ pain, elevated LFTs, but Clostridia spp. infection
causes special features o Crepitusoftheabdominalwall(gaspresentingallbladderwall)o
Imaging showing air-fluid levels in the gallbladdero Mild-moderate unconjugated
hyperbilirubinemia (Clostridia can hemolyze RBCs) o Occurs more commonly in
immunosuppressed/diabetics/vascular compromise * Dx: presentation + imaging +
culture showing gas-forming organisms * Tx: emergent cholecystectomy + broad
spectrum Abx 4111: Anal Fissure � Presentation: painful bowel movements with blood
on toilet paper/in water; pt may withhold bowel movements causing worsening
constipationo Commonly occurs a longitudinal midline-posterior anal canal distal to
the dentate line (most susceptible to tear due to poor blood supply ?? poor
healing)o Painfromdamagetofissurefromstoolpassageandspasmwithbowelmovements o Skin
tag (sentinel pile) may be present at the end of the fissure * Pathophysiology:
trauma (constipation, anal sex, prolonged diarrhea), IBD (Crohn??s or UC), anal
cancer results in hypertrophy/hypertonicity of the internal anal spincter * Dx:
clinical presentation * Tx: soften stools (high fiber diet/adequate water
intake/stool softeners), heal wound (sitz bath, regular gentle cleansing, petroleum
jelly/topical anesthetic/topical vasodilators after washing) o 2nd line:
nitroglycerine ointment (headache side effect) & botulinum toxin injection into the
internal sphinctero 3rd line: lateral internal spinchterotomy (10% risk of
incontinence) 2322/4364: Small Bowel Obstruction 4364: Don??t forget! Adhesions are
the most common cause of small bowel obstruction. If a patient presents with a
small bowel obstruction, the greatest risk factor is prior abdominal surgery.
3179/4609: Prolonged Post-Operative Ileus (PPI) * Presentation: nausea, vomiting,
abdominal distention, obstipation, hypoactive bowel sounds o Normallypost-
opileuswillresolvein3-5days;anylongerisconsideredPPIo
Notethatobstructionformadhesionswillhavehyperactivebowelsounds * Pathophysiology:
ileus is a non-obstructive slowing down of bowel movement. This is an expected
occurrence after general anesthesia, however prolongation may be due to several
factors: o Abdominal instrumentation/local inflammation (edema)/use of opiates for
pain control post-op * Imaging: abdominal X-ray showing large & small dilated loops
of bowel as well as dilated stomach in some cases with no transition point to
normal (thus supporting overall edema of the bowel) * Dx: history/supporting
imaging * Tx: ??? 2972: Sphincter of Oddi Dysfunction * Presentation: colicky RUQ
pain, elevated LFTs (obstructive), Hx of cholecystectomy or cholecystitis *
Pathophysiology: abnormal clamping down of Oddi following an inflammatory process
(infection, surgery, etc.) due to dyskinesia/stenosiso Sustained
dyskinesia/stenosis results in a biliary obstruction pictureo
Useofopioidanalgesics(morphine)mayprecipitatesymptomscausingsphinctercontraction *
Imaging: ERCP showing dilated bile ducts in the absence of stones * Dx: history +
Sphincter of Oddi manometry * Tx: sphincterotomy 2923/2924/2983: Genetic Diseases
of Liver Metabolism * Dubin-Johnson syndrome � conjugated bilirubinemia; jaundice
with body stressors (illness, pregnancy, OCP use) but otherwise no/minor symptoms
(fatigue, abd. pain, weakness) and no hemolysiso MorecommoninSephardicJewso
Clinically normal aside from reactionary jaundice and black liver (epinephrine
metabolites) o Labs:Bilirubin(20-
25mg/dL),normalLFTs,normalcoproporphyrin(predominantlyCoproI) * Rotor syndrome �
Dubin-Johnson syndrome without the black liver * Crigler-Najar syndrome � autosomal
recessive unconjugated bilirubinemia; o
Type1:significantmentalretardation/death;Phototherapy/plasmapheresiscanhelp
conjugate the bilirubin to buy time for curative liver transplant o Type 2: fairly
benign unconjugated bilirubinemia with jaundice; often asymptomatic, but symptoms
(if occuring) can be treated with phenobarbital or clofibrate � Gilbert syndrome �
mild unconjugated bilirubinemia triggered by bodily stressors; very similar to C-N
syndrome II, difference is in the enzyme defect 3178/4462/12142: Perforated Peptic
Ulcer Disease * Presentation: chronic epigastric pain that suddenly worsens, with
rebound tenderness/guarding (peritonitis due to gastric contents in peritoneal
cavity), air under the diaphragm on CXR * Pathophysiology: chronic NSAID use, Hx of
PUD, H.pylori infection, head trauma/severe burns can all presipose to generating a
peptic ulcer * Dx: immediate upright CXR, as diagnosis and prompt treatment (<12hr)
is critical to limit mortality * Tx: immediate surgical repair via open laparotomy
3181: Psoas Abscess * Presentation: subacute fever, lower abdominal/flank pain
radiating to groin, anorexia/weight loss o Painwithdeepabdominalpalpation;??
Psoassign??positive * Pathophysiology: often
previous infection results in hematogenous seeding * Imaging: CT abdomen/pelvis
for localization of abscesso Ultrasound is a poor technique because of how deep the
psoas in the abdominal cavity * Dx: presentation + imaging * Tx: percutaneous
drainage + Abx 4640: Pilonidal Disease * Presentation: subacute sacrococcygeal pain
with intergluteal fluctant mass 4-5mm above the anus with mucoid/purulent/blood
drainageo Oftenworsenswithbendingover(anythingstretchinginterglutealskin!)o Occurs
commonly in men 15-30yr with sedentary lifestyles/occupations/deep gluteal clefts *
Pathophysiology: result of edematous infected hair follicles in intergluteal
region. Constant pressure from sitting causes occlusion/abscess formation as hair
is forced into a formed sinus tract. * Dx: clinical presentation * Tx: drainage +
excision of sinus tracts + open closure + lifestyle changes 4558/3585: Pancreatic
Adenocarcinoma & malignant obstruction of the biliary tree (Uworld medicine notes)
4251/3064 Acute Apendicitis/Apendiceal Abscess General Principles3213: Glasgow Coma
Scale * Used to help triage patients for significant brain injury: 0-3 (non-
responsive), 4-8 (coma), 9-15 (OK) * Eye opening: none (1), to pain (2), to verbal
command (3), spontaneous (4) * Verbal response: none (1), incomprehensible (2),
inappropriate words (3), confused (4), oriented (5) o Intubated patients score a 1T
on this section * Motor response: none (1), extension posture/decerebrate (2),
flexion posture/decoticate (3), withdrawal movement (4), localizes movement (5),
obeys commands (6) 3578: Traumatic Amputation * If you happen to get an amputated
body part on the scene (1) wrap in sterile gauze, (2) moisten with sterile saline,
(3) place in plastic bag, (4) place plastic bag on ice, (5) go with the patient to
the ED * DO NOT place directly on ice (frostbite), in antiseptic/alcohol (chemical
injury), or immerse in water (change to blood vessel structure) 3221: Gunshot Wound
to the Lower Chest * Concern for this area of trauma is that the wound could be in
the chest OR the abdomen * Diaphragm level on expiration is the 4th dermatome R,
5th dermatome left (level of the nipples); on inspiration it goes to about the 12th
dermatome at the flanks. * Because of it??s outstanding excursion with regular
breathing, thoracic gunshot wounds below the nipples are considered to involve the
thorax AND abdomen until proven otherwise. 3227: Intubation � Orotracheal
Intubation � the classic ??intubation?? that everyone thinks about. Fast and able
to establish an airway in most patients without too much trouble. This is the
preferred route.o
Notethatpatientswithcervicalspinalinjuryshouldbefirststabilized...butmaysafelyrecei
ve orotracheal intubation after stabilization! � Nasotracheal intubation � an
option, especially in patients with significant facial trauma (don??t want to jack
up their face more with the intubation blade!). It isn??t preferred as it??s a
blind procedure. Contraindications include: o
Basilarskullfracture�tubecanpassthroughfractureintothecranialvault o
Apneic/hypopneicpatients�notreallysurewhy,butitis. 3503: Tracheobronchial Rupture *
A rare result of chest trauma (this question featured an MVC with driver colliding
on steering wheel) * Presentation: persistent pneumothorax/air leakage into chest
tube following chest trauma; pneumomediastinum may be present (crepitus on chest
palpation)o The idea is that you??re pulling more air into the thoracic cavity with
every breath o Most commonly occurs in the right main bronchus * Imaging:o Upright
CXR: will show air in thorax; the most important 1st imaging after chest trauma o
ChestCT:doneafterpersistentpneumothoraxdespitechesttubeplacement * Dx: presentation
+ confirmation via Chest CT/bronchoscopy/surgical identification * Tx: surgical
repair Rheumatology/Orthopedics 3302: Fat Embolism Syndrome * Presentation:
respiratory distress (hypoxemia, dyspnea, tachypnea), neurologic dysfunction
(confusion, visual field defects) & petechial rash, sometimes fever/sub-
conjunctival hemorrhage o Occurs 24-72hr after inciting incident * Pathophysiology:
o Long bone fracture: fatty bone marrow leaks into blood as embolus (femur/pelvic
fractures) o Orthopedic surgery: similar to long-bone fractureo Pancreatitis: rare;
not totally sure how this works, but remember it! * Imaging:o CXR:unremarkable??
bilateralpulmonaryinfiltrateswithin48hr * Dx: clinical diagnosis; may be definitely
diagnosed on autopsy * Tx: prevent with early fracture immobilization, supportive
care/ventilation are best Tx 3569: MCL Tear * Presentation: injury to knee/leg
causing discomfort/swelling of medial knee; may be associated with medial meniscus
tear * Etiology: severe valgus strain o vaLgus??forcecomesfromLateralside o vaRus??
forcecomesfrommedialside * Imaging: MRI may be used if planning operative repair *
Dx: clinical o Valgusstresstest�laxityinthejointwithvalgus(lateral)strain * Tx:
RICE (rest, ice, compression, elevation) + analgesics o Surgical repair may be
considered in some situations 3566/4485: Stress Fracture * Risk factors: repetitive
physical activity, abrupt increase in activity, poor Ca2+/Vit.D/calorie intake,
female athlete triad (low calories, hypo/amenorrhea, low bone density) *
Presentation: insidious onset of local bone/joint pain with localized tenderness at
fracture site. o Most common site is the 2nd metatarsal; it bears to brunt of
walking weight * Etiology: tension/compression of bones without adequate rest OR
with abrupt increase in use * Imaging: X-ray of affected area may show fracture but
can be normal for up to 6wk! o CT/MRI/ultrasound are all very sensitive, but
typically not needed * Dx: clinical presentation * Tx: o 2nd-4th metatarsal - RICE
for 4-6 weeks + analgesia ?? Persistent pain with these tx may have wide, hard-toe
podiatric shoe applied!o 5th metatarsal � surgical fixation + casting due to worse
bloodflow to this area and increased risk of non-union healing 3415/3526: Scaphoid
Fracture� Presentation: history of fall onto outstretched arm, typically
soreness/pain in wrist (??sprained wrist??) with tenderness upon palpation of the
anatomic snuffbox/scaphoid tubercle (high sens., low spec.)o
Circulationtothescaphoidbonecomesfromthedistalportionofthebone(radialartery)o
Middlescaphoidfracturesoftenhavefinebloodflowandcanbehandledbyfamilydoco
Proximalscaphoidfracturesoftenhavepoorbloodflowandshouldbereferredtoorthodueto
increased risk of avascular necrosis development * Dx: plain radiograph showing
fracture o If initially negative, a cast can be placed on clinical suspicion alone
with follow-up radiographs o Follow-up in 2-4wk often allows for development of
visible fracture to occuro CT or MRI may be used to confirm fracture if plain
radiograph is not initially positive * Tx: thumb spica cast (short arm cast with
wrapping to support the thumb) 3556: Supracondylar Fracture of the Humerus *
Presentation: fall onto an outstretched arm, significant pain/bruising/deformity of
the distal humerus * Etiology: most common fracture in peds due to thin
supracondylar region (just above the elbow) from bone remodeling * Imaging: plain
radiograph of affected area showing fracture * Dx: clinical + imaging * Tx:
analgesia, immobilization, orthropedic fixation (if displaced) * Complications o
Brachialarteryinjury:lossofbrachial/radialpulseso
Mediannerveinjury:weakness/deformity/lossofsensationofdistalhando
Cubitusvarusdeformity:abnormal??bump??ontheareaoffractureduetoremodlingo
Compartmentsyndrome(<1%):rare,butmaycauseVolkmann??scontractureo
NotethatlimblengthdiscrepancyisNOTacommoncomplicationasthedistalhumerusgrowth plate
does not contribute much to longitudinal growth (proximal humerus and distal
forearm are the biggest contributors!) 4250: Meniscus Tears * Presentation:
popping/catching/locking sensation of the knee, reduced range of knee, slow-onset
joint effusion, tenderness of joint, Thessaly test (+; standing on affected leg and
turning)/Mcurray test (+; pt laying, leg rotated and flexed) * Etiology: rotation
on planted foot (younger pt) or degradation of meniscal cartilage (older pt) *
Imaging: o MRI:ifplanningonsurgicalrepairo Arthroscopy:ifunexplainedjointeffusion �
Dx: presentation + imaging � Tx: o Milddiseaseorolderpt�rest/NSAIDso
Youngerptwithpersistentsymptoms(>3wk)�surgicalrepair 3557: Clavicle Fracture *
Presentation: fall on outstretched arm or direct shoulder trauma followed by pain,
immobility, posterior/inferior shoulder displacement, and classically use of the
contralateral arm to support injured one o Middle1/3�mostcommonsiteforinjury o
Proximal1/3�won??tbreakasit??ssowellfixatedtothesternum(sternoclavicularjoint) *
Complications: Brachial plexus injury (nerve palsy) or subclavian artery injury
(bruit beneath fracture) * Imaging o X-ray +/- angiogram (subclavian artery) or
nerve conduction studies (brachial plexus) * Tx: o
Middle1/3�bracing/rest/icewithearlymobilizationtoretainshouldermobility o
Distal1/3�openreduction+surgicalfixationwithearlymobilization 3168/4605: Common
Causes of Shoulder Pain & Differentiating Them * Rotator Cuff
Impingement/Tendinopathy � pain with shoulder movements, subacromial tenderness,
normal passive range of motion with pain reproduction with impingement tests (Neer,
Hawkins) * Rotator Cuff Tear � similar to tendinopathy, but more prominent
accompanying weakness with shoulder movements; more common it pts >40yr; drop arm
test(+); MRI may confirm tear * Adhesive Capsulitis � ??stiffness?? with gradual
onset; decreased active AND passive range of motion * Biceps Tendonopathy �
anterior shoulder pain with weakness/pain upon biceps flexion * Glenohumeral
osteoarthritis � gradual onset of deep shoulder pain with decreased active AND
passive range of motion;
precipitated by trauma and much more rare! 3398/3463/4608: Compartment Syndrome �
Presentation: o Early: extreme pain (out of proportion) increasing with passive
stretch, rapid/intense swelling, paresthesias in affected limb o
Late:decreasedsensation,motorweakness,decreasedpulses,limbpallor,paralysis *
Pathophysiology: direct trauma, prolonged compression, or return of perfusion to
acutely ischemic limb all resulting in massive cellular damage and swelling within
the fascia compartmento Circumferential 3rd degree burn around a limb is a less
common cause. The formed eschar constricts blood/lymphatic vessels resulting in
massive fluid build-up in the limb. * Dx: clinical +/- compartment pressure
measurement (compartment pressure >30mmHg or �pressure [diastolic BP � compartment
pressure] <20-30mmHg is significant) * Tx: emergent fasciotomy (faster time-to-
fasciotomy the better) o Post-op:keepinglegatleveloftorso(keepperfusion),analgesiao
If caused by circumferential 3rd degree burn, escharotomy is also indicated
Hematology/Oncology2590: Anterior mediastinal masses include the 4??T??s (thymoma,
teratoma including germ cell tumors, thyroid cancer, and terrible lymphoma). While
these all have different characteristics and signs, if the patient with mediastinal
is B-hCG(+) and AFP(+)...the only tumor that could possibly produce that is a mixed
germ cell tumor (the multiple germ cell types are able to generate the two tumor
markers!). 4493: Don??t forget! In anyone with End-Stage Renal Disease, LMHW
(enoxaparin)/rivaroxaban/epixiban are all contraindicated as they??re renally
excreted. The only acceptable anticoagulation for a patient in renal failure is
Unfractionated Heparin (bridge) ?? Warfarin. Neurology4599: Various Cranial Nerve
Palsies * CN III/IV/VI � strabismus (different changes depending on individual
nerves injured * CNV2,3 compression � Tic douloureux (trigeminal neuralgia) * CNV3
� jaw asymmetry (paralysis of the muscles of mastication * CNVII � facial droop *
CNX recurrently laryngeal - hoarseness * CNXII � tongue palsy (tongue will move
toward the side that??s damaged) 4604: Various Upper Extremity Nerve Palsies *
Axillary nerve � classically injured from an anterior dislocation of the shoulder
(blow to anteriorly rotated/abducted arm), will cause flattening of the
deltoid/shoulder abduction weakness * Radial nerve � classically injured from
midhumeral shaft fractures, will cause weakness of extension of the forearm/hand *
Ulnar nerve � medial epicondylar fracture, lossof medial hand sensation/intrinsic
hand muscle tone * Musculocutaneous nerve � loss of biceps reflex (C5/C6) with
areas of arm sensation deficit * Long thoracic nerve � winged scapula (loss of
serratus anterior) 11997: Meningioma * Presentation: headache, seizure, localized
weakness/numbness (compression of brain matter) * Pathophysiology: meningothelial
cell origin, benign but may compress brain structures * Imaging: MRI showing extra-
axial, calcified, dural-based mass * Dx: presentation + imaging with confirmation
on surgery * Tx: complete surgical resection without chemo/radiation 4204: Anterior
Cord Syndrome � Presentation: abrupt onset of neurologic symptoms classically
occurring with thoracic aorta surgery o
AnteriorCorticospinaltract:immediatebilateralLEflaccidparalysis?? Upper motor
neuron signs develop over days/weeks (hyperreflexia, spasticity, etc.) o
Spinothalamictract:lossofpain/temperaturesensationfromthelevelofinjurydownward o
Intermediolateralcellcolumn(autonomictracts)urinaryretentiono Note that vibratory
sensation/proprioception are preserved (dorsal column) * Pathophysiology: the
anterior spinal artery (ASA) depends on a thoracic aorta branch called the Artery
of Adamkiewicz. Should this be disrupted, the anterior spinal cord becomes
ischemic/infarcted, leading to the specific signs/symptoms * Dx: clinical
presentation * Tx: rehab and functionality salvage Ear, Nose, Throat3428: Nasal
Septal Perforation � Presentation: whistling noise during respiration sometimes
with obvious defect of nasal septum. o Classiccomplicationofrhinoplasty(25%) *
Pathophysiology: the nasal septum is mostly cartilage and has a poor blood supply.
It relies on small mucosal arteries fed by the well-vascularized nasal side walls.
Thus after trauma (such as rhinoplasty) a defect may not heal well, resulting in
perforation * Dx: clinical presentation + visualization of perforation * Tx:
surgical revision 2846: Retropharyngeal Abscess * Presentation: neck pain, nuchal
rigidity, odynophagia, drooling, fever, and buldging of the pharyngeal wall
following penetrating trauma into the space * Anatomy: o
Anteriorborder:buccolphayngealfascia/constrictormusclesofthepharynxo Posterior
border: alar fasciao
Communicateswiththeparapharyngealspaceanddrainsintothesuperiormediastinum *
Complications: o
Acutenecrotizingmediastinitis:infectiondrainsintothesuperiormediastinumorspreadsint
o the posterior mediastinum via the ??danger zone?? between the alar
fascia/prevertebral fascia. * t �Causes fever, chest pain, dyspnea, and odynophagia
* ?? �Requires prompt surgical incision and drainage o
Carotidsheathinfection:spreadherecancauseinternaljugularthrombosisaswellasCNIX,X,
XI, and XII palsies 3500: Nasophayngeal Carcinoma * Presentation: nasal congestion,
epistaxis, headache, cranial nerve palsies (usually CN V or CN VII), and serous
otitis media (obstruction of Eustachian tube)o Cervical lymph nodes are most
commonly inflammed * Pathophysiology: Epstein-Barr virus infection can result in
cellular damage resulting in this cancer formation. It??s very rare in the USA, but
most common in Southern China 2195/2847: Peritonsilar Abscess (??Quinsy??) *
Presentation: fever, chills, sore throat, muffled ??hot potato?? voice, uvular
deviation, unilateral lymphadenopathy, pooling of saliva, and trismus (unable to
open jaw) from muscle spasmo
Airwayobstructionandspreadtoparapharyngealspace(carotidsheathinvolvement) * Dx:
clinical scenario with signs on oropharyngeal exam * Tx: immediate abscess drainage
via needle aspiration with culture/empiric antibiotics o GAS and respiratory
organsisms should be covered 3427: Torus Palatinus * Presentation: benign ??bony,
fleshy, hard mass?? of the midline suture on the hard palate; has a thin epithelium
and tends to get damaged and bleed with slow healing (poor vascular supply), often
small but may grow throughout life * Pathophysiology: thought to be the result of
genetic predisposition (congenital lesion) o Morecommoninwomen&asians * Dx:
clinical presentation o Biopsy is NOT indicated for any reason * Tx: Reassurance
needed unless symptomatic (pain, interference with eating/speech, etc.)
Renal/Electrolytes 4751: Gross Hematuria � Total Hematuria: blood throughout
urination; result of damage to the kidneyo Differential: renal mass
(benign/malignant), glomerulonephritis, kidney stone, PKD, pyelonephritis, traumao
Note that passage of clots would be very rare for glomerulonephritis. More commonly
there would be RBC casts or microscopic hematuria...although gross is possible *
Terminal hematuria: blood at end of urination; result of pathology within the
bladder/prostate/posterior urethrao Differential: urothelial cancer, UTI, kidney
stone, BPH, prostate cancer o Cystoscopy+Prostateexamisoftenagoodfirststep *
Initial hematuria: blood at beginning of urination; result of pathology in the
anterior urethra o Differential:urethritisortrauma 3348/3349/4557: Trauma to the
Male Urogenital Tract * Anatomy o
Bladderneck�narrowingofbladdertoformintotheprostaticurethra o Posterior urethra
* ?? �Prostatic urethra � runs through the prostate * ?? �Membranous urethra � from
end of prostate to bulbomembranous junction o
Anteriorurethra�frombulbomembranousjunction??tipofpenis * Posterior Urethra Injury
o Classically occurs in the male patient in an MVA suffering pelvic fracture. The
shifting of the bladder/prostate with pelvic bone injury results in tearing at the
bulbourethral junctiono Presentation: blood in urethral meatus, unable to void,
perineal/scrotal bruising, and high- riding prostate?? Note that Foley catheter
placement is AVOIDED as it may cause worse injury! o
Dx:retrogradeurethrogramshowingextravasationofcontrastorinabilityofcontrasttoenter
the bladder o Tx:placementofsuprapubiccatheter+delayedsurgicalcorrection * Anterior
Urethra Injury o Classically occurs with straddle injury. Pressure on anterior
urethra causes shearing o Dx: retrograde urethrogramo
Tx:immediatesurgicalcorrection * Extraperitoneal Bladder Injury o
Contusion/ruptureofthebladderneckoranterior/lateralwallso Presentation: localized
pain of lower abdomen/pelvis (urine extravasation), gross hematuria, urinary
retention, and pelvic fracture may pierce the bladder � Intraperitoneal Bladder
Injury (Bladder Dome Rupture o Contusion/rupture of superior bladder wall often
following blunt abdominal traumao
Presentation:diffuseperitonitis/guarding(leakageofurineintoperitoneum),referredpain
to shoulder (diaphragm irritation, phrenic nerve/C3-C5 nerve root) 4607: Pre-Renal
AKI * Etiology: decreased renal perfusion (volume depletion, decreased effective
arterial blood volume, intravascular fluid displacement, renal artery stenosis,
afferent arteriole vasoconstriction * Presentation: oliguria, BUN:Cr (>20:1),
unremarkable sediment on urinanalysis * Dx: presentation with associated labs * Tx:
depends on etiology, but often occurs due to true volume depleted state; thus a
saline bolus would be a great first step in working up these patients if volume
depleted Cardiovascular4501: Post-Cardiac Catheterization Retroperitoneal Hematoma
* Presentation: sudden onset hypotension, tachycardia, flat neck veins, flank/back
pain; classically occurs within 12 hrs of catheterization
* Pathophysiology: while local complication are much more common, any pt
undergoing cardiac catheterization with puncture site above the inguinal ligament
can bleed into retroperitoneal space o
Pttoavoidstrenuousactivity/liftingfor1weekfollowingthisprocedure(riskofhematoma) *
Imaging: non-contrast CT abdomen/pelvis * Dx: presentation + imaging to confirm *
Tx: supportive care (fluids, rest, transfusion of blood products) + close
monitoring o Surgical repair of hematoma can be done, but is rarely required
4527/4696: Aortic Injury * Presentation: o
LowEnergyinjury:hypotension,alteredmentalstatus/shock,Hxorevidenceoftrauma o
HighEnergyinjury:circulatorycollapseandpromptdeath(morecommon)o Classically car
crashes and falls >10ft should prompt suspicion for aortic injury *
Pathophysiology: blunt trauma (increased pressure or fracture causing puncture) or
deceleration (part of aorta anchored by ligamentum arteriosum does not move, while
the rest lurches forward and rips away from anchored portion) * Imaging: o
UprightCXR:widenedmediastinum(mostsensitive),left-sidepneumothorax,right-ward
displacement of mediastinum/trachea, and disruption of aortic contour (??aortic
knob??) o ChestCT/angiography:eithermaybeusedinequivocalCXRswithclinicalsuspicion *
Dx: history + imaging * Tx: immediate ABCs/emergency workup and stabilization ??
anti-hypertensives if appropriate with immediate operative repair of aorta 4541:
Remember that after chest trauma, shock could occur for a few reasons. A patient is
ALWAYS presumed to have hypovolemic shock following trauma, as it??s most common. A
great clue that hypovolemia isn??t the culprit is pulmonary capillary wedge
pressure. A patient may also be suffering from cardiogenic shock due to cardiac
contusion! * Hypovlemia/Hemorrhage � PCWP decreased (loss of overall blood volume)
* Cardiogenic shock � PCWP increased to due to pump failure (cardiac contusion,
etc.) 4494: Ankle-Brachial Index * Calculated by measuring highest systolic ankle
pressure (doralis pedis OR posterior tibial) and the highest systolic brachial
pressure then dividing the [Ankle Systolic/Brachial systolic]. * Interpretation o
<0.90�poorbloodflowtoperipheralLE,evidenceofPADo
0.91�1.30�normalrange;maybefalselyelevatedintothisrangebymedialcalcific
arteriosclerosis (Mockneberg??s arteriosclerosis) in pt with diabeteso
>1.30�suggestscalcified/incompressiblevessels,thusfurtherstudiesareneeded 4556:
Note that it only takes 100-200mL of fluid to generate cardiac tamponade! Thus CXR
may show a normal cardiac silhouette without evidence of pneumothorax. If clinical
suspicion is high a normal CXR does NOT rule out tamponade and treatment should be
initiated promptly! 2371: Bowel Ischemia * Classic complication following AAA
repair/graft placement due to loss of the SMA from graft leading to left
colon/sigmoid colon ischemia and damage (usually within 1 day of surgery!) *
Presentation: abdominal pain, bloody diarrhea, fever/leukocytosis * Prevention:
checking left colon/sigmoid colon perfusion following AAA repair and grafting 2337:
Acute Mediastinitis * Presentation: subacute post-op fever, tachycardia/chest
pain/leukocytosis with sternal wound drainage with purlulent dischargeo Uncommon,
but can occur in 5% of sternotomies post-op * Imaging: CXR (widened mediastinum) *
Tx: taken to surgery on strong suspicion of infection for
drainage/debridement/immediate closure/prolonged course Abxo Diagnosis is confirmed
intra-operatively with pus in the mediastinum o Mortalityrangesfrom10-
50%evenwithpropertreatment! 4241: Femoral Artery Aneurysm � Presentation: anterior
thigh pain (compression of femoral nerve) with pulsatile mass below the inguinal
ligament; may result in thrombosis and limb ischemia o 2nd most common peripheral
aneurysm (popliteal is #1) o associatedwithAAA Pulmonary Critical Care
Renal/Urinary/Electrolytes 4018/4059: Minimal Change Disease * ?? �Most common
cause of nephrotic syndrome in children under age 10 (very rare in teenage/adult
years) * ?? �Presentation: fatigue, edema (orbital, facial, genital, sacral, LE;
often mild in morning progressing to prominent through the day), & hypoalbuminemia
* ?? �Pathophysiology: T-cell damage to podocytes of glomerular basement membrane
(allows protein permeability). Often idiopathic.o Primary (idiopathic) is the most
common causeo Secondary causes: Hodgkin Lymphoma (Reed-Sternburg Cells)/Thymoma/T-
cell leukemia * ?? �Labs: Urine dipstick (shows protein), 24hr urine
collection/random urinalysis (nephrotic range proteinuria, no hematuria), low serum
bicarbonate, high serum Cl- * ?? �Biopsy: indicated for children >10yr or if not
responding to empiric steroids o Light: no pathologic changes notedo Immuno: normal
glomeruli without deposition of antibodies o Electron: diffuse effacement of
podocyte foot processes * ?? �Dx: presentation + labs; biopsy only indicated in
some situations * ?? �Tx: empiric steroid administration (extremely steroid
responsive) o Further workup needed for those not responding to steroids 4828:
Renal Tubular Acidosis ?? Presentation: o Infants/Young children: failure to thrive
(acidic environment = poor cell division), poor weight gain, normal anion gap
metabolic acidosis + hyperchloremia o
Olderchildren/Adults:recurrentcalculi,muscleweakness,bonepain,myalgias ???
Nephrocalcinosis causing polyuria (failure of nephron)???Normal anion gap metabolic
acidosis + hyperchloremia * ?? �Pathophysiology: genetic disorders that make the
kidneys unable to maintain normal acid-base balance causing acidification of the
blood/serum (acidosis) * ?? �Subtypeso Type 1 (Distal): poor Hydrogen secretion
into urine causing retention of H+ ions ???Metabolic acidosis; more alkaline urine
(pH >5.5); low-normal serum K+???(+)urine anion gap (urine Na+ + urine K+ - urine
Cl-)???Often associated with nephrolithiasis/family Hx of nephrolithiasis (genetic
disorders) ???Medications or autoimmune etiology are also possible???Tx: low dose
oral alkaline solutions o Type 2 (Proximal): poor HCO3- resorption causing wasting
in urine???Metabolic acidosis; normal acidic urine (pH <5.5); low-normal serum K+
???May be part of Fanconi syndrome (glucosuria, phosphaturia, aminoaciduria, K-
wasting) ???Tx: high dose oral alkaline solutions o Type 4: transient poor response
by nephron to aldosterone (failure of Na-K exchange) o ???�Metabolic acidosis; more
acidic urine (pH <5.5); high serum K+ o ???�Associated with obstructive
uropathy/congenital adrenal hyperplasia/poorly controlled Diabetes Mellitus o ???
�Tx: low dose oral alkaline solution + furosemide (lower K+) * ?? �Labs: serum
electrolytes, urine pH/urinalysis * ?? �Dx: presentation + labs * ?? �Tx: (see
subtypes) 3552: Wilms Tumor (Nephroblastoma) * ?? �The most common renal malignancy
in childhood (typically age 2-5yr); often sporadic * ?? �Presentation: asymptomatic
firm/smooth abdominal mass that does not cross the midline. Classically found by
mom during bath time; less commonly symptomatic with abdominal pain, HTN,
hematuria, and fever. Rarely presents with pulmonary metastases/lung symptoms o
WAGR syndrome: Wilms Tumor, Aniridia (no iris), genitourinary malformation, and
retardation o Beckwith Widemann Syndrome: Wilms Tumor, macroglossia, hemi-
hypertrophy, organomegaly o Denys-Drash Syndrome: Wilm�s tumor, progressive renal
failure, male pseudohermaphrodism * ?? �Pathophysiology: deletion of WT1 (WAGR),
mutation of WT1 (B-W S), or mutation of WT2 (D-D S) causing abnormal proliferation
of the metanephric blastema to form the tumor * ?? �Imaging:o Abdominal ultrasound
� best 1st imaging to help characterizeo CT chest/abdomen with contrast � fully
characterize tumor & check for lung metastases * ?? �Dx: clinical presentation +
imaging * ?? �Tx: tumor excision/nephrectomy + chemotherapy +/- radiation o Great
prognosis with treatment (90% 5-year survival)o Rarely stage V disease (bilateral
tumors) making for a less favorable prognosis 2513/3548: Enuresis * ?? �Enuresis
(bed wetting) is urinary incontinence >x2/week in a child age >5yr o Normal until
age 5; girls often potty trained earlier than boyso Primary: child never achieved
�dryness�o Secondary: child achieved �dryness� for >6 months with re-emergence of
bedwetting o ???�Genetic � strong genetic link for familial enuresis on chromosome
13 o ???�Psychologic stress � behavior regression/mood lability/change to
environment (birth of a new child, new home, first time at school, etc.) o ???�UTI
� dysuria, hesitancy, urgency, abdominal/flank pain o ???�Diabetes mellitus �
polyuria, polydipsia, polyphagia, weight loss, lethargy, candidiasis o ???�Diabetes
insipidus � polyuria, polydipsia, large volume dilute urine (rare in children!)
o ???�Obstructive sleep apnea � snoring, dry mouth, fatigue, hyperactivity,
irritability * ?? �Labs: urinalysis, further studies based on suspected etiology
* ?? �Imaging: ultrasound/other imaging if daytime symptoms or Hx of recurrent UTI
* ?? �Dx: clinical presentation * ?? �Tx: o 1st line: Non-pharmacologic behavioral
interventions * ???�Avoid sugary drinks/caffeine before bed, engage in regular
daytime voiding/voiding just before bed, minimize all fluid intake near bedtime,
start a reward system for dry nights * ???�Enuresis alarm to require regular
bladder filling/voiding to �train� the bladder (3-5mo of therapy); best long-term
outcomes o 2nd line: Demopressin (ADH analogue) +/- oxybutynin (anti-cholinergic)
to decrease urine output and promote bladder retention of urine???High rate of
relapse with stopping medications & hyponatremia concerns o 3rd line: TCAs
(imipramine is classic; concern for suicidality/cardiotoxicity) 2233: Alport�s
Syndrome * ?? �Presentation: classic triad of hematuria/proteinuria, sensoneurial
deafness, and familial kidney
failure o May feature vision abnormalities but this is less common (25%) * ??
�Pathophysiology: mutation of a-5 chain of type IV collagen affecting basement
membranes o Kidney (glomerular BM); Ear (cochlear BM); Eye (lens/retina BM) o X-
linked dominant: males (full presentation) and females (isolated hematuria) * ??
�Biopsy: often indicated for nephritic/nephrotic syndrome in children over age 10yr
o Light: may be normal (early) or �basket weaving� if late stageo
Immuno:nothingdetectedo Electron: �basket weaving� alternating thick and thin
capillary loops with GBM splitting * ?? �Other things that might look like Alport�s
o Thin basement membrane disease: AD mutation of a-3/a-4 chains of Type IV
collagen; often results with benign hematuria and a �thin� basement membrane (1/2
normal thickness throughout)o Anti-GBM disease: autoantibody to the �non-
collagenous� domain of a-3 chain of Type IV collagen; Biopsy shows linear IgG
deposits on the GBM characteristically; essentially Goodpasture syndrome but only
of the kidneyo Benign recurrent hematuria: Renal biopsy shows totally normal
architecture and problem likely will resolve on it�s own. 3692/4005/4196: Urinary
Tract Infection (UTI) * ?? �Risk Factors: uncircumsized male <1yr, female any age
(short urethra), renal anomaly (VUR, PUV, etc.), recent sexual activity, poor
vaginal hygiene * ?? �Presentation: o Older child/adult (cystitis): dysuria,
frequency, urgency, suprapubic pain, foul-smelling urine o Older child/adult
(pyelo): fever, chills, flank pain, CVA tenderness, N/V +/- cystitis symptoms o
Infant:fever,fussiness,decreasedurineoutput,dehydrationo Fever >39C (102.2 F) in
any child <3yr should prompt workup for occult UTI * ?? �Pathophysiology: ascending
bacteria �climb� up the urethra/urogenital tract causing infectiono Rarely
hematogenous spread can occur via renal arteries (young children most common) * ??
�Micro: E.coli >>> Staph. Saprophyticus > other bugs * ?? �Labs: Serum BUN/Cr
(estimate renal function); urine dipstick (qualitative urine assessment);
urinalysis (quantitative urine assessment); urine culture (test for/ID bacteria &
susceptibilities) o Mid-stream clean-catch is appropriate in children/adults not in
diaperso Straight Catheterization for urine sample is necessary in children in
diapers, as the presence of feces/skin flora in the diaper make for a high chance
for sample contamination o Urinanlysis may show (+)blood/RBCs/leukocyte
esterase/nitrites/bacteria/WBCs * ?? �Imaging:o Indications for Renal/Bladder
Ultrasound (checks urologic abnormalities??increased UTI risk) ???Any infant <24mo
with 1st febrile UTI???Child of any age with recurrent febrile UTI???Child with UTI
+ Hx of renal/urologic disease, hypertension, or poor growth ???Child not
responding to normal UTI treatments * ?? �Dx: clinical + urinanalysis/urine culture
* ?? �Tx: antibiotics o Prophylactic Abx may be considered in pts with recurrent
febrile UTIs or high grade VUR * ?? �Follow-up: o Repeat bloodwork/urine culture
are NOT indicated as a �test of cure�, but only if patient fails to improve 2-3
days following treatment initiation 2226: Recurrent Cystitis & Constipation * ??
�Presentation: constipation (straining, painful poops, passage of hard �pellet�
stools, crampy abdominal pain, <2 poops/wk) with recurrent UTIso Classically occurs
with initiation of cow�s milk, toilet training, or start of school o Anal fissures,
hemorrhoids, encopresis, vomiting may also occur * ?? �Pathophys: enlarged rectum
from impacted stool compresses bladder leading to outflow obstruction * ?? �Dx:
clinical presentation * ?? �Tx: increase dietary fiber, limit cows milk, oral
laxative/suppository o Resolution of constipation should resolve the recurrent UTIs
and any complications 3688/3694: Vesicoureteral Reflux * ?? �Presentation:
Retrograde flow of urine into the ureter/renal pelvis o Confers risk of recurrent
UTIs, pyelonephritis, renal abscess, renal scarring, chronic renal insufficiency
progressing to renal failure * ?? �Grading o I: retrograde flow into ureter; no
dilationo II: retrograde flow into ureter/renal pelvis; no dilationo III: mild-
moderate ureteral/pelvic dilation; mild renal calyx bluntingo IV: dilation/mildly
torturous path of ureter; obvious dilation of renal pelvis o V: gross dilation of
upper UG tract with marked tortuosity of renal pelvis ?? Dx:o Any child <2yr with
first UTI should have a renal/bladder ultrasound to assess for abnormalities that
may allow for VURo Recurrent UTIs should warrant a voiding cystourethrogram (VCUG),
the gold-standard for diagnosing VUR * ?? �Tx: anatomic anomalies may be surgically
fixed or patients are closely followed +/- prophylactic Abx * ?? �Follow-up: o
Renal scintigraphy (dimercaptosuccinic acid) is best for long-term following of
scarring o Monitoring for chronic renal insufficiency (HTN, anemia, etc.) is
recommended 4548: Posterior Urethral Valves * ?? �Presentation: poor urine stream,
straining to void, urosepsis, failure to thrive, & renal failure (progressive
bladder distention??hydronephrosis)o Oligohydraminos/Potter�s Sequence is a
severe/feared presentation * ?? �Pathophysiology: abnormally folds of distal
prostatic urethra cause outflow obstruction ???backup of urine into the upper UG
tract??damage to kidneys o The most common UG tract pathology & cause of chronic
renal failure in newborn boys * ?? �Dx: presentation + VCUG/cystoscopy o May be
prenatally diagnosed on prenatal ultrasound (bladder distention / bilateral
hydroureter or hydronephrosis) * ?? �Tx: surgical PUV ablation/urinary diversiono
While early Dx is possible, it�s a 50/50 shot for resolution or progression of
disease regardless of treatment/severity upon diagnosis! 3554/4279/7764: Henoch-
Sch�nlein Purpura (�Anaphylactoid purpura�) ?? Presentation: colicky abdominal
pain/intussusception, lower-extremity (buttocks/legs, sometimes arms) palpable
purpura (nonblanching vasculitis), arthralgia (knee/ankles), & renal damage
(microscopic or gross hematuria, non-nephrotic range proteinuria, RBC casts, or
mild creatinine elevations) o Note that renal involvement may occur weeks after
initial presentation! o Often preceded by a viral infection (triggers production of
IgA) * ?? �Pathophysiology: IgA production and deposition into small-medium vessels
causing vasculitis. The inflammation causes damage/limits bloodflow resulting in
pain/poor function/bruising * ?? �Labs: normal CBC/CMP with abnormal urinanalysis
(RBCs/casts/proteinuria) * ?? �Biopsy (immuno): shows IgA deposition in the
mesangium of the glomeruli * ?? �Dx: clinical +/- renal biopsy * ?? �Tx:
hospitalization with supportive care (fluids/NSAIDs) + corticosteroids for severe
cases 4853: Hypernatremia * ?? �Presentation: lethargy, altered mental status,
muscle cramps/weakness, decreased reflexes, seizure * ?? �Pathophysiology: o
Hypovolemic hypernatremia: renal losses (diuresis) or external losses (sweating,
diarrhea) o Hypervolemic hypernatremia: excess Na+ intake or mineralocorticoid
excess * ?? �Labs: markedly elevated serum sodium * ?? �Dx: presentation with high
Na+ * ?? �Tx: gentle fluid resuscitation with isotonic crystaloids (0.9% saline or
Ringer�s Lactate); as using hypotonic solutions may correct the sodium too quickly,
leading to cerebral edema/damage! 3940: Note that Hepatitis B is a major risk
factor for development of membranous nephropathy. This process is rare in children,
but often occurs with concomitant HepB infection! 2234: If a child has a normal UA
but urine dipstick returns proteinuria, the child should have two additional urine
dipsticks on two separate occasions to follow-up for serious pathology. * ?? �If
dipsticks are negative, transient proteinuria is diagnosed and you�re done! * ??
�If dipsticks are still positive on either repeat test, child should be referred to
a peds nephrologist for further renal pathology workup (24hr urine, renal
ultrasound, renal biopsy if necessary!) Allergy/Immunology4479: Vaccinations for
pre-mature babies should be given based on chronologic age, not gestational age.
* ?? �Vaccines are safe in pre-mature babies as long as their immunocompetent (even
live-attenuated!) * ?? �The only restriction is HepB vaccine, which should be held
until the patient is 2kg (4lbs 6oz) * ?? �Vaccines by Class: o Inactive (killed):
Polio, Hep Ao Toxoid(inactivetoxin):Tetanus,Diptheriao Conjugated Subunit: HepB,
pertussis, H.flu (Hib), Pneumococcal, Meningococcal, HPV, flu (IM) o Live
attenuated: MMR, rotavirus, varicella, flu (intranasal) 8951: Rotavirus Vaccine
* ?? �Rotavirus Presentation: gastroenteritis (fever, vomiting, watery diarrhea),
dehydration can occur o Highly contagious via fecal-oral or fomite transmission
(most common cause of gastroenteritis) * ?? �Vaccine: live attenuated vaccine given
in two doses (2mo, 4mo); may be administered with other vaccines, but not alongside
other live-attenuated vaccines (concern for poor response handling multiple
viruses!) o Well tolerated, but classically carries risk of intussusception (live-
attenuated virus reproduces within the gastric tissue causing intestinal MALT
hypertrophy) o Contraindications: anaphylaxis to vaccine, Hx of intussusception/GI
malformation (Meckel�s is classic), SCID (cannot receive any live-attenuated
vaccines), or moderate/severe illness 3236: If a parent makes the decision to not
vaccinate their child their wishes should be respected & the
risks/benefits/consequences should be thoroughly explained/documented * ?? �Its
best to inquire about why, not undermine the mother�s authority & lose relationship
* ?? ��Herd Immunity� � helps keep kids who medically cannot receive vaccines
healthy and safe. Also explains why kids without vaccines can avoid illnesses that
are vaccinated against.
However, it only works if kids are largely being vaccinated! * ?? �School
enrolment � if the child is not medically exempt from vaccination, some states
retain the right to refuse them entry into daycare/school. * ?? �Vaccination
refusal is not something to be reported to the health department * ?? �Court-
ordered vaccination may only be sought if there is an outbreak of a specific
disease at the time. Otherwise (due to herd immunity) there is a vanishingly small
chance for disease acquirement. 3854: Two regular vaccines that can significantly
reduce the risk of cancer are * ?? �HBV: HepB significantly associated with
hepatocellular carcinoma; vaccination minimizes infection risk * ?? �HPV: Human
Papilloma Virus is shown to cause endometrial cancer (as well as other mucous
membrane cancers!), thus vaccination against high-risk strains minimizes this risk
4258: Contraindications for DTaP/TDaP ?? Diptheria/Tetanus component o
Contraindication:anaphylaxiso Cautions: moderate/severe illness, Guillain-Barre
syndrome or Arthus-type Rxn within 6wk of T- D exposure?? Pertussis component o
Contraindication: anaphylaxis, progressive neurologic disorder present, or
encephalopathy within 1wk following the vaccine o Cautions: moderate/severe
illness, seizure within 3 days, >105F temp within 2 days, hypertonia/hypo-
responsiveness within 2 days, or inconsolable/persistent crying within 2 days 3196:
Hyper-IgM Syndrome * ?? �Presentation: severe, recurrent sinopulmonary infections
(otitis, sinusitis, pneumonia) with viruses/encapsulated organisms and
opportunistic organisms (PCP pneumonia, Candida thrush, etc.) o Poor growth/failure
to thrive due to excessive energy needed to fight off disease * ??
�Pathophysiology: X-linked genetic defect of CD-40 ligando CD-40L expressed on T-
cells; when binding to CD-40 on B-cells, it induces class switching o Results in
failure of B-cell class switching away from the IgM default classo Results in poor
plasma cell maturation/production??poor response to infection/vaccines * ?? �Labs:
CBC w/diff, B & T-cell counts, serum IgG/IgA/IgM, HIV testing o Low IgG/IgA with
high IgM * ?? �Dx: clinical presentation with characteristic Ig profile * ?? �Tx:
IVIg administration with Abx prophylaxis 12519: Common Variable Immunodeficiency
(CVID) ?? Presentation: less severe immunodeficiency presenting in late
childhood/teenage years o Recurrent respiratory (pneumonia, sinusitis, otitis) from
encapsulated bugs (H.flu, S.pneumo) + chronic lung dx (bronchiectasis, asthma) o
Recurrent GI infections (Salmonella, Campylobacter) + GI disorders (chronic
diarrhea, IBD) o Commonly Giardia Lamblia infection at least onceo Autoimmune Dx
(RA, thyroid disease, etc.) are commono Failuretothriveiscommon ?? Pathophysiology:
isolated abnormal B-cell differentiation causes impaired humoral immunity due to
decreased Ig levels (IgG, IgA, and/or IgM) o Failure of B-cell development = poor
response to vaccination * ?? �Labs: severely decreased IgG & decreased IgA, IgM, or
both * ?? �Dx: presentation + Ig deficiency * ?? �Tx: avoiding infection + IVIg
(bolster humoral immunity) 3197/4762: Severe Combined Immunodeficiency (SCID) ??
Presentation: severe, recurrent sinopulmonary infections (otitis, sinusitis,
pneumonia) with viruses/encapsulated organisms and opportunistic organisms (PCP
pneumonia, Candida thrush, etc.) o Poor growth/failure to thrive due to excessive
energy needed to fight off diseaseo Chronic diarrhea & Absence of Lymphoid Tissue
(non-palpable lymph nodes despite severe infection, small/absent tonsils,
small/absent thymus)?? Pathophysiology: gene defect resulting in failure of T-cell
development, ultimately leading to failure of B-cell development due to lack of T-
cell stimulation of B-cellso May be X-linked or autosomal dominant inheritanceo
Adenosine deaminase deficiency (ADA) is a classic cause (severely affects DNA
production, thus quickly developing T-cells are largely affected) * ?? �Labs: CBC
w/diff, B/T-cell counts, serum IgG/IgA/IgM, HIV testing o Low IgG/IgA/IgM, low T-
cells (CD4+, CD8+, CD3+), low B-cells (CD19+) * ?? �Dx: clinical presentation +
labs * ?? �Tx: early stem cell transplant * ?? �Screening: detected in newborn
screening via absence of T-cell DNA excision circles, which are excreted by
normally developing T-cells in the thymus, in dried blood 3198/4495: Chronic
Granulomatous Disease (CGD) * ?? �Presentation: recurrent severe
cutaneous/pulmonary infections, supprative adentitis, and osteomyelitis caused by
Catalase(+) organisms o MostcommonlyX-linkedinheritance * ?? �Pathophysiology: gene
defect of NADPH oxidase resulting in weak neutrophil �oxygen burst� o NADPH??O2-
(superoxide)??H2O2 (hydrogen peroxide)??ClO (bleach) is the normal process that
occurs in the O2 bursto Catalase is used by bacteria to neutralize hydrogen
peroxide; most bacteria have superoxide dismutase (neutralize superoxide), thus
without the ClO production, it�s extremely hard to kill catalase(+) organisms??
Labs: CBC w/diff, neutrophil function tests (below) o Dihydrorhodamine-123 Test:
compound reacts to superoxide causing flourscence that can be visualized or picked
up on flow-cytometry o Nitroblue Tetrazolium Test: compound reacts to superoxide
made by neutrophils and turns blue if the neutrophil is functioning properly. A
�negative� test is one that turns blue! * ?? �Micro:o Bacteria: S.aureus, Serratia
spp., Burkholderia spp., Norcardia spp, Listeria spp., Klebsiella spp. o Fungi:
Aspergillus spp., Candida spp. * ?? �Dx: presentation + neutrophil function tests
?? Tx: anti-microbial prophylaxis (Bactrim/Intraconzole) + lifelong INF-Gamma
(boost intracellular killing) 2134/3195: X-linked (Brunton�s) Agammaglobulinemia
* ?? �Presentation: severe, recurrent sinopulmonary infections (otitis, sinusitis,
pneumonia) with viruses/encapsulated organisms and opportunistic organisms (PCP
pneumonia, Candida thrush, etc.) o Poor growth/failure to thrive due to excessive
energy needed to fight off diseaseo Occurs after age of 6 monthso Often
small/absent lymphoid tissue present due to poor B-cell proliferations * ??
�Pathophysiology: defective tyrosine kinase that prevents proper maturation of B-
cells o Occurs after 6mo, as this is when mom�s passive immunization IgG wanes * ??
�Labs: CBC w/diff, Ig counts, B/T-cell counts (will show normal T-cells, low B-
cells, and low Igs) o Note that Total B-cells can be calculated with [Lymphocytes �
CD4+CD8 T-cells] * ?? �Dx: presentation with corresponding labs * ?? �Tx: IVIg
(immunoglobulin replacement therapy), prophylactic Abx if needed o While
immunizations are not contraindicated, they�re useless as the patient has no
humoral production of Ig to generate an immune response 2769: Hereditary Angioedema
(HANE) * ?? �Presentation: rapid onset edema of the hand/lips/face/genitals, GI
tract (colicky abdominal pain), and larynx (life-threatening airway compromise),
often presenting in late childhoodo Nourticariapresento Classically flares with
ACE-inhibitor initiation, trauma, infection, or dental procedure o Note that
acquired forms often present in people age >30yr * ?? �Pathophysiology: C1
inhibitor deficiency/dysfunction, or destruction leading to unopposed activation of
C1 compliment resulting in huge buildup of Cb2/bradykinin (pro-inflammatory
endpoints) * ?? �Labs: compliment level assay (C1q normal if hereditary/low if
acquired, C4 always low) * ?? �Dx: presentation with corresponding compliment
levels * ?? �Tx: ??? 4143: Leukocyte Adhesion Deficiency * ?? �Presentation:
recurrent skin (cellulitis, abscess, omphalitis) and mucosal (periodontal)
infections o Poor wound healing with absence of purulence/neutrophils at site of
infection o Delayed umbilical cord separation (age >3wk) * ?? �Pathophysiology:
defective integrins on leukocyte surface stopping normal adhesion needed for
extravasation, stopping migration of WBCs to areas of inflammationo Inflammation
still occurs but no early WBC neutrophils to direct inflammation * ?? �Labs: CBC
(marked neutrophilia/lymphocytosis); analysis of wound drainage * ?? �Dx:
presentation + labs * ?? �Tx: ??? 3602/3993: Selective IgA deficiency ??
Presentation: often asymptomatic but classically recurrent sinopulmonary/GI
infections due to impaired immunologic IgA barrier on mucosal surfaceso Importantly
any blood transfusion will cause anaphylaxis in these patients, as they will mount
an immune response to IgA present in donor blood. Thus any blood products of a
patient with this disease must be washed for IgA and patients must wear information
bracelets. o In Celiac�s Disease: Selective IgA deficiency may actually mask the
IgA autoimmune bodies, thus is suspicion is high, but IgA is negative??check total
IgA for deficiency and check Anti-IgG antibodies * ?? �Dx: Low IgA, normal IgM/IgG,
normal B-cells/T-cells +/- low IgG2/IgG4 selective deficiency * ?? �Tx: supportive
care with medical alert bracelet 4847: Wiskott-Aldrich Syndrome * ?? �Presentation:
eczema (dry/scaly rashing), microthrombocytopenia (low platelets with small
platelets), petechiae/purpura/severe bleeding (intracranial, GI), and recurrent
infections (B/T-cell dysfunction) * ?? �Pathophysiology: X-linked recessive
mutation on WAS protein gene; causes impaired cytoskeleton remodeling in
hematopeotic cells, screwing up their response to the body�s environment o
Dysfunction in leukocytes??B/T-cell poor migration & immune synapse function o
Dysfunction in platelets??tiny/few platelets cripples primary hemostasis * ??
�Labs: CBC (thrombocytopenia) * ?? �Smear: thrombocytopenia with small platelets
* ?? �Dx: presentation + peripheral blood smear * ?? �Tx: hematopoietic stem cell
transplant 3545: DiGeorge Syndrome * ?? �Presentation: developmental delay,
dysmorphic facies (cleft
palate, short palpebral fissures, small chin, ear malformation), parathyroid
aplasia/hypoplasia (hypocalcemia), thymic aplasia (T-cell dysfunction &
lymphopenia), congenital heart disease (truncus arteriosus >> VSD, ToF, aortic arch
interruption)o Complications: tetany/seizures/arrhythmias (severe hypocalcemia),
bacterial/viral/fungal infections (T-cell/B-cell dysfunction) * ??
�Pathophysiology: sporadic or AD 22q11.2 microdeletion causing abnormal development
of the the pharyngeal pouches??abnormal facial, neck, and mediastinal development *
?? �Labs: serum calcium (hypocalcemia), CBC (low T-cells/lymphopenia) * ??
�Imaging: echocardiography (rule out cardiac defects) * ?? �Dx: FISH study showing
microdeletion * ?? �Tx: aggressive Ca2+ repletion; fixing any abnormalities;
vaccination against disease * ?? �Lookalikes: Velocardiofacial syndrome (22q11.1
microdeletion; �Incomplete DiGeorge syndrome) � developmental delay/hypotonia,
dysmorphic facies (cleft palate, wide/prominent nose with square nasal root, short
chin, fish-shaped mouth), & congenital heart disease (VSD, right-sided aortic
arch); no parathyroid or thymus problems Other Immunodeficiency syndromes mentioned
in this section * ?? �IgG Subclass Deficiency � recurrent sinopulmonary infections;
low-normal IgG with normal IgM/IgA * ?? �Job�s Syndrome (hyper IgE syndrome) �
abnormal Faces, cold staph Abscesses (no inflammation), retained 1o Teeth, high
IgE, Dermatologic problems (eczema)??FATED mnemonic * ?? �Chediak-Higashi syndrome
� failure of lysosomal trafficking enzymes (giant neutrophil blue-grey granules &
neutropenia) causing recurrent infections, ocular albinism (bright blue
eyes/photophobia), dermatologic albinism, hair with silver streaks * ?? �Transient
Hypoglobulinemia of Infancy � IgG levels will dip in newborns around 6mo (mom�s
passive immunization wears off); IgA/IgM/B-cells/T-cells are all normal; typically
resolves by 12mo General Principles 2433/4199/4822/4823/4874/7741: Normal
Developmental Milestones Age Gross Motor Fine Motor Language Social/Cognitive Red
Flags 2mo Lifts head/chest when prone Hands unfisted 50%; tracks past midline
Alerts to voice & sounds, coos Social smile, recognizes parents Fails to alert;
irritability; no social smile; early rolling (hypotonic) 4mo Sits with support;
beings rolling Hands mostly open; reaches midline Laughs; turns to voice Enjoys
looking around Poor head control, no laugh, no visual threat 6mo Begins to sit with
propped hands (unsupported at 7mo) Transfers objects hand-to-hand; raking grasp
Responds to names; babbles mixing vowels & consonants Stranger anxiety No rolling;
head lag 9mo Pulls to stand; cruises 3-finger pincer grasp; hold bottle/cup Says
�mama� �dada� Waves �bye� & plays Pat-a-Cake W-sitting (hypotonia), Scissoring
(hypertonia), primitive reflexes 12mo Stands; walks first independent steps; throws
ball 2-finger pincer grasp 1st words (not �mama� or �dada�) Separation anxiety;
follows 1- step commands & gestures Unable to localize sounds; no protective
reflexes 18mo Runs; kicks a ball Tower (2-4 cubes); removes clothing 10-25 words;
phrases emerge (�Thank you� �Stop it�); IDs 1 body part Understands �mine�; plays
pretend alone Persistent Toe walking (hypertonia) 2yr Scales stairs with both feet
on steps; jumps Tower (6 cubes); copies a line 50+ words; 2 word telegraphic
sentences Follow 2-step commands; parallel play; toilet training starts Poor
transitions, lack of social interactions 3yr Scales stairs with alternative feet;
ride tricycle Copies a circle; uses utensils 3 word sentences; 75% intelligible
speech Knows age/gender, imaginative play Echolalia (autism); extended family fails
to understand speech 4yr Balance/hops on 1 foot Copies a square Identifies colors;
100% intelligible speech Cooperative play 5yr Skins/walks backwards Copies a
triangle; prints letters; ties shoelaces; dresses/bathes independently 5 word
sentences; counts to 10 Makes friends; completes toilet training Strangers fail to
understand speech 3418: Intraosseous IV access (IO) at the proximal tibia is a
common site for venous access when peripheral lines are difficult to start in
children (adults not so much!) * ?? �Easier to start (less risk) than a central
line * ?? �Away from the sternum/chest if cardiac resuscitation is needed
simultaneously ?? Contraindications: active infection in the area, fracture,
previous unsuccessful IO attempts, severe bone fragility (osteogenesis imperfecta,
etc.) 7726: Evaluating Neonatal Hydration/Weight Loss * ?? �Presentation: decreased
wet diapers, decreased tearing, sunken fontanelles, dry mucous membranes, decreased
skin turgor, delayed capillary refillo [# of wet diapers/day = # of days old] in
the first week of lifeo �Pink-stain�/�brick-dust� poop (uric acid crystals) is a
sign of mild dehydration in the 1st week * ?? �Normally, a child should lose up to
7% of their birthweight in the first 5 days of life (excretion of excess fluids
from in-utero & during labor) o Wt loss <7% - continue breastfeeding as normal &
check wt in 1wk (should be gaining)o Wt loss >7% - assess for sucking
failure/lactation failure, daily weightings, & supplement with formula GI4925:
Pediatric Dehydration Assessment & Resuscitation * ?? �Children are more
susceptible to dehydration due to 1high-frequency gastroenteritis, 2high surface-
area to volume ratio (increased insensible losses), and 3possible inability to
access fluids or communicate they�re thirsty to their provider * ?? �First Step:
determine severity o Ideal: regular body weighings (1kg lost = 1L fluid lost); this
is near impossible as it�s hard to pinpoint a child�s �well weight� before the
start of the illness due to rapid growth o Realistic:clinicalhistoryandphysicalexam
* ???�Mild (3-5% loss): Hx of decreased intake/fluid loss but minimal symptoms
* ???�Moderate (6-9% loss): decreased skin turgor, dry mucus membranes,
tachycardia, irritability, delayed capillary refill (2-3sec), & decreased urine
output * ???�Severe (10-15% loss): cool/clammy skin, dry mucous membranes, cracked
lips, sunken eyes/fontanelles, tachycardia, lethargy, delayed capillary refill
(>3sec), and minimal urine output ?? Second Step: rehydration therapy o Mild-
Moderate: oral rehydration therapy (if tolerated) * ???�The glucose-sodium filled
solutions for ORT work on the principle that coupled co- transport for glucose-Na
are maintained even with secretory diarrhea, while other Na absorption mechanisms
are impaired * ???�It�s important to use drinks specifically targeted at oral
rehydration, as their electrolyte profiles are specifically targeted to take
advantage of this. Gatorade does NOT meet these qualifications & may act as osmotic
diuretics due to high sugar content.o Moderate-Severe: IV fluids with isotonic
crystalloids??add dextrose after initial resuscitation ???Emergency Phase: 20mL/kg
IV bolus with appropriate solution???Repletion Phase: electrolyte repletion over 24
or 48hr if hypernatremic (100-50-20 rule) o ?? �+100mL/kg/day � first 10kg body
weight o ?? �+50mL/kg/day � second 10kg body weight o ?? �+20mL/kg/day � each kg
above 20kg previously accounted for o ?? �Consider adding more if increased
insensible losses (respiratory distress or fever) o ?? �Rate is determined by the
4-2-1 Rule o +4mL/hr � first 10kg body weighto +2mL/hr � second 10kg body weighto
+1mL/hr � each kg above 20kg previously accounted for ?? Ex) 24kg child would get
1000mL + 500mL + 80mL = 1580mL/day @ 64mL/hr ???Hypotonic should NEVER be used as
concerns over electrolyte changes can result in cerebral edema/permanent brain
damage/locked-in syndrome 8955: Pediatric Constipation?? Presentation: <2 poops/wk,
crampy abdominal pain, straining to poop, passage of hard stools o Often onset with
some change in life: staring cows milk, starting school, toilet trainingo If
unresolved: anal fissures/hemorrhoids (hard stool damaging anal mucosae),
encopresis (paradoxical diarrhea via relaxation of distended bowel), enuresis/UTI
(big bowel compressing ureters), vomiting (stool backup) can all occur??
Pathophysiology: Although many reasons, classically the child starts something new
and feels uncomfortable stooling. Holding the stool results in
impaction/constipation.o Cow�s milk (as opposed to breast) may also result in lower
levels of fluid in gut = hard poops! o Problem compounds itself, as stooling is
painful/uncomfortable and child�s instinct to hold stools is reinforced * ??
�Imaging: not routinely needed, but in severe cases X-ray Chest/Abdomen can rule
out air-fluid levels & rupture of bowel (air under diaphragm) * ?? �Dx: clinical
presentation * ?? �Tx: increase fiber, decrease cow�s milk (<24oz), laxatives
(polyethylene glycol or mineral oil) ???suppository/enema to open bowel up (if
other treatments are not working) o Note that while juice can work as an osmotic
laxative, it is not encouraged as excessive juice consumption may be needed,
promoting increased dental problems/obesityo Child should sit on the toilet
following every meal to encourage regular stoolingo Treatment should be continued
until stooling is regular and stools are consistently soft 2475/4817/4818:
Pediatric Jaundice?? Physiologic Jaundice of the Newborn o Presentation: universal
jaundice occurring in the first 2-4 days of life o Pathophysiology: * ???�High
hemoglobin turnover (high hematocrit with shorter lifespan; HbF only designed to
last 90 days, as opposed to the 180 days of HbA) * ???�Immature liver uridine-
diphosphgluconate-gluconosyltransferase (UDG-Transferase) activity until 2wk of age
(slower bili conjugation; often more pronounced in Asians) * ???�Sterile gut, thus
lack of bacterial enzymes to convert bilirubin??urobilinogen increasing
enterohepatic circulation * ???�Note that only unconjugated (indirect) bilirubin
(not water soluble) can cross the BBB as it�s high lipid solubility can slip
through the fatty neuron/glial cell membranes; conjugated bilirubin has been made
too polar to cross the fatty BBB * ???�Note that breastfeeding will likely increase
peak bilirubin levels o Labs: unconjugated hyperbilirubinemiao Dx: presentation
with labso Tx: spontaneous resolution by age 1-2wk * ???�Close monitoring for
worsening due to concerns for kernicterus & frequent feeding to speed colonization
of the gut * ???�Sunlight exposure can relieve jaundice but not recommended due to
concern for skin damage in the neonate * ???�Intervention may be needed if rapidly
rising or if total bilirubin >20mg/dL (phototherapy) or >25mg/dL (exchange
transfusion) ?? Breastfeeding Failure Jaundiceo Presentation: jaundice within first
week of life, dehydration, inadequate stooling (dark/sticky meconium should
transition to yellow-green/seedy stools within first week)o Pathophysiology:
inadequate breastfeeding leads to dehydration and slowed passage of bilirubin-laden
meconium in the gut. Bili in stagnant stool gets more time to be re-absorbed,
leading to heightened enterohepatic circulation??unconjugated bilirubinemia ???Mom:
poor milk supply, cracked/clogged nipples, engorgement, infrequent feeds ???Child:
poor latching, ineffective sucking, falling asleep with feedso Labs: unconjugated
hyperbilirubinemiao Dx: presentationo Tx: identification of lactation failure with
specific plan to address it (some common ones below) * ???�Increase Feed Frequency:
neonates are fed 8-12 times/day (every 2-3hr) * ???�Increase Feed Time: feeds
should last approximately 10-20min/per breast during the first month of life * ???
�Maintain Mom Hydration: if mom is dried out, milk may be produced in lower
quantity * ???�Formula Supplementation: if above does not work, supplementation may
be needed o Follow-up: follow-up after 2 days with H&P, weight, and bilirubin
levels to note resolution???If not resolving: phototherapy (>20mg/dL bili) or
exchange transfusion (>25 bili)???Even if breast milk is low, do not discontinue
breastfeeding as the benefits will be lost. Simply continue and supplement as
needed. ?? Breast Milk Jaundice o Presentation: jaundice after the first week of
life, adequate hydration/stoolingo Pathophysiology: high levels of B-
glucuronidase/lipase in mother�s milk causing increased enterohepatic circulation;
although not well understood o Labs: unconjugated hyperbilirubinemiao Dx:
presentationo Tx: none needed; will resolve between weeks 2-10 of life
2923/2924/2983: Genetic Diseases of Liver Metabolism * ?? �Dubin-Johnson syndrome �
conjugated bilirubinemia; jaundice with body stressors (illness, pregnancy, OCP
use) but otherwise no/minor symptoms (fatigue, abd. pain, weakness) and no
hemolysiso More common in Sephardic Jewso Clinically normal aside from reactionary
jaundice and black liver (epinephrine metabolites) o Labs: Bilirubin (20-25 mg/dL),
normal LFTs, normal coproporphyrin (predominantly Copro I) * ?? �Rotor syndrome �
Dubin-Johnson syndrome without the black liver * ?? �Crigler-Najjar syndrome �
autosomal recessive unconjugated bilirubinemia (passes through BBB) o Type 1:
significant mental retardation/death; Phototherapy/plasmapheresis can help
conjugate the bilirubin to buy time for curative liver transplant o Type 2: fairly
benign unconjugated bilirubinemia with jaundice; often asymptomatic, but symptoms
(if occuring) can be treated with phenobarbital or clofibrate ?? Gilbert syndrome �
mild unconjugated bilirubinemia triggered by bodily stressors; very similar to C-N
syndrome II, difference is in the enzyme defect 2478/2479/4868: Breastmilk &
Breastfeeding?? Breastmilk is considered the ideal human nutrition source for full-
term infants & should be given exclusively for the first 6mo of life as long as
child is maintaining normal growth statuso Pureed solid foods are introduced at 6mo
with continuation of breastmilk until age 1yr ???Start with pureed
fruits/vegetables??pureed proteins/meats ???Fruit juice can be started at 6mo, but
no more than 4-6oz/day (risk of dental caries!) ???Introduction of allergenic foods
does NOT decrease allergy development o Cow�s milk introduced at 1yr of age ??
Benefits of Breastmilk for babyo Protein content highest right after birth;
consists of 70% whey and 30% casein proteins (Whey protein = easier to digest &
promotes gastric emptying)o Aids in digestion (lysozymes) & promotes absorption of
nutrientso Aids in passive immunization (contains maternal IgA, lactoferrin) with
decreased rates of otitis media, gastroenteritis, URI, UTI, necrotizing
enterocolitis, Type I diabetes, childhood cancer, and childhood obesityo Associated
with less reflux/colic than traditional formulas ?? Drawbacks of Breastmilk babyo
Less phosphorus/calcium (but better absorbed, thus it�s a bit of a wash)o Vitamin D
deficient � Vit. D supplementation (400IU/day in the first month of life is
mandated with exclusive breast feedingo Iron deficiency � prematuity/maternal iron
deficiency can largely predispose child to iron deficiency. Supplementation should
occur from [birth � 1yr] if risk factors present ???Fe deficiency is the most
common nutritional deficiency of infancy!???Switching to cow�s milk before 1yr of
age increases risk of this o B12 deficiency � if mom is vegan; recommend
supplementation if this is the case * ?? �Benefits of Breastfeeding for mom o
Rapiduterineinvolution/decreasedpost-partumbleedingo Faster weight loss to return
to pre-pregnancy weighto Moderate contraception/less periods/increased bonding with
childo Reduced risk of breast/ovarian cancer (NOT ENDOMETRIAL CANCER!!!) * ??
�Contraindications to Breastfeeding o Baby - galactosemia o Mom � active TB (unless
post-2wk of therapy), maternal HIV (if formula available), herpes of the breast,
active peri-partum varicella infection, active herpes of the breast/nipple, some
medications/chemotherapy/active drug abuse or alcohol consumption 3825: Beckwith-
Wiedemann Syndrome * ?? �Presentation: Abdominal wall defects (omphalocele,
gastroschisis, umbilical hernia), macrosomia, hemi-hypertrophy, macroglossia, and
visceromegalyo Increased risk of Wilms Tumor and hepatoblastoma development o
Hypoglycemia is common and should be monitored closely * ?? �Pathophysiology:
mutation on chr 11p15 (WT1; part encodes insulin-like growth factor 2) * ??
�Imaging (FIRST STEP!): prompt abdominal ultrasound to rule out concomitant
abdominal tumor * ?? �Dx: clinical presentation +/- specific genetic defect o Note
that congenital hypothyroidism may present with macroglossia/umbilical hernia and
should not be confused for this syndrome! * ?? �Follow-up: screening for abdominal
tumors based on ageo Age 0-4: AFP/Abdominal ultrasound every 3 months o Age 4-8:
abdominal ultrasound every 3 monthso Age 8-20: renal ultrasound every 3 months
2452/DiV: Duodenal Atresia Presentation * ?? �Bilious Vomiting: yellow/green
stained vomit proves that the GI tract is patient past the Ampulla of Vater (rules
out pyloric stenosis). Typically, this type of vomiting indicates a surgical
problem o Note that 20% of pts with duodenal atresia will have it before the
Ampulla of Vater; this will lead to non-bileous vomiting. Thus, just because it�s
non-bileous, doesn�t mean it�s not duodenal atresia. * ?? �Polyhydraminos: too much
amniotic fluid; can be an indicator impaired swallowing (which includes GI
obstruction) or urine overproduction (maternal diabetes, twin pregnancy) * ??
�Passage of meconium: yes, even with bowel obstruction, the infant may still pass
meconium. Lanugo, amniotic fluid, bile will not be able to form it, but mucus is
shed throughout the GI tract (even with an obstruction) thus can form meconium * ??
��Double Bubble� sign on CXR: two pouches of gas (stomach and proximal duodenum)
seen due to gas filling the stomach, a stricture point at the pyloric sphincter,
then gas filling duodenum proximal to the atresia point. Pathophysiology * ??
�Bowel obstruction may in intrinsic (duodenal atresia) or extrinsic (annular
pancreas, adhesive Ladd�s bands); but gas throughout the bowel with signs of
obstruction points to partial obstruction vs total * ?? �Duodenal development
involves lumen obliteration around week 8, with subsequent re-canalization
afterward. Failure of recanalization results in obstruction * ?? �Jejunal/Ileal
development does not undergo this obliteration/recanalization process and
obstruction is the result of poor bloodflow causing segmental ischemia??segmental
obstruction * ?? �There are several associated abnormalities with duodenal atresia
with the top 4 being Down�s syndrome, Annular pancreas, Malrotation of the gut, and
congenital heart disease. Workup * ?? �First Step: IV access, fluid resuscitation,
NGT placement for stomach decompression * ?? �If unstable: suspect
malrotation/volvulus??prophylactic ABX + exploratory laparotomy * ?? �If stable:
AP/lateral CXR o No dilated loops of bowel (proximal obstruction) + Double bubble +
no distal bowel gas = duodenal atresia o No dilated loops of bowel (proximal
obstruction) + Double bubble + distal bowel gas??Upper GI contrast study o Dilated
loops of bowel (distal obstruction)??contrast enema to assess Lower GI tract
Management o Workup as indicated aboveo Surgery should be delayed for thorough
workup if patient is stable; but clinical instability warrants emergent trip to the
OR for exploratory laparotomy for repair of malformed gut Areas to Get in Trouble o
Inadequate resuscitation before emergent surgery??hypovolemia can result in
hypotension that�s exacerbated by anesthesia, which may lead to shock! o Not
working up cardiac defects??nearly 20% of
babies with duodenal atresia will have cardiac defects due to comorbidity with
Down�s Syndrome! These may take precedence over the GI problem and should be
addressed first. o Damage to annular pancreas??this is another common co-
malformation with duodenal atresia. In surgery care must be taken to not damage the
pancreas as it may lead to pancreatic enzyme leak! 4890: Ileum/Jejunum Atresia * ??
�Presentation: bilious emesis, abdominal distention, other signs of intestinal
obstruction * ?? �Pathophysiology: in-utero vascular accident often due to maternal
medication use or cocaine/tobacco use. The lack of perfusion causes bowel
necrosis/resorption, sealing off that section of bowel * ?? �Imaging: upright
abdominal X-ray showing triple bubble sign (stomach, duodenum, jejunum/ileum that
isn�t resorbed) and gasless colon (gas can�t pass past resorbed segment) * ?? �Dx:
clinical presentation + imaging * ?? �Tx: adequate fluid resuscitation &
stabilization??surgical resection/re-anastamsosis of bowel 2467/4183: Hirschprung�s
Disease (Congenital Aganglionic Megacolon) * ?? �Presentation: uncomplicated birth,
delayed passage of meconium (>48hr), bilious emesis, abdominal distention/no stool
in rectal vault, increased rectal tone, patent anuso Increased rectal tone with
�squirt sign� (forceful expulsion of gas/feces) with rectal exam o Regular
consistency of meconiumo Highly associated with Down�s Syndrome (trisomy 21) * ??
�Pathophysiology: failure of neural crest cell migration to the gut to form
segments of the enteric nervous system. Thus, GI tract without ENS cannot relax
causing obstruction. * ?? �Imaging: upright abdominal X-ray showing air-fluid
levels and possibly obstructiono Contrast enema if stable showing obstruction
(level of recto-sigmoid colon) and proximal dilation of colon with �transition
zone� (�bird�s beak sign�) * ?? �Dx: presentation + rectal suction biopsy (absence
of ganglion cells) * ?? �Tx: surgical resection of affected colon with re-
anastamosis 2466/2467/4183: Meconium Ileus ?? Presentation: uncomplicated birth,
delayed passage of meconium (>48hr), bilious emesis, abdominal distention/no stool
in rectal vault, patent anuso Inspissated meconium (thick/difficult to pass) may be
seen/notedo Bowel perforation may be noted as will require immediate surgery!o
Highly associated with Cystic Fibrosis (�F508 or other!) & often the first sign
(virtually all children with meconium ileus have CF, but only 20% of pts with CF
have meconium ileus) * ?? �Pathophysiology: abnormal ion Cl/Na transport channels
results in poor water secretion into many hollow viscera (including the gut)
leading to very thickened meconium that isn�t passed well. o Thick meconium causes
clogging??obstruction * ?? �Imaging: upright abdominal X-ray showing micro-colon
(diffusely small colon) & air-fluid levels (sometimes called the �soap-bubble
appearance�) o If stable: Contrast enema if stable (obstruction at the level of the
ileum) o If unstable/air under diaphragm: no further imaging; proceed to ex-lap
* ?? �Dx: presentation + imaging * ?? �Tx: immediate water-soluble contrast enema
(Gastrografin is hyperosmolar & can suck fluid into the gut to break up meconium to
relieve obstruction) & treatment of underlying diseaseo Emergent ex-lap if failure
of Gastrografin/unstable/evidence of bowel perforation o Chloride sweat test needed
to screen for CF after addressing acute GI event 2463/4851/12517: Intussusception o
?? �Presentation: sudden severe episodic/crampy abdominal pain with interspersed
normal feeding/behavior, palpable �sausage-like� abdominal mass, �currant jelly
stools�, Dance�s sign (empty RLQ), �peeking bowel� (bowel intussusception all the
way to anus, where it�s peeking out) o Classically can occur after URI (most common
cause of lead point!) or rotavirus infection (and with rotavirus vaccination in
older versions of the vaccine!) o ?? �Pathophysiology: �lead point� within the bowl
causes telescoping of bowel with normal gut motility, causing
obstruction/pain/ischemia/death if severe. o Possible lead points: none identified
(75%) > Peyer patch hypertrophy following viral illness (most commonly in ileum) >
Meckel�s diverticulum (most common cause of re-current intussusception) > Henoch-
Scholein purpura (small bowel hematoma)/Celiac�s disease (lymphoid
hyperplasia)/intestinal tumor (Burkitt�s lymphoma most common)/intestinal polyp
(check for FAP or others)/Cystic fibrosis (inspissated stool) * ?? �Imaging:
abdominal ultrasound (�target sign�) * ?? �Dx: presentation + imaging * ?? �Tx:
air/water-soluble contrast enema (acute resolution), surgical removal of lead point
(if present or enema failure), treatment of underlying disease process (if present)
o If ongoing bleeding after resolution??Technitium-99m scan for Meckel�s
Diverticulum 4838: Meckel�s Diverticulum * ?? �Presentation: asymptomatic (most
common presentation), painless hematochezia (most common sign), intussusception
(recurrent), intestinal obstruction, or volvulus can all be part of presentationo
Bleeding may be substantial leading to anemia/hemorrhagic shocko Rule of 2�s: 2%
prevalence, x2 incidence in males, presents around 2yr, 2ft from ileocecal valve
* ?? �Pathophysiology: incomplete obliteration of vitilline duct; contains
heterotopic gastric tissue which produces HCl resulting in erosion of gastric
mucosa??bleeding/stricture/obstruction * ?? �Dx: Technetium-99m pertechnitate scan
(�Meckel�s scan�) showing gastric mucosa both in stomach and in diverticulum o
Superior mesenteric angiography & colonoscopy may reveal diverticula but much less
preferred due to invasive nature of both tests * ?? �Tx: often bleeding is
intermittent, but definitive treatment is surgical resection of diverticulum
2456/2474: Necrotizing Enterocolitis * ?? �Risk Factors: prematurity (<32wk), very
low birth weight (<1.5kg), reduced mesenteric perfusion (dehydration, hypotension,
congenital heart disease), enteral feeding (formula > breastmilk) * ??
�Presentation: vital sign instability/lethargy/hypothermia, vomiting, bloody
stools, abdominal distention/tenderness, residual milk in stomacho Complications:
septic shock, bowel rupture, intestinal stricture, short bowel syndrome, death o
Most common cause of death in Pediatric ICUo Most commonly occurs at terminal
ileum/colon * ?? �Pathophysiology: premature bowel has a difficult time totally
digesting/absorbing nutrients???bacterial proliferation/fermentation??mucosal
inflammation??translocation of bacteria/fermenting gasses into the bowel wall * ??
�Labs: CBC (leukocytosis), CMP, ABG (metabolic acidosis) * ?? �Imaging: upright
abdominal X-ray showing pneumatosis intestinalis (�train track�/�double line� bowel
wall; air in intestinal wall) or air in portal veins (bacterial transit into portal
venous system) * ?? �Dx: clinical presentation + imaging * ?? �Tx: immediate broad-
spectrum Abx, ICU admission with close supportive care 2464: Milk/Soy Protein
Colitis * ?? �Presentation: regurgitation/vomiting with feeding, painless bloody
stools, eczema at 2-8wk of age o Family Hx of allergy/asthma/eczema may be a clue *
?? �Pathophysiology: non IgE mediated allergy to proteins in milk causing colonic
inflammation * ?? �Dx: painless bleeding/symptoms ceases with dietary modification
o Should improve within 3 days, but may take up to 2wk for complete resolution * ??
�Tx: avoidance of all dairy and soy until age 1yr (often they can tolerate at this
age) o Momcancontinuebreastfeedingifsheeliminatesdairy/soyfromherdiet o Hydrolyzed
formula should be used in formula fed infants 3872: Choanal Atresia?? Presentation:
depends on severity of obstruction but overall well-appearing except for below o
Unilateral: often undiagnosed until first URI where lack of patency is realizedo
Bilateral: cyanosis/tachypnea at rest; worsening with feeding & resolves with
cryingo May present as part of CHARGE syndrome (Coloboma, Heart defects, Atresia of
Choanae, Retardation, Genito-urinary malformation, Ear abnormalities/deafness w/
cup-shaped ears) o A classic finding is inability to pass NG tube through one or
both of the nasal passages or a failure of condensation on cold metal when placed
under the nares.o Note that infants are obligate nose-breathers until 4mo (unless
crying). Often these children will appear dusky/cyanotic/in respiratory distress
unless crying * ?? �Pathophysiology: failure of posterior nasal passage
canalization with either bony (90%) or membranous (10%) obstructiono Cyanosis with
feeds occurs from child not being able to suck/swallow & breathe simultaneously
* ?? �Imaging: CT scan (choanal narrowing at level of pterygoids, air-fluid levels
at obstruction site) * ?? �Dx: clinical presentation + imaging * ?? �Tx: first step
= oropharyngeal intubation/airway with orogastic tube placement for feeding o
Resolution achieved with endoscopic or surgical repair of obstruction 4856: Crying
in the Newborn * ?? �Normal crying: intermittent, resolves with comforting,
duration <2hr/day * ?? �Excessive crying: >3hr/day for >3days/wk for >3wk in an
otherwise healthy infant o Typically occurs around the same time of day (often in
the evening)o Colic � baby is just excessively cryingo GERD � arching of back
during feeding (Sandifer syn.), frequent spit-ups/vomiting, poor wt gain o Corneal
abrasion � Hx of playing in sand; fluorescein dye instillation to show damageo Hair
tourniquet � hair wrapped around extremity of digito Milk-protein allergy � biliary
symptoms and painless bloody stools * ?? �Tx: H&P for possible etiology; if colic,
review infant comforting techniques with parents & reassure that baby is healthy,
but colicky o Comfort baby with: infant swing, swaddling, quiet dark room (minimal
stimuli), holding/rocking o Assess feeding habits to check for
overfeeding/underfeeding/poor technique 2773/3602: Celiac�s Disease (sprue)??
Presentation: long-standing bulky/foul/floating diarrhea, loss of muscle mass/fat,
fatigue, and malabsorbtion (may cause specific symptoms based on what isn�t being
absorbed properly)o Dermatitis Herpeteformis � itchy, small vesicular rash
appearing on knees, elbows, forearms, and buttockso Iron deficiency anemia � due to
poor intestinal absorptiono Short stature/weight loss � may specifically occur in
children/infantso Other autoimmune diseases: these diseases tend to run in packs,
and if you have one you�re more likely to have another!?? Pathophysiology:
Autoimmune disease causing small bowel destruction in response to gluten ingestion
o Anti-gliadin/Anti-tissue transglutaminase/Anti-endomysial IgA or IgG antibodieso
Gluten found in wheat, rye, barley, and oats (if harvested in fields with wheat
present) ?? Dx: IgA serologic testing, select antibody testing, or intestinal
biopsy (villous blunting, chronic inflammatory cells) o Selective IgA deficiency
may actually mask the IgA-type antibodies, this is suspicion is high, but IgA is
negative??check total IgA for deficiency and check for IgG-type antibodies o
Confirmed with resolution of symptoms with gluten free diet ?? Tx: gluten free diet
2198: D-xylose test for Celiac�s Disease * ?? �Remember! Celiac�s disease is an
autoimmune disease (anti-gliadin antibodies) causing atrophy of the small-
intestinal brush border with gluten ingestion causing chronic diarrhea,
steatorrhea, and weight loss due to malabsorption * ?? �Dx: D-xylose test o D-
xylose is a sugar that can be absorbed in the small intestine without digestion and
will easily be filtered out by the kidney into the urine o Pt drinks 25g of D-
xylose and subsequently has blood/urine sampled to check for levels of D- xylose in
each ???Normal or malabsorption from enzyme deficiency = normal D-xylose levels ???
Celiac�s disease = low D-xylose due to damaged intestinal wall 3581: Tropical Sprue
* ?? �Essentially Celiac�s disease presentation but sub-acute onset after a trip
for >1 month to a tropical endemic area (Puerto Rico, Bahamas, etc.) * ??
�Presentation: malabsorbtion (fatty stools, borborygmi, hyperactive bowel sounds,
glossitis, cheilosis, pallor, edema, diarrhea, gas, cramps, fatigue, progressive
weight loss)o Classically this causes B12/folate malabsorption??megaloblastic
anemia * ?? �Dx: Hx and small intestinal biopsy (villous blunting, lymphocytes,
eosinophils, plasma cells) * ?? �Tx: leave the tropical area, should resolve with
symptomatic treatment 2453: Cyclic Vomiting Syndrome * ?? �Presentation: recurrent,
predictable pattern of acute clusters of vomiting with spontaneous resolution o
More common in pt with migraine headaches or family Hx of migraine headaches o May
result in dehydration, anemia, and social/school impairment * ?? �Pathophysiology:
thought to be a sort of �ENS migraine� causing abnormal firing of enteric ganglia *
?? �Dx: criteria as are follows o >3 episodes within 6mo period, lasts 1-10 days,
occurs >4x/hr at peak intensity o easilyrecognizedbyfamilyo no symptoms in between
episodes & no underlying etiology identified * ?? �Tx: hydration, anti-emetics
(ondasetron), and reassurance (66% of pt have gradual resolution in 5-10yr) o Anti-
migraine therapy (sumatriptan) if history of migraines has proven beneficial 2945:
Biliary (Choledochal) Cysts ?? Presentation: abdominal pain, jaundice, palpable
mass; often presents <10yr; presentation may have additional signs/symptoms based
on age:o Infants � may present with acholic stools; must rule out biliary atresia o
Older Kids � may present with pancreatitiso Adults � vague epigastric pain, RUQ
pain, cholangitis/fevero May transform into cholangiocarcinoma if left untreated
* ?? �Pathophysiology: congenital dilitation of the biliary tree. Many types, but
Type I is the most common (single dilatated extrahepatic cyst). * ?? �Labs:
conjugated hyperbilirubinemia +/- elevated LFTs * ?? �Imaging: abdominal ultrasound
or ERCP visualization of the cyst * ?? �Dx: presentation + labs + imaging * ?? �Tx:
surgical resection (relieve obstruction & prevent malignant transformation) 3970:
Biliary Atresia * ?? �Presentation: normal birth ???jaundice, acholic stools
(light-colored), dark urine ???hepatitis, hepatomegaly, hepatic fibrosis/failureo
Symptoms develop within the first two months of life * ?? �Pathophysiology:
progressive obliteration of the extrahepatic ducts/gallbladder * ?? �Labs: direct
(conjugated) hyperbilirubinemia +/- elevated LFTs * ?? �Imaging: abdominal
ultrasound (first step; abnormal/absent gallbladder) o Hepatic Scintigraphy � shows
failure of radiotracer dye movement into small bowelo Surgical cholangiogram � gold
standard; often obtained in the OR when planning for surgical shunting to set up
eventual liver transplant * ?? �Dx: presentation + imaging * ?? �Tx: Kasai
procedure (hepatoportoenterostomy; buys time/allows for child development to limit
further surgical morbidity/mortality)??liver transplantation 2896/3194: Reye
Syndrome ?? Presentation: rapid onset hepatic dysfunction, encephalopathy, cerebral
edema, & increased ICP causing abnormal behavior & vomiting??lethargy??
seizure/deatho Classically caregiver will give history of viral illness
(flu/chicken pox/etc.) treated for fever o Elevated ICP is the most common cause of
death (brainstem herniation)o Note that aspirin is always contraindicated in
children unless treating Kawasaki�s disease or childhood rheumatologic diseases
(e.g. juvenile idiopathic arthritis) * ?? �Pathophysiology: administration of
aspirin (or other salicylates) in children during viral infection can result in
hepatic mitochondrial dysfunction??fulminant hepatitis??hyperammonemia causing
cerebral toxicity/swelling * ?? �Labs: LFTs (elevated AST/ALT), CMP (normal
bilirubin, elevated NH3, hypoglycemia, possible electrolyte disruption),
coagulation studies (elevated PT, PTT, and INR) * ?? �Imaging: CT/MRI of brain may
show diffused cerebral edema * ?? �Biopsy: liver biopsy will show microvesicular
steatosis * ?? �Dx: presentation/clinical history +/- imaging & biopsy * ?? �Tx:
admission with supportive care 4926: Pediatric GER (physiologic) & GERD
(pathologic) ?? Presentation o Physiologic: �happy spitter�; child asymptomatic
except for little spit-ups after feedingso Pathologic: FTT/sub-optimal nutrition,
irritability/feeding refusal, Sandifer syndrome (torticollis & arching of the back
during feedings from painful esophagitis)???Sometimes may have constant hunger
(child gets a buffering action from milk)???Complications: laryngitis, bronchitis,
wheezing/worsening of asthma, vocal cord nodules, sub-glottic stenosis,
bronchopulmonary constriction, Barrett�s esophagus ?? Pathophysiology o
Physiologic: shorter esophagus, immature LES causing times of incomplete closure,
commonly in the supine position o Pathologic: incomplete closure of LES for any
reason +/- gastric emptying delay?? Dx: clinical presentation + esophageal pH probe
(shows episode of esophageal acidification correlating with clinical signs)o Barium
UGI or scintigraphy showing frank aspiration would be diagnostic but less useful as
this is a severe presentation and much less common ?? Tx o Physiologic: frequent,
small-volume feeds with holding the infant upright or 30min after meals. Typically
improves by 6mo and resolves by 1yr when the child can sit upright & LES matures o
Pathologic: H2 blocker or PPI + thickening feeds (add oatmeal) + upright
positioning ???If this fails, surgical intervention may be needed
2451/2458/2656/8791: Foreign Body Aspiration * ?? �Risk Factors: intellectual
disability, difficulty swallowing/Hx of choking, refusal to feed, vomiting * ??
�Presentation: o Esophageal (most common): persistent/worsening cough, vomiting,
dysphagiao Tracheobronchial: sudden onset stridor, coughing, focal monophasic or
generalized wheezing, dyspnea, diminished air movement on affected sideo Red Flags:
hematochezia, melena, severe/new abdominal pain * ?? �Pathophysiology: children
love to put thing in their mouth. That�s really it.o Coins are the most common item
ingestedo Batteries/magnets/sharp objects are high risk require special attention
with treatment * ?? �Imaging: X-ray (66% normal; 33% object or lung hyperinflation
seen from �ball-valve� obstruction of bronchus), CT (if X-ray shows nothing) * ??
�Dx: presentation + imaging or endoscopic visualization * ?? �Tx: removal of object
by various methods depending on situation o Wait & Watch: * ???�Asymptomatic & non-
high risk object??if passes to stomach within 24hr you can simply monitor the poop
to ensure proper passage * ???�High risk object past the esophagus??close follow-up
for red flag symptoms & stool examination; passage typically occurs without problem
in 90% of children o Flexible endoscopy: preferred for low-risk objects in the
proximal esophagus on imagingo Rigid endoscopy: used for impacted sharp objects in
the proximal esophagus on imagingo Rigid bronchoscopy: if in tracheobronchial
tract; must be done promptly due to concern for asphyxiationo Note that induction
of vomiting/diarrhea will not speed passage process & pushing of the object into
the stomach with endoscopy is not an acceptable treatment 2465/DiV: Malrotation
with Midgut Volvulus Bilious Emesis Differential Based on Age * ?? �Any age �
Adhesions, Hirschprung�s disease, incarcerated inguinal hernia, malrotation
w/volvulus * ?? �Neonate (0-1mo) � annular pancreas, duodenal atresia, imperforate
anus, jejunoileal/colonic atresia, meconium ileus, meconium plug, necrotizing
enterocolitis * ?? �Infant (1-24mo) � intussusception * ?? �Child (2-12hr) � ileus
2nd to appendicitis, intussusception Presentation * ?? �Bilious
or nonbilious vomiting (depends on part that has undergone volvulus) should always
prompt a search for midgut volvulus, as it can be a life threatening condition!
* ?? �Basically any developmental defect (esp of the gut) puts a patient at risk
for volvulus Pathophysiology * ?? �The midgut is defined by receiving blood from
the superior mesenteric artery (starting at the Ligament of Treitz) and includes
the 2nd part of the duodenum through the proximal 2/3 of transverse colon * ??
�Development of the midgut occurs in the 6th week of gestation with rapid
elongation and herniation into the umbilicus. Ultimately this section of bowel
undergoes 270o of counterclockwise rotation, finally finding it�s final resting
spot around week 12. * ?? �Malrotation occurs when midgut starts to take it�s first
90o angle turn and return from it�s herniated position back to the abdominal
cavity. Improper fixation causes the remaining 180o of turning to occur around the
midgut mesentery, giving the classic �corkscrew� appearance. * ?? �Problems occur
when this bowel becomes kinked, resulting in obstruction and strangulation??bowel
ischemia and eventually death/perforation * ?? �While acute volvulus is an emergent
surgical event, malrotation doesn�t necessarily cause volvulus AND volvulus may
�kink and un-kink� causing colicky symptoms chronically. Workup * ?? �If patient is
hemodynamically unstable, skip imaging and go to the OR * ?? �Abdominal X-ray:
exclude perforation (free air under diaphragm) * ?? �Upper GI series with contrast:
show the course of the gut and will be diagnostic for volvulus o Most commonly,
this is a normal study o Classically shows �corkscrew� gut from improper rotation
around mesentery Management * ?? �If free air under diaphragm or hemodynamically
unstable proceed to surgery without more imaging * ?? �Surgical fixation is
necessary for resolution of malrotation/volvulus o IV fluid resuscitation + ABx +
NGT for stomach decompression + emergent laparotomyo If bowel is not infarcted??
Ladd�s Procedure (un-twisting, division of Ladd�s bands, fixation + prophylactic
appendectomy to avoid confusing symptoms later in life should appendicitis occur) o
If bowel is infarcted??bowel resection with Ladd�s Procedure * ?? �During surgery;
large bore NGT should be passed through the end part of the duodenum to rule out
atresia or other malformations of the gut * ?? �If pt is found to have asymptomatic
malrotation, surgery the the earliest convenience should be done 3078/3465/DiV:
Hypertrophic Pyloric Stenosis Differential Dx * ?? �Surgically managed: antral web,
pyoric atresia, pyloric stenosis, GERD from anatomic defect * ?? �Medically
managed: acute gastroenteritis, GERD, metabolic disorders, pylorospasm Presentation
?? Healthy baby with progressive non-bilious, projectile vomiting immediately
following meals; baby will always seem hungry despite vomiting (�hungry baby!�) o
Vomiting only food/mother�s milk directly after or during feeding sessionso Olive
shaped mass can be palpated and visible peristalsis can be seen in upper abdomen o
Sunken fontanelles from dehydration ?? Risk factors: first-born child, erythromycin
administration, formula feeding (late presentation at 3-5wk) Pathophysiology ??
Poorly understood; but histologic evidence points to immature/absent ganglia
resulting in inability of pylorus to relax, resulting in hypertrophy/hyperplasia
and obstruction * ?? �Stomach muscle hypertrophy/dilation occurs due to vigorous
peristalsis in attempts to pass chyme through the obstructing pylorus * ?? �As
stomach peristalsis strength grows, it becomes so intense that is overwhelms the
lower esophageal (cardiac) sphincter, resulting in projectile vomiting Workup * ??
�If palpable �olive� is appreciated ???this is diagnostic, no further workup needed
* ?? �If no �olive� is appreciated??abdominal ultrasound showing pyloric thickness
>3mm & length >15mm are typically diagnostic (although this number can change with
age!) * ?? �If still uncertain or negative ultrasound with high suspicion??upper GI
series with contrast showing delayed emptying, retrograde peristalsis, and �string
sign�/�tit sign� at the pylorus is diagnostico Major concern for aspiration of
contrast fluid (as the child will surely vomit anything in it�s stomach; thus this
test should be done only if needed!) * ?? �CMP may show a hypochloremic,
hypokalemic metabolic alkalosis from protracted vomiting o Hypochloremia � loss of
Cl- ions from HCl in vomito Hypokalemia � dehydration from vomiting results in
aldosterone activation to restore intravascular volume with subsequent Na+
retention and K+ wastingo Alkalosis � with decreasing K+, but still demand for Na+
resorption, the kidney is less able to used the Na+/K+-antiporter. Na+ traveling
more distally in the nephron results in more activation of the Na+/H+ antiporter,
wasting H+ to save Na+ resulting in paradoxical aciduria. Management * ?? �First
Step: IV access with fluid resuscitation for protracted vomiting in this order: o
1st - Isotonic normal saline bolus at 20mL/kgo 2nd � D5 with 1�2NS at 1.5x normal
infusion rateo Once child urinates � add 20mEq/L KCl to the already running fluid o
Electrolyte abnormalities should be corrected before surgery * ?? �Ramstedt
pyloromyotomy � small incision into pylorus with spreading and fixation of the
muscle to relieve the obstruction; air or methylene blue are introduced via NGT to
prove patency/lack of leak. o
Shouldbedelayeduntilproperfluidresuscitation/electrolytebalancinghasoccurredo
Optimal fluid status shows normal urine output, serum bicarb <30mmol/L and normal
K+ o Pt should be able to eat a few hours following surgery, although post-op
vomiting isn�t uncommon. Vomiting 3-4 days following surgery indicated complication
Areas of Trouble * ?? �Inadequate fluid resuscitation may lead to anesthesia
induced hypotension/death * ?? �Leak � fever, tachycardia??feeding intolerance,
leukocytosis??peritonitis, sepsis; must be re- operated on to fix the leak
4290/DiV: Pediatric Abdominal Wall Defects (Umbilical
Hernia/Omphalocele/Gastroschisis) Differential Dx * ?? �Gastroschisis � discussed
below * ?? �Omphalocele � midline abdominal wall defect with herniation of gut
contents; amnioperitoneal membrane covering gut contents, umbilical cord insertion
into this membrane; heightened risk for abnormal formation of other systems; liver
herniation may allow for earlier detection * ?? �Bladder/Cloacal Exstrophy �
exstrophy of sac filled with hemi-bladder/urethra/kidney/intestine; typically
occurs inferior to umbilical stalk, often sac partially divides two hemi-bladders
(inside and outside), often extensive associated developmental defects * ?? �Prune
Belly Syndrome � abdominal wall hyposplasia, gut contents held within collagenous
wall (making it �pruned�), 95% males, associated with UG system underdevelopment
(hypoplastic prostate, bilateral undescended testes, infertility, bladder outlet
obstruction) ?? Urachal Abnormality � communication between bladder/anterior
abdominal wall from poor/absent ablation of the urachus. May be fistula/cystic
sac/small outpouching. Associated with NTDs and omphalocele Umbilical Hernia * ??
�Typically occur in children. Associated with congenital hypothyroidism (cretinism)
* ?? �In children, often are asymptomatic and resolve spontaneously without
intervention * ?? �In adults, associated with high intra-abdominal pressure
(ascites, pregnancy, weight gain, etc.) * ?? �Often close by age 2; repair should
occur if it does not resolve by age 4, a >2cm defect is present or progressive
enlargement after 1yr occurs Gastroschisis * ?? �Risk Factors: <20yr, white race,
single pregnancy, low BMI, frequent UTIs, cigarette smoking, drug or alcohol use
* ?? �Presentation: Paraumbilical (right sided), small (<5cm) abdominal wall defect
with evisceration of gut contents and sometimes associated evisceration of gonads,
bladder, & stomach o Lacks membrane covering cut contents (gut exposed to open air)
o Cord insertion is normal at the umbilicuso Causes matting, dilation, and
thickening of bowels; malrotation is common; Ileus is common o Rarely associated
with other developmental abnormalities; intestinal atresia rarely (10-25%) o
Maternal AFP may be mildly elevated * ?? �Pathophysiology: not totally clear, but
thought to be due to vascular accident in the umbilical ring resulting in poor
development and defect development. Right sided defect is thought to be more common
due to involution of the right umbilical vein o Bowel abnormalities are due to
extended exposure to amniotic fluid causing inflammation * ?? �Workup:
Covering/Peds Surgery consult, blood labs, IV fluids, urine output monitoring, Full
body X-ray for anatomic survey/implanted device location check * ?? �Management: o
Initial: stabilize airway, Central/Peripheral IV access, IV fluids, cover with
sterile plastic wrap, warming lamp, OG-tube decompression, urinary catheter, broad
spectrum Abx o Place viscera in sterile dacron-silastic silo to allow for gradual
reduction as inflammation slows o Attempt reduction & schedule for surgical
reduction when abdominal laxity will facilitate repair o Ventilation/fluid &
nutrition support with intra-abdominal monitoring for healing Omphalocele * ??
�Risk Factors: <20 or >40yr, high BMI, SSRI use/family Hx * ?? �Presentation:
Umbilical/epigastric/or hypogastric variable sized (but often large) abdominal wall
defect with herniation of gut and sometimes the liver into a membrane sac o Covered
in amnioperiotneal membrane (10-20% will rupture)o Cord insertion is into the
amnioperiotneal membraneo Bowl is typically normal appearing; malrotation often
present; bowel function normalo
Commonlyassociatedwithotherdevelopmentaldisorders(Beckwith-Wiedemann,Trisomy 13/18,
Pentology of
Cantrell, various defects of the gut) o Maternal AFP severely elevated * ??
�Pathophysiology: results from arrest of lateral-body fold migration and body wall
closure during organogenesis. When normal gut herniation occurs around week 5,
development arrests, leaving the herniated gut in place until birth. This is
thought to be due to a failure of cell migration, thus the higher association with
concomitant developmental defects. o Note that liver herniation (giant defect) is
rarely associated with chromosomal abnormality! * ?? �Workup: Peds Surgery consult,
blood labs, IV fluids, urine output monitoring, Full body X-ray for anatomic
survey/implanted device location check o Echocardiography for assessment of heart
defects & genetic testing also recommended ?? Management: o Initial: stabilize
airway, Central/Peripheral IV access, IV fluids, cover with sterile plastic wrap
(if sac is ruptured), warming lamp, OG-tube decompression, urinary catheter, broad
spectrum Abx o If ruptured � follow gastroschesis algorithmo <2cm defect �
immediate surgical reduction??support for healingo 2-9cm defect � place viscera
into sterile dacron-silastic silo for reduction??surgery/support o >9cm defect �
apply sclerosant to sac/cardiopulmonary stabilization??sterile dacron-silastic silo
for reduction??surgery/support Which is More Urgent? Why? * ?? �Short Term �
Gastroschisis. The exposed, inflamed, nonfunctional bowel requires immediate
protection and surgical correction. The child also has increased insensible fluid
losses which can also cause problems * ?? �Long Term � Omphalocele. The child has a
protected, functional bowel. However, the high association with other developmental
defects makes the child�s future development very difficult and sometimes, not
viable. Areas to Get in Trouble * ?? �Remember to note respiratory distress and
intubate as necessary * ?? �Remember to carefully check for bowel ischemia/necrosis
and address as needed * ?? �Remember to wrap bowel in plastic wrap & warm with lamp
immediately. Moist gauze is avoided as it is not water-tight and will cause
significant loss of insensible fluids * ?? �TPN should be provided to patients with
slow return of bowel function. Matted/inflamed bowels are likely to be non-
functioning. * ?? �Post-reduction, abdominal compartment syndrome (low urine
output, insufficient ventilation, positive fluid balance) may occur. It should be
monitored with intra-abdominal pressure monitoring. 3849/DiV: Esophageal Atresia
with Tracheo-Esophageal Fistula Presentation * ?? �Excessive drooling with
white/frothy mucus buildup in mouth/nose * ?? �Cannot tolerate feedings with
immediate gagging/choking and vomiting of food * ?? �Oxygen desaturation with
feeding � often implies severe abnormality in tracheo-bronchial anatomy (some of
feedings go into the lungs!)o May result in respiratory distress/pneumonia
development * ?? �EA may manifest via polyhydramnios (failure of swallow) on
prenatal ultrasound Pathophysiology * ?? �Esophageal Atresia: Abnormal development
of trachea-esophageal fold which normally separates the caudal primitive foregut
into the esophagus and trachea * ?? �TEF: thought to be due to defective
epithelial-mesenchymal interactions in a lung bud that fails to develop. This lung
bud wants to hang out with the esophagus and the fistula is formed. Types of TEF
* ?? �Many types with different combinations of defect/TEF * ?? �Type C (proximal
esophageal pouch with distal TEF) is most common (85%) with Type A (pure EA without
TEF) being next most common (8%) Associated Abnormalities * ?? �VACTERL, CHARGE, or
Trisomy syndromes are often diagnosed * ?? �VACTERL = vertebral, anorectal,
cardiovascular, tracheoesophageal, renal, and limb abnormalities * ?? �CHARGE =
coloboma, heart defect, atresia choane, retarded growth, genital defects, and ear
defects Workup * ?? �First Step: Placement of NG-tube with CXR (AP and lateral)o
Gastric bubble presence = some connection between air and stomach (no EA or EA +
TEF)o EA = shows NG-tube coiled in the esophagus/mediastinum or going into the
tracheao Checks for abnormal lungs = pneumonia, primary lung lesions, congenital
diaphragmatic hernia * ?? �Contrast esophagram may be used in equivocal findings;
however, the concern of aspiration pneumonitis should reserve this test only if
truly necessary * ?? �Diagnosis can be made simply with history and radiologic
findings consistent with disease Management * ?? �First Steps: intubate if signs of
respiratory distress, place NG-tube into esophageal pouch/elevate child�s head
(minimize vomiting thus aspiration). * ?? �If pneumonia: broad spectrum Abx &
gastrotomy tube for decompression should be placed * ?? �Surgical repair: able to
undergo repair surgery as soon as patient is stable/able to tolerate surgery o
Physical exam, cardiac/renal ultrasound, ECG, and X-rays for anatomic survey must
be done prior to surgery to ensure anesthesia tolerance/find all defects for repair
* ?? �Complications:o Esophageal anastamotic leak (15%) � often heal with stricture
needing surgical revision o Strictures (80%) � need esophagostomy and balloon
dilationo GERD (100%) with increased risk of Barrett�s esophagus * ?? �Prognosis:
100% survival rates, but often with significant GI complications that will be
addressed Areas of Trouble * ?? �Interrupted IVC (IVC drains into the azygous vein
to get to heart) � the azygous vein is typically divided during EA/TEF repair. If
interrupted IVC is present, this will cause cutoff of lower extremity venous
drainage & death of the patient * ?? �Right-sided aortic arch � rare, but possible
(esp. with developmental defects!). Right thoracotomy is the typical approach for
repair, thus right-sided AA would result in disaster. If present, a left
thoracotomy is the proper approach. * ?? �Avoid intubation/ventilation if possible
as the abnormal connections between the trachea and GI tract may result in pumping
air into the GI tract??abdominal distention. This distention will compress lung
volumes, leading to worsening lung function (the opposite of what you want!)
2480/3089/4302/4839/FA: Vitamin Deficiencies * ?? �Vitamin A (retinoic acid;
eyes/skin) � night blindness, corneal degeneration, Bitot spots (squamous
metaplasia of conjunctiva causing silvery-grey plaques) dry/scaly skin,
immunosuppression, retardation & fullness of the fontanelles in children * ??
�Thiamine (B1) � classically from alcoholism or polished rice consumption in 3rd
world o Wet BeriBeri (heart) � dilated cardiomyopathy??high-output cardiac failure
& edemao Dry BeriBeri (PNS) � polyneuritis & symmetric muscle wastingo Wernicke-
Korsakoff syndrome (CNS) � metabolic damage to medial dorsal nucleus of thalamus &
mammillary bodies; confusion/opthalmoplegia/ataxia??confabulation, antero &
retrograde amenesia, personality changes. Must give thiamine before glucose in
these patients (impaired glucose metabolism = worsening of symptoms!) * ??
�Riboflavin (B2; mouth/eyes) � cheilosis (inflammation of lips causing
scaling/cracking at angles of mouth), glossitis (inflamed/red tongue) & corneal
vascularization (blurring/burning/itching of eyes) * ?? �Niacin (B3) �
glossitis ???pellagra (4Ds = Diarrhea, Dementia, photoDermatitis, Death)o Hartnup
disease, carcinoid syndrome, isoniazid, and corn-based diet can all lead to this
* ?? �Pyridoxine (B6; brain/blood) � convulsions, irritability, peripheral
neuropathy, sideroblastic anemia o Isoniazid, OCPs, and goat�s milk can all cause
this * ?? �Biotin (B7) � rare but classically occurs with consumption of raw egg-
whites (avidin); dermatitis, alopecia, & gastroenteritis * ?? �Folate (B9) �
megaloblastic anemia, hypersegmented neutrophils, glossitis o More common cause of
megaloblastic anemia (low stores in the liver); differentiated from B12 by high
homocysteine/normal MMA levelso Caused by: Medications (phenytoin, sulfonamides,
methotrexate) & goat�s milk o Lack of supplementation in pregnancy increases risk
of neural tube defects * ?? �Cyanocobalamin (B12) � megaloblastic anemia,
hypersegmented neutrophils, beefy-red tongue, stocking-glove neuropathy
paresthesias (myelin degeneration)??subacute combined degeneration o More commonly
due to lack on intrinsic factor/terminal ileum resection; rarely due to veganism;
differentiated from B9 by high homocysteine/high MMA * ?? �Vitamin C (ascorbic
acid) � poor collagen synthesis??scurvy (swollen gums, bruising, petechiae,
hemarthrosis, subperiosteal hemorrhage, anemia, poor wound healing, perifollicular
hemorrhage with corkscrew hairs) & weakened immune response * ?? �Vitamin D �
rickets (kids), osteomalacia (adults), hypocalcemic tetany (severe); must
supplement in exclusively breastfed babies * ?? �Vitamin E (tocopherol) � hemolytic
anemia, acanthocytosis (spikey RBC), muscle weakness (similar to B12, but without
characteristic hematologic findings!) * ?? �Vitamin K (phylloquinone) � neonatal
bruising, bloody stools, or intracranial hemorrhage occurring in 1st week of life;
prolonged aPTT/PT o Neonates are naturally deficient in Vit. K naturally due to
lack of gut colonization, poor placental transfer of Vit.K, immature liver
function, & little Vit.K in breastmilk o Denial of Vit.K shot, long-term use of
Abx, or Cystic fibrosis (AEDK deficiency) are all common scenarios where neonates
are not Vit.K replete & complications occur * ?? �Zinc � delayed wound healing,
decreased adult hair, dysgeusia, anosmia, acrodermtitis enteropathica (symmetric
dry vesiculo-bullous scaly rash, FTT, chronic diarrhea) * ?? �Copper � poor wound
healing/connective tissue formation/microcytic anemia (poor Fe2+ absorption) * ??
�Chromium � decreased glucose tolerance; typically caused by TPN * ?? �Selenium �
increased cell damage/poor wound healing/dilated cardiomyopathy; typically from
TPN use * ?? �Fluoride � dental caries * ?? �Protein (Marasmus) � emaciation,
edema, �broom-stick appendages� * ?? �Calorie (Kwashiorkor) � malnutrition, edema,
anemia, fatty liver, skin lesions (flaky/de-pigmented); this is the classic
starving African child 2480/4302/FA: Vitamin Excess ?? Vitamin A (retinoic acid) o
Acute � nausea/vomiting/vertigo/blurred visiono Chronic � classically occurs in
person on isotretinoin for ance; alopecia, dry skin, hepatic damage/hepatomegaly,
arthralgia, pseudotumor cerebrio Teratogenic � classically in teen on isotetinoin
for acne; must be on two formed of birth control for this medication; cleft
palate/cardiac abnormalities * ?? �Niacin (B3) � niacin flush; avoided by taking
aspirin with niacin * ?? �Vitamin C � nausea, vomiting, diarrhea, fatigue, calcium-
oxalate nephrolithiasis * ?? �Vitamin D � hypercalcemia, hypercalciuria, loss of
appetite, & stupor * ?? �Fluoride � chalky white/brown tooth enamel, ligamentous
calcification, increased bone fracture risk Ethics3623/3624/4846: Informed Consent
* ?? �Medical Circumstances where minors don�t need consent: emergency care
(unstable airway, blood transfusion, or emergency surgery are classic examples!),
STI treatment, substance abuse treatment, prenatal care treatment, contraception
* ?? �Emancipated minors: homeless, parent, married, military, financially
independent, high school graduate or aged 18yr * ?? �Often the hospital ethics
committee gets involved if neither of the above situations are present & the
parent/legal guardian is incompetent or the medical decisions being made will
likely harm the patient * ?? �Refusal of vaccines is typically honored unless there
is a high risk situation or need for vaccination is part of emergency care (such as
tetanus exposure) o Consent may only be given by a parent with legal custody of the
childo If parents share joint custody, only one parent is needed to allow the
medical decision (even if the other does not want the medical decision to be made)o
If both parents refuse life-saving treatment, court-order should be sought for
life-saving Tx 9848: Firearm Injury * ?? �Risk Factors: male adolescent,
behavioral/psychiatric problems, Hx of impulsive/criminal/violent behavior, or low
SES * ?? �Firearm injury occurs almost always due to access in the home/relative�s
home/friend�s home * ?? �Prevention: o Remove all firearms in the home (often the
first & most important step)o If removal is not possible, firearms should be
1stored un-loaded & 2weapon and ammo should be stored in separate locked containers
4320: Child Abuse?? Presentation: can be different depending on situation and child
o Unexplained/unlikely injury (cigarette burns, scalding of the legs/buttocks,
bruising of the legs/buttocks, spiral fracture, shaken baby syndrome, etc.) o
Multiple fractures in different stages of healingo Malnutritiono Sudden changes in
behavior or scholastic abilities ?? Risk Factors:o Caregiver: young/single parents,
low SES, substance abuse, psychicatric conditions, Hx of abuse o Home environment:
unstable (divorce, conflict, poverty, etc.), recent loss of job, lack of social
support, domestic violence in/around the homeo Victim: intellectual disability,
emotional/psychiatric illness, unplanned/unwanted child ?? Remember that physicians
are mandated reporters and must report suspected cases of child abuse to Child
Protective Services 3235: Refusal of Treatment * ?? �While some treatments may be
refused life-saving treatment refusal should not be honored (even if rationale is
for religious/cultural reasons) * ?? �A typical situation is with a disease where
treatment has a good prognosis, but lack of treatment would surely result in
death/disability (Acute Lymphoblastic Leukemia is a good example) * ?? �In these
situations, the physician should: o Continue to explain the benefits of treatment
and consequence of lack of Txo Seek aid from the Ethics Committee, Social Services,
Risk Management, and possibly the Law (in the form of a court ordered mandate for
treatment)o Not engage in un-consented treatment until the proper channels have
been taken Infectious Disease 2782: Different Forms of Infection Precautions * ??
�Contact precautions (gown/gloves) � effective against contact (fecal-oral) * ??
�Droplet precautions (surgical mask) � effective against short-range droplets
(coughs/sneezes) * ?? �Airborne precautions (N95 mask, negative pressure room) �
effective against airborn pathogens * ?? �Hand Hygiene � effective against fecal-
oral, contact, droplets, & secretions 4353/4843: Lymphadenitis * ?? �Presentation:
fever, symptoms of infection (URI/etc.), & lymph node that becomes swollen,
enlarged, tender, erythematous, +/- poorly mobile (often affected submandibular
nodes) o Typically occurs in a well-appearing child <5yr oldo May progress into
fluctuant/indurated masso Unilateral typically = bacterial & bilateral typically =
viral * ?? �Micro: o Acute unilateral: S.aureus > S.pyogenes > Prevotella Buccae or
Anaerobes (+dental caries) > B.henslae (+history of nodule at site of cat scratch)
> Kawasaki�s diseaseo Acute bilateral: adenovirus (pharyngoconjunctivits) > EBV/CMV
(+mono) > Toxoplasmosis > HIV o Subacute: Mycobacterium avium complex (+slow onset;
nodes non-tender) * ?? �Dx: clinical presentation +/- throat swab & cultureo If
unresponsive to treatment � TB/Toxoplasmosis may be considered * ?? �Tx: empiric Tx
with clindamycin (covers Staph/Strep spp) or directed therapy with culture if
needed 2781/3642: Impetigo ?? Presentation (micro) o Non-bullous
(S.aureus/S.pyogenes): painful, non-pruritic papules??pustules that easily rupture
forming �honey-crusted� skin lesions o Bullous (S.aureus): rapidly enlarging bullae
with yellow fluid & collar of scale surrounding ruptured lesions o Previous skin
lesions (eczema, abrasion, bug bite) are risk factors due to breaking skin barrier
* ?? �Dx: clinical presentation o ASO titer is not useful unless complications
arise (takes weeks to rise) o Skin swab is not useful (skin flora contamination
would be extensive) * ?? �Tx: o Limited skin involvement: topical Abx (mupirocin)o
Extensiveskininvolvement:oralAbx(cephalexin,dicloxacillin,clindamycin)o Thorough
hand washing greatly decreases transmission & should be encouraged 2193:
Pharyngitis * ?? �Presentation: very common infection, which can present
differently depending on etiology o Common: sore throat, dysphagia, odynophagia,
pharyngeal/tonsillar erythemao Bacterial: +tonsillar exudates, edema, palatal
petechiae, & lack of viral symptoms o Viral: +viral symptoms (cough, rhinorrhea,
conjunctivitis, oral ulcers) * ?? �Micro: Strep. pyogenes (GAS); viruses vary * ??
�Dx: rapid strep (RSAT) & throat culture (either + means bacterial infection) o
Note that the Centor criteria (use in adults) are NOT accurate in pre-adolescent
childreno Centor Criteria looks for Tonsillar exudates, tender anterior cervical
lymphadenopathy, absence of cough, and history of fever.???0-1 out of 4 (80% neg
predictive): analgesics and supportive care only ???3 out of 4 (60% pos
predictive): rapid strep/delayed strep testing with Tx if positive ???4 out of 4:
Throat culture + antibiotics ?? Tx:o Bacterial: oral amoxicillin or penicillin o
Viral: supportive care only 3285/3286/4850: Rhinosinusitis * ?? �Risk factors:
antecedent viral URI (most common; inflammation = poor ciliary clearance of mucus);
less common include allergic rhinitis, anatomic obstruction, environmental
irritants * ?? �Presentation: o Viral: URI symptoms lasting <7 days; symptom Tx is
only needed Txo Bacterial: symptoms last >7 days; fever, thick/persistent nasal
discharge (yellow/green purulent), nasal congestion, inflammation & swelling of
nasal turbinates, tender maxillary sinuses, facial pain, maxillary tooth pain,
cough/wheezeso Alarm signs: epistaxis, turbinate destruction, palate eschar,
maxillary cyanosis * ?? �Micro:o Acute (S.pneumo = non-typable H.flu > Moraxella
catarrhalis) o Chronic (S.aureus)o Nosocomial/Immunosuppressed (Pseudomonas)o Red
flags present (Fungal) * ?? �Labs: Nasal swab & Cultureo If failure to improve or
worsening on Abx??needle aspiration of maxillary sinus with culture * ?? �Imaging:
CT sinuses (sinus opacification, mucosal thickening, air fluid levels) * ?? �Dx:
clinical presentation o Acute: persistent symptoms >10 days; severe symptoms, fever
>102, face pain >3 days; worsening symptoms >5days following viral URI * ?? �Tx:
Amoxicillin-clavulanic acid, short course (<3 days) decongestants, and
NSAIDs/Acetaminophen o Failure to improve should prompt aspiration & susceptibility
testing for change of Abx 3326/4845/8784: Pre-septal (Peri-Orbital) vs Orbital
Cellulitis * ?? �Risk Factors: sinus infection is the biggest risk factor via local
spread of infection * ?? �Presentation: these diseases differ only in a slightly
different location (superficial vs deep to the orbital septum) and are often
confused. Unfortunately, they have VERY different clinical courses. Either of these
can result from existing infection or local trauma. o Common: eyelid
edema/erythema/tenderness, fever, leukocytosiso Pre-septal: (no additional
features)o Orbital: opthalmoplegia, pain with extraocular movements +/- proptosis &
vision impairment (blurry vision or diplopia)??blindness, subperiosteal abscess,
cavernous sinus thrombosis, intracranial infection, or death! * ??
�Pathophysiology: concern in orbital cellulitis is due to the valve-less ophthalmic
venous system which may allow infection to spread to the skull/braino Nasofrontal
vein/anterior ethmoid vein/lacrimal vein??superior ophthalmic vein o Posterior
ethmoid vein??inferior ophthalmic vein ???Superior/inferior ophthalmic veins??
cavernous sinus??brain * ?? �Micro: S.aureus, Strep.
pneumo, or other Strep spp. * ?? �Imaging: CT of eye orbits used if
differentiating the two is unclear * ?? �Dx: clinical presentation +/- CT of eye
orbits * ?? �Tx: o Pre-septal: outpatient oral Abxo Orbital: admission with IV abx
& close monitoring 2196/2845/3288/3289/4891: Epiglottitis ?? Presentation: o
Prodrome: URI (cough, congestion, rhinorrhea)o Airway compromise:
restlessness/anxiety, muffled �hot-potato� voice, �cherry red� epiglottis,
stridor/trouble breathing, dysphagia, drooling, �tripod� positioning
(upright/forward positioning with neck hyperextension)o Most commonly occurs in
unvaccinated children (didn�t get the Hib vaccine), however vaccinated children can
still contract the disease * ?? �Pathophysiology: acute inflammation of the
epiglottis/arytenoids/aryepiglottic folds * ?? �Micro: Haemophilus influenza (type
b) or S.pyogenes (less common) * ?? �Imaging: lateral neck X-ray showing
�thumbprint sign� (epiglottic swelling) * ?? �Dx: clinical presentation +/- imaging
* ?? �Tx: o Offer humidified O2 (while waiting on intubation) + avoid airway
distress (no tongue depressor) o Immediate endotracheal intubation (protect airway
before it closes)o Abx (based on most likely pathogen); if H.flu rifampin
prophylaxis for family members needed 2424/3288: Laryngotracheitis (Croup) * ??
�URI causing acute inflammation of the trachea/larynx; commonly in fall/winter
months * ?? �Presentation: low pitched "barking/seal-like" cough, stridor,
hoarseness, and trouble breathing worse at night/when excited/with exercise o Most
commonly occurs between age 6mo � 3yro May result in upper airway obstruction
(prominent stridor, respiratory distress) from subglottic edema and intercostal
retraction on inspirationo Spasmodic Croup: significant stridor/difficulty
breathing only at night (better in daytime) with croup-like symptoms; often
relieves itself after onset * ?? �Micro: parainfluenza virus o May be spasmotic
(not caused by infection), but instead due to nighttime laryngospasm * ?? �Imaging:
A-P/lateral neck X-ray showing steeple sign (sub-glottic edema/stenosis) * ?? �Dx:
presentation +/- imaging * ?? �Tx: single dose of dexamethasone, either orally or
intramuscularly, is appropriate to shorten disease course, reduce croup scores and
shorten hospital stays. Prolonged courses of corticosteroids provide no additional
benefit. o Try to avoid irritating procedures (use of a tongue blade) unless
necessaryo If upper airway obstruction present, aerosolized racemic epinephrine
should be added (mucosal arteriolar constriction) and demonstrable improvement must
be shown for discharge o Intubation may be necessary if improvement does not occuro
Spasmodic croup often treated with cool mist in the evenings to sooth the throat
(classically child is exposed to �cool night air� and relief is noted) 3288/3553:
Bronchiolitis * ?? �Acute inflammation of the lower respiratory tract (bronchioles)
* ?? �Presentation: fever, cough wheezing, labored breathing without improvement
with bronchodilators; spleen/liver may seem enlarged due to lung hyperinflationo
Onset age <2 years; may be recurrent, since an infection does not provide immunity
o Often epidemics occur during November - Aprilo Typically, illness takes 10 days �
2wks to resolve entirely (2 day prodrome??3 day respiratory distress??up to 2wk
alternating OK/distress??resolution) o Complications: ???Neonates (<2mo): apnea
spells & respiratory failure ???Children: wheezing past age 5 (10%) &
predisposition to asthma. * ?? �Imaging: CXR (hyperinfiltration/air trapping,
patchy infiltrates of atelectasis) * ?? �Micro: respiratory syncytial virus (RSV) *
?? �Dx: clinical presentation, ruling out life threatening problems * ?? �Tx:
supportive care (O2 supplementation, IV fluids) +/- bronchodilator treatment if
helpful o Typically, a trial of an inhaled albuterol, with treatment continued only
if the initial dose proves beneficial is recommended o Aerosolized ribavirin may be
considered in very sick infants o Corticosteroids, antibiotics, and decongestants
are of no benefit?? Prevention: palivizumab (anti-RSV monoclonal antibody) for
infants with 1preterm birth <29wk, 2chronic lung disease of prematurity, or
3hemodynamically significant congenital heart disease
2869/3007/3131/3444/3611/4354: Infectious Mononucleosis (Epstein-Barr virus)�
Presentation: fever, malaise, lethargy, lymphadenopathy (tonsillitis, swollen
cervical lymph nodes, swollen eyelids), tonsillar exudate, +/- hepatosplenomegalyo
Complications: acute airway obstruction (intense tonsillitis), peritonsilar abscess
(superinfection), post-Abx rash after (amoxicillin or ampicillin;
polymorphous/macropapular pruritic rash covering entire body; poorly understood
mechanism; not considered a true allergy, pt may take these drugs in future without
any concerns) o Initial HIV infection can look similar but will be fever, malaise,
lymphadenopathy, diarrhea, and rash??it�s actually reasonable to test for HIV if
monospot is negative o Autoimmune hemolytic anemia/thombocytopenia is a
complication of EBV-mono from EBV- antibodies (IgM cold-agglutinin anti-I
antibodies) cross-reacting with RBCs/platelets. Occurs approximately 2-3 weeks post
infection o Nasopharyngeal carcinoma/Burkitt�s lymphoma both can we caused by EBV �
Dx: heterophile antibody (monospot) test; Anti-EBV antibody test o Monospot has 25%
false negative on first week of disease & poor sensitivity in children <4yr of age;
viral capsid antigen (VCA), early antigen, & Epstein-Barr nuclear antigen (EBNA)
are preferred in children <4yr (antibody formation isn�t reliable) o Smear showing
variant lymphocytes with convoluted nuclei and vacuolated cytoplasm o Transient
hepatitis (elevated transaminases)� Tx: rest and avoidance of strenuous activities
for >3weeks after onset (risk of splenic rupture) o If acute airway obstruction:
inhaled corticosteroids (decreased inflamed tonsils) o Splenic rupture: abdominal
pain and anemia 2270: CMV mononucleosis-like syndrome� Presentation: mono symptoms
(fever, fatigue, myalgias, arthalgias), no pharyngitis/lymphadenopathy. o Negative
heterophile antibody (monospot) test o Atypical lymphocytes (large, basophilic,
with vacuolated appearance) * Dx: clinical presentation * Tx: ganciclovir 4317: Cat
Bites * ?? �Pathophysiology: due to their long/sharp teeth, cat bites can easily
deposit bacteria deep into the dermis, resulting in an increased risk for infection
& soft-tissue structural damage (nerve, tendon, etc.) * ?? �Micro: Pasturella
multocidia, anaerobic bacteria * ?? �Tx: copious irrigation/cleaning + prophylactic
amoxacillin/clavulanic acid (activity vs the two most common bugs) + tetanus
booster (if last dose >5yr ago) + avoidance of closure (allow for drainage) 11984:
?? Presentation: Hx of cat scratch/bite or flea bite with papule/nodule at site??
fever of unknown origin (>14 days), localized lymphadenopathy starting 1-2wk
following initial presentation o Kittens have a higher incidence of carrying this
disease * ?? �Dx: clinical presentation +/- serology * ?? �Tx: azithromycin
(reduced duration of lymphadenopathy) 3002/4814: Human Rabies * ?? �Presentation:
hydrophobia/aerophobia (causes involuntary pharyngeal muscle spasm), agitation,
aggression, disorientation, spastic paralysis??ascending flaccid paralysiso
Incubation time of 1-3mo; near 100% mortality once symptoms arise * ?? �Pathophys:
virus binds nACh receptors, enters into neurons moving retrograde via the dorsal
root ganglion into the Purkinje/pyramidal cells of of the hippocampus o
Transmissionisfromsalivafrominfectedanimalbite(bat>>>fox,skunk,raccoon) o Often bat
bites are small & go unnoticed; pt may have Hx of caving or camping * ?? �Micro:
rhabdovirus * ?? �Dx: clinical presentation * ?? �Post-exposure Prophylaxis (PEP) �
Thorough cleansing of the wound (reduce risk by 90%) + Rabies vaccine (if person
hasn�t gotten it before) + passive immunization (human rabies Ig) o High risk wild
animal bite � includes bat, fox, raccoon, coyote, skunk ???If animal unavailable
start PEP ???If animal available; euthanize it/test for rabies??PEP if positiveo
Low risk animal bite � squirrel, chipmunk, mouse/rat, rabbit??No PEPo Pet � if a
pet (usually a dog) DOES have rabies, they�ll show signs within 10 days ???If
available for quarantine??observe 10 days??if shows signs of rabies, euthanize pet
and do PEP immediately ???If not available for quarantine??start PEPo Livestock or
unknown wild animal � call the health department 2857/3329/3660/3758: Neonatal
Conjunctivitis * ?? �Chemical (<24hr) � mild conjunctival irritation and tearing o
Pathophys: irritation from any chemical; classically follows routine silver nitrate
prophylaxis o Tx: eye lubricant/supportive care * ?? �Gonococcal (2-5 days;
N.gonorrhea) � severe swelling/chemosis (conjunctival injection), profuse purulent
discharge??corneal edema, ulceration??scarring/blindness o Pathophys: inoculation
by infected vaginal secretions during birth; while moms are screened, most cases
occur with moms that become infected during their pregnancyo Dx: gram stain +
culture on Thayer-Martin agar of eye secretionso Tx: IM injection of 3rd gen
cephalosporin (ceftriaxone/cefotaxime)o Prophylaxis: erythromycin ointment on the
eyes (for all babies in the US) or silver nitrate Cat-Scratch Disease (Bartonella
henslae) (babies in other countries; concern of chemical conjunctivitis) ??
Chlamydial (5-14 days; C.trachomatis) � mild swelling/chemosis, discharge ranging
from watery, serosanguinous, or purulent??corneal edema, ulceration (Trachoma)??
scarring/blindness o Pathophys: inoculation by infected vaginal secretions during
birth; while moms are screened, most cases occur with moms that become infected
during their pregnancy o Dx: PCR
of eye secretions for C.trachomatiso Tx: oral macrolide (azithromycin preferred;
erythromycin linked with pyloric stenosis!) to kill off eye and nasal colonization
(worry of Chlamydia pneumonia!) Childhood Conjunctivitis 2857: Trachoma * ??
�Presentation: eye swelling/chemosis with follicular conjunctivitis (clusters of
follicles on the eye) & pannus formation (neovascularization of the cornea)o
Typically occurs with concurrent nasopharyngeal infection (persistent runny nose) o
The #1 cause of blindness worldwide (repeated infections??scarring) * ?? �Micro:
C.trachomatis serovar Type A/B/C * ?? �Dx: PCR for C.trachomatis or Giemsa stain of
eye secretions * ?? �Tx: topical tetracyclines or oral azithromycin 2428: Neonatal
Sepsis ?? Presentation: often subtle, most commonly with early decreased
activity/poor feeding (esp. <28d old) o Other signs: Temperature instability
(hypothermia or fever), abnormal white count (high or low), left shift
(�bandemia�), jaundice, CNS disturbance (lethargy/irritability/apnea) o Because it
can be subtle & lack the common presenting signs, sepsis/serious infection should
always be high on the differential for neonates! * ?? �Labs: CBC, blood
smear/culture, CSF analysis/culture, urinalysis/cultureo CT is not needed prior to
neonatal LP as the open fontanelles will simply budge with increased intracranial
pressure, stopping post-LP herniation * ?? �Dx: presentation + labs * ?? �Tx:
parenteral empiric abx (gentamicin + ampicillin) after cultures drawn o If neonate
is critically ill, do not wait for cultures and give Abx 9849/SkM: Coxsackie
Viruses * ?? �Both viruses commonly come around in summer months (classically
around when school is starting up) & affects kids ages 3-10yr * ?? �Coxsackie-A o
Herpangina: fever, pharyngitis, grey vesicles/ulcers on tonsillar pillars/posterior
oropharynx o Hand-Foot-Mouth Dx: (+)red vesicular rash of hands/feeto
Asepticmeningitis:typicalmeningitissigns/symptomsfromprogressionofDx * ??
�Coxsackie-Bo �Devil�s Grip�: extreme unilateral throat pain causing difficulty
breathingo Dilated cardiomyopathy: often signs of heart failure with characteristic
imaging * ?? �Dx: clinical presentation * ?? �Tx: supportive care (may need
hospitalization & intense support if severe) 9849: Herpetic Gingavostomatitis * ??
�Presentation: fever, pharyngitis, inflamed gingiva, clusters of small vesicles
(dew-drops on rose petal) of the anterior orophaynx/lipso No seasonality; typically
presents in children aged 6mo � 5yr * ?? �Micro: HSV-1 * ?? �Dx: clinical
presentation +/- Tzank smear or PCR testing * ?? �Tx: oral acyclovir
3243/3257/3261/3636/3836/3900: Lyme disease (Borrelia Burgdorferi from the Ixodes
Scapularis tick) ?? Presentation o Early local (days � 1 month): erythema migrans,
fatigue/malaise, mild headache, neck stiffness, myalgias/arthralgias o Early
disseminated (weeks � months): Heart (5%, AV-block, cardiomyopathy); CNS (15%,
uni/bilateral Bell�s palsy, meningitis, encephalitis); Muscle (60%, migratory
arthralgia), Eye (10% conjunctivitis), Skin (multiple erythema migrans!), regional
lymphadenopathy o Late (month � years): Muscle (60%, migratory polyarthritis), CNS
(encephalomyelitis, peripheral neuropathy) * ?? �Labs: synovial fluid aspiration
(if joint involvement; leukocytosis, negative gram stain, PCR for BB DNA, ELISA for
BB DNA, or Western blotting for BB DNA) * ?? �Dx: Labs + clinical presentation
following tick bite (25% report this) or travel to Lyme Endemic Area (New England
or Minnesota/Wisconsin areas) o Classically occurs with hiking & direct contact
with leaf litter/plants harboring ticks ?? Tx: o Oral Doxycycline � first line;
good as it kills B.burgdorferi AND anaplasmosis (another tick borne illness); bad
as it can cause teratogenic mental retardation and teeth discoloration ???Bell�s
Palsy: artificial eye drops and eye patching at night are recommendedo Oral
amoxicillin � for pregnant women and children <8yrs (concern for doxycycline
toxicity) o IV ceftriaxone/cefotaxime � for disseminated dx, heart block, or
meningitis caused by Lyme Disease; hospitalization required to administer 4662: To
prevent infection with Lyme Disease (B.burgdorferi), any person with a tick
attached to their skin should immediately remove the tick by taking tweezers,
pinching as close to the skin as possible, and gently remove the tick with upward
pressure. * ?? �Prevent tick attachment with tick repellants, protective clothing,
tick checks, and bathing * ?? �Removal of the tick in <24 hr has a low transmission
rate even if the jaw/head are attached * ?? �Pt should seek medical attention if
erythema migrans rash pops up * ?? �Pt should receive doxycycline (or other
appropriate abx) prophylaxis if they meet ALL 5 criteria: o Tick is ixodes
scapulariso Tickattachedfor>36hrsandengorgedo Prophylaxis can be initiated with
72hr of tick removalo Local Lyme disease infection rate is >20% (endemic area)o No
doxycycline contraindications (pregnancy, breastfeeding, <8yrs old) 3005/3571:
Causes of Osteomyelitis in Children * ?? �<2mo: GBS/E.coli * ?? �2mo � 4yr:
Kingella kingae * ?? �>4yr: S.aureus ?? Sickle cell: Salmonella spp./S.aureus
2447/3577: Septic Arthritis in Children * ?? �Presentation: acute onset fever/joint
pain, fatigue/malaise, absolute refusal to bear weight on affected joint, pain with
active/passive movement, swollen joint with erythematous/warm overlying skino Often
preceded by skin infection or URI (hematogenous spread of bacteria into joint
space) o Complications: rapid/permanent joint destruction (4-6hr can result in
this!)o If joint fluid is sterile, consider transient synovitis * ?? �Labs: CBC
(elevated WBCs), blood culture, ESR/CRP (elevated), synovial fluid culture (below)o
Normal synovial fluid � clear, <200 WBCs, <25% neutrophilso Non-inflammatory (OA) �
clear, 200-2000 WBCs, 25% neutrophilso Inflammatory (crystals/RA) � translucent or
opaque, 2000-100,000 WBCs, >50% neutrophils o Bacterial infection � opaque or
purulent, >50,000-150,000 WBCs, >80% neutrophils * ?? �Micro: <3mo (Staph spp, GBS,
gram negative bacilli); >3mo (Staph spp, GAS, Strep. pneumo) * ?? �Imaging:
Ultrasound of joint to assess for joint effusion (if effusion present...tap it!) o
MRI of joint if pt fails to improve after 48hr of Abx (concern for osteomyelitis)o
Pain radiograph of the hip isn�t helpful for Dx, but may help in ruling out other
hip problems that may present with similar symptoms * ?? �Dx: arthrocentesis with
synovial fluid culture * ?? �Tx: Immediate surgical drainage + IV empiric Abx
(shown below) switching to targeted once susceptibilities are available given
immediately after arthrocentesiso <3 mo: anti-staph (nafcillin or vancomycin) + GNR
coverage (gentamicin or cefotaxime)o >3mo: nafcillin, clindamycin, cefazolin, or
vancomycino Surgical drainage/debridement/irrigation = most important factor in
preventing disability 3441/3671/4833: Causes of Meningitis in Children ?? Bacterial
o <3mo: GBS > E.coli (gram neg. bugs) > L. monocytogenes > Herpes simplex (HSV) o
3mo � 10yr: S.pneumoniae > N.meningitiso >11yr:N.meningitis ?? Viral: non-polio
enteroviruses (echovirus/Coxsackie virus) 2442/3441/3442/10904/SkM: Neisseria
meningitides (�meningococcus�) * Gram (-), doughnut-shaped diplococcus; un-
encapsulated * At risk populations: o Infants aged 6mo � 2 yrs - this is the time
frame where mom�s antibodies to the bug are no longer present in the baby, and it
hasn�t had a chance to make it�s own yet o College freshman/army recruits/inmates -
lots of people getting crammed together in an dorm/army barrack often will share
their strains...which can make some sick o People with C5,6,7,8,9 compliment
deficiency - all needed to form the MAC complex which is necessary for killing
Neisseria spp. Diseases it Causes * Meningococcemia - entry of the meningococcus
into the blood causing acute illness o Abrupt spiking fevers, chills, joint/muscle
pain, petechial rash o Worry of acute illness spreading through the body/into the
CNS causing further disease * Fulminant meningococcemia (Waterhouse-Friderichsen
syndrome) - septic shock from infection o Bilateral hemorrhage into the adrenal
glands??adrenal insufficiencyo Widespread inflammation??
hypotension/tachycardia/large petechial rash o DIC/coma may occur with progression,
with death following soon after (near 100% mortality) � Meningitis - entry of
meningococcus to the CSF, often following meningococcemia o Young Infants - ever,
vomiting, irritability, lethargy, bulging fontanelleo Older Kids - fever, vomiting,
photophobia, irritability, lethargy, stiff neck (older), Kernig sign (back/neck
pain with flexion of hip??extension of knee), Bruzinki�s sign (flexion at the knees
with passive flexion of the neck)o Adults - fever, vomiting, photophobia,
irritability, lethargy, stiff neck, Kernig/Brudzinki�s signs petechial rash
(specific for gonococcus) o CSF findings: ???Neutrocytosis - chemotactic response
to infection???Reduced glucose levels - host stress response to limit energy
substrates from bacteria ???Elevated protein - BBB breakdown to allow for
chemotaxis o Complicationsinchildren:???Hearing loss (most common), intellectual
disability, cerebral palsy, epilepsy, visual loss (rare, typically in occipital
lobe infection)???All children with bacterial meningitits should have followup
developmental and audiologic testing Diagnosis * Often strong suspicion should
prompt immediate empiric treatment * Gram-stain/culture on Thayer-Martin VCN (A
chocolate agar with Vancomycin, colistin, nystatin) or rapid antigen test for
pathogenic N.meningititis strains * Maltose/glucose fermentation (specific for
N.meningititis) Vaccine * ?? �First time age 11 � 12 * ?? �Booster age 16 � 21 * ??
�High risk: college dorm, military
recruit, living in sub-Saharan Africa, Muslum Hajj to Mecca 3245/3633: Empiric
Treatment for Meningitis * ?? �Make the Diagnosis or Immediately treat? o If child
is sick but stable: LP for CSF analysis first; treat upon confirmation of infection
o If child is unstable: initiate IV Abx with stat LP for CSF analysis * ?? �Empiric
Treatment options o Age <2: vancomycin + ceftriaxone/cefotaxime + ampicillin
(Listeria coverage!)???Cefotaxime better in neonates (won�t displace bilirubin from
albumin mitigating the risk for induced hyperbilirubinemia & kernicterus)o Age 2-
50: vancomycin + ceftriaxone/cefotaximeo Age 50+: vancomycin +
ceftriaxone/cefotaxime + ampicillin (Listeria coverage!)o Recent
Neurosurgery/shunt: vancomycin + cefepime (4th gen cef)o Penetrating injury to
skull: vancomycin + cefepimeo Immunocompromised: vancomycin + cefepime + ampicillin
o Note that all regimens should also treat with dexamethasone or methylprednisolone
(decreases risk of sensoneurial hearing loss) 4833/Neuro: CSF Fluid Analysis * ??
�Normal: clear fluid; glucose is 2/3 of blood glucose; 40-50mg/dL of protein; <5
WBCs per mm3 with lymphocyte predominance; Opening pressure 60-150 mm H2O in fetal
position * ?? �RBC presence: o No xanthochromia: traumatic tap (may be some in
first few samples of CSF) o Xanthochromia: yellowish discoloration of spun CSF
supernatant due to lysed RBCs in the sample from in vivo bleeding into the CSF * ??
�Positive EBV on PCR: strongly suggests CNS lymphoma in immunosuppressed/AIDS
patients * ?? �14-3-3 protein: specific for Creutzfeldt-Jakob disease Disease Cell
Protein Glucose Other Findings Bacterial Meningitis PMNs (neutrophils) High Low
Culture/Gram stain may be positive Viral meningitis /Encephalitis Lymphocytes
Normal - High Normal Viral PCR may be positive TB meningitis Lymphocytes Very High
Very low Acid-fast bacilli positive Guillain-Barre syndrome Normal Normal - High
Normal Multiple Sclerosis (MS) Lymphocytes Slight increase Normal Oligoclonal Bands
may be present Acute Disseminated Encephalomyelitis PMNs (neutrophils) or
lymphocytes High Normal Ologoclonal Bands often absent (differentiates from MS)
Subarachnoid Hemorrhage Lymphocytes or many RBCs Normal - High Normal Xanthochromia
3458/3905/3906: Pertussis (Bordatella Pertussis; Whooping Cough; �100 Days Cough�)
* ?? �Small Gram(-) coccobacilli; encapsulated * ?? �Presentation: occurs in three
stages of disease o Catarrhal:mildcough/rhinitis/conjunctivalbleeding(1-2wk)o
Paroxysmal: worsening cough with classic inspiratory �whoop� & post-tussive emesis
(2-6wk) +/- weight loss (vomiting); worsens with exercise/laughing/smoke/steam/at
night o Convalescent: slow resolution of symptoms (weeks-months)o Children <6mo:
present with apnea and risk of sudden death! * ?? �Labs: CBC (leukocytosis with
lymphocyte predominance) * ?? �Dx: clinical presentation +/- nasopharyngeal swab
for culture or PCR * ?? �Tx: early Macrolides (azithromycin/clarithromycin/etc) +
respiratory isolation o If given in catarrhal stage??faster resolution; if after
catarrhal stage??decrease transmission o Anti-tussivesareNOTrecommended * ?? �Post-
exposure prophylaxis: even with proper vaccination, pertussis can still spread to
close contacts. Thus, all close contacts should receive Abx prophylaxis with
macrolides o <1mo: azithromycin (5 day course) ???Erythromycin associated with
pyloric stenosis; clarithromycin is not studied in neonates o >1mo: azithromycin (5
days), clarithromycin (7 days), or erythromycin (14 days)o If any contacts are out
of date with their vaccines, they should also receive proper vaccination * ??
�Vaccines: o DTaP: 5 doses from, early childhood � age 6o Tdap: one dose every 10yr
starting in adolescence & during any pregnancyo Waning Immunity: neither vaccine
confers lifelong immunity (thus the large number of boosters); classically
teens/adults who have not received their Tdap are at risk 3788: Neonatal Tetanus
(Clostridia tetani)?? Gram(+) spore-forming cocci classically found in soil & rusty
nails ?? Presentation: classically occurs in children with unhygienic delivery or
poor cord care practices (may have infection of the cord stump in addition to
tetanus) o Jaw muscle contraction = trismus (lock-jaw)??difficulty feedingo Facial
muscle contraction = risus sardonicus (a creepy looking locked grimace)o Extensor
back muscle contraction = opisthotonos (pronounced arching of the back), clenched
hands & dorsiflexed feet can also occuro Exaggerated reflexes = easier to stimulate
response of muscleso Diaphragm contraction = respiratory failure (most common cause
of death) ?? Pathophysiologyo Result of tetanus toxin (tetanospasmin)o Enters at
the NMJ end plate and is retrograde transported to the motor gangliao Binds tightly
to ganglioside receptors on Renshaw cell interneurons to block glycine/GABA
(inhibitory) via cleaving SNARE proteins needed for their release??dis-inhibition
of lower motor neurons causing tonic muscular contraction (tetany) * ?? �Dx:
clinical history/presentation * ?? �Tx: supportive care + wound debridement +
Tetanus Ig (passive immunity) + Abx (penicillin) * ?? �Vaccination: o DTaP: 5 doses
from, early childhood � age 6o Tdap: one dose every 10yr starting in adolescence &
during any pregnancyo Waning Immunity: neither vaccine confers lifelong immunity
(thus the large number of boosters); classically teens/adults who have not received
their Tdap are at risk 3423/3675/SkM: Malaria (Plasmodium spp; Anophales mosquito
transmission)?? Presentation: cyclical fevers with non-specific symptoms (malaise,
headache, N/V, diarrhea, jaundice, hepatosplenomegaly, myalgia, pallor, anemia,
petechiae)o Cyclic fevers have three stages: cold (chills, shivering; incubation),
hot (high fever, with RBC lysis and spread of parasite); wet (sweating/resolution
of fever with re-infection) ???P.vivax/P.ovale: Q3 fever (every 48hr)???
P.Falciparum: irregular fever pattern; banana-shaped on blood smear???P.malariae:
Q4 fever (every 72hr) o Child complications: cerebral malaria (headache, seizure,
coma), hypoglycemia, acidosis o Adult complications: acute renal failure, pulmonary
edema * ?? �Dx: thin/thick peripheral blood smear + Giemsa stain showing Plasmodium
o Typically, travelers who did not adhere to chemo-prophylaxis will contract
malaria even with proper protective gear * ?? �Tx/Prevention: o Anti-malarial
drugs: atorvaquone-proguanil, doxycycline, mefloquine, chloroquine,
hydroxychloroquineo Insecticides & mosquito nets (stop bugs from biting)o Sickle-
Cell (sickled RBCs disrupt normal reproduction of Plasmodium spp) 3259: When
traveling to a malaria endemic region two things must occur: minimize mosquito
exposure and malaria prophylaxis depending on the region. P.falciparum is a bitch
and will dictate your prophylaxis. * ?? �Chloroquine resistant P.falciparum
(Brazil, Sub-saharan Africa/South, Southeast Asia) o Atoraquinona-proguanil o
Doxycycline o Mefloquine (weird dreams and good in pregnancy) * ?? �Choloquine
susceptible areas: o Chloroquine/hydroxychloroquine 1-2 weeks in advance o Any
agents that work with chloroquine resistant P.falciparum?? Areas without
P.falciparum (Mexico/central America/Southern South America/Korea o Primaquine
(will cause crisis in G-6PD deficient pts) 3612/3791: Pinworm (Enterobius
Vermicularis) * ?? �Presentation: nocturnal perianal itching (pruritis ani) o
Additional symptoms: Vulvovaginitis (in prepubescent girls), abdominal pain, N/V o
Commonly occurs in school-aged children * ?? �Pathophysiology: parasite worms live
in the cecum/appendix, but migrate to the anus to deposit eggs in the perianal
region at night (hence the itching)o Transmission from contaminated
objects/unwashed hands after scratching the butthole * ?? �Dx: �tape test�
(application of clear tape to the perianal region at night/in morning??microscopic
visualization of pinworms/eggs) * ?? �Tx: albendazole + household prophylaxis with
pyrantel pamoate 4186: Varicella-Zoster virus (Chicken Pox) ?? Presentation:o
Complications: pneumonia, cerebellar ataxia, superimposed skin infectionso Airborne
transmission thus extremely contagious (90% develop if exposed & not immune) * ??
�Vaccine: VZV vaccine (2 doses at 1yr & 4yr; live attenuated) * ?? �Post-exposure
Prophylaxis: o Child >1yr, not immune, & exposed within last 5 days: simply receive
VZV vaccine doseo Exposed Child <1yr outside neonatal period: reassurance (low risk
of dx development)o Pregnant, immunocompromised, or signs/symptoms 5 days before �
2 days after birth of child: varicella immunoglobulin (within 10 days of
recognition) 3670: Infantile HIV/AIDSo Presentation: FTT, chronic diarrhea,
generalized lymphadenopathy, severe opportunistic infections (PCP pneumonia,
candida, etc.)o Risks include high maternal viral load (most important) &
breastfeeding by infected mother o Transmission typically during delivery, but may
be transplacental o Labs: CBC (normal absolute lymphocyte count with deficient CD4+
cells)o
Thenormallymphocytecountcanalsodifferentiatethisfromimmunocompromisedsyndromes o
Dx: DNA PCR of fetal blood for maternal anti-HIV antibodies or HIV anti-body
presence after 18mo o Tx: HAARTo Prevention: maternal screening with anti-
retroviral therapy for mom & immediately for baby 3969: Scarlet Fever??
Presentation: fever, chills, sandpaper rash (punctate/diffuse over neck/trunk;
desquamates into fine scales) with Pastia�s lines (petechiae localized to skin
creases), strawberry tongue, circumoral pallor (pale perioral region with red
cheeks), & bacterial pharyngitis symptoms (sore throat, dysphagia, odynophagia,
pharyngeal/tonsillar erythema, grey-white tonsillar exudates) o Can follow any
Strep. pyogenes infection (pharyngitis or
wound/burn/skin infection) o Incubation time of 1 � 7 days & most often occurs in
winter/spring???Micro: Caused by GAS (Strep. pyogenes) that have acquired
erythrogenic toxin ?? Dx: ?? Tx: ???Dx: clinical presentation + rapid response to
penicillino Must be differentiated from Kawasaki�s disease, which often features
bilateral conjunctival injection, peripheral extremity changes, or no response to
penicillin ???Tx: Penicillin V (preferred) o If allergic to penicillin:
Clindamycin, erythromycin, or 1st gen cephalosporins 2712/3443/3874/4836: Acute
Rheumatic Fever?? Presentation: symptoms of the JONES criteria with Hx of Strep
throat o Most common in girls age 5-15yro Typically occurs a few weeks after a GAS
pharyngitis (strep throat)o Mitral stenosis/regurgitation: a late complication
presenting as Hoarseness/cough (compression of recurrent laryngeal), elevation of
left mainstem bronchus on CXR, and atrial fibrillation (abnormal conduction through
stretch fibers)o Aortic stenosis and left heart failure/pulmonary HTN may also
occur more rarely * ?? �Pathophysiology: Antibodies formed from infection cross-
react with host antigens (notably in the valves of the heart) due to molecular
mimicry. �Incubation time� is for antibodies titers to build * ?? �Labs: ASO titer,
Anti-DNase titer, Anti-hyaluronidase titer * ?? �Dx: o JONES major criteria o ???�J
� joint pain from migratory polyarthritis o ???�? � pancarditis initially with
mitral/aortic valve damage over years o ???�N � nodules in the skin (often firm,
but painless) o ???�E � erythema marginatum (rash with central clearing a distinct
thin red border) o ???�S � Syndenham�s chorea (�St. Vitus�s Dance�; basal ganglia
damage; chorea/emotionally labile may be part of the picture!) o ???�An ASO titer
being high can also be helpful to confirm diagnosis o JONES minor criteria???Fever,
arthralgia, elevated ESR/CRP, or prolonged PR interval * ?? �Tx: prophylactic IM
benzathine penicillin G (eliminate S.pyogenes pharyngitis to limit antibody
formation) every 4 weeks for a length of time depending on situation: o Rheumatic
fever without endocarditis??5yr or till age 21 (whichever is longer)o
Rheumaticfever+endocarditis,butnoresidualheart/valvulardiseaseonechocardiography???
10yr or till age 21 (whichever is longer)o Rheumatic fever + endocarditis +
persistent heart or valve damage??10yr or till age 40 (whichever is longer)??
Prevention: treat all cases of Strep Throat with Penicillin V 2241: Post-
Streptococcal Glomerulonephritis * ?? �Autoimmune disease in response to a GAS
throat/skin infection occurring 10-20 days post-infection. Classically happens in
kids and young adults; rare before age 2yr o Rarely may be caused by HIV or Hep B *
?? �Presentation: Fever, rash, arthralgia, periorbital edema, hypertension, �tea-
colored urine�, Hx sore throat or impetigo o Urine: oliguria, proteinuria,
hematuria, sterile pyuria, eosinophiluria, WBC casts o Blood: eosinophilia, low
serum C3 compliment levelso Biopsy: sub-epithelial humps due to complement
deposition * ?? �Micro: �nephrtiogenic strains� of GAS (carry M-protein) * ?? �Dx:
clinical presentation with elevated ASO titer or anti-DNase B (ADB) antibodies +/-
renal biopsy o Light microscopy (H&E) � glomeruli enlarged with endocapillary
proliferation. Also hypercellular with neutrophils o Immunofluorescence � �starry
sky� or �lumpy bumpy� granular appearance from IgG, IgM, and C3 desposition in GBM
and mesangium o Electron microscopy � sub-epithelial �humps� originating from
conglomeration of subendothelial complexes. Will progress into the urinary space
and dissipate ?? Tx: supportive care, should resolve on its owno Prognosis good in
children but very bad in adults often leading to renal failure 3742: Toxic Shock
Syndrome * ?? �Bacterial infection (S.aureus most common; GAS is less common) with
Toxic-Shock Toxin-1 (TSST-1), a super-antigen that results in massive T-cell
activation/cytokine release, resulting in loss of intravascular fluids to the
extravascular spaces and shock! * ?? �Presentation: rapid development of high
fever, Hypotension (<90 systolic), diffuse red/edematous rash (looks like sunburn),
skin desquamation of palms/soles, multisystem failureo Classically (50%) associated
with a tampon left in post-menstruation, typically arising 2-3 days after the last
menstrual period o Non-menstrual infections can also cause it (post-surgery,
sinutitis, etc) * ?? �Dx: clinical syndrome with history * ?? �Tx: supportive
therapy for shock, removal of foreign materials causing infection, anti-staph
(penicillin + vancomycin) are all part of treatment 2431/2782/3077/SkM: Measles
(�Rubeola�) ?? Presentation: prodrome (1-3wk post exposure) ???exantherm ???severe
dx o Prodrome: fever, cough, coryza (rhinitis), conjunctivitis, Koplik spots
(irregular red spots on buccal mucosa with white-blue centers) o Viral Exantherm:
blanching red-brown macropapular cephalocaudal spread; spares palms/soles o Severe
Dx: pneumonia (most common cause of death), subacute sclerosing panencephalitis,
blindness, gastroenteritis * ?? �Dx: clinical presentation + anti-measles antibody
titers (IgG/IgM x4 rise) * ?? �Tx: supportive care + Vitamin A (promotes immune
response; often used in hospitalized pts, infants, pregnant women, elderly) * ??
�Vaccine: MMR vaccine (1yr & 5yr doses) * ?? �Prevention: airborne transmission
(most contagious during prodrome) means suspected cases should be under airborne
precautions (negative pressure room + N95 facemask for healthcare workers) 3009:
Mumps * ?? �Presentation: fever/malaise??parotitis (painful swelling at angle of
the jaw), orchitis (painful swelling of testicles post-puberty??infertility), &
aseptic meningitis (headache, fever, nuchal rigidity) * ?? �Dx: clinical
presentation +/- urine culture for Mumps * ?? �Tx: supportive care * ?? �Vaccine:
MMR vaccine (1yr & 5yr doses) 3663/SkM: Rubella (�German Measles�) ?? Presentation:
may present or could be asymptomatic in children/adults o Congenital: FTT,
sensoneurial hearing loss, cataracts, patent ductus arteriosus (continuous machine-
like murmur), microcephaly, blueberry muffin rash, bone lesions, thrombyctopenia o
Children: fever, occipital/auricular lymphadenopathy, cephalocaudal macropapular
rash o Adults: fever, cephalocaudal spread of macropapular rash,
arthralgias/arthritis * ?? �Dx: serologic evidence via neonatal IgM titers * ??
�Tx: supportive care * ?? �Vaccine: MMR vaccine (1yr & 5yr doses) 3256/4852:
Congenital Syphilis ?? Presentation: o Symptoms occur within 2 years of age;
Infection occurs trans-placentally after 1st trimester (Prevented with Tx of mom in
1st trimester) o Early symptoms: �Snuffles� at birth (runny nose), Bullous rash
with desquamation, Snail track lesions/condylomata lata of mucous membranes at
birth, Hepato-splenomegaly o Late symptoms: Neurosyphilis (similar to adult
symptoms with CNVIII deafness), Eye infections (corneal inflammation causing �gun
barrel sight�) & Bone/teeth maldevelopment: ???Saddle nose � cartilage destruction
of palate/nasal septum???Saber shins � inflammation of the tibia leading to bowing
???Frontal bossing � inflammation of skull causing protrusion???Hutchinson�s Teeth
� widely spaced teeth with a central notch ???Mulberry molars � molars with too
many cusps ?? Dx: Clinical presentation + confirmatory testingo Non-treponemal
serologic tests (non-specific tests) * ???�Rapid Plasma Reagent (RPR) test � carbon
particles coated with cardiolipin mixed with patients serum to measure anti-
cardiolipin titers in patient serum via agglutiniation * ???�Venereal Disease
Research Laboratory (VDRL) test � similar to RPR but uses cardiolipin bound to
several different particles to help with visualization * ???�Cheap, sensitive, but
can have false positives * ???�Great test to measure decreasing titers to monitor
treatment o Treponemal Tests (specific tests)???Fluorescent Treponemal Antigen-
Absorption (FTA-ABS) test � non-pathogenic Treponema fixed to microscopic slide is
mixed with patient serum to removed cross- reacting antibodies to that non-
pathogenic strain. You then add the serum to another slide with killed Treponema
Pallidum, then add fluorescent dye-tagged anti-human Ig. Fluorescent visualization
is definitive. o Indirect dark-field microscopy of a sample from lesions can be
done to visualize the tiny, tiny spirochetes before antibodies are formed.
Visualization via refracted light is definitive. o Culture/gram stain is not useful
?? Tx (any stage) o First line: IM penicillin Go If allergic to penicillin: oral
doxycycline or ceftriaxone (3o only)o If pregnant and sensitive to penicillin:
desensitize??IM penicillin G in 1st trimester 2906: Vertical Transmission of
Hepatitis B * ?? �Any pregnant mom with HepB can pass it on to their child
(typically during birth, but may occur trans- placentally if infection occurs
during 3rd trimester)o Mom is HBeAg (-) � 20% chance of transmission overall o Mom
is HBeAg (+) � 95% chance transmission overall * ?? �Infantile Hepatitis B results
in chronic hepatitis in 90% of cases, thus all children of mothers with HepB should
receive HBIG (HepB Ig passive immunization) followed by HepB vaccine at birth
[click through all questions and snag the random/un-covered TORCHES infections]
Pregnancy/Childbirth/Puerperium 2485: Neonatal Clavicular Fracture * ?? �Risk
Factors: fetal macrosomia (>4000g, maternal diabetes, post-term pregnancy),
instrumental delivery (vacuum or forceps), shoulder dystocia * ?? �Presentation:
crying/pain with passive motion of extremity, crepitus over clavicle, asymmetric
Moro (weakness on affected side), pseudoparalysis (refusal to move from pain) o
Often child holds affected limb with opposite hand & tilts head away from injury o
Rarely may injure
 surrounding nerves or vessels * ?? �Pathophysiology: difficulty in birth often
places great force on the fetal shoulder, sometimes causing fracture/displacement *
?? �Imaging: X-ray showing fracture * ?? �Dx: presentation + imaging * ?? �Tx:
reassurance, gentle handling, analgesia, long-sleeve shirt with arm pinned to
chest/elbow at 90o o Fracture typically heals on its own in 7-10 days without
complication 4174: Immediate Evaluation and Care of the Neonate * ?? �APGAR score �
appearance, pulse, grimace, activity, respiration � ensures good
respiration/circulation * ?? �Clear airway secretions � ensures patent airway * ??
�Dry/warm baby � thermoregulatory center in brain is underdeveloped; thus
drying/warming/swaddle are essential components of immediate care * ??
�Erythromycin eye ointment + Vit. K shot � stop gonococcal conjunctivitis/neonatal
hemorrhage 8820: APGAR Scoring & Respiratory Considerations * ?? �APGAR score at 1
minute and 5 minutes o Appearance � totally blue (0), blue at extremities (1),
total pink (2)o Pulse (palpate umbilical cord) � none (0), <100bpm (1), >100bpm (2)
o Grimace � none (0), suction/aggressive stimulation (1), cry on stimulation (2) o
Activity � none (0), some flexion (1), flexion that resists extension (2)o
Respiration - none (0), weak/irregular/gasping (1), strong cry (2) * ?? �When
respiratory interventions are neededo Risk factors: young mom, Hx substance abuse,
Hx diabetes mellitus/maternal HTN o If APGAR is <7 (esp. if pulse & respiration
scores are poor) you must resuscitate! o Cyanosis of face or central body may
indicate respiratory/cardiac problems * ?? �Interventionso APGAR <7 � pulse
oximetry + positive pressure ventilation (bag-and-mask) o If HR <60 � chest
compressions requiredo Failure to improve with pulse ox/pos. pressure � intubation
4889: Small for Gestational Age (SGA) ?? Risk Factors o
Maternal:preeclampsia/eclampsia,malnutrition,placentalinsufficiency,multiparty,drug
use o Fetal: regular variant or chromosomal abnormalities, congenital infection,
in-born error of metabolism causing IUGR?? Presentation: birth weight <10th
percentile o Symmetric IUGR � all components (head, weight, length) are similarly
decreased o Asymmetric IUGR � weight affected > head/length * ?? �Children with SGA
are at increased risk for hypoxia/asphyxia/meconium aspiration (poorly
ventilated/compliant airways), hypothermia (low brown fat & overall fat content),
hypoglycemia (decreased glycogen stores), hypocalcemia (poor Ca placental
transfer), & polycythemia (high EPO from hypoxia!) * ?? �Children with Very Low
Birth Weight (<2600g) may have hyperglycemia (immature pancreas leading to poor
insulin production) 4223: Effects of Maternal Hyperglycemia (Diabetes) on the
Neonate * ?? �Pathophys: maternal hyperglycemia??high diffusion of glucose through
placenta??fetal hyperglycemia??fetal hyperinsulinemia (anabolic hormone)??
abnormal/excessive growth * ?? �1st trimester effects: congenital heart disease,
NTDs, small left colon syndrome, craniofacial malformations, spontaneous abortion *
?? �2nd/3rd trimester effects o Polycythemia � due to increased metabolic demand
from anabolic effects, thus EPO production; neonate appears plethoric upon birtho
Organomegaly � anabolic effects of insulino Neonatal hypoglycemia � continued
hyperinsulinemia after exodus from high sugar womb o Traumatic Birth � macrosomia
from anabolic effect can lead to excessive stress on the fetus during birth??
shoulder dystocia/clavicular fracture/asphyxia/hypoxic encephalopathy Neurology
2280/2680/3514/4841/NN: Seizures * ?? �New onset seizures typically occur in
children and elderly folkso ALWAYS get head imaging on a new onset seizure to rule
out an organic causeo EEG may be useful to catch ongoing seizure or identify a
seizure disorder through EEG waves * ?? �Epilepsy: a tendency to have recurrent,
unprovoked seizures o Lennox Gastaut Syndrome: childhood seizures + retardation (1-
2Hz spike-and-wave); Tx: Valproate; lamotrigine; felbamate; rufinamideo Benign
rolandic epilepsy: childhood seizures often happening at night (centro-temporal
spikes); Tx: Carbamazepine (may not be treated)o Absence epilepsy: childhood/teen
absence seizures (�dropping the juice at breakfast�); triggered by hyperventilation
(3Hz spike-n-wave); Tx: Ethosuximide; valproateo Juvenile myoclonic epilepsy: teen
seizures often happening in the morning (4-6Hz spike-n- wave); Tx: Valproate;
lamotrigine; levetiracetam * ?? �Simple Partial (Focal): seizure confined to one
part of the brain; pt typically stays conscious but may lose consciousness if both
sides become involved o Presentation: ???Motor (motor cortex): stiffening/jerking
of a specific body part; Jacksonian March (spread from fingertips to body as
seizure activity moves along the motor homunculus to involve a general side of the
body) o ???�Sensory: visual (occipital), tactile (parietal), gustatory/olfactory
(temporal) o ???�Autonomic: sweating/epigastric �rising� feeling o ???�Psychic
(temporal lobe): d�j� vu/jamais vu or feelings of fear/anxiety/excitement o EEG may
show specific, discreet changes * ?? �Complex Partial: seizure is confined to one
hemisphere and pt loses consciousness o Arise in parietal or temporal lobeso
Automatisms (repetitive, purposeless motor movements) are a common feature o Pt
will not respond properly to their environment due to impaired consciousness ??
Generalized Tonic-clonic (Grand Mal): o Risk factors: fever, hypoglycemia, sleep
deprivationo Presentation: typically occurs in four major phases +/- tongue biting,
peri-oral cyanosis, or urinary incontinence. Will always have eyes open during
event. * ???�Aura: sensory stimulation (smells/visions); may or may not occur * ???
�Tonic phase: whole body tenses up, sometimes with a �epipeltic cry� from pharynx
muscle contraction causing involuntary expiration * ???�Clonic phase: rhythmic
jerking movements for 1-2 minutes, petering out after * ???�Post-ictal phase:
confusion/somnolence following clonic phase ?? Absence (Petit Mal): generalized
seizure featuring unresponsivenesso Presentation: Consists of staring period with
immediate recovery; these spells are often not noticed by the patient, but they are
not aware of what�s going on around them during the spell ???May be thought to be
learning disability or look like daydreaming on initial presentation ???Typically
occurs in children???Hyperventillation is a common trigger ???3Hz generalized
spike-and-wave on EEG is characteristic o Tx: ethosuximide ?? Febrile: generalized
seizures occurring within context of infectiono Risk Factors: fever,
viral/bacterial infection, recent immunization (DTaP or MMR), FamHxo Presentation:
seizure (any type) with fever (100.4), no prior seizures, no CNS infection or other
organic cause for a seizure (metabolic disorder, seizure disorder, etc.) ???Only
affect children 6 months � 5 years of age???No major risk for epilepsy in the
future if you get these o Tx: reassurance/education; abortive therapy needed if
lasting >5min o Prognosis: no effect on intelligence/development; 30% recurrence &
<5% epilepsy?? Psychogenic Non-epileptic Pseudoseizure: seizure that doe not follow
any recognized EEG pattern, often seen in pts with psychiatric history (often
abuse)o Typical pt is a young person under a lot of stress; thought to be a
psychogenic defense mechanism for extreme stress or trauma. Can be quite
convincing.o Bilateral limb movements, no confusion/loss of consciousness and no
changes to the EEG ?? Status Epilepticus � While most seizure activity is acute,
some may take a prolonged course giving significant risks to the patient cause in
seizure. It�s called status epilepticus. Here�s the algorithm to approach this
event: o Give normal first aid and protect the patiento If pt continues to seize
for more than a few minutes assess ABCs, check glucose levels, and establish IV
accesso Send blood lab studies; give 100mg thiamine IV, followed by 50% dextrose
(may be B1 def.)o Administer Lorazepam 0.1 mg/kg IV � benzo to chill them outo [if
seizure persists] Phenytoin/fosphenytoin 20mg/kg IV � anti-epilepticso [if seizure
persists] Intubate and give phenobarbital 20mg/kg IV � old school anti-epilepticso
[if seizure persists] Induce coma (barbiturates, midazolam, or propofol) and begin
continuous EEG monitoring 2680: Cardiogenic Syncope?? Overview of Syncope:
basically passing out with no warning/prodrome/changes in posture due to poor
cardiac output; the resulting cerebral hypoxia results in pre-syncope symptoms,
then full syncope if hypoxia is persistent o Heart rate <35 and >150 beat/min don�t
give enough cardiac output for consciousnesso Drug induced hypovolemia/peripheral
vasodilation are classic causes of syncopeo Exertional syncope may be the result of
outflow obstruction (aortic stenosis, etc.)o Cough/micturition syncope (natural
Valsalva maneuvers) may decrease venous return to heart o Vasovagal syncope is an
abnormal reflex with intense vagus nerve driven vasodilation resulting in abrupt
blood pressure drop and syncope. Typically pain/sight of blood/etc. trigger ito
Orthostatic syncope: loss of consciousness with changes in position (standing up
from laying) * ???�Young pts: usually from a prolonged posture (standing at
military attention) * ???�Old pts: usually standing up from laying down (pooling in
the lower limbs) and often the result of poly-pharmacy (b-blocker + diuretic +
nitrate = pass out) o Sick sinus syndrome: slow heart rate due to sinus node slowed
function * ?? �Presentation:o Abrupt loss of consciousness with near immediate
return to normal function. Many etiologies o Pt may pee themselves (if they have a
full bladder) but never poop themselves ???Can be confused for seizure ???Usually
peeing + pooping themselves
is classic of seizureo Any form of convulsion, Post-ictal confusion, or Tongue
biting/spiting are classic of seizure * ?? �Dx: thorough history with investigation
to possible precipitating factorso Cardiogenic: consider ECG/echocardiography
testing for arrhythmias/abnormal heart structures o
Iforthostatic:considerpositionaltestingortilt-
tabletestingtodocumentorthostaticevent * ?? �Tx: basically treat whatever causes
the disease; often volume repletion, anti-arrythmatics, and drug review are
mainstays of treatment depending on the cause 3657/3666: Neonatal Intraventricular
Hemorrhage * ?? �Presentation: acute onset lethargy/hypotonia, cyanosis/pallor,
bradycardia, hypotension, high-pitched cry, apnea, rapidly increasing head
circumference, bulging fontanelles, focal neurologic deficits, seizure o
Complications:occurinhighergradebleeds(grade3or4) o ???�Communicating (non-
obstructive) hydrocephalus (blood irritation of arachnoid villi causes failure of
normal CSF flow) o ???�Neurodevelopmental disability (cerebral palsy)o High risk in
premature neonates born <30wk gestation or <1500g (3.3lbs) o 25-50% are
asymptomatic and will be caught on screening imaging * ?? �Pathophys: permaturity
results in increased fragility of the subependymal germinal matrix & immature
autoregulation of cerebral blood flow??increased chance for break/bleed * ?? �Labs:
CBC (decreased hematocrit), CMP (metabolic acidosis) * ?? �Imaging: cranial
ultrasound (bilateral ventriculomegaly, opaque/blood filed ventricles) o
Screening:serialcranialultrasoundsofat-riskprematurechildren(25-50%asymptomatic!) *
?? �Dx: imaging +/- presentation * ?? �Tx: supportive care * ?? �Prevention: o All
babies??prophylactic Vit.K shot to prevent coagulopathy of prematurity o Premature
babies??corticosteroids to help prevent premature labor in mom 4248/4865: Brain
Abscess?? Presentation: preceding otitis media/mastoiditis, morning vomiting,
nighttime headache, seizure, fever, focal neurologic deficits (CN III/CN VI),
papilledema * ?? �Pathophys: preceding infection can directly spread into the brain
causing abscess. Increased ICP gets worse at night when laying head down to sleep
(headaches)??stimulation of area postrema (morning vomiting); growing abscess
results in worsening ICP resulting in nerve deficits & papilledema * ?? �Anatomy:
location of preceding infection will likely dictate location of brain abscess o
Otitis media/mastoiditis � temporal lobe or cerebellum from direct spread o
Frontal/Ethmoid sinusitis � frontal lobe from direct spreado Dental infection �
frontal lobe from direct spread o Bacteremia/Infective Heart Disease � multiple
abscesses along the grey-white junction (MCA distribution) via hematoengous spread
* ?? �Labs: CBC (leukocytosis) * ?? �Imaging: CT with contrast or MRI (hypodense
lesion with ring-enhancement & surrounding edema) * ?? �Dx: presentation + imaging
* ?? �Tx: IV broad spectrum ABx +/- needle aspiration/surgical excision/removal of
infected skull (mastoiditis, otitis media, etc.) o Corticosteroids may be used if
significant inflammation is present (risk of brainstem herniation outweighs risk of
suppressing Abx therapy)o LP is contraindicated if brain lesion present (concern of
immediate brainstem herniation) unless fontanelles are still open (pressure is
equalized) 4871: Non-Communicating Hydrocephalus * ?? �Presentation: poor feeding,
irritability, decreased activity, vomiting, rapidly increasing head circumference,
tense/bulging fontanelles, prominent scalp veins, wide-spaced cranial sutures * ??
�Imaging: o Ultrasound � can be used for quick assessment, but only in children
<6mo old o CT � if acutely asymptomatic, these are faster/more availableo Sedated
MRI � if stable, will give the best images * ?? �Dx: presentation + imaging * ??
�Tx: ventricular shunting 2472: Neonatal Abnormalities of the Skull * ??
�Cephalohematoma (subperiosteal hemorrhage) � scalp swelling limited to the surface
of one cranial bone following birth; no skin discoloration/pulsations;
hyperbilirubinemia may be present and require phototherapy; spontaneous resolution
in approx. 2-3wk * ?? �Caput succedaneum � diffuse, eccymotic swelling of the scalp
(crosses multiple skull bones); often occurs in children with vertex delivery or
vacuum-assisted delivery. * ?? �Cranial meningocele � scalp lesion with spontaneous
pulsations, increased pressure with crying, and X- ray evidence of bony
malformation * ?? �Depressed fractures � thinning of calvarium in spots as a
complication of foreceps-assisted delivery or fetal head compression. Depress and
pop with a �ping-pong ball� like quality 3671: Migraine Headache in Children ??
Presentation: bifrontal headache, nausea/vomiting/photophobia, visual aura o
Migraines are the most common type of headache in children <20yro No imaging is
required if good clinical evidence of headache is presento Occipital headaches,
focal neurologic deficits, numbness, history of increasing headache frequency, or
headaches awakening pt from sleep??imaging with CT/MRI to rule out lesion * ?? �Dx:
clinical presentation, no imaging required * ?? �Tx: sensory deprivation (lying in
cool/dark room with cool cloth on forehead + NSAID o Triptans (oral, intranasal, or
injectable) can all be used if the above fail to work 3658: Pediatric CNS Tumors??
Presentation by Location o Supratentorial � increased ICP (awakening from headache,
morning vomiting, papilledema, macrocephaly), seizures, weakness, sensory changes o
Posterior fossa � increased ICP, cerebellar dysfunction (ataxia, clumsiness) o
Brainstem � ataxia, clumsiness, cranial nerve palsieso Spinal Cord � back pain,
weakness, abnormal gait ?? Presentation by Typeo Astrocytoma (low grade) � the most
common primary CNS tumor in childreno Glioblastoma (astrocytoma, high grade) �
arise in cerebral hemispheres, rare in childreno Craniophayngioma � cystic
structure with calcification in the sella turcica on imaging causing visual defects
(compression of optic tracts) & hormonal deficiency (compression of pituitary)o
Ependymoma�glialcelltumorsarisingintheependymalcellsliningbrainventricles;classical
y arise in the 4th ventricle causing obstructive hydrocephaluso Medulloblastoma �
arise in cerebellar vermis causing cerebellar dysfunction (Opsoclonus- myoclonus
ataxia = �dancing eyes and feet�; rapid vertical/horizontal/rotational nystagmus
with marked ataxia +/- other neurologic impairments)o Neuroblastoma � PNS tumors
sympathetic ganglia in abdomen; may metastasize to CNS 3665: Pinealoma??
Presentation: o Parinaud syndrome: limited upward gaze/downward gaze preference,
upper eyelid retraction (Collier sign; can see upper sclera but not lower), light-
near dissociation (pupils accommodate but don�t react to light) o
Obstructivehydrocephalus:persistentheadache,vomiting,papilledema,ataxia o
�Trilateral retinoblastoma�: bilateral retinoblastoma + pinealoma * ??
�Pathophysiology: mass effect causing pressure on pretectal region near
CNIII/superior colliculi (eye problems) & blockage of aqueduct of Sylvius (outflow
obstruction causing hydrocephalus) * ?? �Imaging: CT head/MRI brain showing mass in
pineal region * ?? �Dx: presentation + imaging * ?? �Tx: ??? 4872: Breath Holding
Spells ?? Presentation: episode of apnea caused by frustration/anger/pain in
children 6mo � 5yr of age o Cyanotic: provocation??crying/breath holding with
forced expiration??apnea, falling limp, & passing out??rapid return to baseline o
Pallid: minor trauma/provocation??passing out??breath-holding, pallor, diaphoresis
for <1min??return to consciousness with confusion and sleepiness for a few minutes
o Child may develop vasovagal syncope later in life * ?? �Pathophys: intense
vasovagal response during provocative event * ?? �Labs: CBC (may show iron
deficiency anemia) * ?? �Dx: presentation + normal physical exam * ?? �Tx:
reassurance of parents that this is not serious and does not impact development o
Fe2+ supplementation if iron deficient 3907: Sudden Infant Death Syndrome (SIDS) ??
Risk factors o Mom: smoking during/after pregnancy, age <20yr, inconsistent
prenatal careo Baby: prone/side sleeping position, soft sleeping surface, loose
bedding, bed-sharing, prematurity, sibling that had SIDS * ?? �Presentation: sudden
unexpected death of child that cannot be explained with post-mortem autopsy o #1
cause of death in children between 1mo � 1yr * ?? �Prevention o Mom: smoking
cessation, routine prenatal careo Baby: supine sleeping position, firm bed surface,
room sharing, & pacifier useo Home apnea monitors are NOT recommended if risk
factors present (no efficacy!) 3985: Friedrich�s Ataxia (Spinocerebellar Ataxia)
* ?? �Presentation: o Neuro: gait ataxia, frequent falling, dysarthriao
Cardio:concentrichypertrophiccardiomyopathy o Endocrine: diabetes mellituso MSK:
scoliosis & �hammer toes� * ?? �Pathophysiology: autosomal recessive disorder
causing progressive degeneration of spinocerebellar tracts, posterior columns, &
pyramidal tract + other deformities * ?? �Prognosis: death within 20yr of onset
from cardiomyopathy (90%) or rarely diabetes (10%) 3661/3669: Muscular Dystrophies
(Duchenne, Becker, Myotonic) ?? Duchenne (DMD) o Presentation: onset at age 2-3yr;
progressive weakness affecting legs first (Gower maneuver, calf pseudohypertrophy
with scar/fat replacement) ???Scoliosis/cardiomyopathy/mild cognitive impairment
associated ???Wheelchair bound by adolescence & death by age 30 (heart or lung
failure)o Pathophys: deletion disrupting reading frame of dystrophin on Xp21 (X-
linked recessive) * ???�Dystrophin is an anchoring protein for actin/other skeletal
proteins; lack of this causes weakness/rupture of the myocyte plasma membrane??
injury/degeneration of muscle * ???�Damage = lymphocyte invasion??fiberous
tissue/fat replacement * ???�Large deletion causes a more severe lack of
structural integrity o Labs: Creatinine Kinase assay (very high), serum aldolase
level (high), EMG (weak/polyphasic muscle impulses with normal nerve impulses),
muscle biopsy (dystrophic pattern) totally absent dystrophin levels
(immunohistochemistery, Western blot, or genetic testing) o Dx: presentation +
genetic testing showing Dystrophin Gene deletion on Xp21o Tx: oral steroids can
help improve function transiently ?? Becker (BMD)o Presentation: onset at age 5-
15yr; same as DMD, but less severe ???Cardiomyopathy associated; death by age 50
from heart failure ???Wheelchair bound in 20s/30so Pathophys: deletion preserving
reading frame of dystrophin on Xp21 (X-linked recessive) ???Same as DMD, but
smaller deletion results in less severe phenotypeo Labs: same as DMD but with
decreased amount of dystrophin on IHC staining o Dx: presentation + genetic resting
showing Dystrophin Gene deletion on Xp21 o Tx: oral steroids can help improve
function transiently ?? Myotonic (Steinert Disease) o Presentation: onset at age
12-30yr, but possibly earlier in severe disease * ???�Fetal: polyhyraminos (poor
swallowing), decreased fetal movements * ???�Neonatal: hypotonia/areflexia, feeding
difficulty & respiratory problems * ???�Child/Adult: facial weakness/dysphagia
(atrophy of masseter/temporalis), hand grip myotonia (cannot release grip on
handshake), weakness of extremities, arrhythmias, testicular atrophy/infertility,
balding, cataracts, mental retardation, insulin resistance o Pathphys: CTG
trinucleotide expansion on DMPK gene (Chrom 19 13.3; Autosomal dominant; typically
passed down by mother & subject to anticipation)???Abnormal protein results in
delayed muscle reaction & weakness???Should be suspected in ANY child with
hypotonia; mother should also be examined o Labs: FISH study looking for specific
mutationo Dx: suspect in all children with hypotonia; presentation + DNA testingo
Tx: supportive treatment; high infant mortality due to respiratory failure 2445:
Niemann Pick Disease * ?? �Presentation: loss of motor milestones around ages 2-
6mo, hypotonia, feeding trouble, protuberant abdomen, hepatosplenomegaly,
hypo/areflexia, & cherry-red macula o 3 types (A,B,C) with type A being the
severe/fatal typeo Increased incidence in Ashkenazi Jewso Universally fatal by age
3yr * ?? �Pathophys: sphingomyelinase deficiency (autosomal recessive) * ?? �Dx/Tx:
clinical presentation/supportive care; must differentiate from Tay-Sachs 2445: Tay-
Sachs Disease * ?? �Presentation: loss of motor milestones around ages 2-6mo,
hypotonia, feeding trouble, protuberant abdomen, hyperreflexia, hyperacusis &
cherry-red macula o Increased incidence in Ashkenazi Jewso Universally fatal by age
4yr * ?? �Pathophys: B-hexosaminidiase A deficiency (autosomal recessive) * ??
�Dx/Tx: clinical presentation/supportive care; must differentiate from Niemann-Pick
3686/3687: Marfan syndrome ?? Presentation: o Marfanoid body habitus (tall/slender
build, increased arm:height ratio, decreased upper:lower segment ratio,
arachnodactyly (long fingers, �thumb sign�), joint laxity, pectus excavatum,
scoliosis/kyphosis) o Eye: Upward lens subluxation & retinal detachmento Cardio:
aortic root dilation, aortic regurgitation, increased risk of aortic dissection
(esp. with HTN or trauma), mitral valve prolapse, increased risk endocarditis o
Neuro: Normal IQ * ?? �Pathophys: autosomal dominant mutation of fibrillin-1 gene
(chom. 15) * ?? �Labs: rule out homocytinuria * ?? �Dx: presentation + FISH study
for mutation + negative homocystinuria * ?? �Lookalikes: o Congenital Contractural
Arachnodactyly � fibrillin-2 mutation; basically Marfan�s without the heart
problems & eye problems + contractures of large joints 3687: Homocysteinuria ??
Presentation: o Marfanoid body habitus (tall/slender build, increased arm:height
ratio, decreased upper:lower segment ratio, joint hyperlaxity/skin elasticity,
pectus excavatum, scoliosis) � no arachnodactyly o Eye: Downward lens subluxation,
blue eyeso Cardio: aortic & mitral regurgitation (no aortic dilatation)o Heme:
hypercoagulability (DVT, stroke, MI risk all increased), megaloblastic anemia o
Skin: fair complexiono Neuro: decreased IQ * ?? �Pathophys: autosomal recessive
mutation of cystathioneine synthase * ?? �Labs: urine/plasma methionine
(increased), urinary cyanide nitroprusside test (+) * ?? �Dx: presentation + labs *
?? �Tx: methionine-restricted diet, dual anti-platelet/anti-coagulation (lower risk
of clot), and Vit B6/B12 supplementation (lower homocysteine levels) 3912: Kallmann
Syndrome * ?? �Presentation: hypogonadotropic hypogonadism (no puberty,
underdeveloped genitals, short stature, & secondary sexual characteristics),
anosmia (no sense of smell) * ?? �Pathophysiology: x-linked recessive disorder
resulting in failure of migration of GnRH neurons & olfactory neurons from the
olfactory placode??hypothalamus/olfactory bulb * ?? �Labs: low FSH/LH levels * ??
�Dx: presentation 2763: Sturge-Weber Syndrome * ?? �Presentation: generalized
seizures at early age, mental retardation, & nevus flammeus (�port wine stain�) of
trigeminal nerve distribution (congenital unilateral cavernous hemangioma)o
Complications: Hemianopia, hemiparesis, hemisensory disturbance, & ipsilateral
glaucoma * ?? �Imaging: X-ray head >2yr of age shows gyriform intracranial
calcifications with �tram-line appearance� * ?? �Dx: clinical presentation * ??
�Tx: control of seizure, reduce intraocular pressure, argon laser therapy for skin
lesions 2763: Tuberous-Sclerosis ?? Presentation: o Skin: ash-leaf spots
(hypopigmented macules, illuminate with Wood�s lamp), adenoma sebaceum
(angiofibromas on nose/face), shagreen patches (thickened �orange-peel� patches) o
CNS: infantile spasms (�West Syndrome�), intracranial calcifications, mental
retardation o Systemic: renal cysts, cardiac rhabdomyoma (#1 neonatal cardiac
tumor), retinal astrocytoma/hamartoma * ?? �Pathophys: mutation of TSC1/TSC2 genes
* ?? �Dx: presentation * ?? �Tx: (If West Syndrome??vigabatrin for infantile spasm
Tx) 3871: McCune-Albright Syndrome * ?? �Presentation: precocious puberty,
large/irregularly bordered pigmented macules (�Coast of Maine� spots), multiple
fractures (fibrous dysplasia of bones)o +/- Endocrine dysfunction (hyperthyroidism,
pituitary adenoma, & adrenal hypercortisolism) * ?? �Pathophysiology: sporadic
mutation in G-protein cAMP causing constituent activation of FSH/LH receptors on
the gonads & in other areas ?? Dx: presentation 3550: Neurofibromatosis?? Type 1
(von Recklinghausen disease) o Presentation: * ???�Skin: caf�-au-lait spots
(hyperpigmented macules), axillary/inguinal freckles, multiple neurofibromas, Lisch
nodules (Hamartoma of the iris) * ???�CNS: optic glioma, intracranial
calcifications, neurofibromas, mental retardation * ???�MSK: osseus lesions,
scoliosis o Pathophys: mutation of NF-1 (tumor suppressor gene encoding
neurofibromin) on Chrom 17 o Imaging: MRI brain if signs of intracranial lesion
(chronic headache, early morning vomiting, vision changes, etc.)o Dx: clinical
presentation ?? Type 2 (central neurofibromatosis)o Presentation: hearing loss +
bilateral acoustic neuromas (Schwannoma) +/- skin stuff of NF-1 o Pathophys:
mutation of NF-2 (tumor suppressor gene encoding merlin) on Chrom 22o Labs:
audiometry +/- MRI braino Dx: clinical presentation 2444: Fetal Alcohol Syndrome ??
Presentation: o Facial dysmorphisms: microcephaly, small palpebral fissures,
long/smooth philtrum (lack of vertical grooves on upper lip), thin vermillion
border o Neuro: Microcephaly, mental retardation, ADHD, social withdrawal, delay in
motor/language milestones o Cardio: ventricular septal defect (most common)??
Pathophys: teratogenic damage from EtOH during fetal development o The most common
cause of mental retardation in the world * ?? �Dx: clinical presentation * ?? �Tx:
aggressive speech/physical/occupational therapy 2444/2452/2467/4840: Trisomy 21
(Down Syndrome) ?? Pre-natal Signs: o 1st trimester: Associated with elevated hCG
and decreased PAPP-A * ???�Combined with ultrasonographic imaging for nuchal
transparency (fluid collection at the fetal neck; an early sign of trisomy 21)
* ???�When noting these markers, genetic council, 2nd trimester CVS/amnio are
offered o 2nd trimester: * ???�Quad screen � Decreased: AFP, unconjugated estriol &
Increased: B-hCG, Inhibin A) * ???�Ultrasound � nuchal fold, ventriculomegaly,
echogenic bowel, shortened femur/humerus, absent nasal bone, pyelectasis ??
Presentation: o Craniofacial � epicanthal folds, upslanting palpebral fissures,
Brushfield spots (speckling of irises), low-set small ears, flat facial profile,
short neck with skin folds, furrowed tongueo Extremities � clinodactyly of 5th
digit (hypoplasia/distal incurving), single transverse palmar creases, sandal toe
deformity (widened space between 1st/2nd toes)o Spine � atlanto-axial instability
+/- subluxation (unstable articulation between atlas/axis)???spinal compression
(torticollis, behavioral changes, urinary incontinence, dizziness/vertigo) o
Neuro/Endo � mental retardation, early Alzheimer�s disease, hypotonia, obstructive
sleep apnea, conductive hearing loss, hypothyroidism o Optho � cataracts, glaucoma,
refractive errorso Cardio � endocardial cushion defects (Complete A-V septal defect
is most common)o Heme � leukemia (ALL, AML)o GI � duodenal atresia, Hirschprung�s
disease, omphalocele, pyloric stenosis, Celiac�s disease o Renal � horseshoe kidney
* ?? �Additional Screeningo Annual hearing screenings, ophthalmologic exams, & TSH
o Total IgA/IgA anti-endomysium antibodies (age 2)o Flexion/extension cervical
spine radiographs (age 3) * ?? �Pathophys: nondisjunction
(95%), Robertsonian translocation (4%), mosaicism (not mom�s fault; 1%); increased
risk with advancing maternal age due to increasing nondisjunction risk * ?? �Dx:
clinical presentation/screening + chromosomal analysis (karyotype) 2444/2468/2488:
Trisomy 18 (Edwards Syndrome) * ?? �Pre-natal signs: o 1st trimester: decreased B-
hCG/PAPP-A o 2nd trimester: quad screen (all decreased) * ?? �Presentation: o
Craniofacial � delicate/small facial features)/micrognathiao Extremities � clenched
hands, overlapping digits (2nd over 3rd & 5th over 4th), limited hip abduction,
dorsiflexed big toes, & rockerbottom feeto Cardio: VSD (most common anomaly; >50%)o
Neuro � mental retardation, hypertonia, scissoring gait (leg swings
circumfrentially around to cross the other leg during a step, �scissoring� with the
other leg to maintain balance standing) o Death within the 1st year of life
(cardiac or respiratory failure) ?? Dx: clinical presentation/screening +
chromosomal analysis (karyotype) 2444/2488: Trisomy 13 (Patau Syndrome) * ?? �Pre-
natal signs: o 1st trimester: decreased B-hCG/PAPP-A * ?? �Presentation o
Craniofacial � cleft lip/palate, cutis aplasia (missing scalp)o Extremities �
polydactylyo Ocular � microphtalmia (small eyes), retinal dysplasia, colobomas, &
single eye (rare!) o Neuro � holoprosencephaly (prosencephalon fails to divide into
two hemispheres), microcephaly, severe mental retardation, seizures o Death within
the 1st month of life ?? Dx: clinical presentation + chromosomal analysis
(karyotype) 2441/2444: Fragile X syndromeo Presentation: mental retardation,
long/narrow face, prominent forehead/jaw, large ears, thickened nasal bridge, blue
iriseso Macroorchidisim (Large testes) developing during pubertyo Behavior problems
including emotional instability, autism, or ADHD o Most common hereditary cause of
mental retardation in the USA o Pathohys: X-linked disorder caused by CGG repeat
increases; as the triplet increases rise, the X- chromosome becomes less stable??
damage/phenotype o Dx: clinical presentation + southern blot for FMR-1 mutation
3123: Phenylketonuria (PKU)?? Presentation: initially asymptomatic, may progress to
symptoms if not picked up early o Mild:earlydevelopmentaldelay/hyperactivityo
Severe: mental retardation, developmental delay, seizure, hypotonia, eczema,
mousey-musty odor, hypopigmentation (blue eyes/blonde hair/lack of pigmented brain
structures) ?? Pathophys: autosomal dominant mutation of phenylalanine hydroxylase
o Failure of phenylalanine??tyrosine results in phenylalanine accumulation allowing
it to enter alternative metabolism pathways resulting in neurotoxic metabolites o
Lack of PHE??TYR also stops production of melanin (lack of pigmentation!) ?? Dx:
screening tests +/- clinical presentation o Tandem Mass spectrometry: dried blood
samples are used to detect PHE alternative pathway metabolic products; best/most
cost effective newborn screen o Quantitative Amino Acid analysis: shows elevated
phenylalanine levels (inc. PHE:TYR ratio) ?? Tx: PHE-restricted diet initiated <1mo
age (normal development if achieved) 3193: Galactosemia * ?? �Presentation:
vomiting, diarrhea, FTT, jaundice/hepatic dysfunction/hepatomegaly, cararacts
(�oil- droplet appearance�), renal tubular acidosis, seizureso Symptoms onset after
breastfeeding/routine formula/cow�s milk ingestion for the 1st time o Liver
cirrhosis/Mental retardation occurs if left untreatedo Females suffer form ovarian
failureo Should be suspected in any newborn with 1hepatomegaly, 2hypoglycemia, or
3E.coli sepsis * ?? �Pathophys: autosomal recessive galactose-1-phosphate
uridyltransferase (full phenotype) but other, less common mutations can result in
this disease o Galactokinase deficiency: only cataracts, no other symptomso Uridyl
diphosphate galactose-4-epimerase deficiency: typical presentation + hypotonia +
sensoneurial deafness * ?? �Labs: urinalysis (shows non-reducing substance in
urine), RBC enzyme testing * ?? �Dx: pre-natal screening +/- labs * ?? �Tx:
lactose/galactose free diet (Soy-based formula like Isomil or ProSobee are good
ones) o Early Dx/Tx stops & even reverses liver/renal damage and cataracts 3192:
von-Gierke Disease (Type 1 Glycogen Storage Disorder) * ?? �Presentation:
hypoglycemic seizures, lactic acidosis, hyperuricemia, hyperlipidemia,
hepatomegaly/protuberant abdomen, enlarged kidneys, & doll-like faces (rounded
cheeks, thin extremities, short stature) o Onset around age 3-4mo o Increased risk
of hepatocellular carcinoma * ?? �Pathophysiology: Glucose-6-phophatase (G6P)
deficiency in the liver, kidneys, and intestinal mucosae (unable to break down
glycogen??glucose) causing glycogen accumulation & damage * ?? �Labs: urine
ketones, metabolic acidosis, high serum triglyceride/uric acid * ?? �Dx:
presentation + labs * ?? �Tx: frequent feeding with high complex-carbohydrate diet
Other Mentioned Genetic Diseaseso Fabry Disease � a-galactosidase deficiency;
angiokeratomas, peripheral neuropathy, asymptomatic corneal dystrophy; increased
risk of thromboembolism (heart/renal risk is high)o Krabbe Disease �
galactocerebrosidase deficiency; early developmental regression, blindness,
deafness, paralysis/hypotonia, & reflexia; Tx: cord blood transplant before disease
onseto Gaucher�s Disease � glucocerebrosidase deficiency; hepatosplenomegaly,
thrombocytopenia, and classic Erlenmeyer flask-shaped distal femur; death by age
4yr is common; enzyme replacement therapy is possibleo Hunter�s Syndrome � X-linked
recessive lysosomal hydrolase deficiency o Hepatosplenomegaly, mental retardation,
hearing loss, progressively stiffening/contracted joints, papules over the shoulder
girdle, & dysostosis multiplex (skeletal malformations) o NO blindness (to
differentiate from Hurler�s syndrome)o Dx: clinical presentation + heparin sulfate
in urineo Tx: early bone marrow transplant, but poor prognosis (death within 10-
15yr) o Hurler�s Syndrome � autosomal recessive lysosomal hydrolase deficiencyo
Hepatosplenomegaly, mental retardation, kyphosis, progressively coarsening facial
features, progressively stiffening/contracted joints with corneal clouding o Dx/Tx
= same as Hunter�s syndrome o Hereditary Fructose Intolerance � fructose-1-
phosphate aldolase B deficiency; onset of hypoglycemia, vomiting, diarrhea, FTT,
and seizures with introduction of fruit juice. Avoidance of fructose, sucrose, and
sorbitol resolve problems o Arnold-Chiari II malformation � downward displacement
of cerebellum/medulla through foramen magnum blocking CSF flow (hydrocephalus);
associated with lumbrosacral meningomyelocele o Tx: ventriculoperiotneal CSF shunto
Dandy-Walker malformation � absent/hypoplastic cerebellar vermis/cystic enlargement
of 4th ventricle blocking CSF flow (hydrocephalus), mild mental
retardation/language disorders o Tx: ventriculoperiotneal CSF shunt o Congenital
Aqueductal Stenosis � X-linked stenosis of CSF outflow tracts; associated CNS
abnormalities (abnormal thumb development or spina bifida) & severe mental
retardation o Tx: ventriculoperiotneal CSF shunt Ophthalmology3681: Retinoblastoma
* ?? �Presentation: leukoria (absence of the red reflex) +/- strabismus, decreased
vision, ocular inflammation, eye pain, glaucoma, orbital cellulitis o Tumor is
highly malignant and will metastasize to liver or brain without prompt treatment
* ?? �Pathophys: inactivation of the Rb tumor suppressor gene (familial or
sporadic) * ?? �Imaging: CT or MRI of the brain showing brain mass with
calcifications * ?? �Dx: presentation + imaging * ?? �Tx: referral to ophthalmology
(this is out of the general pediatrician�s scope!) 4531: Regular Vision Assessment
of Children * ?? �Visual assessment should occur at EVERY well child visit for
undiagnosed eye problems can result in blindness. Visual testing modality based on
age. * ?? �Infancy o Observation (pupil/cornial assessment, look for ptosis) fixing
and tracking with eyes (normal extraocular movements) o Red reflex: looks for
leucoria, a sign of retinoblastoma/cataracts o Corneal light reflex: shining light
into eye produces symmetric light reflections; if not symmetric, misalignment may
be present o Cover-uncover test: assesses eye deviations & pupil changes when eyes
are covered/uncovered ?? Age3 o Monocular Snellen Chart or Tumbling E Chart???20/40
or worse at age 3-5yr = refer to ophthalmologist ???20/30 or worse at age >6yr �
refer to ophthalmologist 3711: Strabismus (ocular misalignment)?? Presentation:
ocular misalignment represented by eye deviation after 4mo, asymmetric corneal
light reflexes, asymmetry of red reflex, deviation on cover-uncover test,
torticollis/head tilt (compensatory) o Nasal deviation (esotropia) or temporal
deviation (extropia) are both possibleo Complications: amblyopia (permanent vision
loss from dis-use of the eye), diplopia (double vision, from imperfect alignment of
eyes) * ?? �Pathohys: asymmetric weakness/neurologic dysfunction of the extraocular
eye muscles o Below the age of 4mo, intermittent strabismus can be totally normal
due to immaturity of the extraocular muscles (ocular instability of infancy); it
should resolve with time * ?? �Dx: presentation * ?? �Tx: occlusion therapy (eye
patch of normal eye to encourage lazy eye to snap back into shape!) or penalization
therapy (cycloplegic eye drops to blur vision, similar effect to occlusion therapy)
Poisoning & Environmental Exposure 2378: Caustic Ingestion * ?? �Presentation:
chemical burn/liquefactive necrosis causing Laryngeal damage (hoarsness/stridor),
esophageal damage (dysphagia, odynophagia), gastric damage (epigastric
pain/bleeding) o Immediate complications: upper airway compromise, perforation,
aspiration o Short-term complications: esophageal stricture/stenosis (2-3wk)o Long-
term complications:
ulcers/cancer of upper GI tract * ?? �Imaging: see Tx * ?? �Dx: history + imaging
* ?? �Tx: to be done in this order: o Assess Airway, Breathing, Circulation &
address in that ordero Remove any contaminated clothingo CXR if respiratory
signs/symptoms are presento Hospitalization with upper GI endoscopy within 24hr to
assess extent of damage (immediate endoscopy may not show extent of damage &
perforation risk is high).???NG feeding tube may be placed under endoscopic
visualization, but not blindly o Barium swallow 2-3wk following acute ingestion if
persistent swallowing issues remain present o DO NOT provoke vomiting (milk, water,
activated charcoal, vinegar, nasogastric lavage) as it may push the caustic
substance back into the esophagus/airway.o DO NOT give vinegar to �neutralize� an
alkaline substance. It could invoke an exothermic reaction causing worse damage to
the upper GI tract 2655/3827: Iron Poisoning?? Presentation: often history of child
eating someone�s pills, but they can�t remember which. Classically pills belong to
mom (prenatal vitamins) or grandma (Fe2+ pills)o 30min � 2 days: abdominal pain,
vomiting/hematemesis, diarrhea/melena, hypotensive shock, metabolic
acidosis/compensatory respiratory alkalosis o Around2days:hepaticnecrosis o 14 � 56
days: gastric scarring, pyloric stenosis * ?? �Pathophys: Fe2+ is corrosive to GI
mucosa in large quantities (abdominal symptoms/bleeding/scarring), a potent
vasodilator (hypotensive shock/metabolic acidosis) & causes lipid peroxidation at
the cellular level killing cells (liver necrosis, damage to GI tract) * ?? �Labs:
metabolic acidosis/respiratory alkalosis compensation, low bicarbonate level * ??
�Imaging: abdominal X-ray showing radiopaque pills * ?? �Dx: Hx/Presentation + labs
+ imaging * ?? �Tx: whole bowel irrigation + deferoxamine (Fe2+ chelator) +
supportive care for ABCs (fluids, intubation) 4837: Lead Poisoning (Plumbism) in
Children * ?? �Risk Factors: Home build before 1978, around construction/renovation
of house (peeling paint), pica, parent working with batteries/pottery,
playmate/sibling with lead poisoning, low SES, immigranto Screen any child at 9mo
with risk factors with fingerstick blood specimen (capillary lead)o If screening
(+), venous lead level is a confirmatory test for Pb2+o While lead does accumulate
throughout the body, hair, teeth, bone, or urine is not acceptable * ??
�Presentation: often asymptomatic with appearance of learning deficits once school
starts o GI: abdominal pain, nausea/vomiting, constipation, anorexiao Neuro (short
term): listlistness, irritability, seizure, encephalopathy/loss of consciousness o
Neuro (long term): behavioral problems, cognitive impairmento Heme: microcytic
sideroblastic anemia (peripheral smear shows basophilic stippling; bone marrow
shows ringed sideroblasts); does NOT respond to Fe2+ replacement therapy * ??
�Labs: CBC (microcytic anemia), venous lead levels (high), RBC protoporphyrin
(high) * ?? �Imaging: X-ray (abdomen shows flecks of lead, limbs show �lead lines�
in knees/wrists caused by increased density of metaphyseal bands due to lead
deposit) * ?? �Dx: presentation + venous lead level * ?? �Tx: o Mild (5-44 mcg/L) �
minimize risk factors + repeat test in 1 montho Moderate (45-69 mcg/L) � Meso-2,3-
Dimercaptosuccinic acid (succimer/EDTA)o Severe (>70 mcg/L) � Dimercaprol (British
Anti-Lewisite) + Calcium Disodium Edetate (EDTA) Miscellaneous Poisonings * ??
�Acetaminophen � nausea/vomiting 24hr following ingestion. Sodium Bicarb is the
antidote (alkaline urine to help pull drug out of blood) * ?? �Aspirin � tinnitus,
fever, metabolic acidosis/compensatory hyperpnea (increase rate/depth of breathing
to make for a compensatory respiratory alkalosis); no radiopaque pills on abdominal
X-ray differentiates from Fe2+ poisoning. N-acetylcysteine is the antidote
(minimize NAPQI production) Miscellaneous Antidotes * ?? �Lithium � hemodylasis
(Li2+ is easily removed) * ?? �TCAs � Sodium Bicarb (alkaline urine helps remove) *
?? �Hyperkalemia � Calcium gluconate infusion (stabilize cardiac myocytes)
Dermatology2746/4704: Tinea Corporis (Ring-Worm) ?? Risk factors: athlete�s with
skin-to-skin contact (wrestling/gymnastics), humid environments, contact with
infected animals * ?? �Presentation: scaly/itch ring-shaped patches with
centrifugal spread/well demarcated border ???forms central clearing with raised
edge * ?? �Micro: Infection with any dermatophyte, however Trychophyton rubrum is
classic o May illuminate with different colors under Wood�s Lamp ???Coral-red
fluorescence = tinea infection by Corynebacterium ?? Erythromycin, either systemic
or topical, is the treatment of choice ???Green fluorescence = Tinea infection by
Microsporum ???No fluorescence = Tinea infection by Epidermophyton or Trichophyton
* ?? �Dx: presentation + KOH scraping/prep showing hyphae * ?? �Tx:o 1st
line/Local: 2% antifungal lotion/cr�me (clotrimazole or terbinafine) o 2nd
line/extensive: oral terbinafine or griseofulvin ???Note that extensive infection
should prompt search for immunosupperative disease * ?? �Lookalike: nummular eczema
10553: Tinea Capitis * ?? �Presentation: scaly erythematous plaques of the scalp??
patchy alopecia with residual regular broken hair shafts (black dots) +/-
inflammation/pruritis/lymphadenopathy/scarring o Most common in African American
people * ?? �Micro: Trichophyton tonsurans or Microsporum Sppo Transmission via
skin-to-skin contact or fomites (shared combs) * ?? �Dx: presentation + KOH
scaping/prep showing hyphae * ?? �Tx: Oral terbinafine, griseofulvin, itraconazole,
or fluconazole o Requires systemic therapy to penetrate the affected hair shafts.o
Household contacts should be given prophylactic selenium sulfide (selsun blue) or
ketoconazole shampoo (prevent penetration of hair follicles) ?? Lookalikes: o
Alopecia areata � autoimmune alopecia without black dotso Discoid lupus � well
demarcated plaques causing alopecia/scarring/photosensitivityo Pressure-induced
alopecia � transient hair loss due to constant pressure, usually from surgery o
Trichotillomania � compulsive hair picking with irregular broken hair shafts 2747:
Tinea Versicolor (pityriasis versicolor) * ?? �Presentation: hypopigmented area
noticed during summer months or vacation (infected skin fails to tan due to acid
production from the fungus), may also feature fine scale or pruritis * ?? �Micro:
Malassezia globose classically in hot/humid weather * ?? �Dx: KOH scrape/prep
showing hyphae & yeast cells (spaghetti and meatballs appearance) * ?? �Tx: topical
ketoconazole, topical terbinafine, or selenium sulfide (selsun blue) 4113: Sunburn
* ?? �Presentation: red/painful ???peeling ???blue/purple, bullous * ??
�Complications: skin cancer (melanoma, basal cell, squamous cell) & photoaging * ??
�Pathophys: UVA/UVB rays cause damage to skin cell DNA * ?? �Dx: clinical
presentation * ?? �Tx: o Mild-moderate: NSAIDs/cool compress, calamine lotion, aloe
vera o Moderate-severe: IV fluids/analgesia, wound care * ?? �Prevention: o Avoid
the sun: remain indoors between 10AM-4PM (peak sunlight hours), wear protective
clothes (hats, pants, long sleeves, dark/women cloth), & avoid tanning beds (�base
tan� does not protect against sun damage) o Sunscreen: apply sunscreen 30 min
before exposure, re-apply sunscreen every 2hr; infants <6mo should not be exposed
to chemicals in sunscreen, SPF50 Broad Spectrum provides 98% protection against
UVA/UVB & higher SPF provides diminishing returns 3755: Dermal Melanocytosis
(Mongolian Spots) * ?? �Presentation: Benign, flat, blue-grey patches in infants
classically over the lower back/buttocks o Occurs most commonly in African
American, Native American, Hispanic, Asian chidlren o Fades spontaneously in the
first decade of lifeo Must be documented, as these may be mistaken for bruises * ??
�Tx: reassurance 2758/4104: Atopic Dermatitis (Eczema; �the itch that rashes�) * ??
�Risk factors: relatives with eczema, allergies, or asthma * ?? �Presentation: o
Infant: persistent itch??red/scaly/crusted lesions on extensor surfaces, trunk,
cheeks, & scalp o Child/Adult: lichenified plaques on flexure creaseso Eczema
herpeticum: HSV superinfection = fever, pain, lymphadenopathy, new
vesicular/pustular �punched out� eruption in area of eczema??hemorrhagic crustingo
Increased risk of: impetigo, molluscum contagiosum, tinea corporiso Triggers:
anything to dry the skin (dry air, excessive bathing, irritating laundry detergent,
etc.) * ?? �Pathophys: improper synthesis of the stratum corneum result in an
incomplete epidermal barrier???allergen infiltration into the skin causing
localized allergic reactions * ?? �Dx: presentation + relief with
emollients/steroids * ?? �Tx: topical emollients/topical steroids 4711: Seborrheic
Dermatitis (�cradle cap�) * ?? �Presentation: erythematous/plaques and yellow
�greasy� scales on scalp/eyebrows/eyelids/posterior ear creases/nasolabial folds,
umbilicus, or diaper area + mild itching * ?? �Micro: Malassezia spp. * ?? �Dx:
presentation * ?? �Tx: often spontaneous resolution, but appearance/itching can be
eased by o First line: emollients/non-medicated shampooso 2nd line or widespread:
topical glucocorticoids/topical ketoconazole 2778: Staphylococcal Scalded Skin
Syndrome (SSSS; �Ritter Disease�) ?? Presentation: typically occurs in children
<10yr; adults with kidney disease/immune compromise o Prodrome: fever,
irritability, skin tendernesso Exantherm: facial erythema??generalized erythema
(within 48hr)??superficial flaccid bullae form (Nikolsky sign +, bursting with
crusting common) * ?? �Pathophys: exfoliative toxin targets/destroys desmoglein 1??
failure of keratinocyte adhesion in the superficial dermis resulting in
bullae/exfoliation (approx.
1-2wk) * ?? �Micro: S.aureus producing exfoliative toxin o Cultures of bullae are
often STERILE as the toxin is doing the damage, not the bacteria * ?? �Dx:
presentation * ?? �Tx: anti-staphylococcal Abx (nafcillin, oxacillin, or
vancomycin) + care of denuded skin o Low mortality in children; high mortality in
adults 4404: Superficial Infantile Hemangioma (Strawberry Hemangioma)??
Presentation: bright red, sharply demarcated, blanching superficial plaque arising
in the first days/weeks of life and rapidly growing within 1st two years of life.o
May appear on any organ which may cause problems; eyelid
(strabismus/disfigurement), liver (bleeding), trachea (airway compromise)o Most
common benign vascular tumor of children * ?? �Pathophys: bed of capillary growth
separated only by bits of connective tissue * ?? �Dx: presentation * ?? �Tx:
spontaneous regression with no treatment unless causing problems o If causing
problems: Propranolol 10742: Signs of Deliberate Scalding Injury * ?? �Accidental:
non-uniform depth, poorly defined margins, & �splash injuries� * ?? �Deliberate:
involving buttocks/back/legs with sparing of flexor surfaces (lowered into water),
or a stocking/glove distribution (forced limb into water); uniform depth of burns,
sharp line of demarcation & delay in seeking medical help; CPS must be contacted
3122: Erythema Toxicum Neonatorum * ?? �Presentation: asymptomatic blotchy
erythematous papules/pustules ???more generalized/diffuse pattern which spares
palms/soles common to full-term neonates in the first two weeks of life * ?? �Dx:
presentation * ?? �Tx: reassurance Various Dermatologic Conditions * ?? �Nummular
Eczema: similar to tinea corporis; appears as itchy, red, annular rash, but
improves with emollients & topical corticosteroids (opposite of tinea) * ?? �Nevus
Simplex (macular stain, stork bite, salmon patch, angel kiss): blanching, pink-red
patches often appearing on the eyelid, glabella, or midline posterior neck
presenting at birth; often regress spontaneously but may persist as benign lesions
* ?? �Erythroderma (exfoliative dermatitis): erythema/scaling on over 90% of the
body; individual plaques pop up and coalesce * ?? �Purpura fulminans: life
threatening N.meninigidis or S.pneumo infection causing intense fever/shock, DIC,
and blue-purple hemorrhagic skin lesions Psychiatric/Behavioral 3386: Pyromania
* ?? �Presentation/Dx: impulse control disorder consisting of deliberate fire
setting >1 time, tension/arousal prior to act with relief/pleasure witnessing fire,
actions are for no external/secondary gain/attention o Often fascinated with things
tangentially related to fire (firefighters, fire stations, etc.) * ?? �Tx: CBT
4924: Child Sexual Abuse * ?? �Normal (Toddler): exploring own/others genitals,
masturbatory movements, undressing self/others * ?? �Normal (School aged):
interested in sexual words/play, questions about reproduction/sex, masturbatory
movement (progressively sophisticated) ?? Abnormal: repeated object insertion into
anus/vagina, sex play depicting oral/anal/genital-genital contact, use of
force/bribes/threats in sex play, inappropriate sexual knowledge o Abnormal
behavior of sexual abuse should prompt further investigation o May also coincide
with anal/genital trauma (which should be assessed) oo o o 2470/4855: ADHD??
Presentation/Criteria: inattentive or hyperactive symptoms >6mo, present before age
12, occurring in >2 locations, and causing significant impairmento Inattentive:
difficulty focusing, distractibility, does not listen/follow instructions or may
�half- heartedly� complete tasks, disorganized, forgetful, loses/misplaces objectso
Hyperactive: fidgety, unable to sit still, �driven by a motor�, hyper-talkative,
interrupts, blurts out answers even after prompting to stopo Often getting a
parent�s assessment (home) and a teachers assessment (school) with validated ADHD
scales gives good insight into the problem, aiding with diagnosis ?? Tx: o
?????????o ??????2516/3379: Autism Spectrum Disorder * ?? �Presentation: o o o ?? o
?????????o ????????????o o * ?? �Tx:o o o Typically, perpetrator is male and knows
the victim Girls are far more likely the be victims of such abuse; especially
during pre-adolescence Considered the most invasive form of abuse, often leading to
long-term sequelae If a child EVER mentions or hints at sexual abuse, it must be
taken seriously immediately Pharmacotheray + Educational/Behavioral interventions
(not just Adderall!) Pharmacotherapy First line: methylphenidate,
dextroamphetamine, mixed amphetamine salts (stimulants) Second line: Atomoxetine
(NE reuptake inhibitor) Guanfacine or Clonidine (a2-agonists) may be used as
adjunct therapy Educational/Behavioral Behavior modification/social skills training
Accommodation at school A wide-range of social impairment and restricted &
repetitive behaviors/interests Can be mild (formerly known as Asperger's disorder)
to very severe Often recognized between 1 and 2 years old Genetic correlates with
fragile X syndrome, trisomy 21, Rett syndrome, tuberous sclerosis Criteria Problems
with social interaction and communication including: impairment in normal
social/emotional interactions deficits in nonverbal communication skills
difficulty/lack of interest in establishing interpersonal relationships Restricted,
repetitive patterns of behavior, interests, and activities including: intense,
peculiar interests inflexible adherence to rituals ("rigid through patterns")
stereotyped, repetitive motor movements (hand flapping) hyper/hyporeactivity to
sensory stimulation (reactivity to certain textures) Begins in early childhood
development Cause significant social/occupational impairment Level of intellectual
impairment and level of language impairment is best predictor of prognosis Early
interventions can help maximize these pts communication/ability to function
socially Remedial education/behavioral therapy are mainstays Low dose atypical
antipsychotics may be used to help limit aggression/irritability o o 3760/8923:
Obsessive Compulsive Disorder (OCD) ?? Presentation: o o ?????????o ?? Tx:o o
????????????4898: Imaginary Friends are common in children aged 3-6yr but may
persist throughout school age. These serve no detriment to social relationships and
often aid in developing communication/story-telling skills. These are totally
normal development for these ages. 3384: Trichtillomania ?? o o o ?? o o o ?? Tx:o
o 4893: Neonatal Abstinence Syndrome?? Opiates/Heroin: irritability, high-pitched
cry, tremors, seizures, sweating, sneezing, tachypnea, poor feeding, loose stools,
vomitingo Heroin (48hr post-natally), Methadone (72hr post-natally) present at
different times, but may be delayed up to 4wk post-natalo Tx: small/frequent feeds,
swaddling, low stimulation +/- heroin weaning Ultimate goal is to recover as much
social skill as possible for these kids Assess for potential causes of
pain/discomfort in the child. Apparently the pain can drive these children to these
more intense behaviors. Disorder comprised of obsessions and compulsions:
Obsessions: recurrent/intrusive/undesired thoughts that cause anxiety Compulsions:
repetitive behaviors or mental rituals; failure to complete a compulsion = anxiety
Performed in response to an obsession Done to relieve stress or avoid disaster Not
realistically linked with their trying to prevent ?? Criteria o Pt experiences
obsessions and/or compulsions that consume >1hr of their day or cause significant
distress Not from substance/medication/disease CBT + Pharmacotherapy CBT focuses on
gradual exposure to stimuli that trigger rituals and prevention of the compulsion
done to alleviate it Pharmacology 1st line: SSRIs (often high dose) 2nd line:
serotonin selective TCAs or clomipramine Antipsychotics may be used in augmentation
Last resort: brain surgery or ECT Presentation: Chronic compulsion to pull out hair
More common in women (10:1 ratio) Usually onset with puberty/associated with
stressful events Often involves scalp, eyebrows, eyelashes, but can be any hair
Criteria: Recurrent pulling of hair, resulting in hair loss Repeated attempts to
stop/decrease pulling hair Causes significant stress/not caused by something else
CBT is the best evidenced therapy SSRIs, anti-psychotics, N-acetylcysteine, or
lithium all can have some benefit ?? Cocaine: jitteriness, excessive sucking,
hyperactive Moro reflex * ?? �Phenytoin (fetal hydantoin): nail/digit hypoplasia,
dysmorphic facies, mental retardation, poor growth * ?? �Valproic Acid: increased
risk of NTD, cardiac malformations, and abnormal facies (cleft lip, narrow head,
midface hypoplasia, broad/depressed nasal bridge, long philtrum) 3380: Selective
Mutism ?? o o o ?? o o ??????o 3375: Tourette�s Disorder ?? o o o o o ?? o o o ??
Tx: o o o Oppositional Defiant Disorder ?? o o o o ?? o o o o ?? Tx: o For the
Child: Behavior modification/problem-solving skills training Presentation: Rare
condition where a patient does not speak in specific situations often manifests in
childhood usually occurs in social situations pt may be silent, quietly whisper, or
only use non-verbal means of communicating Criteria: Consistent failure to speak in
select social situations despite normal speech in others Mutism not the result of
language difficulty or communication disorder Last >1 month (cannot be the 1st
month of school) Significant impairment in academic/occupational/social function ??
Tx:o 1st line: CBT or family therapy SSRI may be used if anxiety is present (not
uncommon for these pts) Presentation: A severe tic disorder comprised of both motor
and vocal tics Tics are common at some point in childhood, but persistent tics are
abnormal
Often onset around age 5, sometimes alongside a stressful life event Tics may wax
or wane/change in type Often tics lessen in adolescence and diminish in adulthood
Increased incidence of development of Obsessive compulsive disorder (OCD)/ADHD
Criteria Multiple motor tics AND at least 1 vocal tic occurring for >1yr after
onset of 1st tic Onset prior to 18 years old Not caused by a substance or another
medical condition Behavioral interventions (habit reversal therapy) to minimize
tics are a mainstay of treatments + Medications are used if the tics begin to
impair function First line: Guanfacine (a2-agonist) Second line: Clonidine (a2-
agonst; more sedating) Atypical/typical antipsychotics may be used in severe cases
Presentation: Irritability/anger, defiance, or vindictiveness causing
dysfunction/distress Commonly seen in pre-adolescent boys May transform into
Conduct Disorder (most do not however) Classically the child has no trouble with
peers but lots of trouble with teachers/parents Does NOT involve physical
aggression or violation of others' basic rights Criteria Anger/irritable mood
(losing temper, touchy, often angry) Argumentative/Defiant Behavior (breaks rules,
argues with authority figures, annoys others) Vindictiveness (spiteful at least 2x
in past 6 months) Behavior causes distress or has negative impact on pt or people
around pt o For the Adult: Parent Management Training (improve limit
setting/enforcement) Conduct Disorder Criteria ?? o o ?? o o o o o
Hematology/Oncology
3172/3571/3640/3713/3785/3786/3838/3916/4341/4342/4439/4468/4825: Sickle Cell
Disease ?? Presentation: vaso-occlusive pain crisiso Acute, severe pain somewhere
in the body, low-grade fever, redness/warmth of affected region, sometimes after a
trigger (exercise, dehydration, etc.)o Dactylitis (hand-foot syn; symmetric
swelling & tenderness of hands/feet) is the earliest visible manifestation of a
pain crisiso X-ray may show soft tissue swelling/mottled bone (recurrent) ??
Complications:o Isothenuria�polyuria,nocturia,andhematuria(microscopicorgross) ???
Infarction of renal vasa recta??impaired concentrating ability of kidney ???Most
common complication of sickle cell diseaseo Acute Chest Syndrome � cough, SOB,
chest pain, hypoxemia + new pulmonary infiltrate resulting from damage to pulmonary
vasculature/vascular congestiono Megaloblastic Anemia � due to folate deficiency
from high RBC production to compensate for high RBC turnover (B12 can occur but
rare)o Aplastic Crisis � acute severe anemia (<6 g/dL), low reticulocyte ct (<1%),
no splenomegaly; normal WBCs and platelets; may have functional heart murmur from
hyperdynamic flow * ???�Secondary to Parvovirus B19 infection (Fifth�s disease:
fever, nausea, flu-like symptoms, slapped cheek rash); virus infects RBC bone
marrow precursors and halts erythropoiesis * ???�Tx: Blood transfusion to keep
counts up till virus resolves o Splenic sequestration crisis � acute severe anemia
(<6g/dL), thrombocytopenia, high reticulocyte count, rapidly enlarging spleen;
normal WBC count???Vasoocclusion/outflow obstruction causing pooling of RBCs within
the spleen ???Can becomes severe enough to cause hypovolemic shock???Occurs prior
to autoinfarction of spleen o Functional Asplenia � by age 5, susceptibility to
encapsulated organisms; Howell-Jolly Bodies o Priapism � penile outflow obstruction
(common in children/adolescents)o Other � Osteomyelitis (S.aureus most common;
Pseudomonas more common than average person), avascular necrosis of the femoral
head (sickling occlusion), pediatric stroke (SCD is most common cause), Increased
risk of MI (chronic anemia/overworking heart), gallstones (increased RBC turnover
causing pigment overload), Serious disorder where pt will willfully violate the
rights of people/animals May be cruel to animals or cause physical/sexual violence
without remorse Associated with anti-social personality disorder (should be
assessed for this at age 18) Criteria Must be younger than age 18 Aggression to
people and animals (bullying, threats, physical fights, cruelty, theft, forcing
people to undergo sexual acts) Destruction of property (Fire setting or other modes
of destruction) Deceitfulness or Theft (Engaging in break-ins, stolen items
with/without confrontation) Serious violation of rules (stays out late before 13
years old, run away from home overnight at least twice, truant from school before
age 13) ?? Pathophysiology: autosomal recessive mutation in the B-globin gene for
Hb (Glu??Val) producing HbS o Sickle cell Disease = both hemoglobin genes affected
and encode for HbSo Hb distribution: HbA (0%), HbS (95%), HbF (5%)o Low O2 tension
causes polymerization of Hb??sickling of RBCs??adhesion??occlusion * ?? �Micro:
functional asplenia results in difficulty fighting off encapsulated organismso
S.pneumo (Non-vaccine serotypes) � most common cause of pneumonia (even with
vaccines) o H.flu/N.meningitidis � encapsulated, but rarely cause problems in
vaccinated kidso Salmonella/S.aureus � most common causes of osteomyelitis * ??
�Dx: presentation + hemoglobin electrophoresis (shows HbS) * ?? �Tx: o Acute Crisis
� hydration/analgesia +/- RBC transfusion o Long-Term Maintenance ???Regular
baseline CBC + regular CBC/reticulocyte counts; CXR at 2yr of age +
periodically ???Hydroxyurea (increase HbF to >15%; concern of reversible
myelosuppression)???Vaccination against encapsulated organisms (S.pneumo,
N.meningititis, Hib, etc.)???Prophylactic penicillin until age 5 (helps protect
against S.pneumo) ???Folic acid supplementation (prevents megaloblastic anemia)
3967/3787/4825: Sickle Cell Trait * ?? �Presentation: typically, no features of
sickle cell trait, but sub-clinical damage may contribute to long- term
complications of diseaseo May have family members or relatives with sickle-cell
anemiao More common in African, Middle-Eastern, and Mediterranean people * ??
�Complications: o Renal: ???Episodic renal papillary necrosis (massive hematuria
that resolves spontaneously) ???Inability to concentrate urine (infarction of vasa
recta)???Distal renal tubular necrosis???Renal medullary carcinoma o Splenic
infarction (more common at higher altitudes) o Venous thromboembolismo Priapism
* ?? �Pathophysiology: autosomal recessive mutation in the B-globin gene for Hb
(Glu??Val) producing HbS o Sickle cell Trait = only one hemoglobin gene affected
and encode for HbS * ?? �Dx: gel electrophoresis showing HbA & HbS with higher
proportion of HbA 4436: Hyposthenuria * ?? �Impaired ability to concentrate urine
in the glomerulus often resulting in frequent urination and frequent nocturia seen
in patients with sickle cell trait/diseaseo RBC induced blood thickening within the
thin vasa recta along the glomerulus in the inner medulla (high solute
concentration), causes impaired countercurrent exchange with the glomerulus
inhibiting free water absorption * ?? �NOTE that this does not damage this kidney
in any way. It�s really a blood/vascular problem. The kidney is actually
functioning just fine! 4249/4861: Hemophilia A & Hemophilia B (Christmas Disease)
?? Presentation: delayed/prolonged bleeding after minor trauma/procedure o
Hemarthroses (bleed into joint), intramuscular hematomas, GI bleeding, hematuria
(without kidney damage), and spontaneous bruising are all common signs o Hemophilic
arthopathy: chronic worsening joint pain, swelling, limited range of motion ???
Hemarthrosis??deposition of iron/hemosiderin into joint??synovitis/fibrosis ???Best
seen on CT scan of affected joint (shows fibrosis/deposition) * ?? �Labs: Prolonged
aPTT, decreased Factor VIII or Factor XI, normal platelet count/bleed time/PT * ??
�Pathophysiology: X-linked recessive disorder causing lack of clotting factors (A =
factor VIII def; B = factor IX def); male severely affected; females mildly
affected * ?? �Dx: presentation + labs * ?? �Tx: Administration of missing factor
through injection o Desmopressin can promote Factor VIII production and be used in
mild Hemophilia A 4112/4183: Vitamin K Deficiency * ?? �Vit K is a critical co-
factor for enzymatic carboxylation of clotting factors II, VII, IX, X. Typically
vitamin K stores can last 30 days but in sick folks only last about 1 week! * ??
�Presentation: bleeding diathesis with evidence of pathologic anticoagulation o
Classically lack of supplementation at birth, malabsorption for any reason, or
liver disease will lead to Vit.K deficiency * ?? �Dx: clinical presentation * ??
�Tx: Fresh Frozen Plasma administration with vitamin K injection 4819: Neonatal
Polycythemia ?? Presentation: neologic signs (irritability, jitteriness), ruddy
skin, hypoglycemia/hypocalcemia/ hypomagnesemia (increased RBC metabolism),
respiratory distress/cyanosis/apnea, or abdominal distention o Often child�s
glucose levels stabilize by 24-48hro Hypocalcemia may result in tetany which will
not resolve until 72-96hr (calcium gluconate infusion may be necessary to stop
deterioration)?? Pathophysiology: extremely high hematocrit (>65%) causing
increased viscosity of blood causing �sludging� and poor flow to end-organso
Increased erythropoiesis from neonatal hypoxia from placental insufficiency
(maternal diabetes, maternal HTN, smoking, & IUGR)o Erythrocyte transfusion:
delayed cord clamping or twin-twin transfusion syndrome * ?? �Labs: CBC (hematocrit
>65%), CMP (hypocalcemia/hypomagnesemia/hypoglycemia) * ?? �Dx: presentation +
hematocrit >65% * ?? �Tx: o Asymptomatic: hydration (feeding or IV fluids)o
Symptomatic: partial exchange transfusion (take out whole blood & infuse normal
saline) until hematocrit normalizes 3647/4359: Characteristic Findings on
Peripheral Blood Smears * ?? �Basophilic Stippling: multiple blue granules in RBCs
resulting from ribosome precipitation
from lead poisoning, heavy metal poisoning, or thalassemias * ?? �Howell-Jolly
Bodies: basophilic dots within RBC seen with Wright Stain; consist of residual DNA
left over from cell division, typically are removed by the spleen; occur due to
asplenia/functional asplenia * ?? �Pappenheimer Bodies: basophilic clusters of
heme-Fe2+ in RBCs that stain with both Wright/Prussian Blue stains. Appear most
frequently with increased hemolysis, but are found in normal smears * ?? �Heinz
Bodies: basophilic dots on RBCs peripherally caused precipitation of Hb proteins
from G6PD- deficiency due to oxidative damage form lack of glutathione to serve as
a reducing agent * ?? �Degmacyte (Bite Cell): RBCs with small �bites� taken out of
them; result of normal functioning spleen removing precipitated Heinz bodies
splenic macrophages (they bite out the Hb, leave RBC intact) * ?? �Spherocyte:
smaller RBCs with no central clearing, result of blebbing off the RBC membrane
resulting in increased surface area & loss of central clearing; hereditary
spherocytosis * ?? �Schistocytes (Helmet cells): fragmented RBCs typically due to
microangiopathic hemolytic anemia (RBCs get sheared in intravascular platelet clots
due to some patholologic process) * ?? �Echinocyte (Burr cells): spiny RBCs with
small spines of uniform size/shape; classically occurs in uremia, but may also
occur in anorexia nervosa, long-distance running, dialysis, or other things * ??
�Acanthrocyte (spur cells): spiny RBCs with large spines of varying size/shape;
wide variety of pathology can cause these (must look at clinical picture) * ??
�Dacrocyte (Teardrop cells): occur with hematopoiesis outside of the bone marrow
after myelofibrosis; may occur in Thalassemias, esp. post-splenectomy * ?? �Sickle
Cells: smooth, �sickle-shaped� cells caused by abnormal B-globin chain
precipitation in SCD * ?? �Target Cells: abnormal RBCs with central clearing and
small cleared out ring; result of abnormal RBC membrane interactions due to
thalassemia * ?? �Microcytosis/Hypochromia: small RBCs with more prominent central
clearing; iron deficiency anemia (less Hb to fill up the RBC �doughnut�)
4331/3609/4347: G6PD deficiency (glucose-6-phosphate dehydrogenase) o ?? �X-linked
recessive disorder which can result in acute anemic crises in response to certain
situations. G6PD typically used to generate glutathione to minimize oxidation
damage to RBCs. Should a oxidizing stressor come on, G6PD deficiency pts are not
able to compensate. o Classically triggered by infection, oxidant drugs (anti-
malarials, sulfa drugs, etc.), and fava bean o ?? �Presentation: acute hemolytic
crisis (fever, jaundice, abdominal pain, dark urine) due to hemoglobin denaturation
and disruption/lysis of RBCs. o Labs: normal G6PD levels are typical (as the
deficient cells were destroyed and new reticulocytes have normal G6PD levels)??re-
test in 3 months after crisiso Smear: degmocytes (�bite cells�) and Heinz bodies
(denatured basophilic hemoglobin) o Urine may stain with Prussian Blue (+ is
presence for iron, thus hemolysis is occuring * ?? �Dx: clinical scenario/blood
smear * ?? �Tx: supportive care during crisis with avoidance of precipitating
substances 3440/4383/4860: Immune Thrombocytopenia (ITP) * ?? �Presentation: recent
viral infection, asymptomatic petechiae/ecchymosis, mucocutaneous bleeding
(epistaxis, hematuria, GI bleeding)o In children; occurs most common between 2-5yr
* ?? �Pathophysiology: Platelet destruction/inhibition of megakaryocyte production
by IgG anti-platelet membrane glycoprotein antibodies * ?? �Labs: isolated
thrombocytopenia (<100,000) * ?? �Peripheral Blood Smear: megakaryocytes with no
other abnormalities * ?? �Dx: clinical presentation, CBC, Labs with HIV/HCV testing
(may be cause of disease) * ?? �Tx: o Kids: Skin only = observe | bleeding = IVIG
or glucocorticoidso Adults: Plt >30k + no bleed = observe | Plt <30k or bleed =
IVIG or glucocorticoids 2870/3062/3282/4333: Hereditary Spherocytosis??
Presentation: hemolytic anemia, jaundice, splenomegaly classically in European-
descent folks o Complications: ???Aplastic anemia in Parvovirus B19 infection???
Pigmented gallstones (increased hemolysis causing increased bilirubin)???
Overwhelming sepsis from encapsulated organisms if spleen has been removed as Tx
* ?? �Pathophysiology: Autosomal dominant defect in spectrin or ankyrin RBC
structural proteins resulting in RBC membrane blebbing and eventually deformation
into fragile spheres (not bi-concave disks) * ?? �Labs: anemia, inc. MCHC
(>36%)/dec. MCV (small RBCs), indirect hyperbilirubinemia * ?? �Peripheral Blood
Smear: abundant spherocytes with some shearing of RBCs * ?? �Dx: Osmotic fragility
test (increased fragility), acidified glycerol lysis test (increased lysis), or
abnormal eosin-5-maleimide binding test, with negative Coomb�s test and blood smear
* ?? �Tx: o Definitive: splenectomy (stop RBC destruction) with following
additional interventions o ???�Anti-pneumococcus, Haemophilius, and meningococcus
vaccines before splenectomy o ???�Folate supplementation o ???�Daily oral
penicillin for 3-5yrs after surgery due to risk of sepsis post-splenectomy, which
apparently lasts for >30yrs even though our prophylaxis only goes on for about 5
years. o Symptomatic: blood transfusions (often needed in neonates who cannot
produce new RBCs quickly enough) 3774: Anemia of Prematurity ?? Presentation:
asymptomatic (most common); tachycardia, apnea, poor weight gain o Diagnosis of
exclusion after ruling out hemolysis, enzyme defects, Hb-opathies, infection o
Typically, physiologic RBC nadir in childhood is around 2-3mo * ??
�Pathophysiology: low EPO/decreased reticulocyte production (increased O2 after
birth limits EPO production), short RBC lifespan (HbF only lasts 50 days), &
frequent phlebotomy if in NICU (lab draws) * ?? �Labs: CBC (low
Hb/Hct/reticulocytes), smear (normocytic, normochromic RBCs) * ?? �Dx: presentation
+ labs * ?? �Tx: iron supplementation, minimize blood draws, RBC transfusions (only
if necessary; will prolong disease course from further EPO suppression)o EPO
administration is NOT effective for decreasing need for RBC transfusion
2875/2877/4358: Iron Study Characteristics in Microcytic Anemias o ?? �Iron
Deficiency: not much iron around, thus the body is looking to take up as much as
possible o Decreased: MCV, serum iron, ferritin, transferrin saturation (iron/TIBC)
o Increased:TIBC o ?? �Thalassemia: poor production of hemoglobin leaves iron out
in the blood o Decreased: MCV, TIBC o Increased: iron, ferritin, transferrin
saturation o ?? �Anemia of Chronic Disease: the body takes inflammation to mean
�bacterial infection� and sequesters iron in hopes that it�ll limit bacterial
reproduction.o Decreased: MCV, iron, TIBC, transferrin saturationo
Increased:ferritino Typically, a chronic inflammatory disease (autoimmune is
classic!) can be noted from vignette. Treatment is as follows: ???Underlying
condition treatment (autoimmune disease will be immunosuppressed) ???If no
improvement??administer EPO to stimulate RBC production???If no improvement??packed
RBC transfusion to get RBC count back up 2857/4858/4876: Iron Deficiency Anemia
* ?? �Risk Factors: prematurity, lead exposure, consuming low-iron formulao <1yr:
consuming low-iron formula, cow/soy/goat milk, exclusive breastfeeding after 6mo o
>1yr (toddler): >24oz cows milk/day, <3 servings of iron rich foods/dayo Also
classically occurs in teenage girls (poor diet, rapid growth, menstruation losses)
* ?? �Presentation: tiredness, pallor, pica, koilonychias (spoon nails)??
CHF/cardiac dilatation (very severe) o The most common nutritional deficiency in
childhoodo Must be differentiated from thalassemias (very common cause of childhood
anemia) * ?? �Pathophysiology: many many reasons (bleeding, RBC problems, poor
intake, etc.)o Cow�s Milk <24oz (700mL)/day: low Fe2+ content & bioavailability;
may induce milk-protein colitis causing blood loss in stool (children cannot handle
the milk protein) * ?? �Labs: CBC (anemia (Hct <30%), low MCV, high RDW >20%), iron
studies (decreased iron/ferritin, increased TIBC), normal Hb elecrophoresis o RDW
elevations occur in nutrient deficiencies because nutrient levels vary through the
day; often RDW is the 1st abnormality that can be spotted in iron deficient anemia
o Mentzer index (RDW/RBC) usually >13 (due to decline in RBCs) * ?? �Peripheral
Blood Smear: hypochromia/microcytosis of RBCs * ?? �Dx: presentation + labs + smear
o Childhood Screening: CBC of all children 1yr of age * ?? �Tx: empiric oral iron
supplementation (4-6mg/kg/day) + Vitamin C (enhance iron absorption) o Re-check CBC
in 4 weeks following iron initiation; if Hb has risen by 1g/dL then continue for 2-
3mo and make appropriate diet changes. Re-check at next well-child visit o Blood
transfusions are rarely needed in children, even if Hb <4g/dLo If oral iron does
NOT resolve anemia, Hb electrophoresis (thalaseemias), colonoscopy (GI bleed), or
serum creatinine (renal dysfunction) may be indicated 4348: Pica/Pagophagia?? Pica
� appetite for substances other than food (clay, dirt, or paper are common) o May
have exotic appetite (hair, light bulbs, etc.) when associated with psychiatric
disease * ?? �Pagophagia � appetite for ice * ?? �Both classically associated with
iron deficiency anemia and may appear before iron deficiency is present, thus any
patient with these signs/symptoms should have bloodwork done 4343/4440/4875: A & B-
Thalassemia Minor * ?? �Presentation: fatigue/mild microcytic anemia which does NOT
respond to iron supplementation o Often anemia is picked up on 1yr screening &
doesn�t respond to supplemental iron! * ?? �Pathophysiology: Defect in one of the
genes for a or B-hemoglobin resulting in reduced
hemoglobin production, thus mild chronic anemia refractory to iron supplementation
o More severe variants (major variants) involve more than 1 globin genes o Classic
in people of Mediterranean origin * ?? �Labs: CBC (low Hct (>30%), low MCV, normal
RDW/RBCs), iron studies (normal-increased iron/ferritin), Hb electrophoresis
(Alpha-thal = normal, Beta-thal = increased Hb-A2) o Mentzer Index (MCV/RBC) <13
due to normal/increased RBCs * ?? �Peripheral Smear: target cells & dacrocytes
(teardrop cells) * ?? �Dx: failure to respond to Fe2+ supplementation, genetic
testing or or elevated HbA2 on electrophoresis (if B-thalassemia minor) * ?? �Tx:
symptomatic treatment 3818: Diamond-Blackfan Anemia (Congenital Pure Red Cell
Aplasia or Congenital Hypoplastic Anemia) * ?? �Presentation: neonate with
progressive pallor, FTT, congenital anomalies (webbed neck, cleft lip, shield
chest, triphalangeal thumbs; 50% of cases), mental retardation (50%) * ??
�Pathophysiology: sporadic mutational defect in erythroid progenitor cells
resulting in accelerated apoptosis (some AD & AR defects, but much less common 15%)
* ?? �Labs: CBC (macrocytic anemia, low reticulocyte ct), Hb electrophoresis
(elevated HbF) * ?? �Smear: macrocytic RBCs without hypersegmentation of
neutrophils * ?? �Dx: presentation + labs + smear * ?? �Tx: corticosteroids (limit
apoptosis) or blood transfusions (if unresponsive to steroids) 3200/4438: Aplastic
Anemia * ?? �Presentation: pallor, fatigue, weakness, appetite loss, easy bruising,
petechiae, mucosal bleeding, fever * ?? �Pathophysiology: injury to the bone marrow
results in severely impaired hematopoiesis o Chemotherapy, Abx (chloramphenicol),
drugs (NSAIDs, sulfonamides, carbamazepine), insecticides, toxins (benzene, glue,
CCl4), infections (HIV, EBV, parvovirus B19), thymoma and MANY other things can
cause this * ?? �Labs: CBC (normo/macrocytic anemia, leukopenia, thrombocytopenia,
low reticulocyte ct) * ?? �Dx: bone marrow biopsy (marked hypocellularity in all
lines, fatty infiltration) * ?? �Tx: (depends on cause) 4438: Fanconi Anemia ??
Presentation: congenital aplastic anemia (most common cause) + congenital
abnormalities o Bone marrow: aplastic anemia & progressive bone marrow failureo
MSK: short stature, microcephaly, microphthalmia, absent/hypoplastic thumbs,
hypogonadism o Skin: caf�-au-lait spots, hypo/hyperpigmented areas, large freckleso
Eyes: strabismuso Ears: low-set ears, middle ear abnormalities (hemorrhage, poor
development, chronic infections, deafness) * ?? �Pathophysiology: autosomal or X-
linked recessive mutations in DNA repair genes * ?? �Labs: CBC (pancytopenia), bone
marrow biopsy (marked hypocellularity, fatty infiltration) * ?? �Dx: presentation +
genetic analysis showing chromosomal breaks * ?? �Tx: hematopoietic stem cell
transplant 3437/3438: Hemolytic Uremic Syndrome (HUS) * ?? �Presentation:
antecedent bloody diarrhea followed by classic triad: o Microangiopathic hemolytic
anemia: jaundice, pallor, fatigueo
Thrombocytopenia:petetchiae,bruising,increasedbleedingo Acute kidney injury: poor
urine output, edema, elevated BUN/Creatinine * ?? �Pathophysiology: Shiga toxin
invades colonic endothelium & kills the cells causing bloody diarrhea & damages
endothelium of vasculature (platelet activation/shearing of RBCs) o Classically
child ate undercooked hamburger, unwashed fruits or vegetables, or visited a
petting zoo before the EHEC started * ?? �Micro: E.coli (EHEC) producing Shiga-like
toxin (O157:H7) or Shigella (Shiga toxin) * ?? �Labs: CBC (anemia,
thrombocytopenia, inc reticulocyte ct), indirect hyperbilirubinemia, iron studies
(normal-increased ferritin, decreased haptoglobin), renal function (increased
creatinine, proteinuria, microscopic or gross hematuria) * ?? �Smear: schistocytes
(helmet cells) * ?? �Dx: presentation + labs + smear * ?? �Tx: supportive care
(fluids??blood transfusions,??dialysis) o Do NOT use anti-motility agents in EHEC
(will retain toxin = worse damage)o Do NOT use antibiotics for Tx of hemorrhagic
diarrhea (may increase incidence of HUS) 2867/3284: Acute Lymphoblastic Leukemia
(ALL) * ?? �Presentation: non-specific systemic symptoms +/- bone pain,
lymphadenopathy, hepatosplenomegaly, pallor (from anemia), petechiae
(thrombocytopenia)o Most common childhood cancer (occurs typically age 2-5yr; male
predominance; ^Down syn.) * ?? �Pathophysiology: abnormal proliferation of
lymphoblasts in bone marrow causing WBC hyperproduction and crowding out of
erythroid progenitor cells * ?? �Labs: CBC (anemia, thrombocytopenia, leukocytosis
with lymphocyte/lymphoblast predomience) * ?? �Imaging: CXR showing widened
mediastinum (thymic hyperplasia) * ?? �Smear: lymphoblasts/atypical
lymphocytes/lymphocyte predominance o Lymphoblasts can be confirmed with staining
(PAS+, TdT+) o Myeloblasts (like in AML) would stain positive for peroxidase+
granules * ?? �Dx: bone marrow biopsy with >25% lymphoblasts * ?? �Tx:
corticosteroids + multi-drug chemotherapy/bone marrow transplant ENT2830/3972:
Acute Otitis Media (AOM) * ?? �Risk Factors: formula intake (in lieu of
breastmilk), cigarette smoke exposure, allergic rhinitis, recent URI, craniofacial
abnormalities, chronic middle ear effusion * ?? �Presentation: fever, URI symptoms,
unilateral or bilateral ear pain (tugging on ear), decreased hearing,
immobile/inflamed/distorted tympanic membrane o Pus/drainage may occur if rupture
of tympanic membraneo Complications: Bullous Myringitis (serous, fluid-filled
blisters on the tympanic membrane), chronic supprative otitis media, eardrum
perforation/conductive hearing loss, mastoiditis, labrinthitis, cholesteatoma,
tympanic sclerosis, meningitis * ?? �Pathophysiology: accumulation of infected
fluid in the middle ear; common in children aged 6-36mo due to Eustachain tubes
being narrow/short, thus easily clogged * ?? �Micro: o Most common: Streptococcus
pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis o If
persistent/recurrent: Penicillin-resistant S. pneumoniae (B-lactamase production) *
?? �Dx: inspection of the ear +/- pneumatic otoscopy showing abnormal movement o
Tympanocentesis may be done to drain/culture, esp. with failure to standard therapy
* ?? �Tx: 10-day course amoxicillin (80 mg/kg/day); close follow-up o If
mild/unilateral, child >2yr, normal immune system: observationo If not responding
to amoxicillin (return of symptoms with 1 month): amoxicillin-clavulanic acid o If
allergic to penicillins: azithromycin 5-7 dayso If recurrent despite Abx (>3 inf in
6mo; >4 inf in 12mo): myringotomy with tympanostomy tube + tympanocentesis/cultureo
Decongestants/antihistamines are NOT appropriate as part of treatment 2839: Otitis
Media with Effusion (OME) * ?? �Presentation: Middle ear effusion resulting in mild
conductive hearing loss without infectious symptoms. Ear canal shows dull tympanic
membrane with hypomobility on pneumatic otoscopyo The most common middle ear
pathology in HIV/AIDS due to lymphadenopathy obstructing the Eustachian tube * ??
�Dx: presentation +/- pneumatic otoscopy ?? Tx: Children with serious otitis media
(usually from a Hx of sinus/ear infections) can likely be observed for spontaneous
resolution. o Tympanostomy tubes: If hearing changes persist for 3 months or
greater; aid in draining middle ear fluid and offset obstruction o Surgery:
helpful, but only used in chronic caseso There is NO medical therapy shown to help
serous otitis media Otitis externa (�Swimmer�s Ear�) * ?? �Presentation: ear
discomfort/pain/itching with traction (pulling on the ear), tenderness with tragus
manipulation, inflammation of the external ear canal +/- white discharge; overall
otherwise healthy o Classically occurs with some impairment of regular protective
mechanisms (swimming, cerumen removal, trauma, etc.)o Tympanic membrane will appear
normal * ?? �Dx: presentation ?? Tx: o Mild: topical application of acetic acid
(vinegar) to restore natural acidic environment o More severe: topical Abx
(floroquinolone)/corticosteroid + wick insertiono Perforated oral & topical Abx +
wick insertion 2828/3260: Malignant (necrotizing) Otitis Externa * ??
�Presentation: intense, unrelenting ear pain that�s worse at night & does not
respond to Abx o Purulent ear drainage/feeling of fullness; Ear canal shows
granulation tissue/edema.o Complications: osteomyelitis of the skull base with
cranial nerve involvement (facial droop) or TMJ involvement (pain radiating to jaw
& worsened by chewing) o Associated with poorly controlled
diabetes/immunosuppression in elderly patients * ?? �Micro: 95% of these are caused
by P.aeroginosa (classic if you�re also diabetic!) * ?? �Dx: clinical presentation
with CT/MRI evidence of infection * ?? �Tx: IV ciprofloxacin (first line) o
Fluoroquinolone resistant: other IV anti-pseudomonals (Pip-
tazo/cefepime/ceftazidime) o
FailuretorespondtoAbx:surgicaldebridement/biopsytoexcludecancer 2831: Cholesteatoma
* ?? �Presentation: chronic ear discharge +/- formation of heterogenous mass of ear
debris o Should be suspected in any pt with chronic ear drainage despite proper Abx
therapy o Complications: Hearing loss, cranial nerve palsies, vertigo, brain
abscess/meningitis * ?? �Pathophysiology: collection of debris within the middle
ear against the tympanic membrane that can lead to surrounding damage/destruction
of local tissueo Congenital:collectionofdebris/etcpresentfrombirtho Acquired:
chronic middle ear disease forms a contraction pocket within the tympanic membrane;
over time granulation tissue/skin debris collect in this pocket * ?? �Imaging: CT
head (assess damage to surrounding structures) * ?? �Dx: presentation + full
otologic exam + visualization * ?? �Tx: removal of cholesteatoma by ENT 4090:
Hearing Impairment in a Child * ?? �Etiology:
recurrent ear infections (most common), congenital hearing loss, etc. * ??
�Presentation: inattentiveness, not responsive to commands until modality other
than speech is used (tapping on the shoulder), poor language development, social
isolation o ADHD kids will have strong language development and are often quite
social ?? Dx/Tx: full otologic workup & addressing underlying problem 4201: Non-
Allergic vs Allergic Rhinitis * ?? �Non-allergic Rhinitis o Nasal congestion,
rhinorrhea, sneezing, post-nasal drip o Red, boggy nasal mucosao No obvious
allergic trigger with symptoms year-round o Typical onset >20y/o o Tx: intranasal
anti-histamine and/or intranasal glucocorticoid * ?? �Allergic Rhinitis o Watery
rhinnorhea, sneezing, with eye symptoms (red, watery, itchy eyes)o
Pale/bluishnasalmucosao Obvious allergic trigger or associated allergic disorder
with seasonal patterns o Typical onset <20y/o o Tx: intranasal glucocorticoid
2195/2847: Peritonsilar Abscess (�Quinsy�) * ?? �Presentation: fever, chills, sore
throat, muffled �hot potato� voice, uvular deviation, unilateral lymphadenopathy,
pooling of saliva, and trismus (unable to open jaw) from muscle spasmo Airway
obstruction and spread to parapharyngeal space (carotid sheath involvement) * ??
�Dx: clinical scenario with signs on oropharyngeal exam * ?? �Tx: immediate abscess
drainage via needle aspiration with culture/empiric antibiotics o GAS and
respiratory organisms should be covered 2432: Laryngomalacia * ?? �Presentation:
otherwise health infant (4-8mo most commonly) with stridor/�noisy breathing�
worsening when supine/feeding/URI & improving when prone or upright o GERD symptoms
are very common * ?? �Pathophysiology: laxity of the supraglottic structures * ??
�Dx: presentation + direct or flexible laryngoscopy (omega-shape epiglottis,
collapse of supraglotic structures during inspiration) * ?? �Tx: spontaneous
resolution by 18mo with normal function until then o If severe: surgical
supraglottoplastyo Appropriate treatment of GERD symptoms should always be attended
to Pulmonary/Critical Care 2466/3531/3830/3926/4030/4183/4187/8952: Cystic Fibrosis
?? Presentation: extremely wide-spread effects throughout multiple organ systemso
Disrupted Growth: early normal growth??deceleration of weight gain??deceleration of
length (poor feeding, poor absorption, recurrent sinopulmonary illness, etc.)o
Respiratory: chronic rhinosinusitis/nasal polyps, wheezing, extremely thick mucous,
pan- opacification of sinuses on X-ray, obstructive lung disease??
bronchiectasis/�barrel chest� with distant breath sounds, recurrent pneumoniao GI:
meconium ileus (inspissated meconium), pancreatic insufficiency/fibrosis with
exocrine dysfunction/pancreatitis (25%) (thick secretions/blockage??steatorrhea,
AEDK deficiencies???FFT, poor growth/development, epistaxis/easy bruising often of
extremities) & endocrine dysfunction (Diabetes, 25%), biliary cirrhosis/liver
failure, anal prolapse o Heme: Vitamin K deficiency (lack of Factors V, VII, IX, X
& protein C/S) = bleeding diathesis o Renal: nephrolithiasis/nephrocalcinosis (fat
malabsorption??sequrestration of gut Ca2+???increased free oxalate??oxalic acid
hyper-absorption??hyperoxaluria??Ca2+ oxalate stones) o Repro: men (infertility
from obstructive azoospermia >95%; congenital absence of Vas deferens; failure of
canalization due to inspissated mucus in genital tract; sperm production normal),
women (infertility 20%; thick cervical mucous, secondary amenorrhea from
nutritional deficiency) o MSK: osteopenia/fractures/kyphoscoliosis (Vit. D
deficiency), digital clubbing (lung dx) o Ears: hearing impairment (50%) secondary
to ototoxic Abx (aminoglycosides for Pseudomonas) * ?? �Pathophysiology: mutation
of CFTR (cystic fibrosis transmembrane conductance regulator) protein (chrom. 7) =
defective Na/Cl transporter causes inadequate passage of water into mucous
secretions ??extremely viscous secretions of lungs/GI/UG systems o The most common
autosomal disorder of white people o �F508 mutation most common; but many different
mutations are possible * ?? �Micro: recurrent pneumonia most commonly features
S.aureus (0-20yr) or Pseudomonas (+20yr); sometimes fungal infections of the lungs
can occur as well (Aspergillus most common) * ?? �Imaging: CXR may be indicated for
pulmonary disease, abdominal x-ray/enema for GI disease * ?? �Dx: clinical
presentation +/- specific mutation for CF * ?? �Newborn Screening: sweat chloride
test (elevated sweat chloride), immunoreactive trypsinogen assay (trypsinogen in
pancreas is poorly release, thus backs up into blood) * ?? �Tx: o Lung Problems:
chest physiotherapy, bronchodilators, corticosteroids, DNA-ase ???Lung transplant
is an option for very severe disease o Caloric supplementation: offset high
metabolic demand & malabsorptiono Pancreatic insufficiency: AEDK & pancreatic
enzyme supplementation +/- diabetes treatment ???Pancreas transplant is an option
for severe diseaseo Liver failure: liver transplanto Empiric Abx for pneumonia:
Cefepime (covers MSSA/Pseudomonas) + Vancomycin (MRSA) o ???�Fungal Pneumonia:
itraconazole or voriconazole (Aspirgillus) o ???�Prophylaxis: Azithromycin or
Ibuprofen (decreased inflammation & to slows development of bronchiectasis)o Nasal
polyps: intranasal corticosteroids or surgical removal 4638/4699: Anaphylaxis * ??
�Presentation: sudden development of respiratory distress, hoarseness, & urticarial
following some food/substance exposure * ?? �Pathophysiology: abnormal immunologic
response to certain normally tolerated proteins; pre-formed IgE antibodies against
these proteins results in rapid Type 1 reaction anaphylaxis (bronchoconstriction,
wide-spread inflammation and vasodilation/edema/hypotension) when encountered * ??
�Dx: presentation * ?? �Tx: IM epinephrine (Epi-pin) o B2 agonist activity �
bronchodilation & decrease in inflammatory mediator releaseo A1 agonist activity �
vasoconstriction (minimize upper airway edema)o Pts should carry a rapid injection
of IM epinephrine on them at all timeso If Bee-Sting (hymenoptra) allergy is cause
of anaphylaxis??venom immunotherapy from an allergist can be done to decrease
anaphylaxis risk from 30%??5% 4617/3027: Asthma Classification and Treatment * ??
�Intermittent: daytime symptoms <2x week | nighttime symptoms <2x month | short-
acting B-agonist use <2x week with normal baseline PFTs and no impairment of
function o Tx: PRN albuterol * ?? �Mild Persistent: symptoms >2x week but NOT daily
| nighttime symptoms 3-4x month | normal PFTs baseline with minor limitations of
activities o Tx: PRN albuterol, inhaled corticosteroid * ?? �Moderate Persistent:
daily symptoms, weekly nighttime awakenings, moderate limitation of activities,
with FEV1 60-80% predicted valueo Tx: PRN albuterol, inhaled corticosteroid,
inhaled LABA * ?? �Severe Persistent: symptoms throughout day, frequent nighttime
awakenings, very limited activity, FEV1 <60% predicted value o Tx: PRN albuterol,
high-dose inhaled corticosteroid, inhaled LABA, +/- oral prednisone 4105/4706:
Acute Asthma Exacerbation * ?? �Presentation: dyspnea, SOB, cough, accessory
respiratory muscle use, difficulty speaking, hyperventilation/tachypnea
(respiratory alkalosis, low PaCO2), lung hyperinflation, tachycardia * ??
�Pathophysiology: airway reactivity toward some irritant results in acute
inflammation, bronchoconstriction, and mucus plugging causing a failure of
ventilation o Common irritants are dust mites, animal dander, smoke, pollution,
allergens, URIs, GERD, exercise, Aspirin (AERD)/medications, or many other thingso
Exacerbations cause an acute release of IgE causing inflammation/fluid
accumulation/ pulmonary constriction/mucus productiono 2-4hr after an exacerbation,
the Late-Phase Reaction (LPR) occurs allowing for inflammatory WBC infiltration,
ultimately resulting in more long-term airway hyper-responsiveness * ?? �Labs:
blood gas, O2 monitoring * ?? �Dx: clinical signs/symptoms with history of asthma;
concerns for airway collapse are following: o Drowsiness/lack of breath sounds �
person is failing to move air (likely severe obstruction) and retaining CO2 causing
altered mental consciousnesso Normal PaCO2 on arterial blood gas � everyone will
hyperventilate, BUT if they�re so fatigued from the attack that they�re starting to
wear out, they can no longer hyperventilate, PaCO2 will go back to normal and
they�re getting towards the point where they�ll stop breathing from fatigue. ?? Tx:
o Assess ABCs??does patient need oxygen? Intubation?o SABA (albuterol)??+IV
corticosteroid (prednisone)??+ipratropium nebulizer??+one-time IV infusion of
magnesium sulfate (after 1-hr without response to other therapies)???
intubation/mechanical ventilation ???Wheezes may actually increase as air starts to
move again???Note that B-agonists will halt acute reactivity, but fail to stop
late-phase reactions and the subsequent airway hyper-responsiveness 4335: Asthma
exacerbation due to GERD?? Presentation: recent worsening of asthma symptoms with
normal lung exam. Often sore throat, morning hoarseness, worsening cough when
laying down (at night is common), need for inhaler following meals, dysphagia,
chest pain/heartburn, regurgitation sensation o Result of microaspirations causing
irritation and vagal hypersensitivity resulting in proclivity to bronchospasm o
Often coincides with weight gain (possibly due to a stomach ulcer!) ?? Tx: PPI
trial 3050: Exercise Induced Bronchoconstriction?? Presentation:
Bronchoconstriction/difficulty breathing often triggered by high volumes of dry,
cold air. o Classically occurs in athletes with current or previous diagnosis of
asthma! ?? Tx: o First line: Albuterol (short acting B-agonist) inhaler 10-20
before exerciseo Second line: Anti-leukotriene
inhaler 15-20 minutes before exercise (cannot tolerate albuterol!) o Can be
combined in high-performance athletes 2842/4065: Aspirin-Exacerbated Respiratory
Disease (AERD)?? Presentation: asthmatic symptoms (cough, wheezing, chest
tightness), allergic symptoms (chest congestion, rhinorrhea, periorbital edema),
and facial flushing within 30 min � 3hr of NSAID useo Associated with Nasal polyp,
asthma, and chronic rhinosinusitiso Very similar to allergic/asthmatic flare-up,
thus symptoms may not be attributed to NSAIDo Nasal polyp development can cause
bland tasting food (caused by anosmia), recurrent nasal discharge with grey-
glistening mucoid mass in the nasal canal.o Considered a pseudo-allergic reaction
that is not IgE mediated. Instead the aspirin diverts the arachidonic acid pathway
to produce high amounts of leukotrienes = inflammation ?? Dx: Clinical scenario
3531/3974: Primary Ciliary Dyskinesia (Kartagener Syndrome) * ?? �Presentation: o
Pulmonary:nasalpolyps,chronicsinopulmonaryinfections,bronchiectasis o Cardiac:
situs inversus/dextrocardia (50%; displaced PMI on right)o MSK: digital clubbing;
normal growtho Repro: infertility (immotile spermatozoa) * ?? �Pathophysiology:
autosomal recessive mutation in cilia dynein arms ???absent/immotile cilia causing
poor mucociliary clearance & other symptoms of disease * ?? �Labs: low nasal nitric
oxide levels * ?? �Imaging: bronchoscopy (direct view of poor mucociliary
clearance) or electron microscopy (directly view lack of cilia movement) * ?? �Dx:
presentation + labs/genetic analysis/imaging * ?? �Tx: ??? 4753/4467/12419: Pleural
Effusion * ?? �Basically a transudate or exudate moving form the lung airspace into
the lung pleural cavity * ?? �Transudate � the result of increased hydrostatic or
decreased oncotic pressure. Requires no further workup outside of treatment of
underlying condition causing the exudate * ?? �Exudate � due to
inflammation/irritation of the pleural lining. Defined by the Light Criteria
(having only ONE of these three means its an exudate):o Fluid Protein/Serum protein
ratio >0.5??high protein in fluido Fluid LDH/Serum LDH >0.6??high LDH level in
fluido Pleural LDH >2/3 the upper limit of normal serum LDH??high LDH in fluid o
Note that low glucose (<60mg/dL) is a classic sign of WBCs/bacteria using the
glucose for energy, denoting another sign for exudate. <30mg/dL is highly
suggestive of empyema! ?? Don�t forget! If the pleural fluid shows exudate, that
often means there�s an infection and local cytokine release has increased capillary
permeability to allow for WBC transit! 4087: Malignancy Pleural Effusion * ??
�Presentation: progressive SOB with signs of malignancy (weight loss, fatigue, etc)
and consolidation that eliminates the costo-vertebral angle on CXR o Typically, due
to Lung carcinoma, Breast Carcinoma, or Lymphoma * ?? �Dx: diagnostic
thoracocentesis with pleural fluid analysis o Biggest first step is transudate vs
exudate (Light�s Criteria) o May show malignant cells indicating underlying cancer
* ?? �Tx: drainage of fluid with treatment of underlying cancer 12419: * ??
�Presentation: pleural effusion (increased work of breathing, tachypnea, hypoxia,
percussion dullness) * ?? �Pathophysiology: obstruction/disruption of lymphatic
outflow causes buildup of chyle in pleura * ?? �Etiology: surgical/accidental
trauma, congenital malformation, Down syndrome/Noonan syndrome, malignant
obstruction of lymphatic tracts * ?? �Dx: thoracocentesis with pleural fluid
analysis (milky-white exudative effusion with predominant lymphocytes and
triglycerides * ?? �Tx: drainage of effusion + chest tube + limitation of dietary
fat +/- thoracic duct ligation 4829: Thymus on CXR * ?? �The Thymus is a pediatric
organ responsible for development/maturation of T-lymphocytes * ?? �It�s located in
the anterior mediastinum behind the sternum and in front of the heart * ?? �In
children <3yr, the thymus can be seen on CXR as a uniform mass in the upper thorax,
often appearing as a triangular extension of the cardiac silhouette (sail sign)o
The thymus often shrinks during illness and undergoes rebound hyperplasia after
recovery! 3457: If you ever get a child with severe coughing fits and you note
subcutaneous emphysema (crackles) of the anterior chest??always get a CXR
immediately to rule out pneumothorax 2473/4831: Respiratory Distress Disease
(Hyaline Membrane Disease) * ?? �Risk Factors: prematurity, maternal diabetes, very
low birth weight (<1500g), C-section without labor, perinatal asphyxia, male sex,
Caucasian race * ?? �Presentation: tachypnea, intercostal retractions, grunting,
nasal flaring, & cyanosis at birth o Acute complications � pneumothorax, pulmonary
interstitial emphysema, hemorrhage, sepsis, persistent PDA o Chronic complications
� bronchopulmonary dysplasia (progressive pathologic dysplasia of lung tissue
requiring prolonged ventilatory support from failure for lung tissue to mature) &
retinopathy of prematurity (early supplemental oxygen gets eyes �used to� high O2
levels; withdrawal causes retinal vascular hyperplasia??worry of
hemorrhage/bleeding into eye) ?? Pathophysiology: inadequate surfactant
production ???alveolar collapse ???respiratory failureo Prematurity results in
inadequate amount of surfactant (begins at wk 23-24 but not enough produced until
week 32 for proper function)o Maternal diabetes/hyperglycemia ???neonatal
hypoglycemia ???neonatal hyperinsulinemia ???Chylothorax Pleural Effusion insulin
antagonizes cortisol blocking maturation of sphingomyelin (vital part of
surfactant) o C-section without labor results in decreased stress on neonate??
decreased cortisol ?? Labs: o Pre-natal Lecithin:Sphingomyelin ratio � higher
ratios point to more mature lungso Pre-natal phosphatidylglycerol detection � a
phospholipid component of surfactant. Presence is the best indicator of fetal lung
maturity * ?? �Imaging: CXR (diffuse ground-glass opacities + air bronchograms)
* ?? �Dx: presentation + CXR/pre-natal labs * ?? �Tx: maternal antenatal
corticosteroids (speed surfactant production) + respiratory support (early CPAP or
intubation if severe + supplemental oxygen) + exogenous surfactant till lungs
mature 2473: Other Causes of Respiratory Distress in a Newborn Persistent Pulmonary
Hypertension of the Newborn * ?? �Presentation: variable respiratory distress &
cyanosis due to any non-heart malformations o Commonlyoccursinterm/post-termbabies
* ?? �Pathophysiology: increased Right-to-Left shunting due to increased pulmonary
resistance = hypoxemia * ?? �Imaging: CXR (clear lungs with decreased pulm.
vasculature), echocardiogram (rule out heart defects) * ?? �Tx: respiratory support
(O2, PEEP, intubation, ECMO) & nitric oxide to cause pulmonary vasodilation
Transient Tachypnea of the Newborn * ?? �Presentation: respiratory distress in the
newborn with tachypnea resolving by day 2 of life * ?? �Pathophysiology: inadequate
pulmonary fluid clearance at birth ???pulmonary mild edema * ?? �Imaging: CXR
(bilateral perihilar streaking) Meconium Aspiration Syndrome * ?? �Presentation:
aspiration of meconium causing respiratory distress/respiratory failure * ??
�Pathophysiology: in-utero distress can result in passage of meconium manifested as
meconium- stained amniotic fluid (can be slightly green??thick �pea soup� stuff).
This meconium in the amniotic fluid can be �gulped� and aspirated into the lungs
* ?? �Workup: examination of amniotic fluid (shows meconium staining), CXR
(increase lung volume with diffuse patches of atelectasis), sometimes
pneumothorax/pneumomediastinum can occur * ?? �Tx: suction of the perineum/trachea
to remove as much meconium as possible. Respiratory support if needed. 2435/DiV:
Congenital Diaphragmatic Hernia Differential Dx: * ?? �Transient Tachypnea of
Newborn: most common cause of respiratory distress in term babies; residual
pulmonary fluid remains in lungs after birth o Benign and should only last hours-
days o CXR: diffuse pulmonary infiltrates + �wet silhouette� around the heart * ??
�Hyaline membrane disease (Respiratory distress syndrome): most common cause in
premies o Poor surfactant production in premature Type II alveolar cells o CXR:
homogenous pulmonary infiltrates + �air bronchograms� * ?? �Meconium aspiration
syndrome: meconium stained amniotic fluid will be noted at birth * ?? �Persistent
pulmonary HTN, bronchial atresia, pulmonary agenesis, pneumonia, and non-pulmonary
etiologies are less common but possible Presentation * ?? �Prenatal Screening: will
be picked up at the latest around 24wk gestation on ultrasound (bowel loops in
thoracic cavity, contralateral displacement of heart/mediastinum) * ?? �Displaced
heartbeat: loops of bowel is moving the heart/mediastinum away from hernia * ??
�Tachypnea/tachycardia/absent breath sounds/bowel sounds in chest:
displacement/poor development of lung tissue from infiltrating bowel causing
respiratory distress/poor formed lung tissue * ?? �Scaphoid abdomen/ Barrel shaped
chest: loops of bowel moving out of abdomen and into the chest * ?? �Supracostal
retractions/grunting: sign of severe respiratory distress/impending cardiovascular
collapse. Baby should be intubated and placed on mechanical ventilation.
Pathophysiology * ?? �Failure of the septum transversum to divide the pleural &
coelomic cavities during development (typically finished by week 12) allows for
bowel herniation during critical lung development resulting in lung hypoplasia.
* ?? �Mediastinal shifting also causes compression of the contralateral lung * ??
�When the baby takes their first breath; normally pulmonary circuit pressure goes
from high resistance ??low resistance, allowing for pressure changes in the heart
to allow for adult circulation to be established (closure of foramen
ovale, ductus arteriosis, etc.) * ?? �Lung hypoplasia + contralateral lung
compression keeps pulmonary vasculature resistance high. Resultant
hypoxemia/acidosis/hypotension cause pulmonary vasoconstriction, further worsening
flow into the pulmonary circuit * ?? �The poor pulmonary flow results in acute
respiratory distress/hypoxemia/retention of CO2 Anatomy * ?? �Side of defect: Left
side most common (85%), right side (10%), and bilateral (5%) is most rare. * ??
�Portion of diaphragm affected: o Bochdalek hernia: posteriolateral defect (most
common; cause classic symptoms)o Morgagni hernia: parasternal or retrostenal (rare;
often no pulmonary problems, but symptoms of bowel obstruction)o Diaphragmatic
eventration: thinning of intact diaphragm due to poor muscularization (rare!) o
Diaphragmatic agenesis: no diaphragm; very severe ?? Many children have additional
accompanying anatomical defects (malrotation/non-rotation, ASD/VSD, horseshoe
kidney, polydactyly, NTDs, hydrocephalus, Trisomeies, etc.) Workup * ?? �Child
unstable ???immediate intubation * ?? �Child stable or recently intubated ???
undergo NGT/OGT tube placement * ?? �NGT tube placement where NGT fails to pass ???
Choanal atresia * ?? �NGT/OGT passes past pharynx + CXR o Tube won�t pass through
esophagus + gas in abdomen??esophageal atresia + TEFo Tube won�t pass through
esophagus & no gas in abdomen??esophageal atresia & no TEFo Tube in stomach but
abdominal contents in thorax??CDHo Tube in stomach with normal abdomen??cystic lung
lesion or bronchopulmonary sequester Prognosis ?? Survival rate between 60-80% and
directly correlates with degree of hypoplasia Management * ?? �First Step: intubate
if in respiratory distress o Best to intubate immediately without bag-mask oxygen
delivery, as the air rush of the bag-mask can cause significant barotrauma to the
already poorly functioning lung tissue & cause increased air distension of the
invading bowel * ?? �Second Step: placement of NGT/OGT with suction to decompress
stomach (open up more space for compressed lungs) & search for atresias * ?? �Third
step: admission to NICU with proper blood pressure/ventilator supporto FiO2 100%;
PEEP at 3-5cmH2O; permissive hypercarbia (PCO2 <60mmHg) and O2 saturation levels
between 80-95% are acceptable to minimize barotrauma of aggressive ventillation o
Nitric oxide inhalation may be used to decreased pulmonary HTN o Extracorporeal
membrane oxygenation (ECMO) may be used if child is refractory to these things * ??
�Surgical Repair of Defect: delayed until evidence of lung maturation in NICU
(simply with time and support). Whenever pt is being weened down on vent settings,
surgery can be considered. * ?? �Work-up for further congenital anomalies is also
warranted Endocrine, Diabetes, Metabolism 2171/2184: Diabetic Ketoacidosis (DKA)
* ?? �Often can be the initial presentation of a young person with Type I diabetes
mellitus. Often pt will have weight loss/polydipsia and be able to compensate by
simply drinking more. However, anything disrupting oral intake (recent illness) can
throw this off and send them into DKA * ?? �Presentation: polydipsia/polyuria,
burred vision, weight loss, altered mentation, hyperventilation, abdominal pain o
Labs: hyperglycemia (250-500s), bicarb <18 (acidosis), elevated anion gap, (+)serum
ketones * ?? �Dx: presentation with specific labs * ?? �Tx: High-flow IV fluids, IV
insulin, close watch/replacement of potassium o Note the ketone level (B-
hydroxybutryate) or anion gap are the best methods by which you track response to
treatment 4247/4514: Hyperkalemia in DKA [HIGH YIELD] * ?? �When DKA occurs, pts
often show paradoxical hyperkalemia due to 1extra-cellular shift of K in exchange
for H+ ions to limit the acidosis and 2impaired K+ entry into cells due to low
insulin levels (insulin helps K+ enter into cells o Called �paradoxical� because
the body is actually wasting K+, and overall levels are low, however serum
concerntration is high due to extracellular shift * ?? �Thus pts in DKA should be
given supplemental K+, insulin, and IV fluids because once insulin is on board, the
K+ level can tank quickly, unless it�s very high 3662/3721: Congenital
Hypothyroidism * ?? �Presentation: initially normal (mom�s thyroid hormone still
present) with gradual development of apathy, sluggish movement, weakness,
hypotonia, macroglossia (large tongue), abdominal bloating, umbilical hernia +/-
jaundice, difficult breathing, hoarse/weak cry, dry skin, poor feeding,
hypothermia, or persistent macrocytic anemia o Cretinism: severely stunted
growth/mental retardation from maternal hypothyroidism in-utero or failure to
replete thyroid hormone; will be obvious at birth (mom�s thyroid hormone was never
present) or with development (thyroid hormone not replaced) * ?? �Pathophysiology:
thyroid dysgenesis (aplasia, hypoplasia, or ectopic gland; 85%), error of thyroxin
synthesis (10%), or maternal trans-placental thyrotropin-receptor blocking
antibodies (5%) * ?? �Screening: mandated neonatal T4 (low)/TSH (high) levels * ??
�Dx: presentation or (+) screening test * ?? �Tx: levothyroxine (10mcg/kg titrated
up as needed) 3867/3868/3875: Precocious Puberty ?? Presentation: premature
adrenarche (body odor, oily hair/skin, acne, increased appetite), pubarche
(axially/pubic hair growth), premature menarche, & secondary sexual characteristics
before age 8 (girls) or 9 (boys) o Most common in African American and Hispanic
children o Complications: PCOS, Type II DM, metabolic syndrome ?? Pathophysiology:o
Peripheral: activation of the gonads outside of the HPG axis (low FSH/LH) ???
Typically caused by functional peripheral tumor (adrenals or gonads) o Central:
premature activation of the HPG axis (high FSH/LH) ???Typically idiopathic (80%)
but may be driven by functional brain tumoro Obesity: large adipocytes in childhood
obesity drive increased insulin & leptin secretion * ???�Insulin stimulates adrenal
activation (adrenarche) & ovarian estrogen production (thelarche) stimulating
peripheral activation * ???�Leptin weakly stimulate the HPG axis increasing FSH/LH
causing central activation ?? Labs:o Common: advanced bone ageo Central: high basal
or post-GnRH stimulation test FSH/LH, high estrogen/testosterone, o Peripheral: low
FSH/LH, increased DHEA-S * ?? �Imaging: MRI brain (if central), ultrasound
adrenals/gonads (if peripheral) * ?? �Dx: presentation + labs/imaging o If bone-age
is normal, then presentation may be isolated adrenarche/thelarche/etc. and NOT
precocious puberty ?? Tx:o Central/no tumors: GnRH agonists (inhibitory feedback)
to maximize growth potential o Tumor (central or peripheral): surgical resection
3600/4239: Congenital Adrenal Hyperplasia (Andrenogenital Syndrome) ?? Cortisol
deficiency resulting in bilateral growth of adrenal glands o Cortisol is the major
negative feedback drug in the HPA axis (constant stimulation from ACTH on the
adrenals) o Results in marked thickening/lobulation of adrenal glands o Often due
to a key enzyme deficiency * ?? �21-hydroxylase deficiency (impaired
aldosterone/cortisol production; 90%) o Classical presentation (Neonatal) o ???
�Virilization/ambiguous genitals (females) due to androgen exposure o ???
�Hypernatremia/hyperkalemia/hypovolemia/life-threatening hypotension due to
impaired mineralocorticoid production o Non-classical presentation (Childhood) ???
Precocious puberty (males) or hirsutism/irregular menstruation (females)???Normal
electrolytes & blood pressure???Later in life ???diagnosed with ACTH stimulation
test/17hydroxyprogesterone test o Pathophysiology: Most common (90%) due to
mutation in CYP21A2 gene???Steroidogenesis shunting toward androgens because
aldo/cort production is blocked ???High 17-hydroxyprogesterone level * ?? �11B-
hydroxylase deficiency (impaired aldosterone/cortisol production; 9%) o
Presentation: ???Virilization (shunting toward androgen production) ???HTN
(hypernatremia/mild hypokalemia because 11-DOC is a weak mineralocorticoid) o Labs:
low renin/angiotensin/aldosterone/cortisol; mild hypernatremia/mild hypokalemia ???
High 11-deoxycorticosterone (11-DOC) & 11-deoxycortisol * ?? �17a-hydroxylase
deficiency (impaired cortisol/androgen production; 1%) o Presentation ???
Pseudohemaphodism or phenotypic female (boys) or primary amenorrhea/no pubic hair
(girls) due to loss of androgen production ???Severe HTN
(hypernatriemia/hypokalemia) due to shunting to aldosterone production o Labs: low
renin/angiotensin/aldosterone/cortisol; mild hypernatremia/mild hypokalemia ???High
corticosterone (weak mineralocorticoid) ?? 3B-hydroxysteroid dehydrogenase (<1%) o
extremely rare form causing failure of all adrenal hormone production o High 17-
hydroxypregnenolone ?? Screening: o Increased 17-hydroxyprogesterone levels = 21 or
11-hydroxylase o Decreased 17-hydroxyprogesterone levels = 17-hydroxylase ??
Treatment: o Replace what�s missing � glucocorticoids (all) with mineralocoticoids
(21) or sex steroids (17) Pathways of Adrenal Steroidogenesis Female Reproductive
System 3543/4142/4764/4765/9563/9566: Turner�s Syndrome ?? Presentation:o MSK:
short stature, shield/square chest, widely spaced nipples, decreased bone mineral
desnsity/fractures, cubitus valgus (forearm is angled away from body), narrow/high-
arched palate, low hairline, nail dysplasiao Cardiovascular: bicuspid aortic valve,
aortic coarctation, aortic root dilation/dissection risk o Lymphatics: webbed neck
(lymphatic malformation), congenital lymphedemao Renal: horseshoe kidneyo Repro:
delayed puberty, primary amenorrhea or normal puberty with early menopause,
infertility, infantile uterus, absent thelarce, primary ovarian dysgenesis (�streak
ovaries�) * ?? �Complicationso Decreased breast cancer but increased other cancers
(meningioma & gonadoblastoma)
o Osteoporosis (lack of protective estrogen) * ?? �Pathophysiology: complete or
partial deletion of one X-chromosome in a female (45X0 or Mosaic) o Short stature
result of lost X-chromosome, NOT GH deficiencyo Primary ovarian dysgenesis??lack of
sex hormones??�menopause before menarche� * ?? �Labs: hormonal studies (decreased
estrogen/progesterone, high FSH/LH, low Inhibin A, normal GH) * ?? �Imaging:
Echocardiography or Thoracic MRI (assess aortic valve & aorta); Pelvic ultrasound
(streak ovaries) * ?? �Dx: karyotype (30 blood lymphocytes showing 45X) or
fluorescence in-situ hybridization (45X/46XX mosaic) if clinical phenotype is
present but karyotype is normal or chromosomal microarray to detect mosaic
chromosomal imbalance o Buccal swab for Barr Bodies is an old test that is outdated
by modern techniques * ?? �Tx: Hormone replacement (GH, estrogen, testosterone) &
Vit. D/Ca2+ supplement (help offset osteoporosis) + addressing any other issues
(cardiac, renal, lymphatic, etc.) 4830: Constitutional Growth Delay * ??
�Presentation: normal birth height/length/head circumference??�dropping off� of
growth velocity between age 6mo � 3yr??normal growth tracking around the 5-10%
until puberty??late puberty with normal growth spurt and normal adult height o The
most common cause of childhood short stature and puberty delay * ??
�Pathophysiology: slower rate of maturation of the hypothalamus * ?? �Labs: Bone
age younger than chronologic age * ?? �Dx: presentation + labs * ?? �Tx:
reassurance and continued follow-up to ensure normal growth o Hypothyroidism will
show an abrupt drop off in growth when it develops; usually doesn�t occur at the
young age that Growth Delay will occur o Pts are not deficient in sex hormones or
GH, thus supplementation is not needed 8871: Refeeding Syndrome ?? Presentation: o
K/Mg Deficiency: Arrhythmias (sustained V.Tach), CHF (SOB/JVD/edema), Seizureso
Thiamine Deficiency: Wernicke�s Encephalopathy (retrograde/anterograde amnesia,
confabulation, rotational nystagmus) ?? Pathophysiology: o Catabolic (starvation):
Decreased insulin/increased glucagon & cortisol??ketone body use in brain??
glycogenolysis/lipolysis/protein catabolism??depletion of fat, minerals, vitamins,
and intracellular electrolyes o Anabolic (re-feeding): Insulin surge??abrupt
glycogen synthesis (sugar), protein synthesis (amino acids), & intracellular uptake
of Phos (ATP)/K/Mg/thiamine (DNA)??precipitous drop in serum phos/K/Mg/thiamine??
metabolic derangements * ?? �Dx: presentation * ?? �Tx: slow re-feeding (oral or
parenteral) with aggressive electrolyte resuscitation to prevent 4242: Fibroadenoma
* ?? �Presentation: firm, rubbery, single, unilateral, mobile breast mass,
typically in the upper/outer quadrant of the breasto Typically, tenderness/size
increase just prior to menses (estrogen responsive) * ?? �Workup o Child/adolescent
� serial examinations throughout menstrual cycle; if decreasing in size/tenderness
after menses, be reassured as it�s likely benigno Young adult or persistent mass �
breast ultrasonography (breast tissue often too dense to be well assessed by
mammogram o Adult � mammogram 3773/4244: Maternal Withdrawal of Estrogen * ??
�Presentation: neonatal vaginal discharge/bleeding, breast buds (boys & girls),
vaginal engorgement * ?? �Pathophysiology: maternal estrogen crosses placenta ???
neonatal uterine lining grows ???after birth, withdrawal from estrogen causes
sloughing & resolution within a few days * ?? �Dx: presentation * ?? �Tx:
reassurance, observation, & routine neonatal care 4870: Vaginal Foreign Body * ??
�Presentation: foul vaginal discharge, vaginal bleeding or spotting, pelvic
discomfort, urinary complaints o Examination of the genitals in knee-to-chest or
frog-leg positions for obvious foreign bodies o NEVERdoapelvicexamonapre-
pubertalchild(extremelypainful,riskofhymenperforation) * ?? �Pathophys: toilet
paper (most common), small toys/objects cause irritation * ?? �Imaging: CT pelvis
may be needed if foreign body is not visualized on physical exam * ?? �Dx:
presentation + visualization of foreign body * ?? �Tx: topical anesthetic + calcium
alginate swab or warm saline irrigation o Examination under Anesthesia + removal
may be needed with larger objects or if above techniques are unsuccessful
Dysmenorrhea ?? Primary � excessively painful menstruation (disrupting normal
activities) without discernable underlying pathology; commonly occurs in young
womeno Pathophys: release of prostaglandins causing intense uterine contractions
(physiologically to clamp spiral arteries to slough off endometrium)o Tx: NSAIDs
(first line); prostaglandin synthase inhibitors (2nd line) ?? Secondary �
excessively painful menstruation due to some underlying pathology (often pt
previously had normal menstrual pain/bleeding) o Endometriosis � endometrium
outside of the uterus; often presents with uterosacral nodularity (growth of
extrauterine endometrium) and adnexal tenderness preceding menses by 1-2 days o
Adenomyosis � endometrium growing into the myometrium of the uterus; often presents
with boggy/globular/tender/enlarged uterus o Pelvic infection � cervical motion
tenderness/purulent cervical discharge + infection signso Uterine leimyomata
(fibroids) � abnormal growth of endometrial smooth muscle; associated with heavy
bleeding and irregular/lumpy uterine contour 2388/9566: Amenorrhea * ?? �Primary �
pt aged >15yr has never had a menstrual period o Pelvic ultrasound??uterus or no
uterus???Uterus??Serum FSH??increased or decreased? o ?? �Increased??concern of
gonadal dysgenesis??karyotype o ?? �Decreased??concern of central dysregulation??
MRI brain ???No Uterus??Karyotype + testosterone o ?? �46XX & female testosterone
level??Muellerian dysgenesis o ?? �46XY & male testosterone level??Androgen
insensitivity syndrome * ?? �Secondary � pt has menstruated but has now ceased o
Let the search for an underlying cause begin 4217: Complete Androgen Insensitivity
Syndrome * ?? �Presentation: primary amenorrhea despite normal female phenotype,
absent uterus/ovaries, short vagina (distal 1/3 present), larger than average
breasts, no pubic or axillary hair, cryptorchid palpable testes in labia or present
in inguinal canal/abdomen, no penis/scrotum o Complications:
dysgerminoma/gonadoblastoma (5% risk) * ?? �Pathophys: XY male with X-linked
mutation in androgen receptor, thus developing as a female phenotypically; high
testosterone is aromatized peripherally allowing for estrogen driven development
* ?? �Tx: testicular removal post-puberty (allow for attainment of adult height,
then remove due to risk of malignant transformation in gonads) + post-op estrogen
replacement + psychosocial counsellingo Pre-puberty gonad removal may be done if
concern for cancer presence (large mass, enlarging mass, B-signs of cancer,
+imaging, or +tumor markers) 3911: M�ellerian Agenesis (Mayer-Rokitanski-K�ster-
Hauser Syndrome) * ?? �Presentation: female phenotype, normal secondary sexual
characteristics (breasts, hips, axillary/pubic hair), regular functioning ovaries,
primary amenorrhea, short vagina, absent uterus/cervix/upper vag. * ??
�Pathophysiology: 46XX genotype with failure of Muellerian ducts to form proper
internal female genitals; gonads and external sexual anatomy are normal * ??
�Imaging: pelvic ultrasound showing abnormal internal gentials * ?? �Dx:
presentation + imaging * ?? �Tx: ??? 2390: Abnormal Uterine Bleeding * ?? �Teens??
immature HPA axis causing cycles of anovulation followed by heavy bleeding * ?? �If
stable: high-dose combined OCPs or high dose progestin (if contraindication to
estrogen) * ?? �If unstable: emergency D&C 3241: Emergency Contraception * ??
�Copper IUD: copper-induced inflammatory reaction killing sperm/ova & stopping
implantation; effective 0-120hr following intercourse with 99% efficacy * ??
�Ulipristal Pill: anti-progestin (delays ovulation); effective 0-120hr after
intercourse with >85% efficacy ?? Levonorgestrel pill/OCPs: progestin (delays
ovulation); effective 0-72hr after sex with 85% & 75% efficacy (respectively) 4230:
Granulosa Cell Tumor of Ovary * ?? �Presentation: o Child: precocious puberty
(begins <8yr), leukorrhea, large adnexal mass o Adult: abnormal uterine bleeding,
endometrial hyperplasia, large adnexal mass * ?? �Pathophysiology: malignant
estrogen producing neoplasm * ?? �Labs: elevated estrogen levels * ?? �Imaging:
pelvic ultrasound (shows adnexal mass/thickened endometrium) * ?? �Dx: presentation
+ labs/imaging * ?? �Tx: surgical removal Cardiovascular 3546: Innocent Heart
Murmurs ?? Presentation: heart murmur with normal appetite/energy/growth
patterns/activity, no significant family history, & structurally normal hearto
Typically maneuvers that decreased blood return to the heart (Valsalva, sudden
standing) decrease the intensity of the murmuro Nearly 50% of children will have a
benign (�innocent� or �functional�) physiologic heart murmur ?? Types of Murmurso
Still�s Murmur: Grade I-III/VI at Left Mid-sternal border
vibratory/twanging/buzzing murmur loudest when supine or exercisingo Pulmonic
Ejection Murmur: Grade I-II/VI upper left sternal border blowing/high-pitched
systolic murmur loudest when supine or exercisingo Venous Hum: continuous murmur
heard at the neck/infraclavicular regions due to �buzzing� of the jugular vein;
only appreciated when pt is sitting or standing, but disappears when supine * ??
�Pathophysiology: simply caused by turbulent blood flow in the growing heart tissue
* ?? �Dx: presentation * ?? �Tx: reassurance 4497: Vascular Ring/Pulmonary Artery
Sling ?? Presentation: symptoms onset age <1 and depend on structure compressed o
Tracheal: coughing, wheezing, and biphasic stridor (expiration > inspiration; not
relieved with albuterol
or epinephrine; improves with neck extension) o
Esophageal:dysphagia,difficultyfeeding,vomiting o Other cardiac defect: may show
murmur (up to 50%) ?? Anatomy: o Complete Vascular Ring � formation of double
aortic arch or other anomaly that wraps circumferentially around surrounding
structures o Aberrant Aortic Vessel � aortic vessel branches off earlier than
normal running against surrounding structures o Pulmonary Artery Sling � L.
pulmonary artery aberrantly runs between the trachea/esophagus * ??
�Pathophysiology: abnormal development of aortic arch or other major vessels
resulting in vasculature wrapping around & compressing the trachea, bronchi, and/or
the esophagus * ?? �Imaging: ultrasound or X-ray may show aberrant vessels * ??
�Dx: presentation * ?? �Tx: surgical correction 4826: Post-Pericardectomy Syndrome
?? Presentation: abdominal pain/vomiting/decreased appetite (infants); pericardial
friction rub/pleuritic chest pain exacerbated by laying supine (older kids) in kids
with Hx cardiac surgeryo Cardiac Tamponade: Beck�s triad (hypotension, JVD or scalp
veins in infants, muffled heart sounds), tachycardia, narrowed stroke volume,
hepatojugular reflex, pulsus paradoxus, & electrical alterans; CXR shows
cardiomegalyo Pleural Effusion: SOB, chest pain; CXR shows blunted costovertebral
angles * ?? �Pathophysiology: inflammation from tissue damage during surgery leads
to reactive pericarditis or pleuritis??fluid accumulation within those tissues * ??
�Dx: presentation * ?? �Tx: supportive care + addressing any emergent complications
4854: Myocarditis ?? Presentation: o Viral prodrome/flu-like illness (as most cases
are due to viral etiology)??worsening respiratory distress (progression into heart
failure) o Heart failure (dyspnea, syncope, tachycardia, nausea, vomiting,
hepatomegaly) * ?? �Etiology: many, many things o Viruses (most common): Coxsackie
B virus, adenoviruso Bacteria: C.diptheriae, S.pyogenes, S.aureus, M.tubeculosis o
Fungi: Candida spp., Cryptococcus sppo Protozoa: T.cruzi (Chagas� disease)o
Autoimmune: SLE, rheumatic fever. Sarcoidosiso Kawasaki�s disease * ??
�Pathophysiology: infective infiltration/autoimmune inflammation & damage to
myocardiocytes causing damage??systolic & diastolic dysfunction * ?? �Labs:
elevated CRP/ESR, elevated CK-MB * ?? �Imaging: Endomyocardial biopsy (Gold
Standard; ID organism or inflammation type), EKG (T-wave/ST- segment changes,
sometimes arrhythmias develop), echocardiogram (global ventricular
dysfunction/hypokensis, decreased ejection fraction), CXR (cardiomegaly,
pericardial effusion) * ?? �Dx: presentation + labs + imaging * ?? �Tx: supportive
care (diuretics/inotropes) + treatment of underlying etiology; treatment-refractory
cases require heart transplant eventuallyo Mortality: newborns (75%; heart is
poorly adapted for insult), older children/teens (25%) o Full recovery (66%) &
long-term heart failure (33%) 2678/2688/2691/2711/4673: Hypertrophic Obstructive
Cardiomyopathy (HOCM) ?? Presentation: young person experiencing dyspnea, chest
pains, syncope, chest pain with exertion; classic reason for young athlete to
suddenly collapse and die on the fieldo MorecommoninAfricanAmericanso Increased
risk of ventricular fibrillation (aberrant myocardium = abnormal conduction) o May
be totally symptomatic (50%) & should be screened for: ???In all sports physicals
(history/physical exam) ???If pt has Family Hx of sudden, unexplained death at
<50yr (No sports until H&P + EKG) o Murmur: creshendo-decreshendo murmur best heard
on the left, lower sternal border/apex ???Decreased with increased blood in the
left atrium * ?? �Sustained handgrip (increased afterload), squatting from standing
(increased afterload/preload) or passive leg raise (increased preload) * ?? �These
all increase distention of the ventricle, minimizing outflow obstruction ???
Increased with decreased blood in left atrium * ?? �Valsalva, abrupt standing
(decreased preload), and nitroglycerin * ?? �All increased obstruction, thus the
intensity of the murmur???Can sound like aortic stenosis; however AS would be quite
rare in a young person if they have no family Hx or risk factors for it.o Dual
Impulse Carotid upstroke may be noted (mid systolic cardiac obstruction) & strong
apical impulse (isolated LVH) may be noted on exam ?? Pathophysiology: autosomal
dominant mutation typically of myosin binding protein C or cardiac beta- myosin
heavy chain gene resulting in abnormal myocardial hypertrophy in left
ventricle/septumo Physical activity causes increased flow along the narrowed
ventricle, which can pull the mitral valve leaflets into the ventricle creating
outflow obstructiono Outflow obstruction commonly occurs when resting just after
physical activity (physiologic ventricular dilation starts to wane, accentuating
the obstruction) * ?? �Imaging: echocardiography (eccentric LVH), EKG (signs of
LVH) * ?? �Dx: presentation + imaging * ?? �Tx: o Everyone: refrain from
sports/physical activityo If symptomatic: CCBs, antiarrythmatics??pacemakers, and
surgical myomectomy can all be used depending on situation 3910: Congenital Long-QT
Syndrome * ?? �Presentation: lightheadedness/syncope/palpitations incited by
exercise or sudden surprise o Seizures/sudden death can all also occur (less
common)o Jervell-Lange-Nielsen Syndrome: AR; Long-QT syndrome + sensoneurial
deafness o Romano-Ward Syndrome: AD; Long-QT syndrome (no deafness) * ??
�Pathophysiology: caused by dysfunction of ion-channels responsible for cardiac
conduction within the myocardium; different types are caused by different
dysfunction * ?? �Imaging: EKG (shows QT segment >450ms) * ?? �Dx: EKG +/-
presentation * ?? �Tx: refrain from vigorous exercise/surprise; Propranolol (class
II antiarrhythmic, shortened QT), pacemaker treatment, & avoidance of QT-prolonging
drugs/electrolyte derangements (listed below) 3910: Non-Congenital Causes of QT
Prolongation (>450ms) * ?? �Electrolyte derangements: hypocalcemia, hypokalemia,
hypomagnesemia * ?? �Abx: floroquinolones, macrolides * ?? �Psychiatric Drugs: all
antipsychotics, all SSRIs, all TCAs * ?? �Opioids: methadone, oxycodone * ??
�Antiemetics: ondasetron, granisetron * ?? �Antiarryhmatics: quinidine,
procainamide, flecainide, amiodarone, sotalol 4661: Classic Signs Associated with
Congenital Heart Defects ?? Left to Right Shunting (L-R) � pushing oxygenated blood
into the pulmonary circuit often causing pulmonary HTN and CHF if left untreatedo
Tachypnea, poor weight gain, & sweating during feeds are all classic signs * ??
�Right to Left Shunting (R-L) � pushing deoxygenated blood into systemic circuit,
lowering the O2 content of the systemic blood o Central cyanosis is a classic sign
* ?? �Interruption of Left Ventricular Outflow � pallor/shock/severe acidosis
[Acyanotic Congenital Heart Disease] Atrial Septal Defect (ASD) ?? Presentation:
often is asymptomatic unless involving other structures of the hearto Ostium Primum
defect: less common (20%); defect in lower portion of atrial septum; may cause
malformation of mitral valve anterior leaflet causing mitral regurgitationo Ostium
Secundum defect: most common (70%); defect in middle portion of atrial septum;
often totally asymptomatic + murmuro Sinus venosus: rare (10%); right pulmonary
veins drain into SVC or R.atrium (brings oxygenated blood from right lung into
heart) instead of L.atrium = L-R shunt; asymptomatic + murmuro Murmur: systolic
ejection murmur heard at ULSB (high pulmonic flow) with fixed splitting S2 (always
increased filling of R. ventricle) +/- systolic rumble (increased flow across
tricuspid) o Complications: CHF, pulmonary HTN, atrial arrhythmia, paradoxical
embolism * ?? �Imaging: echocardiography or CXR (R. atrial enlargement), EKG (R.
ventricular hypertrophy) * ?? �Dx: presentation + imaging * ?? �Tx: surgical
closure to prevent complications 3990/4705: Ventricular Septal Defect (VSD) ??
Presentation: the most common congenital heart defect (25% of all defects) o Small
VSD: likely no symptoms + grade IV/VI holosystolic murmuro Moderate VSD: signs of
CHF/growth failure + grade I-II/VI holosystolic & diastolic murmuro Large VSD:
signs of CHF/growth failure + diastolic murmur +/- mild holosystolic murmuro
Murmur: holosystolic murmur at LLSB (turbulence through L-R shunting) or diastolic
rumble at the apex (increased flow across mitral valve from L-R shunting)???The
larger the VSD, the less turbulence, the softer the murmur o Eisenmenger Syndrome:
chronic L-R shunting results in high flow through pulmonary vasculature causing
pulmonary HTN. Increasing pulmonary vascular resistance (PVR) results in physiology
right ventricular hypertrophy. Eventually the R. ventricle gets strong enough that
it overwhelms the left, causing R-L shunting??late cyanosis/dyspnea ?? Anatomy:o
Inlet (3): occurs near & may involve the mitral/tricuspid valve (areas of in-flow
to the venticles); may be part of an AVSDo Trabecular (muscular; 4): most
common/least concerning; hole through muscular septum (lower portion); if small,
may close on its owno Membranous (2): through the membraneous septum (upper
portion); most concerning type as it�s likely the result of endocardial cushion
defects; higher chance of concomitant defectso Outlet (supracristal; 1): occurs
near & may involve the pulmonic/aortic valves (areas of out-flow from the
ventricles) * ?? �Pathophysiology: L-R shunting causes increased bloodflow into the
pulmonary circulation (also causing less outflow into systemic circulation)??heart
failure * ?? �Imaging: echocardiogram (evaluate size/character of defect) * ?? �Dx:
presentation + imaging * ?? �Tx: o Spontaneous closure suspected??medical
management of CHF (diuretics/propranolol) & serial Echocardiograms to ensure
closure;
75% of small VSDs close by age 2 without sequelae o Spontaneous closure not
suspected??surgical closure; indicated with:???CHF refractory to to medical Tx???
Large VSD with pulmonary HTN (closure at 3-6mo)???Small/moderate VSDs not suspected
to close spontaneously (closure at 2-6yr of age) 3539: Complete A-V Septal Defect
(CAVSD)?? Presentation: FFT/poor feeding (newborns), exercise intolerance (older
children), tachypnea, cough/wheezing/rales/crackles, tachycardia, cardiomegaly,
sweating/pallor with feeding or activity, peripheral edema, hepatomegaly??all signs
of CHF o Most common heart defect in Down Syndrome (trisomy 21); stigmata of
disease present o Murmur: loud S2 (pulmonary HTN), systolic ejection murmur @ LUSB
(high flow across pulmonic valve) +/- holosystolic murmur at LLSB (VSD; will be
absent if very large) * ?? �Pathophysiology: poor endocardial cushion formation
results in an ASD, VSD, and common A-V valve (poor mitral/tricuspid valve
formation)??L-R shunting causes increased pulmonary blood-flow & return to the
heart??ventricular overload & CHF * ?? �Imaging: echocardiography * ?? �Dx:
presentation + imaging * ?? �Tx: surgical repair 4912: Patent Ductus Arteriosus
(PDA) ?? Presentation: o Small PDA: often asymptomatic + murmuro Large PDA: may
cause CHF/pulmonary HTN + murmur, widened pulse pressure, brisk pulses, and
sometimes an end-diastolic rumble at the apex (increased flow across mitral valve)
o Murmur: continuous �machine-like� murmur best hear in LUSB ?? Pathophysiology:o
In-utero: Ductus arteriosus serves as a R-L shunt; diverting blood away from
immature lungso Normal neonatal: PDA contracts and scars down to the ligamentum
arteriosuso Abnormal neonatal: PDA remains open & the change in circulation
pressures reverses it into a L-R shunt, diverting flow into the pulmonary circuit *
?? �Imaging: echocardiogram showing abnormal flow * ?? �Dx: presentation + imaging
* ?? �Tx: indomethacin (NSAID) typically helps the PDA clamp/scar down o Surgical
resolution may be needed in larger/persistent PDAs 11968: Coarctation of the
Aorta ?? Presentation: o Neonates: minimally symptomatic at birth??CHF (poor
feeding, fussy, tachypnea, lethargy)???cardiogenic shock (hypotension, cyanosis,
metabolic acidosis, prolonged capillary refill, diminished urinary output) ???
Severe pre-ductal coarctation severely off bloodflow into the aorta; PDA is only
source of good systemic bloodflow (R-L shunt from low post-coaractation pressure)??
cut off when PDA closes causing systemic outflow failure o Older Children: upper
extremity HTN (R arm > L arm), decreased lower extremity flow (decreased O2 sat in
LE, decreased BP in LE, diminished/delayed femoral pulses), bicuspid aortic valve
(50%), �bruit of turbulence� audible in upper left back near left scapula o Adults:
Older children signs/symptoms + lower extremity claudication & palpable pulsations
of intercostal arteries * ?? �Pathophysiology: thickening of the tunica media of
the aorta, typically around the ductus arteriosus (can be pre- or post-ductal)
resulting in compromised bloodflow distally * ?? �Dx: presentation/bruit * ?? �Tx:
immediate PGE2 + low-dose dopamine (+inotrope) ???surgical repair (end-to-end
anastomosis) o If �re-stenosis� following surgery occurs: Symptoms should return;
Check all extremities BP???Balloon angioplasty (widen the narrowed segment)
[Cyanotic Congenital Heart Disease] 2429/3541/4842: Tetralogy of Fallot ??
Presentation: the most common cyanotic congenital heart disease with following
features:o Cyanosis: pulmonic stenosis & L-R shunting cause deoxygenated blood to
flow into systemic circulation; PDA closure results in severe hypoxia resulting in
a blue baby! o 4 classic defects: ???1. Over-riding aorta (overlies a portion of
ventricular septum??pulmonic stenosis) ???2. Pulmonary stenosis/atresia (right
ventricular outflow tract obstruction)???3. Right ventricular hypertrophy (reactive
to pulmonary outflow obstruction)???4. Ventricular septal defect (VSD; allows for
R-L shunting & into PDA if present) ???Often, but not classically, Patent Ductus
Arteriosus present (PDA; aids with oxygenation) o Hypercyanotic �Tet� Spells:
sudden cyanosis/decreased murmur intensity due increased pulmonary vascular
resistance (agitation, feeding, crying, hyperventilation from playing/running
around) causing increased shunting away from pulmonary circulation; child becomes
irritable/cries/becomes dizzy & learns to squat down (increased SVR & transient
increased venous return causes increased flow to lungs = better oxygenation) o
Murmur: creshendo-decreshendo at left-upper upper sternal border (pulmonic
stenosis) + single S2 (aorta snapping shut, pulmonic valve inaudible) * ??
�Pathophysiology: poor blood oxygenation due to limited flow through pulmonary
vasculature * ?? �Imaging: echocardiography (RVH), CXR (�boot-shaped heart�,
decreased pulmonary vascular markings, right-sided aortic arch) * ?? �Dx:
presentation + imaging * ?? �Tx: surgical repair around 4-8mo o Tet Spell � knee-
chest position (�squatting�) + IV fluids, oxygen, propranolol if needed 4260: D-
Transposition of the Great Arteries ?? Presentation: central cyanosis in first 24hr
(most common to present in neonatal period!) o Murmur: single S2 (aortic valve
abnormally set in anterior position; sound overshadows pulmonic valve closure) +
VSD (holosystolic, LLSB) or PDA (continuous �machine-like� murmur radiating to
neck/arms/supraclavicular region) depending on defect present ???If ASD is present
allowing for survival, no murmur is heardo Note that L-transposition of the Great
Arteries reverses the vessels & the heart (double negative that cancels each-other
out!) * ?? �Pathophysiology: abnormal rotation of the septum dividing the
aorta/pulmonary arteries due to failure of neural crest cell migration??two
independent circulatory systemso Not compatible with life unless PDA, ASD or VSD
are present to allow mixing between systems * ?? �Imaging: CXR (�egg on a string�
narrowed mediastinum), echocardiography (abnormal connections) * ?? �Dx:
presentation + imaging ?? Tx: immediate PGE2 (keep patent ductus)??emergent balloon
septoplasty (enlarge defect to ensure blood mixing)??definitive repair with
�arterial switch operation� (switch around great vessels & incise/re-implant
coronaries to proper bloodflow) 3991: Tricuspid Atresia?? Presentation: central
cyanosis, clear lung sounds, murmur/EKG findings o ASD/VSD must be present for
survival???VSD Present: L-R shunting allows for acceptable oxygenation???VSD
Absent: cyanosis as PDA constricts with eventual hypoxia w/out intervention o
Murmur: holosystolic murmur at Left Lower Sternal Border (if VSD present)o EKG:
left axis deviation (hypoplastic R. ventricle/LVH), small/absent R-waves in pre-
cordial leads (V1, V2, V3; hypoplastic R. ventricle), large �peaked� P-waves in
lead II (R. atrial hypertrophy) ?? Pathophysiology: lack of communication between
the R. atrium/ventricle & concomitant septal defects results in the left ventricle
doing the work in-utero that the right ventricle normally does. This causes greater
development of the left ventricle & a hypoplastic R. ventricle o Normally, neonates
are born with right-axis deviation & prominent R-waves in V1/V2/V3 due to shunting
away from the left ventricle in neonatal circulation o Decreased R. ventricular
flow results in poor pulmonary circulation, thus decreased pulmonary valve/artery
development??decreased pulmonary markings * ?? �Imaging: CXR (normal sized heart,
decreased lung markings), echocardiography (hypoplastic R. ventricle, ASD, VSD)
* ?? �Dx: presentation + imaging * ?? �Tx: Surgical repair (Glenn shunt + Fontan
Procedure) Persistent Truncus Arteriosus * ?? �Presentation: mild cyanosis + murmur
o Murmur: single S2 (single pulmonic-aortic valve), systolic ejection murmur at
LUSB, & diastolic murmur at apex * ?? �Pathophysiology: malformation of the
pulmonary arteries/aorta so that there is only one big outflow vessel from the
ventricles; VSD is nearly always present * ?? �Imaging: Echocardiography (shows
abnormality); CXR (enlarged heart +/- right-sided aortic arch) * ?? �Dx:
presentation + imaging * ?? �Tx: Tx for CHF + surgical repair Total Anomalous
Pulmonary Venous Return (TAVR) * ?? �Presentation: severe cyanosis within 24hr of
birth + murmur o Murmur: pulmonary ejection murmur heard in LUSB (right sided over-
filling) * ?? �Anatomy: o Supracardiac: lungs feed into SVC or innominate artery o
Cardiac: lungs feed into R.atriumo Infracardiac:lungsfeedintoportalsystem * ??
�Pathophysiology: venous return from lungs only feeds into the right heart (not
into left heart); R-L shunting occurs across the PFO or ASD to fill the left heart
after * ?? �Imaging: CXR (enlarged heart with �snowman appearance� from anomalous
drainage) * ?? �Dx: presentation + imaging * ?? �Tx: surgical revision
Rheumatology/Orthopedics/Sports Medicine 12422: Juvenile Idiopathic Arthritis (JIA)
?? Presentation: child <16yr with chronic, symmetric
polyarthritis/fatigue/inflammation of joints +/- other constitutional symptoms
(fever, rash, etc.) occurring for >6weekso Oligoarticular (<5 joints affected) can
be early onset (<8yr) or late onset (>8yr) ???Early onset � females, ANA+,
uveitis/blindness (50%), hips/sacroiliac joints spared ???Late onset � males, HLA-
B27+, spondyloarthropathies risk, hips/sacroiliac joints involved o Polyarticular
(>5 joints affected) can be Rheumatoid factor (RF)+ or RF- ???RF+??females, late
onset, often severe widespread joint involvement ???RF-??females, early or late
onset, may cause deformity of jointso Systemic (Still�s Disease) � high spiking
fevers (often �of unknown origin�), transient salmon colored rash on
trunk/extremities with fevers, hepatosplenomegaly, & lymphadenopathy
Pathophysiology:
autoimmune attack of joints o Females more commonly have overall; but men more
likely to have oligoarticularo Anemia due to inflammatory stimulation of hepcidin
(inhibits gut iron absorption, limits release of iron from liver
reticuloendothelial system & macrophages) * ?? �Labs: ESR/CRP elevation, anemia of
chronic disease (chronic inflammation), elevated acute phase reactants
(hyperferritinemia, hypergammaglobulinemia, thrombocytosis), +RF or +ANA * ?? �Dx:
presentation * ?? �Tx: NSAIDs/immunomodulatory drugs (steroids, MTX, etc.) +
Physical therapy (joint mobility) 4873: Supracondylar Fracture of Humerus * ??
�Presentation: child age 2-12yr with Hx of fall onto outstretched arm with elbow
extended. Immediate pain, swelling, refusal to move arm at elbow * ??
�Complications: o Median nerve damage: runs near the bone; nerve deficit in
distribution of median nerve (palmar aspect thenar compartment/digits 1/2/3/half of
4 + dorsal aspect tips of digits 1/2/3) o Median artery damage: runs through this
area directly adjacent to bone; always check the distal radial/ulnar pulses to
ensure this has not occured o Compartment syndrome: severe pain (despite
analgesia), pallor, pokilothermia, paresthesias +/- late findings
(pulselessness/paralysis) due to intense inflammation * ?? �Imaging: plain X-ray
(fracture of the bone + anterior/posterior triangular lucency from fat pad
inflammation �posterior fat pad sign�) * ?? �Labs: compartment pressures (if
concern for compartment syndrome) * ?? �Dx: presentation + imaging * ?? �Tx:
setting of bone + address any complications 4064: Spondylolisthesis * ??
�Presentation: child with slowly developing back pain +/- neurologic dysfunction
(urinary dysfunction, loss of dermatomal cutaneous sensation) & palpable �step off�
of the lumbosacral area * ?? �Pathophysiology: developmental disorder causing
forward slipping of vertebrae (typically L5 slipping over S1) causing spinal cord
compression * ?? �Imaging: AP/lateral/oblique views of the spine (shows anterior
subluxation) * ?? �Dx: clinical presentation + imaging * ?? �Tx: surgical
resolution (if nerve impingement, persistent pain, or progression) 3404/4533: Legg-
Calv�-Perthes disease (idiopathic avascular necrosis of femoral capital epiphysis)
* ?? �Presentation: persistent hip/groin/knee pain of insidious onset + antalgic
gait (stance-phase shortened vs swing phase; done to avoid pain; �anta � alga� =
pain avoidance), thigh muscle atrophy, decreased range of motion o Most common in
boys ages 4-10 (pre-puberty) * ?? �Pathophysiology: unknown; but suspected to be
underlying thrombophilia * ?? �Imaging: X-ray hips (flattened/fragmented femoral
head �Crescent sign�, loss off femoral joint space, head contained within the
acetabulum; often alternating areas of lucency and density representing
necrotic/new bone) o Often early X-rays are negative and mis-diagnosis of transient
synovitis may occur o MRI:mustbedonetoconfirmDx * ?? �Dx: presentation + labs * ??
�Tx: conservative bracing/observation with avoidance of weight bearing by the hip
girdle +/- surgery if femoral head dislodged 3079/4834/4835: Kawasaki�s Disease
(Mucocutaneous Lymph Node Syndrome) ?? Presentation: persistent high fever (>5
consecutive days, refractory to antipyretics) o Diagnostic criteria: 1cervical
lymphadenopathy, 2bilateral non-exudative conjunctivitis,
3swelling/inflammation/peeling of palms & soles, 4mucositis (strawberry
tongue/fissured lips), 5widespread rash o Classically occurs in children 18-24mo,
especially of east-Asian descent; almost always occurs in children <5yr (rare to
occur afterward!) o Complications: coronary artery aneurysm??thrombosis/myocardial
ischemia/death; hydrops of the gallbladder (RUQ pain), arthritis/uveitis/urethritis
* ?? �Pathophysiology: poorly understood but thought to occur in three phases:o
Acute Phase: 1-2wk; classic presenting signs for diagnosiso Subacute Phase: weeks-
months; palms/soles rash/formation of aneurysms/thrombocytosis o Convalescent
Phase: weeks-years; gradual resolution of aneurysms * ?? �Labs: elevated ESR/CRP,
leukocytosis with neutrophilia, reactive thrombocytosis, sterile pyuria * ??
�Imaging: echocardiography at time of Dx & 6-8wk later (rule out coronary artery
aneurysm) * ?? �Dx: characteristic fever + 4 out of 5 diagnostic criteria o
Atypical presentation may be suspected with lab findings * ?? �Tx: high-dose
aspirin + IVIg (minimize inflammation to decrease cardiovascular problems) within
10 days of fever (acute phase); low-dose aspirin (subacute or convalescent if
aneurysms present for the anti-platelet effects to limit thrombotic occlusion) o
Spontaneousresolutionwithin12days 3403/4844: Slipped Capital Femoral Epiphysis
(SCFE) * ?? �Risk Factors: Obesity (#1), endocrinopathies (#1 for bilateral), renal
failure, radiation of the hips * ?? �Presentation: limping/pain with activity
typically of upper-anterior thigh, but may be referred into the lower thigh/knee
(33%) o Limited internal rotation of the hip + obligate external rotation when hip
is flexed to 90� is a hallmark & often limited hip extension/abduction are also
foundo Most common hip disorder between ages 8 and 15; more common in
boys/overweight/obese children undergoing physical activity (obesity = greatest
risk factor)o NotethathypothyroidismputsptsatespeciallyhighriskofbilateralSCFEo
Complications: avascular necrosis of hip (33%), SCFE of contralateral hip (33%), or
chrondrolysis ?? Pathophysiology: Slipping from disruption of the proximal growth
plate causing displacement medially/posteriorly often without acute injury o The
physis (junction between femoral neck/head) weakens due to rapid expansion of
growth plate cartilage during pubertal growth (not as strong as bone) o Being
overweight causes excessive traction * ?? �Imaging: frog-leg & lateral X-ray hips
(epiphysis widening??posterior displacement of femoral head; epiphyseal cap appears
as �scoop slipping off the ice cream cone�; Klein Line doesn�t pass thru epiphysis)
* ?? �Dx: clinical presentation + imaging * ?? �Tx: Pt should not bear weight;
emergent referral to orthopedic surgery (surgical pinning/fixation of the femoral
head to stop slippage)o Close follow-up for other hip & weight loss should occur
2486: Rickets * ?? �Risk Factors: dark skin complexion, exclusive breast feeding
(without supplementation), poor absorption of Vit.D (CF, etc.), anticonvulsant
medications (interfere with liver metabolism) * ?? �Presentation: delayed
fontanelle closure, craniotabes (�ping-pong ball skull�), skull frontal bossing,
�rachitic rosary� (palpable bone �bumps� on ribs), �pidgeon-chest deformity�
(sternal protrusion), �wrist widening�, & genu varum (�bow legged�) * ??
�Pathophysiology: o Vit. D dependent: Vitamin D deficiency or Ca2+ deficiency (less
common) causing weak formation for hydroxyapatite crystals, thus poor bone strength
& deformity o Vit. D independent: familial hypophosphatemia (X-linked dominant
disorder) causing low phosphorus due to renal wasting??failure of hydroxyapatite
crystal formation * ?? �Labs: 25-OH Vit.D (low), Ca (low-normal), phos (low-
normal), alk.phos (very high), PTH (high) * ?? �Imaging: X-ray (osteopenia,
metaphyseal cupping/fraying, epiphyseal widening from lack of bone) * ?? �Dx:
presentation + imaging * ?? �Tx: Vit.D repletion (1000-2000 IU/day) with
maintenance of 400 IU/day after repletion 3684/3685: Congenital Foot Deformity * ??
�Metatarsus Adductus o Presentation: bilateral medial deviation of the forefoot
with neutral hindfoot position ???Foot able to be corrected with passive or active
motion (�flexible foot�)???The most common congenital foot deformity???More common
in 1st born infants (less space in primigravid uterus) o Pathophysiology: crowding
in uterus causes deviation of foot bones o Dx: presentationo Tx: reassurance
(spontaneous resolution with normal use) * ?? �Congenital Clubfoot o Presentation:
rigid medial/upward deviation of both forefoot & hindfoot (does not correct with
active or passive movement)o Pathophysiology: several etiologies;
congenital/teratogenic/uterine crowding can all occur o Labs: karyotyping to rule
in/out congenital genetic problem should be soughto Dx: presentationo Tx:
orthopedic examination + serial manipulation/casting soon after birth 3770:
Osteogenesis Imperfecta ?? Presentation: o Structurally brittle bone � often
multiple fractures (may mimic child abuse), short stature, scoliosis, hearing loss
(fracture of the conducting bones of the ear), & dentogenesis imperfecta
(small/misshapen teeth with opalescent blue-grey or yellow-brown discoloration) o
Weakened connective tissue: joint instability, easy bruisability o Blue sclerae �
decreased collagen in the eye revealing choroidal veins * ?? �Pathophysiology:
Autosomal Dominant genetic defect in COL1A1 gene (?1 or ?2 chain of Type 1 collagen
synthesis)o Type I = normal lifespan with defects; may not be noticedo Type II =
perinatal lethal from in-utero fractureso Type III/IV = moderate defects; often
recurrent fractures/full phenotype * ?? �Dx: presentation * ?? �Tx: bisphosphonate
use (even in children <2yr) with internal fixation of long bones 3555: Growing
Pains * ?? �Presentation: bilateral lower extremity pain occuring at
night/resolving by morning in an otherwise unaffected & healthy childo Typically
occurs in children 2-12yr (pre-puberty) * ?? �Pathophysiology: unknown cause; but
totally unrelated to growth (despite name) * ?? �Dx: presentation * ?? �Tx:
education, massage/muscle stretching exercises/OTC NSAIDs + monitoring for changes
in pain 4584: Serum Sickness-like Reaction * ?? �Presentation:
fever/urticarial/polyarthralgia with no mucosal involvement 1-2wk following
exposure to new medicationo Less commonly: headache, edema, lymphadenopathy,
splenomegaly o Most commonly occurs with antibiotics (B-lactams/sulfa drugs) * ??
�Pathophysiology: type III hypersensitivity reaction (not a true allergy) * ??
�Labs: elevated ESR/CRP * ?? �Dx: Presentation * ?? �Tx: cease/avoidance of
offending drug +/- steroids if severe o Resolution typically occurs within 48hr of
offending agent 4399/4761: Congenital Torticollis ?? Presentation: infant (1-6mo)
with head tilt to one side/chin tilt toward the other (contraction of SCM), limited
range of neck motion, & a neck mass (does not trans-illuminate; on inferior portion
of contracted SCM, often bleeding into the muscle) o Positional plagiocephaly
(flattening of occiput/forehead with ipsilateral anterior ear displacement) may
result if not corrected causing craniofacial asymmetry o Risk Factors: multiple
gestation, oligohydramnios, breech positioning (uterine crowing) * ??
�Pathophysiology: crowding within the uterus causes abnormal posture and formation
of the neck mass causing pulling on the SCMo Associated with other conditions also
caused by uterus crowding (developmental dysplasia of the hip, metatarsus adductus,
and clubfoot * ?? �Dx: presentation * ?? �Tx: positioning (tummy time), passive
stretching, and physical therapy * ?? �Lookalike: Acquired Torticollis may be the
result of a posterior fossa tumor. Tonsillar herniation or compensation for visual
disturbance from the tumor can result in secondary head tilt. This is extremely
rare and would like present with other neurologic sequelae. 2629/4642/8772/11441:
Characteristics of Common Childhood Bone Tumors * ?? �Common Symptoms: bone pain in
a teenage boy without constitutional symptoms; may have pathologic fracture leading
to discovery * ?? �Osteosarcoma - o Presentation: chronic localized bone pain with
swollen soft tissue mass; most common bone tumor of children o Imaging: X-ray
showing mix of radiodense/lucent areas +/- sunburst pattern/Codmann triangle o Dx:
presentation + imagingo Tx: excision/chemotherapy to treat ?? Ewing Sarcoma �
extremely malignant tumor of bone; typically occurring in the lower extremity
(femur most often); 2nd most common bone tumor of children o Presentation: bone
pain/swelling/inflammation of local area???May have osteomyelitis-like symptoms
(intermittent fever, leukocytosis, anemia, ^ESR) ???Lung or lymph node involvement
may be present on initial exam o Imaging: X-ray showing lytic lesion with endosteal
scalloping + periosteal retraction causing �onion skin appearance�??�moth-eaten�
mottled appearance + involvement of soft tissue o Dx: presentation + imaging o Tx:
surgical resection + chemoradiation?? Osteoid Osteoma - Benign tumor typically in
proximal femur; other long-bones/spine may be affected o Presentation: focal bone
pain/tenderness worse at night, unrelated to physical activity ???Children may
develop swelling/deformity; this is rare in adolsecents/adults o Imaging: X-ray
showing sclerotic bone lesion with obvious central lucencyo
Dx:imaging+bonepainreliefwithNSAIDso Tx: serial X-rays of lesion every 4-5mo; most
resolve spontaneously, surgical excision is reserved for refractory symptoms??
Langerhans Histiocytosis (LCH, Langerhans Cell Granulomatosis, or Histiocytosis X)
o Presentation: focal bone pain/swelling + hypercalcemia/pathologic fracture o
Imaging: Xray showing solitary lytic long-bone lesiono Dx: presentation +
hypercalcemia + imagingo Tx: conservative management (will spontaneously resolve)
3402/4534: Developmental Dysplasia of the Hip (DDH) * ?? �Risk Factors: breech
presentation, female sex, Caucasian, family history of DDH o Most commonly (75%) pt
has no risk factors for this problem * ?? �Presentation: palpable �clunk� on
regular serial hip stability exams o Equivocal signs � soft click, leg-length
discrepancy, asymmetric inguinal folds o Complications: limp (Trendelenburg gait),
scoliosis, arthritis, avascular necrosis of the hip * ?? �Screening: all children
should receive serial hip screening at every well-child visit up to 1yr o Barlow
maneuver � pt supine with hips flexed/hips abducted, adduction of the hips with
gentle posterior pressure; (+)if hips dislocate during maneuver indicating hip
dysplasia o Ortolani maneuver � following Barlow??knee flexed/gentle anterior
pressure at the greater trochanter is applied and his are abducted; (+)if �clunk�
is heard with abduction indicating hip dislocation occurring during Barlow and
reversed with Ortolani (�clunk� is reduction of the hip) o Galeazzi sign � flexion
of hips/knees of supine child so feet touch resting surface and ankles touch
buttocks; if knees are even, it�s normal; asymmetry indicated DDH ??
Pathophysiology: dislocation of the femoral head from the acetabulum due to weak
hip joints or abnormally flat acetabulum groove (poor fit for femoral head) o Hip
instability is acceptable <2wk of age (often it resolves spontaneously as child
develops) * ?? �Imaging: o <2wk: no imaging needed; watch/re-examine after 2wk of
ageo 2wk � 6mo: bilateral ultrasound of hips (ossification has largely not occurred
yet) o >6mo: bilateral X-ray hips (ossification sufficient for X-ray detection)
* ?? �Dx: (+)Barlow/Ortolani (no imaging required)o If (-)Barlow/Ortolani but
evidence of hip asymmetry??get imaging depending on age o Early diagnosis is
crucial; as intervention must be done before 6moo Delayed diagnosis is one of the
most common reasons for malpractice of a pediatrician * ?? �Tx: (+)Barlow/Ortolani
or (+)imaging ???orthopedics referralo <6mo: Pavlik harness (keeps hips in
flexion/abduction) for regular growtho >6mo: Reduction under general anesthesia
(higher risk of complications later) 3416/3668: Radial Head Subluxation
(�Nursemaid�s Elbow�) * ?? �Presentation: child distressed keeping arm extended &
pronated +/- mild tenderness of radial head; child should be in pain with movement
but no swelling or angular deformity should be present o Common elbow injury in
children aged 1-5yro Often due to �pulling child�s arm from harm� or �swinging
child around for play� * ?? �Pathophysiology: axial traction on the child�s forearm
pulls the radial head down, allowing the annular ligament to get trapped between
the radial-humeral articulation o In children <5yr the annual ligament if somewhat
weak, thus cannot hold the radial head firmly in place; after age 5yr, it�s
sufficiently thickened to stop subluxation * ?? �Imaging: often X-rays are normal;
post-reduction films are not needed if maneuvers are successful * ?? �Dx: clinical
presentation + success of treatment maneuvers * ?? �Tx: forced hyper-pronation OR
forced supination with flexion; an audible click with full return to function
should be noted afterward if successful 4849: Osgood-Schlatter Disease * ??
�Presentation: adolescent athlete with knee pain (esp. over the tibial tubercle)
exacerbated with exercise, relieved by rest & reproducible with knee extension
against resistence;o Tenderness/swelling/inflammation +/- palpable mass over tibial
tubercle (heterotopic bone formation from traction injury) may also be noted * ??
�Pathophysiology: rapid growth in adolescents causes traction on the apophysis of
the tibial tubercle by the quadriceps tendon via the quadriceps tendon-patella-
patellar tendon complex o Athletic endeavors cause additional traction resulting in
pathologic changes * ?? �Imaging: X-ray (anterior soft tissue swelling, lifting of
tibial tubercle from tibial shaft, irregular fragmentation of tubercle) * ?? �Dx:
presentation +/- imaging * ?? �Tx: activity restriction/stretching exercises/NSAIDs
for pain o Banding of the tibial tubercle may also provide relief during athletic
events 4857: Transient Synovitis ?? Presentation: transient joint (often knee or
hip) pain, decreased ROM, & limping following a viral infection or mild trauma;
often well-appearing and pain not severe enough to restrict daily lifeo Most common
cause of knee pain in children (typically 3-10yr of age)o Must be differentiated
from septic arthritis (fever, unable to bear weight, leukocytosis, ESR >40 or CRP
>2mg/dL)??if seen prompt joint aspiration is necessary?? Pathophysiology: synovial
inflammation somehow caused by antecedent event (poorly understood) * ?? �Dx:
presentation + ruling out septic arthritis * ?? �Tx: rest/NSAIDs; spontaneous
recovery around 1-4wk - * ?? �Glasgow Coma Scale * ?? �Childhood Conjunctivitis
* ?? �Rocky Mountain Spotted Fever Neurology 2671: In apparent unprovoked first
seizure pt should have imaging done ASAP to check for masses/bleeds that may have
caused the seizure. This patient also fell while seizing, making CT w/out a great
choice for initial imaging because they might have a traumatic bleed * CT w/out
contrast is the imaging of choice in emergent situations * MRI is imaging of choice
for non-emergent situations * EEG is useful, but more pressing matters may need to
be addressed. This may be done later if assessing the patient for a possible
seizure disorder3630: C.Jejuni is the most common precipitant of Guillian-Barre
Syndrome. Often it??s manifested by bloody diarrhea prior to the ascending
weakness. Apparently people with lymphoma/SLE get it more often. Other ways of
getting it could be: * Less common infection: Herpes virus, Mycoplasma spp, H.Flu *
Recent HIV infection or immunization2316: Lumbar spinal stenosis presents
classically as low back pain, worse with standing/walking uphill (causes greater
compression) and better with sitting/walking downhill (opens up spine). Typically
caused by degenerative joint disease (DJD) resulting in disc herniation/osteophyte
impingement on the spinal cord. * Neurologic exam may be normal (straight leg raise
only positive in 10% of pts) but there can be signs of nerve compression in lower
extremities (numbness/tingling/etc) * Best next step ?? MRI
of the spine to look for degenerative changes in spine3726: Cerebellar hemorrhage
is a type of intracranial hemorrhage presenting as: Headache (occipital/radiates to
shoulder); facial weakness/gaze palsy/nystagmus; neck stiffness (blood in the 4th
ventricle causing irritation); gait ataxia; N/V * Classically there is no
hemiparesis * Often comes on as progressive for minutes � hours (as opposed to
immediate) * Best next step ?? non-contrast head CT to visualize bleed * Tx ??
emergent surgical decompression 3446: Workup of Multiple Sclerosis (MS) includes
the following: * T2 weighted MRI: check for hyper/hypodense lesions due to white
matter demyelination (periventricular regions/corpus callosum, optic nerves,
brainstem, spinal cord) * LP: check for IgG oligoclonal bands, often with normal
opening pressure/CSF 3631: Atrophy of the caudate nucleus is a classic sign on
imaging for Huntington??s disease 4130: Shy-Drager Syndrome (multiple systems
atrophy) is a Parkinson+ syndrome consisting of: * Parkinsonism (tremor, gait
disturbance, etc.) * Autonomic dysfunction (orthostatic hypotension, abnormal
lacrimation/sweating, bladder/bowel dysfunction, etc.) * Widespread neurologic
signs * Parkinsons drugs are not effective here (as is the case with most Park+
syndromes) * Tx ?? expand intravascular blood volume to keep BP up as orthostatic
hypotension is a problem (salt- supplementation, fludrocortisone, a-adrenetgic
agonists, etc.)4513: Brain abscesses classically present as a triad of headache,
focal neurologic signs, fever (20%) although some may not even have fever (50%).
Ring-enhancing lesions are highly specific on MRI/CT. Typically infection is due
to: * Direct spread from head/neck infection (50% sinusitis) � Viridians group step
(S. intermedius, mutans, mitis, oralis) or anaerobic bacteria (prevotella,
peptostreptococcus, bacteriodes) * Hematogenous spread (25% lung inf./endocarditis)
� Staph aureus * Rarely direct inoculation may occur � Staph aureus * Best next
step ?? MRI/CT with contrast to see ring-enhancing lesions * Tx ?? 4-8 weeks of
antibiotics (decide via culture/like source) with drainage if possible 4691: Spinal
Cord compression typically presents as: gradual worsening of severe lower back
pain, worse when lying down/at night, with lower extremity weakness/sensory signs *
If more advanced, UMN signs (Babinski, exaggerated reflexes) in the lower
extremities, loss of sphincter tone, paraplegia, and sensory loss can occur * Best
next step ?? MRI of the spine/IV glucocorticoids * Tx ?? aimed at underlying cause
(this case was metastatic cancer, so we??d treat that) 2938: Wilson??s disease is
autosomal recessive disease with abnormal copper absorption in the gut *
Presentation in kids ?? liver disease of unknown etiology * Presentation in young
adults ?? neuropsychiatric disease (Parkinsonism, depression, catatonia) with liver
disease * Best next step ?? ceruloplasmin levels (<20 diagnostic), urine copper
levels, slit-lamp eye examination (look for Kayser-Fleischer rings) 12028:
Myasthenia Gravis exacerbation may be precipitated surgery, infections, and
medications (aminoglycosides/B-blockers are classic). The ice pack test is
supportive for MG by improving muscle weakness (often ptosis) by decreasing ACh
breakdown from the cold temperature � +Ice pack test should prompt confirmatory ACh
antibody testing4378: Seizures may be precipitated by strong emotions, sleep
deprivation, alcohol withdrawal, or flashing lights with a delayed return to
baseline. Syncope may occur with upright positioning, strong emotions, heat, and
crowded spaces with an immediate return to baseline2634: If a patient has signs of
Myasthenia Gravis (weakness with repetitive use, often of small muscles): � � �
2673: � � Dx ?? Bedside testing (ice pack/Tensilon testing) and confirmatory Ach
Antibody testingNext best step ?? chest imaging as MG is often due to thymoma
(thymus makes the antibodies) Removal of the thymus can greatly improve MG symptoms
When evaluating facial hemi-weakness, the distribution can tell you where the
lesion is:Above the pons (central lesion): forehead is spared, pt can raise the
eyebrow; this is due to contralateral connections in the CNS that will link up with
the LMNs of the foreheadBelow the pons (tu palsy): whole hemi-face is affected,
eyebrow cannot be raised; typically, recovery will occur within 3 weeks and total
recover in 6 months 3724:spinothalamic tract) and is associated with Arnold-Chiari
malformation I (caudal displacement of the cerebellum into the foramen magnum)
Syringomyelia typically presents with a cape-like distribution of sensory loss
(pain/temp sensation; 4376: Acute Angle-closure glaucoma: sudden narrowing/closure
of the anterior angle chamber, stopping the flow of aqueous humor and increasing
intraocular pressure. * Presentation: acute onset of orbitofrontal headache, N/V,
severe eye pain with injection, poorly reactive, dilated pupil, excessive
lacrimation, poor visual acuity. * Permanent vision loss may occur from damage due
to increased intraocular pressure 4072: When assessing brain metastases, the
clinical picture will direct therapy: * Surgical resection followed by
radiation/radiosurgery ?? single mass, good performance status, mass is accessible
for surgery * Whole brain radiation or supportive therapy ?? multiple masses, poor
performance status, mass in not accessible for surgery * Note that brachytherapy is
implantation of a radioactive device next to the tumor to limit radiation exposure
to the other organs 3919: Dexamethasone depression testing may be helpful in
assessing depression causing pseudodementia. This is a weird, and often useless
test for this reason; but the clinical picture for pseudo vs genuine dementia can
be difficult, so this MAY be helpful in delineating that line 3738: Anterior lobe
lesions may result in weakness of the contralateral body and Broca�s (expressive)
aphasia (Broca??s area is present in the posterior frontal lobe). Temporal lobe
lesions will cause Wernicke??s (receptive), anomic, or conduction aphasias. 3300:
Anterior Cord Syndrome: often due to burst fracture of the vertebrae (vertebrae is
burst open, typically due to high energy impact) with total loss of motor function
and bilateral loss of pain/temperature sense below the lesion. Proprioception is
intact. 2289: Tick paralysis is classically an ascending paralysis with
predominance to one side (left weaker than right but weakness present in both).
Typically occurs within hours-days (faster the guillian-barre) * Occurs due to
release of neurotoxin from an attached tick; pt may have history of hiking and NO
prodromal illness. Tick must be attached about a week before symptoms onset.
Metriculous search for a tick is the next best step. Removal of tick / supportive
care will often result in recovery. Typically autonomic function/sensory
function/CSF are normal * Guillian barre can have a similar history but onset of
symptoms will be bilateral and over the course of days to week. Autonomic
function/sensory function may be messed up! CSF may show high protein. Tx is IVIG
or plasmapheresis to remove the autoantibody causing disease. 3461: Carbamazepine
is the treatment of choice for Trigeminal Neuralgia (80%); note that it can cause
aplastic anemia and CBCs must be monitored on this drug; if this drug does not
work, then surgical decompression of the trigeminal nerve (CN V) may be warranted.
3715: Early symptoms in carbi/levodopa treatment are
hallucinations/dizziness/headache/agitation. After 5- 10 years of treatment,
dyskinesias and tardive dyskinesia are more likely to come up. 4702: always choose
non-contrast CT over contrast CT when evaluating a stroke initially. The contrast
can be confused for blood and obstruct the clinical evaluation. 3727: When treating
myasthenic crisis (worsening weakness/difficulty breathing and swallowing)
intubation for declining respiratory status is immediately done and
plasmapheresis/IVIG/corticosteroids is done after patient is stable to minimize
symptoms. AChE drugs (typically used to treat) are held to minimize secretions as
these can further worsen respiratory status. 4394: HCTZ is a K+ wasting diuretic
and pts may suffer from hypokalemia on it (always supplement K+ when pt are on
HCTZ). Signs of hypokalemia are as follows: * Minor: cramps, weakness, fatigue *
Major: flaccid paralysis, rhabdomyolysis, hyporeflexia, tetany, heart abnormalities
(premature ventricular beats, broad T-waves, U-waves, and ST depression) with fatal
arrhythmias can all occur! * Tx: potassium repletion 4372: Pt with spinal cord
compression (low back pain, parasthesias in leg, butthole working poorly) in the
setting of an infection should be examined for epidural abcess. * Best next step ??
MRI of spine with gadolinium contrast, blood culture, inflammatory markers * Tx:
immediate Abx (typically staph aureus) and surgical consult for de-
compression/drainage/culture 4443: Corticosteroid-induced myopathy may be confusing
as it can be in the presence of inflammatory disorders that can cause muscle
weakness/pain. Classically it presents in a patient taking chronic corticosteroids,
with proximal muscle weakness, no pain/tenderness, normal ESR/CK, and more
involvement of the lower extremities * Occurs weeks-months of starting high-dose
corticosteroid treatment; presents with the classic ??can??t climb stairs, comb
hair, etc.?? * Tx: taper/discontinuation of corticosteroids yields recovery in the
following months 3809: Remember! Pts with myasthenia gravis may have an
exacerbation with infection and drug treatments (floroquinolones [-floxacin],
aminoglycosides, beta-blockers, or macrolides) * Classically it??s generalized
weakness and difficulty breathing after an infection treated with antibiotics! * Tx
(if respiratory
status decline) ?? ICU monitoring with intubation 4022: Remember that ACA stroke
will produce contralateral weakness/loss of sensation with lower>upper extremity
weakness. This is due to the homunculus distribution of the motor cortex perfused
by the ACA. It may even feature urinary incontinence. 3327: Remember that infection
of the periorbital region/face can move into the cavernous sinus (ophthalmic/facial
venous system is valveless) and cause thrombosis. This may result in nerve palsies
and intracranial hypertension. This is beyond a normal cellulitis as nerve symptoms
would not be present if it was just a superficial cellulitis. 3691: Exertional heat
stroke is best managed with ice bath immersion (although cold water shower can
work), fluids/electrolyte repletion, management of any end-organ damage.
Temperatures can skyrocket above 104F, which results in symptom presentation. 3637:
Idiopathic intracranial hypertension (pseudotumor cerebri) is best managed with: *
acetazolamide (inhibits choroid plexus carbonic anhydrase ?? decreases CSF
production). Lasix (furosemide, etc.) may be added in pts that continue to have
symptoms. * Optic nerve sheath decompression may be used in patients refractory to
medical treatment (stop damage to eye nerves and blindness). * Corticosteroids/LPs
may be used as bridging therapy until definitive treatment is initiated * Mannitol
is not used in treatment; it require in-patient monitoring and only used for severe
intracranial hypertension (pt is obtunded) Cardiovascular 8879: Patients with IV
drug use and heart problems should immediately be considered for infective
endocarditis. This question was tricky as you had both an early diastolic murmur at
the left sternal border (indicating aortic regurgitation) AND a 2:1 second-degree
AV heart block (indicating progression of endocarditis into the myocardium via a
perivalvular abscess). This occurs in 30-40% of people with endocarditis! � Note
that early diastolic murmur at the RIGHT sternal border indicates aortic root
disease 4093: If a guy starts having a heart attack and then passes out it??s
likely that the guy has sudden cardiac arrest (passes out from lack bloodflow,
heart beat is irregular) due to arrhythmia. >50% of the arrhythmias due to
myocardial infarction occur within the first hour after the MI. There are two
types: * Phase 1a (immediate) ventricular arrhythmia: patient has
arrhythmia/cardiac arrest within 10 minutes of the MI onset. Due to re-entrant
myocardial conduction. * Phase 1b (delayed) ventricular arrhythmia: patient has
arrhythmia/cardiac arrest between 10-60 minutes after MI onset. Due to abnormal
automaticity causing uncoordinated heart contractions 3994: Isolated systolic
hypertension: a type of HTN that happens in the elderly due to a loss of elasticity
in the arterial walls. Typically the patient feels good, has a normal ejection
fraction, and elevated systolic BP with normal diastolic BP. * Important to note
elevated systolic BP and widened pulse pressure in elderly patients as it is a
treatable risk factor for further cardiovascular events * Tx: low dose thiazide,
ACE inhibitor, or long acting Ca++ channel blocker 4649: In any patient with Atrial
Fibrillation, the CHA2DSs- VASc score should be calculated in order to determine
the optimal therapy. It goes like this: * Congestive heart failure ------------- 1
if yes * Hypertension --------------------------- 1 if yes * Age
>75*--------------------------------- 2 if yes * Diabetes
Mellitus---------------------- 1 if yes * Stroke/TIA/Thomboembolism------ 2 if yes
* Vascular disease----------------------- 1 if yes * Age 65-
74*------------------------------ 1 if yes * Sex
category--------------------------- 1 if male Depending on the score, you??ll get a
certain anticoagulative therapy to minimize stroke risk: * 0: no therapy * 1: none
or aspirin or anticoagulation * 2 or more: anticoagulation (Apixaban, dabigatran,
rivaroxaban, edoxaban, or Warfarin) 3766: Mobitz I (Wenckebach) vs Mobitz II second
degree heart block have distinct features on EKG: * Mobitz type 1: occurs in the AV
node, has progressively longer PR intervals until a non-conducted ?? dropped?? QRS
complex (??group beating??), with narrow QRS, and low risk for complete heart block
o Exercise/atropine improves this heart blocko
Vagalmaneuvers(carotidmassage)worsensito
Tx:observationortreatmentofreversiblecauses * Mobitz type 2: occurs in the bundle
of His/Purkinje fibers, randomly drops QRS complexes with a normal rhythm, with
widened QRS and is high risk for complete heart block o Exercise/atropineworsenso
Vagalmaneuvers(carotidmassageimprove o Tx:pacemakerimplantation * NOTE that if
assessing the rhythm, look at the rhythm strip at the bottom of the EKG 3826:
Percutaneous coronary intervention (PCI) is threading a catheter into the heart and
inflating a balloon on the end to open up a stenotic artery causing MI. A stent is
usually placed to keep it upon until about 3 months when it??s removed, as the
artery has adapted. * PCI or fibrinolytic therapy should be initiated within 90
minutes of a heart attack, and within 90 minutes of first medical contact (if PCI
available) or 120 minutes (PCI not available, time for transport) * Fibrinolysis
used typically if patient presents within 12 hrs and cannot tolerate PCI * O2, full
dose aspirin (chewed), clopidogrel/ticagrelor (platelet inhibition),
nitroglycerine/morphine for pain control, beta blocker, and anticoagulation should
all be initiated for initial stabilization 3958: Old people with orthostatic
hypotension/syncope is usually the result of hypovolemia or autonomic baroreceptor
failure. Hypovolemia can be due to: * Diarrhea, decreased fluid intake, diuretic
therapy, and other reasons * Often mucous membranes are dry * Prerenal azotemia:
Increased BUN or BUN: creatinine ratio (>20:1) occur with hypovolemia because
glomerular filtration decreases and urea absorption increases to maximize water
retention by the kidney. These two lab values can clue you in to the etiology of
syncope. 2742: Patient presents with burning chest pain that often occurs with
lifting heavy boxes at work. He is on chronic prednisone for SLE (which are risk
factors for atherosclerosis) * The FIRST step in management is to get an EKG (it
could be an MI). * If that is normal, get an exercise EKG as the pain may be due to
ischemia, but only with exercise. * If that is normal, GI causes should be
investigated (GERD, etc.) 2148: Atypical symptoms for acute coronary syndrome
include: dyspnea, epigastric pain, N/V * The elderly, women, and those with
diabetes more likely have atypical presentation * 20% of these patients DO NOT
PRESENT WITH CHEST PAIN 2141: Sinus bradycardia (<50 bpm) with symptoms
(dizziness/syncope) approach: * ID/treat any underlying causes, get EKG, monitor
cardiac rhythm, get IV access, and pulse oximetry for oxygen levels * Persistent
bradyarrythmia + [hypotension/shock, mental status change, chest discomfort, or HF]
requires further intervention. If it??s just a slow heart rate, then just observe *
If symptoms: atropine (0.5mg IV bolus, up to 3mg) to inhibit parasympathetic system
* If persistent: Transcutaneous pacing, DA IV, or epinephrine IV to increase
sympathetic system * If persistent: consult cardiology and transvenous pacing 4911:
Mitral valve regurgitation classically presents as: holosystolic murmur radiating
to the axilla, progressive exertional dyspnea, and dry cough (pulmonary
edema/congestion) 4395: Don??t perform testing for coronary artery disease in
patients with low pre-test probability! A positive result could lead to unnecessary
testing and causing harm to the patient. � Young age (men <40, women <50), female
gender, no cardiac risk factors (smoking, diabetes, family Hx, etc.), and character
of chest pain (exertional, relieved with rest, signs of angina) that suggest non-
cardiac etiology put people at LOW RISK 2310: After and MI successfully treated
with cardiac catheterization, there??s a good chance, especially with risk factors,
that cholesterol plaques could rupture and send cholesterol emboli showering
throughout the body causing ischemia. This can be manifested through livedo
reticularis, blue toe syndrome, renal failure, gangrene, ulcers, Hollenhorst
plaques (yellow, shiny plaques in the retina), stroke, or GI bleeding. * Tx: statin
therapy with support for any other problems * May happen immediately or delays (up
to 30 days after) 4243: In heart failure, there??s decreased cardiac output,
eventually backing up the CV system where forward flow is impaired and organ
perfusion is poor. Neurohumoral functions (epinephrine, NE) will cause increased
vascular systemic resistance to keep BP high and perfuse the organs. Eventually the
afterload on the heart will start to take a toll and LVEDV will increase (less
forward flow) and cardiac index will drop (Cardiac output /Body surface area) 4673:
Hypertrophic Obstructive Cardiomyopathy (HOCM) should be suspected in a young
person experiencing syncope, chest pain, and has a creshendo-decreshendo murmur on
the left sternal border. While aortic stenosis CAN cause this murmur, it is
unlikely if the patient does not have a familial syndrome/risk factors that leads
to aortic stenosis. Aortic stenosis would be more common in older people. 4455:
Exertional syncope is passing out when exerting yourself, often due to outflow
obstruction or arrhythmia, although it could have many causes. With fixed-outflow
obstruction you have obstruction in bloodflow that cannot meet the demands your
body needs, so your brain is underperfused and you pass out. Classic signs for
exertional syncope due to fixed-outflow obstruction: * Pulsus parvus et tardus
(delayed, diminished carotid pulse) * Single soft S2 sound (not much pressure
closing
the tricuspid) * Mid to late peaking systolic murmur at 2nd right intercostal and
radiating to carotids 4054: When you get a patient with suspected angina pectoris
BUT they cannot undergo exercise testing (like they have a leg amputation)... you
can administer adenosine or dipyramidole (coronary vasodilators) � If coronary
artery disease is present, the disease artery is already dilated to provide blood
to the tissue is perfused (there would be ischemia if it was normal size). This it
cannot further dilate. The other, non- diseased vessels will dilate with the
medication and cause coronary steal, revealing ischemia in the diseased tissue
2678: Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant
mutation typically of myosin binding protein C or cardiac beta-myosin heavy chain
gene resulting in abnormal myocardium � The murmur is decreased with increased
blood in the left atriumo
Sustainedhandgrip(increasedafterload),squattingfromstanding(increasedafterload/prel
oad) or passive leg raise (increased preload)o These all increase distention of the
ventricle, minimizing outflow obstruction * The murmur is increased with decreased
blood in left artriumo Valsalva,abruptstanding(decreasedpreload),andnitroglycerin o
All increased obstruction, thus the intensity of the mumur * Murmur is best heard
on the left, lower sternal border/apex 2729: Acute pericarditis is a complication
of recent MI occuring within the first few days of MI: * Pleuritic chest pain worse
when supine, better with sitting up/leaning forward * Diffuse ST elevations with PR
depressions 3765: First degree heart block: normal contraction of the
atria/ventricles, but transmission below the AV node is slowed for some reason.
This causes normal QRS complexes but prolonged PR intervals (the conduction is
fine, it??s just slow going from the atria to the ventricles. * Considered benign,
although associated with higher risk of MI/more severe heart block * Tx if non-
symptomatic: no intervention with follow up monitoring * Tx if cardiac symptoms or
prolonged QRS: electrophysiology studies to uncover nature of disease. 8472:
Myocardial sleeves are these bits of myocardial tissue that extend into the
pulmonary veins to act as a sphincter, decreasing reflux of blood in the pulmonary
veins. Because the pulmonary tissue is so different, this puts this myocardial
tissue at risk for ectopic/aberrant conduction. For this reason, the pulmonary
veins are the most likely anatomic spot for generating atrial fibrillation. �
Atrial fibrillation ?? irregularly irregular pulse with narrow QRS complexes, and
absent P waves 4650: Costochondritis is an important cause of chest pain that??s
sharp, non-radiating, lasts for hours, worsens with inspiration/movements, and
importantly REPRODUCABLE WITH PALPATION. It??s not a heart problem, it?? s a joint
tenderness problem. 3769/4453/3506: Amiodarone is an antiarrhythmic drug that??s
great for atrial and ventricular arrhythmias... but has many, wide-ranging side-
effects. The top 5 are: * Pulmonary fibrosis � associated with cumulative dose, not
serum levels. The longer you take the drug the more likely you??ll get this *
Thyroid dysfunction � hyper>hypothyroid. Amiodarone is made with iodine. Always
check TSH before initiation and 3-4 months after using amiodarone * Hepatotoxicity
� often asymptomatic, but drug should be stopped/switched if seen * Corneal
deposits � often secreted by the lacrimal gland. These are not a big deal and do
not warrant drug cessation * Blue-grey skin discoloration, especially on the face
4738: Abdominal Aortic Aneurysm (AAA) expansion is most closely linked to active
smoking (likely due to aortic wall damage/degeneration) * Risk factors for
development: Caucasian, >60yrs, smoking, and atherosclerosis * Risk factors for
expansion: large diameter, high rate of expansion, and current cigarette smoking
4042: Any person (especially younger) presenting with agitation, dilated pupils,
atrophic nasal mucosa, HTN, and acute myocardial ischemia should be suspected for
cocaine abuse! * a/B adrenergic stimulation = HTN/pupil
dilatation/agitation/ischemia * cocaine also potentiates thrombus formation * Tx:
immediate benzodiazepines/O2 + aspirin, nitrates, calcium channel blockers * NEVER
GIVE A B-BLOCKER: it will cause unopposed a-adrenergic activity and HTN crisis!
4298: The best treatment for long-term medical prevention of MI following acute
myocardial ischemia is ALL of the following: * Dual antiplatelet therapy (aspirin +
P2y12 receptor blocker) * Beta blocker * ACE inhibitor or ARB * Statin *
Aldosterone antagonist (eplenerone/spironolactone) in pts with EF <40% or in
diabetes mellitus 2172: Fibromuscular dysplasia: a chronic resistant hypertensive
syndrome due to abnormal cell development (no inflammation/atherosclerosis) often
involving the renal/carotid/vertebral arteries * Presentation:o
Renalarterynarrowing??inappropriatereninactivity??HTNo Symptomsofcarotidstenosis??
amorousisfugax,TIA,Horner??s,strokeo SymptomsofcarotidorvertebralAstenosis??
dizziness,pulsatiletinnitus,headache * Screening should be done on women aged
<50yrs witho Severe, resistant hypertension...especially before age 35 o Creatinine
increase after starting an ACE or ARBo Suddenincreaseinbloodpressurefrombaseline *
Dx � CTA of the abdomen or duplex ultrasound showing fibromuscular stenosis. If
nothing is seen, cathather based arteriography should be used * Tx �
antihypertensive drugs or vascular surgery3768: Remember that complete (3rd degree)
heart block shows P-waves that are NOT followed by QRS complexes. This is treated
with immediate pacemaker placement (cardiac pacing) � These patients may show T-
wave inversion indicating myocardial ischemia, BUT if they do not have ST
elevation, MI treatment is NOT indicated. 2743: Ca++ channel blockers are poor
choices in acute MI as the vasodilation can result in reflex tachycardia causing
increased oxygen demand on the myocardium ?? worsening of MI ischemia * If a
patient has acute pulmonary edema associated with an acute MI (??flash pulmonary
edema??) the best bet is a loop diuretic. Furosemide is a great choice, as you??ll
pee out fluid (decrease preload) AND cause venodilation (decrease preload). *
Venodilators (IV nitroglycerine) are a good choice if loop diuretics cannot be used
4108: Remember! Specific changes to EKG can clue you into where the MI is occuring.
It??s actually pretty complicated and I??m SUPER tired right now so I don??t want
to go through it all. But suffice it to say that if you note AV block on the ECG,
likely the RCA is occluded because it supplies the AV node. 2737: Patients that
cannot comply with dual-antiplatelet medication following MI and stenting are at
high risk for stent thrombosis. Apparently all this question said was that the guy
was unemployed (a nice clue). However, premature cessation of dual-antiplatelet
therapy with a stent is the highest risk factor for this! 3094: The most helpful
non-pharmacologic treatment to decrease HTN is: * In obese patients ?? weight loss
* In non obese patients ?? the DASH diet (low salt, high fiber, emphasis on
fruits/veggies and low fat) o
Followedbyexercise,isolatedsaltrestriction,andalcoholcessation 3093: DON??T just
say HOCM when you see a young person with a heart murmur. Bicuspid aortic valve can
be a familial defect resulting in aortic regurgitation (AR) * AR: diastolic
decreshendo murmur best heard in the left sternal border in the 3rd/4th intercostal
space * Congenital bicuspid aortic valve = the most common cause in developed
countries * Rheumatic heart disease = the most common cause in developing countries
2153: Aortic Stenosis: presents with the following: * Exertional syncope: pt will
be doing something (jogging) and will get lightheaded/pass out without confusion
afterward * Pulsus parvus et tardus (??delayed and diminished carotid pulse??):
because the aortic valve is obstructing bloodflow the carotid pulse will be delayed
after the S1 sound; the bicuspid valve closes but the blood won??t make it out of
the heart until later * Single/soft S2 with an S4: the S2 is diminished as the
aortic valve doesn??t ??click?? shut, it??s fused together. S4 from increased
pressure of contraction to maintain perfusion (LVH) * Harsh ??creshendo-
decreshendo?? murmur that radiates to the carotids: due to bloodflow past the
stenotic arteryFirst step in working up AS ?? EKG because it??s suspected to be due
structural heart disease. 4003: Most common cause for Aortic Stenosis: * Elderly:
age-related calcific changes * Young: congenital anomaly (bicuspid aortic stenosis)
4681: The renin-angiotensin-aldosterone system (RAAS) is a major target for HTN
treatment * In response to decreased perfusion in the kidney ?? renin released from
the JG cells * Renin cleaves angiotensinogen ?? angiotensin I * Angiotensin
converting enzyme (ACE) converts angiotensin I ?? angiotensin II * Angiotensin II =
potent vasoconstrictor and promotes aldosterone production * Aldosterone = acts on
collecting ducts to increase sodium resorption/water resorption * Blocking any of
these steps will ultimately decrease BP but buildup the previous steps; thus a
direct renin inhibitor will decrease both angiotensin II AND aldosterone 4456:
Syncope in a patient with a prolonged PR interval (P wave to QRS) AND prolonged QRS
would suggest a conduction abnormality in the myocardium suggesting bradyarrythmia
or high grade AV block. Note that this can be intermittent and seeing the patient
with a heart rate within normal range does NOT exclude bradyarrhythmia. 4235: In
cardiogenic shock, the patient??s heart is failing so bad that they??re failing to
perfuse vital organs. Characteristic signs of cardiogenic shock are: cold/clammy
extremities, high right atrial/pulmonary wedge
pressure (backup into pulmonary circuit), very low cardiac index, high systemic
vascular resistance (afterload) 4532: USPTF guidelines recommend screening for AAA
with abdominal ultrasound in men who have previously smoked aged 65-75. Men that??
ve never smoked...there??s no recommendation so it doesn??t hurt to do it but it??s
not needed. 4518: High BNP or N-terminal Pro-BNP (the inert peptide cleaved off it)
correlates with LV systolic dysfunction/overfilling. Lack of high BNP is a great
negative predictor of good LV systolic function. 2666: Acute arterial occlusion is
the result of arterial blockage for some reason (a classic is cardio-embolism)! *
Presentation: Pain, Pallor, Pulselessness, Polkiothermia (cold limb), paresthesia,
paralysis * Tx: IMMEDIATE anticoagulation (usually heparin IV). While that??s
going, order other things. 2156: Right Ventricle Myocardial Infarction (RVMI): MI
with accompanying JV distention, clear lung fields, and hypotension. The
hypotension can be so profound it can cause cardiogenic shock. � Tx: Normal MI
protocol + IV saline bolus; apparently when the right heart is dying, it needs more
pre- load to allow for proper cardiac output. Giving something to increase heart
contractility (inotrope/adrenergic) would further demand on the heart and cause
worsening infarction. Vasodilators may worsen the depressed BP. 2224: Uremic
pericarditis: in the setting of renal failure, a BUN >60 mg/dL can result in
pericardial sac inflammation and ultimately a pericarditis (friction rub, chest
pain relieved by leaning forward). * May have abnormal, but not classic EKG due to
only low level of inflammation * Tx: immediate dialysis (typically yields quick
recovery from symptoms) 10763: Nitroprusside is a fantastic IV drug for acute
control of hypertensive emergency. It is metabolized into nitrous oxide and cyanide
ions and leads to rapid correction of HTN. The drawback is that it cannot be used
in prolonged settings as the cyanide ions will build up and can cause toxicity.
Cyanide toxicity is more common in folks with renal damage as they cannot filter
out the CN- as well. * Cyanide toxicity: altered mental status, lactic acidosis,
seizure, coma * Also...severe hyperkalemia does NOT cause seizure. It causes
weakness/cardiac arrhythmias 4592: Peripheral Edema due to Venous insufficiency: a
common condition that presents as leg discomfort, pain, and swelling especially
after prolonged standing. Improves with leg elevation. Abnormal venous distention,
skin discoloration, dermatitis, and skin ulceration (esp. as the medial ankle) are
all signs � Tx:o 1.Legelevation,exercise,andcompressionstockingso 2. Venous duplex
ultrasound to ID the area of venous reflux/insufficiency o 3. Endovenous ablation
3635: Constrictive Pericarditis: occurs when the pericardium is damaged, loses
elasticity, and becomes fibrous resulting in altered heart function * Etiology:
idiopathic, viral, cardiac surgery, radiation/chemotherapy, or tuberculosis *
Presentation: fatigue/dyspnea on exertion with peripheral edema/ascites, and
increased JVP with sharp X/Y waves (forward flow compromise) o
Pulsusparadoxus/abnormalseptalmovement:systolicBPdropsuponinspiration;heartcan??t
distend well and when you breathe in, more blood flows into the right
ventricle...so the septum compensates moving into the left ventricle, diminishing
outflowo Calcifications on X-ray of the pericardiumo Kussmaul??
ssign:failureofcentralvenousBPdecreaseoninspiration � Tx: Diuretics (temporary
relief) with pericardiectomy (definitive Tx) 2711: A CLASSIC reason for a young
athlete to get syncope/abnormal heart sounds is HOCM. Oddly, this can become more
severe as the outflow of blood along the narrowed ventricle can pull the mitral
valve leaflets into the ventricle creating outflow obstruction. This outflow
obstruction is largely blamed for clinical manifestations AND the harsh systolic
murmur that worsens with standing up suddenly. 4346: Note that chronic GERD
patients may have chronic cough (stomach HCl into lungs) or hoarseness (HCl into
the larynx) as part of their clinical picture. 4697: S4 heart sound can be heard in
a variety of pathologic/non-pathologic processes; all of which result in stiffening
of the left ventricular wall, causing a sound of blood sloshing into a stiffened
heart wall� MI, acute ischemia, HTN, aortic stenosis, hypertrophic cardiomyopathy,
and normal aginging in older adults can all result in the stiff heart wall
responsible for an S4 3689: Exertional Heat Stroke: body temperature >40C (104F) +
central venous dysfunction that??s most common in young people exerting themselves
too much in the heat. * Dehydration is common causing tachycardia, hypotension,
hemoconcentration, elevated BUN * Tx: ice water bath and rehydrationNon-exertional
heat stroke: is the same symptoms as exertional, but in elderly people who simply
cannot stand the heat or are not able to compensate for it properly with
homeostasis � Tx: external evaporative cooling (luke-warm water with a fan on them)
4484: Marfan44s syndrome (fibrillin-1 mutation) can have major cardiac implications
due to weakened elastic tissue in the aorta! * Aortic dissection: painful tearing
sensation, radiating toward the back. Uneven BP in the left vs right arm. Aortic
root dilatation causing aortic regurgitation (decrescendo diastolic murmur) *
Mitral valve prolapse may also occur causing backflow into the pulmonary circuit.
2713: Cardiac myxomas are most typically (80%) present in the left atrium �
Symptoms: o Constitutionalsymptoms(fever,weightloss,Raynaud??s)duetoIL-
6overproductiono
Massintheheart;maymimicmitralvalveproblemsorearlydiastolicsound(tumorplop) o
Invasion of cardiac or lung tissueo Embolization possible causing stroke or
ischemic organ damage * Dx: transesophageal or transthoracic echocardiogram
demonstrating heart mass * Tx: prompt surgical resection 2663: B-blocker overdose:
bradycardia, AV-block, hypotension (all causing cardiogenic shock), diffuse
wheezing (due to bronchospasm, specific!), and hypoglycemia � Tx:o
1.ABCs,isotonicsaline(getBPup)andIVatropine(getHRup)o 2. IV glucagon: increases
intracellular AMP, limits effect of B-blocker on cells 4445: Cardiac Tamponade due
to Pericardial effusion can occur due to many different reasons (most often
idiopathic!). However it will always present with similar symptoms! *
Enlarged/globular cardiac silhouette (??water bottle?? shape) * Clear lung fields *
Inability to palpate the point of maximal impulse (PMI) * Beck�s triad:
hypotension, JVP, muffled heart sounds 2692: Any patient presenting with heart
failure with signs of chronic alcoholism (macrocytic anemia / liver damage AST>ALT
were given here) should be considered for alcoholic cardiomyopathy * Etiology:
chronic alcohol can have direct damaging effects on the heart tissue * Dx: rule out
ischemic cardiomyopathy; heart failure in the setting of chronic alcoholism * Tx:
cessation of all alcohol intake (mainstay) + low salt diet/HTN drugs/etc. 4742:
Oddly enough this question painted a picture of a guy with asthma via telling us
that he had chronic rhinitis, nasal polyps, and eczema. He likely had unstable
angina and treatment may have caused him to have a dry cough! * Aspirin = common
trigger for bronchoconstriction for asthmatics * Non-selective B-blockers = limit
ability to bronchodilate, thus exacerbating asthmatics This guy was also on an ACE
inhibitor...which has a classic side effect of dry cough 9648: SPECT-scan of the
heart with stress testing can clue us into areas of the heart that are ischemic *
Tc-99 is injected into the body and is passively taken up by perfused myocardial
cells; if there is ischemia, the Tc-99 will not be taken up and he radioactive
signal will be diminished in that area * We can use this to check for ischemic
areas in the heart o Same normal uptake at rest/during exercise = low chance of CAD
o Normal uptake at rest with decreased uptake in areas in exercise = likely
inducible CAD o Decreaseduptakeatrest/exercise=scarfrompreviousdamage * If we see
the signs of inducible CAD then treatment must be given! * Tx: anti-platelet
therapy, b-blocker, and modifying risk factors 3056: Recognizing aortic dissection
can be as easy as seeing a false lumen on a chest CT scan. * Hypertension is a
necessary feature to cause tearing and dissection o
StanfordA:goesbacktowardtheheart??B-blockerwithsurgicaltreatment o
StanfordB:goesdownthedescendingaorta??B-blockerandfollow-up * Tx: Labetalol (or
possibly another b-blocker) ?? these will decrease BP and heart rate reducing
stress on the aortic wall quickly4469: Lone Atrial Fibrillation is AF with a CHADS-
VASc of 0 ?? it requires no intervention at this time 4676: New onset Atrial
Fibrillation without a discernable underlying etiology (relatively normal EKG with
loss random dropping of beats) should be checked for hyperthyroidism, as it??s a
major cause of spontaneous-onset atrial fibrillation! � EKG of hyperthyroid:
irregularly irregular rhythm, variable R-R interval, no discernable P-waves 4127:
Stable angina pectoris is predictable chest discomfort occurring with exertion and
relieves with rest due to insufficiency of coronary bloodflow during increased
myocardial oxygen demand. * 1st line: beta blockers ?? avoided in low
BP/bradycardia, or if side effects aren??t tolerated well; work well as they
decreased blood pressure and contractility of the heart * 2nd line: Ca++ channel
blockers (-??dipines??) or long acting nitrates ?? used after B-blockers fail 3820:
Remember! Digoxin has NOT been shown to decrease mortality in CHF patients! It only
reduces symptoms by increasing contractility! It??s honestly considered to be a
poor drug to due toxicity! * Digoxin toxicity: nausea, vomiting, fatigue,
confusion, weakness, yellow-halo/scotomas,
and life threatening arrhythmias (can cause nearly any type!), and elevated K+. *
If starting amiodarone, pt digoxin dose should be reduced by 25% 3526:
Cardioembolic embolus: Patients with myocardial infarction will subsequently have
worse contractility (thus stasis) predisposing heart attack patients to possible
cardiac thrombus formation. If the left ventricle myocardium is damaged, then this
predisposes to mural thrombus and and systemic embolization (stroke, acute limb
ischemia). � Tx: immediate anticoagulation, vascular surgery consult, transthoracic
echocardiogram (check for mural thrombi in hear to find source of ischemia) 4270:
elevated BNP is one of those lab values that you simply do NOT ignore! >100 pg/mL
BNP has sens90, spec76, and predictive acc83 3521: Pericarditis: sharp, stabbing
chest pain that??s worse with inspiration (more preload = more stretching of
pericardium) and better with leaning forward; classically occurs with a friction
rub * Characteristic EKG: diffuse ST elevation with depression in aVR * Post-MI
Acute pericarditis: occurs a few days after MI * Dressler�s syndrome: an
immunologic pericarditis against heart tissue that occurs a few weeks after a heart
attack (takes time for the titers to rise to do damage)o
Fever/malaise/elevatedESRareallsignstolookoutfor o Tx: NSAIDs or Corticosteroids
for refractory cases 10764: Constrictive pericarditis: pathologic thickening of the
pericardium which results in heart constriction and ultimately failure of diastolic
function * Dx: signs of right heart failure (fatigue/dyspnea, elevated JVP, cardiac
cirrhosis/nutmeg liver); Kussmaul�s sign (lack of JVP decrease on inspiration),
pericardial calcifications, or midsystolic pericardial knock (like the beat is
knocking against something hard) * Etiology: idiopathic, viral, cardiac surgery,
prior chest radiation, TB (endemic) * Tx: if new and not severe ?? anti-
inflammatory drugs followed by pericardectomy; if severe then immediate
pericardectomy * Note that normal JVP is <8cm H20) 4707: Heart failure with
preserved ejection fraction: basically you have a heart who??s left ventricle has
hypertrophied so much that it cannot fill with an adequate volume of blood to
properly perfuse the body. * Etiology: several reasons, the classic is long-
standing hypertension causing LV hypertrophy * Dx: Signs of left heart failure
(orthopnea, lung crackles, possibly edema/liver cirrhosis), normal (>50%) ejection
fraction, evidence of diastolic dysfunction via echocardiograpyo
DecreasedLVcompliancecausesincreasedLVpressure??LApressure(lossofatrialkick,atrial
enlargement, atrial fibrillation) ?? pulmonary congestion ?? right heart failure *
Tx: no specific regimen; Tx centers around fixing contributing factors (HTN) to
stop progression 4227: Statins inhibit HMG-CoA reductase thus decreasing intrinsic
cholesterol synthesis ?? forcing increased cholesterol uptake from blood to meet
demands on the liver. Side effects include: * Myalgias � common, may have increased
creatine kinase; thought to be due to decreased CoQ10 synthesis which is necessary
for muscle energy production * Liver dysfunction � rare but serious 4741: Nitrates
are fabulous drugs to stop angina (ischemic chest pain). They are venodilators that
work in two ways to decrease wall stress in the heart: * Pool blood in systemic
veins: this decreases preload, thus wall stress. The Frank-Starling forces are
minimized and cardiac contraction is less intense, thus oxygen demand is decreased
* Lowers systemic BP: plays a minor role in decreasing ventricular wall stress
4126: Hyperthyroidism can be manifest with atrial fibrillation (most common
arrhythmia in hyperthyroid) along with other classic symptoms (increased HR, heat
intolerance, weight loss, myxedema, eye bulge, hyperreflexia, lid lag, goiter,
etc.) � Tachycardia is due to thyroid hormone induction of B-adrenergic receptors
(pro-adrenergic) � Tx: o Propranolol(immediately)�slowsheartrate(blocksB-
adrenergicreceptors)ANDmildly decreases T3/T4 production by the thyroid o
Thyroidablationwiththyroidhormonereplacement(definitive) 4380: Remember! Aortic
dissection can go proximal toward the heart and rip the aorta causing blood to
flood into the pericardium ?? cardiac tamponade! * Increased pericardial
pressure ?? diastolic failure ?? decreased preload and heart failure * Dx:
hypotension, tachycardia, distended JVs, pulsus paradoxus * Tx: emergency
pericariocentesis to drain fluid with surgical repair of dissection 8819: Aortic
coarctation (late presentation): remember that this is a congenital aortic
stricture which can cause significant cardiac signs/symptoms: * Associated
findings: bicuspid aortic valve, Turner??s disease, ventricular septal defect (VSD)
* Dx: classically presents with asymptomatic HTN and epistaxis in a young person o
Mayalsohaveclaudication,headache,heartfailure,aorticdissectiono Brachial-
femoraldelay,upperextremityhypertensionwithlowerextremityhypotension, continuous
cardiac murmur (from collateral flow)o CXRcanshow:LVhypertrophy,notchingof3-
8ribs,??3-sign??ofaorticindentation o Confirmwithechocardiography � Tx: balloon
angioplasty +/- stenting to open stricture point 3962: Pts with strong clinical
suspicion of vasovagal syncope and normal EKG can be clinically diagnosed without
further testing! � Uncertain cases can be confirmed with tilt-table testing 4291:
Poor response to anti-hypertensive regimen can be due to a number of factors: *
Poor adherence to diet/lifestyle changes: typically weight loss, DASH diet,
cessation of excessive alcohol consumption, and regular aerobic exercise are big
ones * Medication non-compliance * Use of medications that can raise BP: NSAIDs
(decrease renal perfusion thus increased RAAS), decongestants or glucocorticoids
2744: Premature Atrial beats (APBs) are benign arrhythmias, usually manifest on EKG
by an early P wave generated by a pacemaker that isn??t the SA node. Typically,
these are no big deal but can cause symptoms and may precede atrial fibrillation. �
APBs can be exacerbated by tobacco, alcohol, caffeine, and stress. Thus these
should be decreased/eliminated if the patient is experiencing symptoms due to APBs
4910: Aortic regurgitation is characterized by: * Diastolic ??decreshendo murmur??:
sound of blood rushing back into the LV * ??Hyperdynamic??, ??Bounding??, ??water
hammer?? pulse: because of increased LV filling, stronger LV contractions occur
(increased systolic BP) and due to aortic backflow, decrease diastolic pressures
occur. This widens the pulse pressure making peripheral pulses feel much more
intense. 4061: Dilated cardiomyopathy is CHF due to myocardial damage resulting in
dilation of the ventricles and diffuse hypokinesia (ventricles can??t pump as well,
thus heart failure occurs) * Dx: classically acute heart failure in a young person
suggests dilated cardiomyopathyo Recentviralinfectionisacommonprecipitant(3-
5%)duetodirectviralandimmuneresponse damage to the myocardium (Coxsackie B,
Parvovirus B19, HHV-6, adeno, and enteroviruses) o
Thiaminedeficiency(wetberiberi)isanotherclassiccauseo Dilated ventricles with
diffuse hypokinesia on echocardiogram confirms diagnosis * Tx: supportive for CHF
and tx for precipitating factor 2159: While most HTN patients have essential HTN,
initial workup should ALWAYS be for secondary causes (as they may be treatable!).
Thus, your approach should be: * History of HTN: duration, evidence of end organ
damage, aggravating/alleviating factors, etc * Basic Labs: o
Urinanalysis:BUN:creatinineandocculthematuriao
Chemistrypanel:riskassessmentforcoronaryarterydisease(CAD) o Lipid profile: risk
assessment for coronary artery disease (CAD)o Baseline EKG: to evaluate for CAD or
left ventricle hypertrophy * If pt has malignant HTN, HTN refractory to >3 drugs,
sudden rise in BP, or onset <30yrs of age without family history, additional workup
should be done as they suggest secondary cause 3920: Remember that Ca++ channel
blockers (-dipines) have a classic side effect of edema! * This is because they
induce vasodilation. It is NOT an allergic reaction * Typically if you have a
person that just started a ??dipine?? and has normal vitals/labs, they likely are
having this adverse drug event * Tx: discontinue the drug and find an alternative
2740: Mineralocorticoid receptor antagonists (MRAs; spironolactone/eplerenone) are
the only heart failure drugs clinically proven to increase survival in pts with LV
systolic heart failure. � Typically we use MRAs when HF symptoms persist despite
ACE inhibitor/ARB/Beta-blocker therapy 3973: Niacin (Vit B3) flush is observed in
high-dose niacin (needed for dyslipidemia therapy). This is a drug- induced and NOT
an allergic release of histamine/prostaglandins. * Can be prevented by taking low-
dose aspirin 30 minutes before niacin dose * Often goes away 2-4 weeks after
initiation of therapy 2722: Variant (Prinzmetal) Angina: a vasospatic angina that
typically occurs in young women without cardiovascular risk factors, onset in the
middle of the night, and often exacerbated by smoking. * May be precipitated by
exercise, hyperventilation, emotion, cold exposure, cocaine abuse; but will not be
consistently exacerbated with exercise like Typical Angina * EKG can show transient
ST elevation with complete return to baseline after ischemic vasospasm * May be
associated with other vasospastic disorders (such as migraines or Raynaud�s
phenomenon) * Tx: nitrates or Ca++ channel blockers (vasodilation) 3096: The most
SPECIFIC (not necessarily the most common) arrhythmia induced by digoxin
(digitalis) is an atrial tachycardia with AV block * Atrial tachycardia: digoxin
can make ectopic pacemakers more pronounced * AV block: digoxin can decrease vagal
tone, thus AV nodal transmission, leading to AV block * Both
of these things happening together is pretty rare, so if you see this and the
patient is on Digoxin, it�s likely due to the medication! 3069: In Wolff-Parkinson-
White (WPW) syndrome, an abnormal accessory pathway between the atrial and
ventricles that bypasses the AV node (slow down for coordination) is present �
Atrial fibrillation is a common, and possibly deadly, arrhythmia in WPW; the quick
atrial depolarization means you??re getting consistent quick ventricular impulses
due to the accessory pathway. Thus AFib can deteriorate in the ventricular
fibrillation ?? sudden cardiac arrest! � Tx:o Hemodynamicallyunstable??
immediateelectricalcardioversiono Hemodynamicallystable??
IVibutilideorprocainamideforrhythmcontrolareused 2731: Late complications (on the
order of months) of MI are post-infarction angina, autoimmune pericarditis
(Dressler??s syndrome) and left ventricular aneurysm. While these may occur earlier
in the post-MI course, they are the only ones that can occur months after! * Left
ventricular aneurysm presents with progressive heart failure, and characteristic
EKG of persistent ST-segment elevation with deep Q waves in same leads after MI *
These are a bit academic BUT it??s possible. * Remember that these aneurysms rarely
rupture, typically scaring over causing much decreased wall mobility and
predisposing to mural thrombi and other complications! * Dx: echocardiography
showing dyskinetic wall motion of the left ventricle wall * Tx: treat symptoms of
heart failure 4719: Sudden Cardiac Arrest (SCA) is a bad time. Typically, only 33%
of patients are resuscitated and make it to the hospital with 10% of those patients
being discharged. The single most important factor in determining survival is time
to rhythm analysis and defibrillation. * The most common cause of SCA is
ventricular fibrillation/tachycardia often induced by ischemia or MI * Ventricular
fibrillation never terminates on its own * Thus effective CPR alongside prompt AED
defibrillation to re-establish perfusion is the best thing for any patient with SCA
as longer time for systemic ischemia = more organ damageo Note that compression
only CPR is recommended for SCA first aid (not rescue breathing)o
Whileadvancedcardiacintervention(catheterization/pressors)serveanimportantpurpose,
they will not have as much impact as promptly halting the arrhythmia to regain
perfusion 2728: Heart free wall rupture is a serious complication following a
myocardial infarction * Typically occurs between 5 days � 2 weeks following
anterior MI * Presentation: acute shock/chest pain, JVD, distant heart sounds,
pulseless electrical activity (PEA) ?? the free wall rupture results in
hemopericardium leading to cardiac tamponade. * Tx: EKG (shows PEA), supportive
care, pericardiocentesis, and emergent surgery for free wall repair 2700: Rheumatic
heart disease most commonly affects the mitral valve classically presenting with an
abnormal heart sound of loud S1 and mid diastolic rupture. The back-pressure of the
stenotic valve can cause atrial dilatation resulting in atrial fibrillation (up to
70% of rheumatic heart disease patients). * AFib � ??irregularly irregular??
heartbeat with loss of P-waves * Dyspnea may occur due to poor flow out of the left
atrium 4277: Three major signs of aortic stenosis are as follows: * Pulsus parvus
et tardus: a delayed carotid pulse due to delayed opening of the aortic valve *
Mid-to-late peaking systolic murmur: often ??creshendo-decreshendo?? murmur
corresponding to the maximal amount of bloodflow across the stenotic aorta * Soft,
single (S2) heart sound: reduced aortic mobility diminished the ??snap?? of the S2
and delayed opening causes it to coordinated better with the pulmonic valve ??
single/soft 4459: Basically what happened to this guy is he got a knife wound that
was sutured and began having abnormal cardiac signs. Apparently you can acquire an
arteriovenous fistula from trauma. This leads to shunting directly into the venous
system which significantly decreases systemic vascular resistance, increases venous
return (preload), and increases cardiac output. * Presentation: widened pulse
pressure, strong peripheral pulsation (brisk carotid pulse), systolic flow murmur,
tachycardia, and flushed extremities * Displacement of PMI/abnormal EKG due to LV
hypertrophy are both possible signs * Because capillary beds are not being perfused
well, the heart may not be able to perfuse tissue adequately, which by definition
is heart failure. Thus, AV-fistula can result in high-output cardiac failure. 3504:
Central Venous catheters should always be placed using portable chest x-ray.
Because the chances for complication due to poor placement are good (perforation
being a major worry), visualization with CXR is necessary. Ideally, the catheter
tip should be in the superior vena cava (proximal to cardiac silhouette OR between
the tracheal-right mainstem bronchus angle) 4709: If a person is having heart
failure (failure to perfuse organs) in the setting of an abnormal heart rate/rhythm
the first step is always immediate electrical cardioversion. It??s a great way to
shock them back into a normal rhythm and get perfusion back. � This patient had
persistent, narrow-complex tachyarrythmia (HR >240...that should scare the fuck out
of you) 3823/4336: Guidelines for Lipid-Lowering therapy (typically a statin) *
Symptomatic atherosclerotic disease ?? high or low intensity based on age (> or <
than 75yr) * LDL >190mg/dL ?? high intensity statin therapy * Age 40-75 with
diabetes ?? high or low depending on 10-year ASCDV risk * Estimated 10-year ASCVD
risk >7.5% ?? moderate to high intensity statin therapy [Note that the difference
between statin intensity is the dose] 4345: Infectious (viral or bacterial)
pericarditis can cause a buildup of fluid in the pericardium causing cardiac
tamponade. * Classic signs are known as ??Beck??s triad?? (hypotension, distended
neck veins, muffled heart sounds) * Pulsus paradoxus is another sign. This is a
decrease in Blood Pressure with inspiration. This occurs due to restriction to
heart distention from the fluid buildup. On inspiration the right side of the heart
will expand due to negative intra-thoracic pressure. Because it cannot expand well,
the increased bloodflow will push the interventricular septum into the left atrium,
resulting in decreased LV filling (preload) and decreased blood pressure *
Hepatojugular reflex is another classic test. You essentially do a Murphey??s sign
and watch the jugular veins. It??s not very sensitive but very specific. o Rising
veins that shortly return to normal = negative o Rising veins that do not return or
persistently deflate after releasing pressure = positive 2723: Variant (Prinzmetal)
angina is a vasospastic angina that often occurs in female smokers with few/no
cardiovascular risk factors, classically awakening them at night. While cessation
of smoking is the most important intervention, Calcium Channel blockers (??-
dipines?? and verapamil/diltiazem) or nitrates are good interventions to prevent
coronary vasoconstriction. 2698: Common causes of Aortic Stenosis: * Senile
calcific aortic stenosis: accumulation of calcium deposits in the aorta due to
aging. Only affects people aged >70 * Bicuspid aortic valve: an inborn abnormality
of the valve. An important cause of aortic stenosis in people under the age of 70
(usually younger than this though!). If the patient is in their 40s...has no
history or signs of Rheumatic fever...and has aortic stenosis ?? consider bicuspid
aortic valve! * Rheumatic heart disease: classic infectious cause of aortic
stenosis. Presents with several signs and aortic stenosis (while uncommon and
severe) can occur. Will nearly always occur alongside mitral valve damage.
Rheumatic damage to the aorta is actually less commonly that bicuspid aortic valve!
4395: Pulmonary embolism should be suspected with pleuritic chest pain,
cardiovascular risk factors, and history of hypercoagulable situation
(coagulopathy, prolonged stasis, etc.) � CXRs are NOT very good at diagnosing PEs,
but often are gotten to rule out other causes of chest pain. There are some fun
findings BUT often the CXR is NORMAL. 4682: Renal artery stenosis has two classic
findings: * Systolic-diastolic periumbilical bruit: apparently if you hear this,
think renal-artery stenosis. Don??t get it confused with AAA...which will produce a
systolic bruit and have a pulsating abdominal mass! * Refractory HTN: the patient
in the vignette has a BP 190/120 on 4 different BP lowering drugs...that ain??t
right son. If you see this, consider secondary causes...of which, renal artery
stenosis is the most common. 3822: (refer to 2698) A patient with Type II Diabetes
Mellitus over the age of 40 should always be on a statin and initiate positive
lifestyle changes according to lipid lowering guidelines. Refer to 2698 for the
complete guidelines. 4725: If a patient FOR ANY REASON goes into Pulseless
Electrical Activity (heart still showing up on EKG but no pulses) the patient is
obviously dying in front of you and guidelines recommend immediate CPR,
Epinephrine, gain IV access, and maybe an advanced airway. * If you do all these
things and the patient has a shockable rhythm...then defibrillate * If you do all
these things and the patient is still in PEA you do two more rounds of CPR and
treat possible reversible causes of PEA Possible reversible causes of PEA are the
5Hs/Ts * H: hypovolemia, hypoxia, hydrogen ions (acidosis), hypo/hyperkalemia,
hypothermia * T: tension pneumothorax, Tamponade (cardiac), toxins (benzos,
narcotics), thrombosis (coronary or pulmonary), trauma 4238: Tachycardia-medicated
cardiomyopathy: with a long-standing tachyarrythmia of any nature (a-fib, a-
flutter, rapid ventricular rhythm, etc.) the myocardium can undergo
responsive changes eventually leading to heart failure * Symptoms: tachyarrhythmia
(of any nature), CHF signs, heart palpitations * Dx: abnormal EKG, rule out CAD,
echocardiography showing diffused changes/hypokinesia * Tx: aggressive rate/rhythm
control of arrhythmia (ablations, AV node blockaid, anti-arrythmatics) 4191: PDE-5
inhibitors (sildenafil, etc.) have a major interaction with a1-blockers (??-
zosins??) and nitrates as the additive effects of vasodilation can result in
precipitous drop in blood pressure. If you??re going to prescribe these drugs
together you must: * Prescribe the lowest possible doses of each with careful
titration up for effect * Make sure drugs are taken 4 hours apart at minimum 4390:
Apparently UWorld LOVES people getting respiratory infections and causing
infectious cardiac tamponade! A pathognomonic finding for cardiac tamponade is
electrical alterans with sinus tachycardia. * This is alternating higher/lower
deflections on EKG due to swinging of the heart within the increased pericardial
fluid resulting in changes in the electrical deflection on EGK * Tx: emergency
pericardiocentesis with examination of causative factors 11126: Remember how we
made fun of people for misdiagnosing heart attacks for GERD? Well that shit is real
because GERD can sound a whole lot like coronary artery disease! A patient with
GERD might come complaining of chest pain with radiation!! Note the characteristic
GERD signs: * Prolonged pain >1hr, post-prandial symptoms, heartburn/dysphagia,
relief with anti-reflux drugs * Often cardiovascular workup is necessary in these
patients, but will remain unremarkable 2732: Post-MI remodeling is part of the
normal healing process in the heart and will result in a white scar. However,
ventricular dilatation can be significant and actually change the ventricle so much
that it can result in eventual CHF. * Ventricle will be dilated, globular, and
thinned with scarring * Tx: ACE inhibitor treatment within 24hrs of MI has been
shown to limit this dilatation/remodeling and reduces the incidence of remodeling-
induced CHF 2695: The most common cause of mitral regurgitation in the US is
myxomatous degeneration of the mitral valve leaflets. * Initially: mid-systolic
click with late systolic murmur * Severe: holosystolic murmur, displaced apical
impulse, 3rd heart sound. Also the backflow can cause dilatation of the left atrium
eventually causing atrial fibrillation. Long-standing regurgitation will lead to
heart failure. 2741: Viral myocarditis due to Coxsackie B virus infection is the
most common cause of diliated cardiomyopathy in a young, healthy patient. If you
get a young, healthy person getting progressive dilated cardiomyopathy...shoot for
coxsackie B. 8927: Patients with intermittent claudication due to peripheral artery
disease are at an extremely increased risk for myocardial infarction in the next 5
years. Claudication often remains stable, however worsening claudication simply
increases the risk of future MI. It??s actually rare for intermittent claudication
to progress to the severity needed to cause critical limb ischemia warranting
amputation (1-2%). 2686: Hypertrophic cardiomyopathy is medically treated with
negative inotropic agents (things to slow down the heart and decreased
contractility) as these will increase filling and widen out the left ventricle,
minimizing obstruction! * 1st line: B-blockers (metoptolol or atenolol) *
Additionally, verapamil (Ca++ blocker) or disopyrimide (Class B anti-arrhythmia)
can be added if symptoms persist. 2745: Long-term prognosis in a heart-attack is
most greatly influence by how fast coronary artery perfusion is re-achieved. There
are two major ways of going about this: * Percutaneous transluminal coronary
angioplasty (PCTA): better outcomes, Door-to-balloon time must be <90 minutes. The
treatment of choice. * Fibrinolysis: not as good, Door-to-needle time of <30
minutes. A good option for those who cannot tolerate the cath lab 2157: 3-5 days
following an MI is the riskiest time for mechanical complications (ruptures) *
Acute Mitral Regurg. from Mitral Valve papillary muscle rupture is a classic
presenting dramatically with sudden onset pulmonary edema, a MR murmur, and
possibly cardiogenic shock. Silent MR (no murmur) can occur if it??s very severe. *
Ventricular wall rupture is another classic presenting with acute onset
hypotension, pericardial tamponade and heart failure * Interventricular septal
rupture often causes hypotension, CHF, pansystolic murmur heard best at the the
left sternal border...often with an accompanying thrill! 11252: Pulmonary HTN is
defined as mean pulmonary pressure >25mmHg. Some classic signs/symptoms include:
heart failure signs (dyspnea, weakness, syncope, edema), pansystolic tricuspid
valve murmur (increases with inspiration), right sided 3rd heart sound, etc. � Tx:
ACE inhibitor or ARB + loop diuretic (and possibly a B-blocker) 3697: Atrial
fibrillation with rapid ventricular response: supraventricular tachycardia with
unorganized atrial activity (heart rate is fast, but irregularly irregular;
essentially the atrium is beating oddly and the ventricles follow suit) * If
hemodynamically stable: attempt rhythm control (controlling atrial rhythm = no more
problems) with beta blockers, diltiazem, digoxin o
DONOTcardiovertthesepatients,itactuallyraisesthechanceforsystemicembolizationinthe
next 48 hrs!! * If hemodynamically unstable (signs of end organ ischemia):
immediate cardioversion * Pt CHADS-VASc score should be calculated and if >1 should
be started on some form of anticoagulation 3777: Norepinephrine (B1/B2/a1/a2) is
used as a first line vasopressor in shock, however it can actually induce
peripheral arteriole spasm resulting in lack of bloodflow ?? gangrene, kidney
damage, bowel ischemia! 2699: Restrictive cardiomyopathy: uniform/symmetric
thickening of the myocardium typically starting with prominent right heart failure,
eventually progressing to right and left heart failure. * Etiology: sarcoidosis,
amyloidosis, hemochromatosis, endomyocardial fibrosis, or idiopathic *
Hemochromatosis (iron overload) is the only REVERSIBLE cause, treated with
phlebotomy * Sarcoidosis/amyloidosis are both slowed with corticosteroids but
cannot be stopped! 4237: Here are some classic lab values for septic shock and why
they happen; highlighted ones are very specific findings in regard to septic shock!
* Low normal right atrial pressure/pulmonary capillary wedge pressure: while we??re
losing blood volume to the extravascular space, the heart is OK and will be able to
compensate to a degree, often keeping pressures within low normal range * High
Cardiac index: remember how the heart is keeping things low normal? It??s doing
that by working as hard as possible, thus it??s pumping a lot of whatever blood is
left * Low Systemic vascular resistance: systemic inflammation results in global
vasodilation, thus low resistance! * High mixed venous O2 levels: tissue infection
(and thus dysfunction) results in an inability to extract oxygen, which actually
results in high oxygen in the veins! 2659: There are TONS of reasons why you may
acquire a long QT syndrome resulting in torsade de pointes (loads of drugs,
electrolyte abnormalities, cardiomyopathy, HIV, the list goes on) HOWEVER they all
have the same treatment: * If hemodynamically unstable: immediate cardioversion *
If hemodynamically stable: intravenous magnesium for stabilization with
search/removal of offending agent o Note that IV magnesium is effective EVEN IF THE
MAG LEVELS ARE NORMAL! 2701: Don??t get confused! Primary pulmonary HTN is
pulmonary HTN without discernable cause. A more common cause of pulmonary HTN is
severe left heart failure. This patient happened to have rheumatic fever
(apparently indicated by her being from the 3rd world AND having signs of heart
failure/A-fib). The mitral valve supposedly was affected resulting in progressive
heart failure. * Progressive exertional dyspnea, nocturnal cough, and hemoptysis �
all possible signs of /41 due to left sided heart failure * Palpitations/irregular
heart beats � signs of atrial fibrillation due to increased pressure and LA
dilatation * Sudden onset left sided weakness � likely a cardiogenic stroke due to
a formed thrombus in the LA that embolized to the brain 4771: There are only two
major mechanisms for pulsus paradoxus: * Cardiac tamponade (we??ve discussed this
one!) * Severe asthma/COPD: typically, there??s a small variation in intrathoracic
pressure with inspiration (gets air to flow in); but in asthma/COPD, air trapping
raises pressure in the lungs, resulting in a much more intense decrease in lung
pressure during inspiration to allow for inward flow (nearly 20x greater pressure
drop). This results in blood pooling in the lung vasculature (decrease preload),
and inflation causes impingement on the heart (decrease outflow). Both of these
things result in less blood coming out of the heart upon inspiration, resulting in
a drop in BP with inspiration! 3698: Ventricular fibrillation is a terrifying
complication of MI, electrolyte imbalance, cardiomyopathy, or drug therapy. It??s
characteristically seen as an EKG with no normal QRS complexes and fibrillatory
waves. Treatment differs by how long the patient has been in fibrillation: * <5
minutes: immediate defibrillation * Unwitnessed or >5 minutes: a round of CPR
followed by defibrillation 3933: Renal stenosis causing renovascular HTN is a
classic secondary cause of resistant HTN (pts on >3 drugs for control of
HTN...which isn??t working!!). You should check for renovascular stenosis when you
see a paitent with resistant HTN + [diffused atherosclerosis, asymmetric kidney
size, recurrent flash pulmonary edema, or creatinine increase >30% from baseline
after starting an ACE/ARB]
3945: Never forget! Nitrates mechanism of stopping stable angina is by pooling
blood in the systemic veins via dilation and decreasing left ventricular wall
stress (thus contractility, thus O2 demand). It??s NOT due to coronary vasodilation
(although this does happen) because the stenotic artery will get less perfusion
(it??s already maximally dilated, while the others now dilate to take more away
from it). 3956: If you see a person with emergent aortic dissection and you need to
confirm the diagnosis you: * Order a CXR ?? if suggestive of something else, treat
that * If not, get a serum creatinine and check for contrast allergy o
IfnormalCr/noallergy??getchestCTwithcontrast o IfCr^/allergy??
getTransesophagealechocardiography * MRI may be used if it??s a non-emergent
situation 4101: As a general rule of thumb: diastolic murmurs and continuous
murmurs are nearly always pathologic. The next step is to evaluate with
transthoracic ultrasonography. Mid-systolic murmurs in young, healthy patients
typically require no workup! 4326: Hypovolemic shock isn??t hard to remember as
long as you relate it back to one thing: intravascular volume loss! * Decreased
blood pressure/pulmonary capillary wedge pressure: bleeding out to the point of
shock means everything works...except you cannot maintain blood pressure to the
vital organs! Thus your BP and PCWP (proxy for left ventricular pressure) are
tanked * Decreased cardiac output: CO=HR*SV ?? you??re blood volume is
tanked...thus you??re SV is tanked. So even though you??re HR increases, the SV is
so low from blood loss that you??re CO is failing * Increased systemic vascular
resistance: another response to tanking BP; your vasculature will try and
compensate to attempt continued organ perfusion 4922: Class IC antiarrythmatics
(flecanide, encanide, propafenone) notoriously exhibit ??use dependence?? where
their QRS prolongation effect are more pronounced with increased heart rate. This
is why they??re useful against supraventricular tachycardias (they??ll kick in when
the arrhythmia arises) � Class IC binds the Na+ channels, but they??re very slow to
dissociate. If the heart rate is slow, they can bind, then dissociate before the
next impulse comes along. However, if faster, they won??t dissociate in time and
end up blocking Na+ conduction, leading to slower depolarizations and widened
(slower) QRS complexes 4593/4297: Cor pulmonale: process of increased lung-vascular
pressure. Untreated, causes right heart failure. * Etiology: COPD (most common),
idiopathic pulmonary HTN, interstitial lung disease, obstructive sleep apnea. Note
that LVF causing RVF is NOT cor pulmonale. * Dx: o
Sym:Dyspnea,syncope,oranginaonexertiono
Sign:Peripheraledema,increasedJVD,hepatojugularreflex,pulsatileliver,edema,ascities
,etc. o Imaging:EKGorechocanbeusedbutrightheartcatheterizationwithelevatedpulmonary
artery systolic pressure >25mmHg is confirmatory � Tx: vasodilators/anti-HTN drugs
3950: Cholesterol Crystal Embolization typically occurs after cardiac
catheterization or recent vascular procedure in the setting of cardiovascular risk
factors. * Features: livedo reticularis, ulcers/gangrene, blue toe syndrome, renal
injury, stroke, Hollenhorst plaques (in the eye), GI ischemia/pancreatitis * Dx: o
Labs:elevatedcreatinine(renaldamage),eosinophilia/eosinophiluria,hypocomplementemia
o Skin/renalbiopsy:biconcave,needle-shapedcholesterolcleftsinoccludedvesselsand
perivascular inflammation with eosinophils 8928: Peripheral Artery disease is
essentially CAD but in the periphery! * Classic presentation is intermittent muscle
cramping/pain with exertion (usually walking) in an older smoker, with
hyperlipidemia/overweight (possibly may be just the smoker!) * Tx: low dose aspirin
+ lipid lowering therapy (usually a statin) + supervised exercise program o
Exerciseshouldbe12weeks,30-45minx3aweeko The goal is to produce the claudication
symptoms during exercise and gently push the limit so they come on with greater
levels of exertion 4740: Acute mitral regurgitation typically occurs in the setting
of MI where you have normal MI symptoms accompanied by/followed by (2-7 days)
severe dyspnea/orthopnea (backwards flow) * Will be associated with increased LVDP
because the backflow of blood into the atrium simply adds onto the blood heading
into the ventricle with the subsequent cardiac cycle. This constant back-forth
increases pressure in the left ventricle, which is reflected back into the
pulmonary circuit * Chronically, the pressure will increase the compliance of the
normally non-compliant left atrium (causing left atrial dilatation chronically),
and concentric reactive thickening of the left ventricle. 4377: Apparently
prolonged recumbence (esp. in an old person!) increases the risk for orthostatic
hypotension. This person may never have experienced it before, but after a
prolonged period of bed rest, they get it transiently until they get back on their
feet! 4720: Acute aortic dissection is a life-threatening, terrifying tearing of
the aortic lumen media layer * Signs/symptoms: tearing chest pain radiating to the
back, hypotension, but other signs can result from involvement of arteries coming
off the aorta getting involvedo Pericardium:pericardialeffusion??
cardiactamponade/pulsusparadoxuso Aorta:aorticregurgitationo
Carotid/subclavianAs:pronouncedhypotensioninheat/limbtheirfeeding(bloodpressurein
the left arm < right arm)o Renalartery:stenosis/compression??renalhypoperfusion *
Dx: clinical signs + radiologic evidence of tear (possibly chest CT) 3158: There
are two major side effects of statin therapy and they??re both have lab values: *
Muscle damage: elevated CPK with myalgias which may progress to severe
rhabdomyolysis and renal failure (would acutely raise BUN and Creatinine). Stop the
statin if this happens * Liver damage: not as pronounced usually, but can cause
elevated liver transaminases (ALT/AST). Usually these will trend back to normal
with stopping the statins. 4398: IV drug users are at high risk for right sided
infective endocarditis (tricuspid valve) because they introduce skin bacteria to
the veins with the IV, and it hits the tricuspid first. * Typically S.aureus,
increased risk with HIV infection, less systemic signs, but often lungs involved *
Tricuspid valve endocarditis ?? holosystolic murmur at the left lower sternal
border (apex), that increases with intensity on inspiration (100% sensitive, 88%
specific). * Septic emboli to the lungs are more common ?? chest pain, cough,
hemoptysis, multiple round alveolar infiltrates on chest x-ray 3090: A younger
person with a creshendo-decreshendo murmur at the right sternal border should be
assumed to have bi-cuspid aortic valve with aortic stenosis unless other
signs/symptoms point to something else. Oddly enough, these patients can present
with stable angina. This is due to chronic increased LV systolic pressure against
the bicuspid valve and reactive concentric hypertrophy of the LV. � Because the LV
gets so jacked, it eventually can require more O2 than it??s getting, resulting in
stable angina due to increased O2 demand from physiologic hypertrophy 3763: Wide
complex tachycardia is going to be any tachycardia where the QRS complex is wide
(the QRS doesn??t shoot straight up/down but slopes up/down). When considering a
tachycardia, two major ones to consider are: * Sustained monomorphic Ventricular
tachycardia: wide QRS complexes and ??fusion beats?? on the EKG are diagnostic here
o Ifstable??treatwithIVamiodarone(ratecontrol) o Ifunstable??
treatwithsynchronizedcardioversion * Paroxysmal Supraventricular tachycardia:
narrow QRS without fusion beats on EKG o Ifstable??
docarotidmassageandtreatwithratecontrol o Ifunstable??
treatwithsynchronizedcardioversion 3092: Classic signs for diagnosing aortic
regurgitation: diastolic decrescendo murmur, widened pulse pressure (this guy had
150/45 mmHg) with ??water hammer?? pulse, and signs/symptoms of heart failure.
4133: Hepatojugular reflex is not specific for any one disease process, but rather
just tells you that the right ventricle is failing and cannot accommodate increased
venous return to the heart. � Press on upper abdomen (essentially on IVC) for 10-15
seconds; persistent elevation JVD >3cm is a positive test (as a normal right
ventricle would accommodate the increased venous return) 4660: When considering an
EKG, always remember your 3 major deviations, the P-wave, QRS complex, and T- wave.
The T-wave and P-wave can actually be quite close together and the forms overall
can vary quite a bit, BUT if you first establish you P/QRS/T then you??ll be able
to move from there. � This question was a Mobitz I AV heart block; which normally
is asymptomatic BUT can present with significant bradycardia causing
syncope/dizziness 3881: Syncope due to underlying structural heart disease may have
no prodromal symptoms. Thus if you have someone with a history of cardiac disorder
(previous MI, heart surgery, etc.) consider arrhythmia as the cause. This question
was a bit confusing as they said the person had several muscle jerks...I??m
guessing this can happen regardless of why the person passed out. 10179: Ca++
channel blockers (CCBs) are classically associated with edema, flushing, headache,
and dizziness (dihydropiridines more than verapamil/diltiazem) due to preferential
pre-capillary (arteriole) dilatation. Essentially the arterioles dilate, but the
venules don??t as much, so capillary hydrostatic pressures go up and you get
transudate. � CCB + ACE/ARB = less chance for edema/side effects due to ACE/ARBs
preferential dilation of the post- capillary venules! 3188: If a patient comes in
with signs of heart attack, dilated pupils, and blood in the nose consider cocaine
abuse induced MI. � Tx: (same as normal MI) cardiac catheterization/thrombolysis
with aspirin/clopidogrel/nitrates/Ca++ channel blockers or a-blockers/morphine. DO
NOT USE A B-blocker as it will cause hypotensive crisis due to cocaine + B-blockade
= unopposed a-activity 4894: Wolff-Parkinson White syndrome occurs due to an
abnormal accessory pathway (bundle of Kent) that connects the atria/ventricles, by-
passing the AV node. This causes pre-mature ventricular excitation (delta wave of
the ECG), and can result in a re-entrant circuit resulting in supraventricular
tachycardia (chest fluttering or palpitations are usually described by the patient)
and possible sudden death. 4129: Thoracic Aortic aneurysms (NOT a AAA) are
dilatations of the aorta above the abdomen * Ascending TAA: occur somewhere between
the aortic root and the innominate (brachiocephalic) artery due to cystic medial
necrosis (aging, 3o syphilis) or connective tissue weakness (Marfans, Ehlers
Danlos) * Descending TAA: occur distal to the left-subclavian, but before the
diaphragm due typically to atherosclerosis (look out for HTN, dyslipidemia,
smoking, etc.) * CXR should show widening of the mediastinum, increased aortic
knob, and tracheal deviation but often chest CT is needed to confirm the diagnosis.
4190: Hyponatremia can be an independent indicator of heart failure severity AND
predicts worse clinical outcomes! Because the heart isn??t perfusing organs well in
severe CHF (notably the kidney/baroreceptors) resulting in BP being maintained by
RAAS, epi/NE, and ADH (vasopressin). Vasopressin??s effect of retaining water (acts
of V2 receptors) along with the other systems limiting kidey excretion of H20
results in dilution hyponatremia ?? [worse CHF = more RAAS = more H20 retention =
more severe dilution hyponatremia] 4334: First thing: if a patient has a history of
panic attack and is having chest pain YOU CANNOT GO THINKING IT??S AN ANXIETY
EXACERBATION UNLESS YOU GET A NORMAL ECG TO RULE OUT ACS. * If a patient presents
with chest pain ?? get a focused H&P, vitals, and venous access o Ifunstable??
checkABCs,stabilize,andassessforunderlyingcauseso Ifstable??
ECG+CXR+aspirinifthechanceofaorticdissectionislow * ?? �If ECG is weird then assess
for STEMI/NSTEMI * ?? �If ECG is not weird look at the CXR * If CXR is
diagnostic ?? treat whatever it is * If CXR is NOT diagnostic ?? look for
underlying causes * If you went through all that crap and they don??t have any
cardiopulmonary problems or GERD...then maybe (MAYBE) you can give them some benzos
for their panic attack. 3979: Uremic pericarditis is pericardial inflammation due
to high blood nitrogen (BUN) levels. * Typical signs of pericarditis (chest pain,
friction rub, better with leaning forward) * Elevated BUN (>60 is classic) with
elevated creatinine will clue you into renal failure * Does not present with
typical EKG findings due to a lack of inflammatory penetration with this one * Tx:
hemodialysis (gets rid of the nitrogen waste and will eventually resolve the
pericarditis) 4454: Digoxin is a cardiac glycoside used to treat arrhythmias and
heart failure, it helps slow down heart rate and allows for greater cardiac
contractility. The downside is it has a low therapeutic index and it??s cleared by
the kidneys * Digoxin toxicity occurs with decline in kidney function (viral
illness, AKI), excessive diuretic use (volume depletion), hypokalemia (enhanced
effects of digoxin). * Symptoms: N/V, decreased appetite, confusion, weakness,
visual changes (yellow-green vision, halos, blurry vision) * Dx: Check digoxin
level, get EKG (rule out arrhythmia) * Tx: bring down the digoxin level, and assess
why it??s high for resolution 4908: Remember! The S3 heart sound is a more dull
version of S1/S2 that occurs with S2 (S4, S1...S2, S3). You can kind of cheat
because the first sound you hear in a recording will always be S1. It??s associated
with ventricular overfilling (like in CHF) 4300: A cardiac stress test is important
screening/diagnostic tool for coronary artery disease (CAD) which either has pts
exercise to induce angina or drugs (like dobutamine) are administered to stress the
heart. * If you??re testing efficacy of anti-angina therapy, then do not stop any
drugs before the test * If you??re trying to diagnose CAD in new onset angina you
must: o Stopanti-anginaldrugsfor48hours(B-blockers,Ca+
+channelblockers,nitrates)andifyou??re doing pharmacologic stress dipyramidole as
well. o Stopcaffeinefood/drinksfor12hourso ACE/ARBs, statins, digoxin, and
diuretics should be continued as they do not affect the onset of angina in patients
with CAD� Potassium levels should be checked before stress testing as
hypo/hyperkalemia can cause abnormal EKG findings in the stress test; if they??re
not normal, delay the test until they are normalized 4668/4483/10972: Infective
endocarditis can present with weird, vague symptoms that may not be entirely
obvious * Systemic emboli (cerebral, pulmonary or splenic infarcts) * Mycotic
aneurysms or infections due to septic emboli * Janeway lesions: nontender, red,
raised lesions on palms/soles from emboli in superficial emboli * Roth�s spots:
hemorrhages of the retina from emboli * Osler nodes: painful fingertips, sometimes
with nodules * Arthritis: swollen joints, especially of the hands/feet *
Proteinuria or hematuria from kidney damage Still�s disease is a rare inflammatory
disorder of recurrent high fever, rash (macropapular/non-pruitic, on trunk and
extremities, during febrile episodes), and arthritis 4680: Adult (autosomal
dominant) Polycystic Kidney Disease is a progressive renal degenerative disease
where the kidneys slowly enlarge with cysts and lose function until complete renal
failure. * Symptoms: often asymptomatic, but can have hematuria/flank pain (cyst
rupture, infection, hemorrhage) * Clinical signs: HTN, bilateral palpable abdominal
masses, proteinuria, CKDo Mayalsoaffectextra-
renalstructures:cerebralaneurysms,liver/pancreaticcysts,GIdiverticula, hernias, and
even heart-valve disorders * Dx: family history/genetic testing, abdominal
ultrasonography demonstrating multiple renal cysts * Tx: close follow with
aggressive control of cardiovascular risk factors (esp. ACE inhibitor use);
ultimately dialysis and renal transplant are necessary4451: When a person presents
with signs of acute decompensated CHF your initial management is the loop diuretics
(get the fluid off), supplemental oxygen (get as much O2 to the heart as needed,
offset dyspnea), and possibly nitrates (take stress off heart). � After they??re
stable, B-blockers, digoxin, and other drugs may be used to for long-term
management 3699: New onset atrial fibrillation is a common complication of coronary
artery bypass surgery (40% of pts or 50% of pts who also had aortic valve
replacement). If the patient has A-fib (or really any other arrhythmia) and is
hemodynamically unstable...immediate cardioversion is necessary. 3977: Some
definitions/complications of hypertension: * HTN: blood pressure >140/90 * HTN
urgency: blood pressure >180/120 with no end organ damage * HTN emergency: blood
pressure >180/120 with end organ damage o
MalignantHTN:retinalhemorrhages,papilledema,orexudatesandsometimesrenaldamage o
HTNencephalopathy:cerebraledemacausingheadache,confusion,seizure,coma 4727:
Viridians Group Strep are often highly susceptible to penicillins. These little
guys live in our teeth and it??s a classic scenario where someone has a previously
damaged heart valve and get infective endocarditis (IE) from one of these guys
after dental procedures. * IV penicillin G or IV ceftriaxone for 4-6 weeks is the
typical treatment regimen for Virdians strep IE that??s susceptible to penicillins
* Patients with penicillin allergy should be treated with vancomycin. * NEVER use
oral antibiotics against infective endocarditis, IV only! 4594: Remember that the
RAAS??s ultimate goal is to maintain blood pressure for perfusion of the kidney!
Don?? t forget, RAAS activation is often a feature of CHF because of poor
perfusion! � Angiotensin IIo Constricts the afferent AND efferent vessels, but
preferentially constricts efferent to promote renal glomerular pressure and
filtrationo Increased Na+ resorption in proximal tubules (less distal Na+ delivery)
o Stimulatetheadrenalglandtosecretealdosterone � Aldosterone: re-absorb Na+ in the
collecting ducts to keep water in the blood ?? maintain blood volume ?? maintain BP
2707: Amyloidosis is a systemic disease where abnormal amyloid protein polymers are
deposited into tissue causing damage and dysfunction. Primary (AL) or Secondary
(AA) from a systemic inflammatory condition (rheumatoid arthritis, IBS, chronic
infections, malignancy, etc.) � Symptoms:o
Kidneydeposit:Nephroticsyndromeorasymptomaticproteinuriao Heart deposit:
restrictive cardiomyopathyo Liverdeposit:liverenlargemento
Skindeposit:waxythickeningandeasybruisingoftheskino Other involvement: enlargement
of any deposited organs (macroglossia is classic) o Bleeding diathesis * Dx:
abdominal fat biopsy deposit showing amyloid protein * Tx: no real treatment.
Hopefully it??s secondary and you can slow down the process causing it! 4722:
Primary hyperparathyroidism is a classic cause of secondary hypertension, typically
due to a parathyroid adenoma (80% of cases). The PTH causes excessive Vit D
activation, leading to renal calcium resorption, GI absorption, and bone breakdown
* ??Stones, bones, groans, psychiatric overtones?? * Hypercalciuria (renal stones),
bone pain (resorption of calcium from bone), GI upset/constipation (intense
absorption) and confusion/depression/psychosis (not sure!) * It??s actually NOT
entirely clear how PHPT causes hypertension, but significant HTN may be related to
pheochromocytoma in the context of MEN 2A. 10767: Scleroderma renal crisis: a
syndrome of coagulation cascade activation, vascular permeability,
and increased renin secretion within the context of systemic scleroderma * Dx:
sudden onset malignant HTN, renal failure without prior kidney disease,
microangiopathic hemolytic anemia/thrombocytopenia (often featuring schistocytes) *
Not really sure how to treat this but it??s pretty intense! 11104: Sudden onset
chest discomfort with mediastinal widening and pericardial effusion should prompt
you to think ??proximal aortic dissection??. This is a surgical emergency and needs
to be rapidly assessed with trans- esophageal ultrasonography (better picture for
better Dx) 4472: Warfarin is a touchy drug and it??s effects and get too high or
low depending on a LOT of factors * CYP450 inhibitors increase warfarin�s effects:
acetaminophen, NSAIDS, antibiotics, amiodarone, and a whole mess of others! *
CYP450 inducers limit its effects: green vegetables, ginseng, OCPs, and a whole
mess of others! * Warfarin is a mess of a drug. 4920: Any paroxysmal
supraventricular tachycardia in a patient that??s stable should be investigated
with vagal maneuvers or IV adenosine to slow the heart and ??unmask?? the P-waves
for proper arrhythmia diagnosis. Sometimes these will terminate the arrhythmia,
giving time for working out treatment. Once the diagnosis is made, proper rate or
rhythm control can be initated. 2164: Pt??s on Lasix diuretics must be watched for
hypokalemia and hypomagnesemia as the drug is K/Mg wasting. Low K/Mg can lead to
arrhythmias and seizures. Thus any patient on Lasix that starts having symptoms of
either of these should have a basic metabolic panel or serum electrolytes checked.
* Note that pts on Lasix AND digoxin are in double trouble as the hypokalemia could
potentiate digoxin resulting in arrhythmias. * Don�t forget! The potassium sparing
diuretics are Spironolactone, Eplerenone, Amiloride, Triamerterine (K+ takes a
SEAT) Infectious Disease 4867/4517: S.aureus typically does NOT cause pneumonia,
however it often affects certain subgroups: hospitalized patients, nursing home
residents, IV drug users, cystic fibrosis pts and pts with recent influenza
infection. Typically these pts will have the flu (fever, myalgia, N/V, etc.), get
treated and recover, only to find they get pneumonia (this is prominent in older
adults). Some other classic pneumonias: * Pneumocystis jiroveci (PCP) � HIV pts *
Klebsiella pneumoniae � diabetics, alcoholics (aspiration), and nosocomial;
classically has the ??currant jelly sputum??, cavitation, and empyema. *
Pseudomonas aeruginosa � cystic fibrosis/bronchiectasis (poor sputum release) *
Mycoplasma pneumoniae � ??atypical pneumonia?? (productive cough, headache, rash;
often better in morning and worse in evening) * Anaerobic infection pneumonia �
aspiration (often pts have poor dentition from vomiting) and typically features
lung abcess! 2236: Urethritis in men: dysuria, penile discharge, urinary urgency,
increased voiding frequency * Bugs: N. gonorrhea (gram� diplococcus), C.trachomatis
(will not grow/stain), mycoplasma genitalium, Trichmonas (rare parasite,
asymptomatic in men) * Dx: gram stain/urinanalysis/culture will get most o Nucleic
acid amplification of first catch urine sample is diagnostic for C.trachomatis o
Wet prep with smear will get Trichmonas * Tx: Azithromycin or doxycycline +
ceftriaxone (always treat the gonococcus/trachomatis co-infection) 4475:
Vaccinations are now important to memorize...great. * Tetanus-diptheria booster
(Td) � give every 10 years * Tetanus-diptheria-pertussis (Tdap) � one dose vaccine
in adulthood (esp. in close contact with kids) * Flu vaccine o
Intramuscular(killed)�givetoanyhealthyadultonceperyear o Intranasal(live-
attenuated)�healthy,non-pregnantpeople<50yearsold,notimmune-comp. * S.pneumoniae
(pneumococcus) vaccine o PCV-13�givetoall>65,followedbyPPSV-236-
12monthslaterorinhighriskgroupso PPSV-
23alone�givetopts<65withchronicmedicalconditions,thengivenormalvaccines once they
hit 65 2274/8959: HIV esophagitis occurs with CD4+ count <100; occurs with painful
swallowing/substernal burning * Candida albicans � white plaques in mouth/esophagus
(oral thrush!) o Tx:3-5daysoforalfluconazolewithHAARTassessment o
Ifpatientfailsthis,furtherworkupforviralcauses * HSV � herpetic vesicles with
round/ovoid ulcers in esophagus, sometimes w/ HSV infection elsewhere o
Severeodynophagia(painfulswallow)WITHOUTdysphagia o Dx:biopsywithhistopathology *
CMV � Deep, linear ulcers in the distal esophagus o Severe odynophagia (painful
swallow WITHOUT dysphagia o Dx:biopsywithhistopathology * Aphthous ulcers �
idiopathic presenting with apthous ulcers Pill esophagitis can cause some similar
symptoms but DOESN??T typically occur in HAART regimens 3917/3590: Diarrhea in
HIV/AIDS typically occurs with different etiologies based on CD4+ count *
Cryptosporidium (<180) � severe watery diarrhea, wt loss, fever o
Classicallyfromanimalcontact,water,orperson-persono Dx:modifiedacid-
faststainshowscryptosporidialoocytes(4-6mcg) o Tx:anti-
retroviraltherapy(resolveswithCD4receovery) * Microsporidium or isosporidium (<100)
� watery diarrhea, wt loss, cramps, no fever * Mycobacterium Avium Complex (<50) �
watery diarrhea, wt loss, high fever (>102F) * CMV (<50) � bloody/small volume
diarrhea, abdominal pain, wt loss, fever o
Dx:colonoscopywithbiopsy�intracytoplasmiceosinophilic/basophilicinclusions o
Tx:gancicloviro MustexamineeyestoruleoutCMVretinitis 4163: Infectious endocarditis
in non-IVDU typically occurs as infection on an already damaged heart valve. This
most commonly occurs from mitral regurgitation (delineated by it??s tell-tale
systolic murmur). 2268: Disseminated Mycobacterium Avium Complex (M. avium or M.
intracellulare): non-specific symptoms (fever, cough, abdominal pain, diarrhea,
night sweats, weight loss), splenomegaly, and elevated alkaline phosphatase. *
Typically, in HIV pts with CD4+ <50; pts with this low of CD4 should be given
azithromycin prophylaxis * Dx: blood culture or lymph node/bone marrow biopsy * Tx:
clarithromycin or azithromycin Other prophlaxis for pts with AIDS with low CD4+
counts: * PCP � TMP-SMX (Bactrim) or dapsone * Esophageal candidiasis � fluconazole
* CMV � ganciclovir * Latent TB with pt having >5mm induration on skin tuberculin �
isoniazid o Don??tgiveBacilleCalmette-Guerin(BCG)livevaccine * MAC - azithromycin
3002: When a person is bit by a possible rabid animal, there are really 4 avenues
for Rabies post-exoposure prophylaxis depending on the situation: * High risk wild
animal bite � includes bat, fox, raccoon, coyote, skunko
IfanimalunavailablestartPEPo Ifanimalavailable;euthanizeit/testforrabies??
PEPifpositive * Low risk animal bite � squirrell, chipmunk, mouse/rat, rabbit ?? No
PEP * Pet � if a pet (usually a dog) DOES have rabies, they??ll show signs within
10 days o Ifavailableforquarantine??observe10days??
ifshowssignsofrabies,euthanizepetanddo PEP immediately o
Ifnotavailableforquarantine??startPEP * Livestock or unknown wild animal � call the
health department PEP for rabies consists of: * Thorough cleansing of the wound
(reduce risk by 90%) * Administer rabies vaccine (if person hasn??t gotten it
before) + passive immunization (human rabies Ig) 4373: Bacillary angiomatosis is a
B.henselae or B.quintana infection in an immunosuppressed pt � Sym: o
Nonspecificsymptoms(abdominalpain,wtloss,fatigue)o
Skinlesions:pedunculated,exophyticpapulewithcollaretteofscale;angiomatoushistology
and identified microscopic bacteriao Visceral lesions: look like skin lesions in
viscera. Prone to hemorrhage * Dx: biopsy with characteristic
histopathology/staining * Tx: susceptible to must antibiotics...but make sure to
help pt regain some immune function 3007: Infectious mononucleosis (Epstein-Barr
virus infection): fever, lymphadenopathy (tonsillitis, swollen cervical lymph
nodes, swollen eyelids), exhaustion, +/- hepato-splenomegaly * Dx: Positive
Monospot (25% false negative on first week), atypical lymphocytosis, transient
hepatitis * Tx: rest and avoidance of strenuous activities for >3weeks after onset
(risk of splenic rupture) o Splenicrupture:abdominalpainandanemia 3249: Traveler�s
diarrhea is not uncommon, however it often lasts a <1 week and remits. If it lasts
>2 weeks parasitic infections should be considered: * Cryptosporidium,
Cystoisospora, Giardia or microsporidia spp are major parasites to be considered. *
Dx: stool examination should reveal parasites 4938/4939: Histoplasmosis is an
endemic fungal infection to the Mississippi/Ohio river delta present in soil, bird
and bat droppings. It??s typically breathed in and resides in the lungs, but may
disseminate in immunocompromised. � Sym:o Immunocompetent:mildrespiratoryinfectiono
Immunocompromised:pancytopenia,hepatosplenomegaly,adenopathy;pneumoniawith diffuse
reticular nodules and cavitary lesions; mucocutaneous lesions * Dx: urine/serum
antigen testing is the most rapid/sensitive/specific o Blood fungal cultures should
be obtained, but are often slower and less sensitive * Tx: o Mild-
moderate:itraconazoleo Severe:IVlipomalamphotericinB(2weeks)thenitraconazole 3105:
After renal transplant, it??s smart to vaccinate and prophylactically treat pts for
common infections as they??ll be immunocompromised to prevent transplant rejection:
* TMP-SMX (Bactrim): PCP, toxoplasmosis, nocardiosis, and others * Val-ganciclovir:
CMV infections * Vaccinations against influenza, pneumococcus, and Hep B 3037/2999:
Blastomycosis is an endemic fungal infection of the Great Lakes (Wisconsin is
classic) and Mississippi/Ohio river valleys. Typically presents with constitutional
symptoms (often looks like TB or histo), lung lesions, ulcerated, wart-like crusted
skin nodules, lytic bone lesions, and prostatitis/orchitis * The skin/bone
manifestations with regional exposure should make the diagnosis.
* Dx: sputum culture of broad-based budding yeast (snowman!) or fluid antigen
testing * Tx: itraconzole (mild to moderate) or Amphotericin B (severe
disseminated) 3259: When traveling to a malaria endemic region two things must
occur: minimize mosquito exposure and malaria prophylaxis depending on the region.
P.falciparum is a bitch and will dictate your prophylaxis. * Chloroquine resistant
P.falciparum (Brazil, Sub-saharan Africa/South, Southeast Asia) o Atoraquinona-
proguanil o Doxycycline o Mefloquine (weird dreams and good in pregnancy) *
Choloquine susceptible areas: o Chloroquine/hydroxychloroquine1-2weeksinadvance o
AnyagentsthatworkwithchloroquineresistantP.falciparum * Areas without P.falciparum
(Mexico/central America/Southern South America/Korea o Primaquine (will cause
crisis in G-6PD deficient pts) 3938: PCP pneumonia is one of the most common
infections in AIDS patients * Sym: dry cough, fever, exertional dyspnea (out of
proportion to CXR findings) * Signs: CXR (bilateral interstitial infiltrates),
elevated lactate dehydrogenase * Dx: bronchioalveolar lavage demonstrating
P.jiroveci * Tx: TMP-SMX (Bactrim) for 21 days + corticosteroids (PaO2 <70) o IV
pentamidine is an alternative for those that cannot take TMP-SMX but it has a lot
of side effects (damage to kidney, liver, heart, etc.) 3003: HSV viral encephalitis
is the only treatable viral encephalitis * Sym: altered mental status, headache,
seizure, hyperreflexia, progressing to coma o
CSF:elevatedWBCs(lymphocytes),normalglucose,elevatedprotein,RBCs/xanthrochromia o
MRI: temporal lobe damage/hemorrhage * Dx: CSF PCR demonstrating viral DNA * Tx: IV
acyclovir 2295: TB re-activation is common in AIDS patients. The infection is kept
latent in the lungs in a granuloma (macrophages make up much of this), so when the
immune system craps out...these do too, releasing the mycobacteria. * Sign/sym:
subacute mild cough, low-grade fever, fatigue prominent in the morning (due to
secretion accumulation) o
CXR:superiorlobeconsolidation(higherO2levels)withcavitarylesions o
SubstanceabuseisahugeriskfactorforTBactiveinfection * Remember that PCP is a common
AIDS pneumonia, but cavitary lesions are uncommon 10301: HIV screening is an assay
detecting HIVp24 antigen and HIV antibodies recommended at: * Initial screen if:
Ages 15-65, being treated for TB, or being treated for any STI * Annual screening
if: IVDU (person AND sex partners), MSM, homeless, incarceration, possible sexual
contact with a HIV+ individual * Additional screening if: new pregnancy,
occupational exposure, prior to any new sexual relationship 2304: Detecting PCP you
can do bronchioalveolar lavage (high sensitivity/spec) or sputum culture (high
specificity but low sensitivity) 3257/3243/3636: Tx for Lyme Disease: * Oral
Doxycycline � first line; good as it kills B.burgdorferi AND anaplasmosis (another
tick borne illness); bad as it can cause teratogenic mental retardation and teeth
discoloration * Oral amoxicillin � for pregnant women and children <8yrs * IV
ceftriaxone/cefotaxime � will work BUT require hospitalization to administer
2993/2994: Mucormycosis (Rhizopus fungal infection) * Classically occurs in
diabetic patients with diabetic ketoacidosis * Presentation: Fever, facial pain,
blood nasal discharge, necrosis of nares/turbinates, eye involvement (chemosis,
proptosis, or diplopia) ?? blindness, coma, and death may occur! * Dx: hyphae from
nasal scrapings on KOH prep * Tx: aggressive surgical debridement and IV
amphotericin B 3264: If anyone on the USMLE eats rice and gets nausea (within 1-6
hours) ?? bacillus cerus (spore former, pre-formed toxin; activated by cooking and
accumulates, especially if stored and re-heated!) 2986: Hepatitis B infection
basically has 3 outcomes: * Acute, mild infection which resolves with time (90%) *
Chronic infection (8%) * Fulminant Hepatic Failure (<2%): occurs most often with
simultaneous HepB/HepD infection o
Signs:hepaticencephalopathy/liverfailurewithin8weeksofHepBinfection * ?? �Meth,
alcohol, and Tylenol users more likely get this (probably worse liver function)
* ?? �High mortality (>80%) o Dx:clinicalscenariowithpositiveHepBliverserology o
Tx:livertransplantation * Note that general contraindications to liver
transplant ?? irreversible cardiopulmonary disease, cancer outside of the liver,
active alcohol or drug abuse 4169/3475: Acute Pyelonephritis treatment depends on
the clinical situation: * Uncomplicated: infection is present but there??s no
chronic medical condition or urinary obstruction o Mild ?? outpatient with oral
antibiotics (usually Bactrim, 10-14 days) o Severe??
IVBactrim,usuallyswitchingtooralwithin48-72hrsifimproving * Complicated: some
obstruction (stones, catheter, etc) or condition (diabetes, azotemia,
immunosuppression, old age, etc.) that would make clearing the infection difficult
o HospitalizationandIVantibioticsbasedonsusceptibility * Pregnancyo
Hospitalizationand[IVceftriaxone+/-gentamicin,andaztreonam * Typically imaging of
the kidney is used when pt doesn�t show improvement within 48-72 hrs, complications
are present, or abnormal presentations (bloody urine, etc.) 4388: Infective
endocarditis is typically due to S.aureus infection and there??s an even higher
chance with concurrent HIV/AIDS. � Typically, right sided (tricuspid) endocarditis
has differences than the typical mitral valve version: o
Murmurlesslikely(lowerpressureflowacrossthetricuspidvalve)o
Lesssystemicsignswithmoreprominentlungproblems(assepticemboligetinthelungs) o Chest
CT can show abscesses, infarction, pulmonary gangrene, cavities at lung periphery
3561: Actinomyces Israeli is an anaerobic gram+, branching, filamentous bacterium;
slow growing! * Sign/sym: chronic progressive non-tender indurated mass at the
manfible, draining sinus-tract like abcess with yellow sulfur granules. Poor dental
hygiene/dental surgery are common co-morbidites * Dx: culture showing
characteristic bacteria * Tx: High dose, prolonged (12 weeks) penicillin and
sometimes surgical debridement 3530: Ludwig angina is a rapidly progressive
submandibular/sublingual gland cellulitis often due to an infected 2nd or 3rd molar
due to S.aureus or anaerobic infection * Signs/sym: fever, dysphagia, painful
swallowing, drooling, firm indurated mass in submandibular space; crepitus often
indicates infection with an anaerobe * Tx: monitor respiratory function,
antibiotics, removal of infected tooth * Most common cause of death in the pt is
aphyxation 3613: Typically, if a post-transplant pt shows lung problems (cough,
dyspnea, CXR infiltrates) and GI problems (abdominal pain, dysphagia, diarrhea) you
should immediately consider CMV infection. * Bone marrow suppression (fatigue,
cytopenias), and myalgias are other possible manifestation * Dx: bronchoalveolar
lavage with PCR for CMV * Tx: IV acyclovir 3888: Basically, if your CD4+ count is
>200 then you can receive any vaccine (simple!) but: * All HIV pts should receive a
pneumococcal conjugate (once) and polysaccharide (every 5 yrs) vaccines * HIV pts
who are sexually active with men should get HepA vaccine (once) * If CD4+ count is
<200 ?? cannot receive live-attenuated vaccines o
MMR,varicellazoster,intranasalinfluenza,yellowfever 4624: Asplenic patients should
be vaccinated for certain pathogens as the spleen serves a very important immune
function via splenic macrophages to kill intracellular/encapsulated organisms via
compliment antibody recognition/phagocytosis * S.pneumoiae (pneumococcus) ??
PCV13+PPSV23 with PPSV23 repeat every 5 years * H.flu ?? Hib vaccine (once) *
N.gonorhea (gonococcus) ?? quadrivalent vaccine every 5 years * Influenza ?? every
year (flu shot) * HAV/HBV vaccines (once) * Tdap (once) with TD booster every 10
years 4120: Vertebral osteomyelitis most commonly spreads through the blood from
recent UTI * Presentation: back pain (severe with palpation), back muscle spasm,
decreased range of motion of the back, +/- fever, possibly with epidural abcess *
Labs: ^CRP, ^ESR, +/- ^WBCs * Dx: first get spinal CXR, if normal ?? MRI of the
back should show soft tissue degeneration/abscess ?? ultimately to get a CT-guided
needle aspiration/biopsy for testing * Tx: antibiotics with surgery to remove
infected bone 3256: Treatment of syphilis (any stage) * First line: IM penicillin G
* If allergic to penicillin: oral doxycycline or ceftriaxone (3o only) * If
pregnant and sensitive to penicillin: desensitize ?? IM penicillin G (concern of
transplacental inf.) 3251: If you??re exposed to HIV you immediately stop what
you�re doing and initiate PEP for HIV * Immediate prophylactic triple therapy
(tenofovir, embricitabine, and raltegrevir preferred) for 28 days * Serologic
testing at immediately, 6 weeks, 3 months, 6 months * High risk exposure: blood,
CSF, genital secretions, needle-stick * Low risk exposure: urine, feces, other
bodily fluids 4714: Splenic Abscess presents with fever, chills, left-upper-
quadrant pain, splenic fluid collection, and sometimes with left sided chest
pain/left pleural effusion/splenomegaly * Classically splenic abscesses are from
septic emboli to the spleen (usually Staph, Strep, or Salmonella) * Tx: splenectomy
or rarely splenic abscess drainage (abx only cure 50% of the time) 2269: Profuse
watery diarrhea in HIV/AIDS patients is typically from a opportunistic infection
(bloody would be more high infectious things). � First step in diagnosing what is
causing the diarrhea is stool examination for ova/parasites as often parasitic
infections will be the cause here! 3248: In normal, healthy folks, there are TONS
of reasons why you??d get GI problems and the specific organism is based off the
symptoms and cultures (often USMLE wants to diagnose based off scenario!) So here??
s some classics to remember:
* B.cereus ?? diarrhea within 6 hours of eating re-heated rice * S.aureus ?? rapid
onset of vomiting and sometimes diarrhea * C.difficile ?? post-antibiotic Tx with
diffuse, watery stools * C.perfringens ?? brief cramps, fever, diarrhea associated
with unrefridgerated food * V.vulnificus ?? raw/undercooked shellfish causing
vomiting/cramp/diarrhea o Maybelife-
threateningwithinvasiveinfectioninimmunocompromised! * E.coli ?? watery or bloody
(shiga-toxin) diarrhea typically from undercooked hamburger beef * Shigella ??
bloody diarrhea/bacteremia classically with travel outside the US *
Campylobacter ?? bloody diarrhea, can cause Guillian-Barre 2927: If you have a
patient who was exposed to HepB via accidental needle stick there??s two routes: *
If they have HepB antibodies ?? give a booster for HepB and reassure, they??ll
fight it off * If no HepB antibodies ?? give immediate HepB Ig and HepB vaccine
followed with two boosters at scheduled later times 2997: Invasive aspergillosis
only occurs in immunocompromised patients and is common in all US regions *
Presentation: fever, cough, sometimes with hemoptysis * CXR: rapidly progressing
consolidation with cavitary lesions showing air pockets or ??halo sign?? noting the
fungus moving around within the cavity based on the patient??s position 4662: To
prevent infection with Lyme Disease (B.burgdorferi), any person with a tick
attached to their skin should immediately remove the tick by taking tweezers,
pinching as close to the skin as possible, and gently remove the tick with upward
pressure. * Removal of the tick in <24 hr has a low transmission rate even if the
jaw/head are attached * Pt should seek medical attention if erythema migrans rash
pops up * Pt should receive doxycycline prophylaxis if they meet ALL 5 criteria o
Tick is ixodes scapulariso Tick attached for >36 hrs and engorgedo Prophlaxis can
be initiated with 72hr of tick removalo LocalLymediseaseinfectionrateis>20%
(endemicarea)o Nodoxycyclinecontraindications(pregnancy,breastfeeding,<8yrsold)
3987/4327: Crystalline nephropathy * Presentation: typically, asymptomatic but may
causeelevated creatinine within 1 week of starting the new drug. May also cause
worsening creatinine. Typically with high doses/IV infusion.o UA: RBC or WBC casts
with frank crystalso Note that precipitation occurs in the renal tubules (higher
solute!) and the glomeruli are fine * Drugs: SAME � ??navir?? (Sulfa drugs,
Acyclovir, Methotrexate, Ethylene glycol, and protease inhibitors) * Tx:
discontinue drug and volume repletion o Aggressive hydration during infusion can
prevent this complication 4071: Ventillatory Associated Pneumonia (VAP) is
typically arise 48hr after being intubated/on a ventilator. * Presentation: fever,
purulent secretions, poor ventilation, leukocytosis * Typical infections: o
Gram+cocci(MRSA,streptococcus) o Gram- rods (Pseudomonas, E.coli, Klebsiella) *
Approach: o CXRo Ifabnormal??sputumsamplesforculture&empiricabx o Get cultures back
and treat based off results 10904: Apparently N.meningitis vaccination
(meningococcus) should be given to all of the following: * First time age 11 - 12 *
Booster age 16 - 21 * High risk: college dorm, military recruit, living in sub-
Saharan Africa, Muslum Hajj to Mecca Also note: a person on TNF-antagonists
(infliximab, etc.) should NOT receive live vaccines...we don??t know if they??d be
a problem or not, so don??t risk it ?? [intranasal flu, yellow fever, MMR,
varicella] 4166: S.pneumoniae is THE most common cause of CAP/HCAP/HAP (not VAP but
hey whatever) 2968/3819: Entamoeba Histolytica can cause amebic liver abcess *
Travel history into endemic area (Mexico is classic) * Single cyst in the right
lobe of the liver with upper right quadrant pain +/- radiating to shoulder * Bloody
diarrhea (from primary infection) * Dx: trophozoites in stool, serology, liver
imaging; typically aspirate is sterile * Tx: metronidazole (clears the primary
infection) + paromycin (clears intestinal infection) 3262: Proteus miribalis is a
classic urease+ infection causing UTI * Pt will present with normal UTI symptoms
but urine pH will be alkaline (>7) * The urease enzyme will cleave urea into
ammonia ?? basic molecule * Promotes struvite staghorn calculi, which must be
entirely removed to cure the UTI! * MANY other urease+ organisms, but this is the
most commonly clinically relevant * In-dwelling catathers often raise the risk for
UTI, especially with urease+ bugs 3054/4233: Legionnaire�s Disease (L.pneumophilia;
lives in water inside protozoa) * Presentation: pneumonia, watery diarrhea, high
fever with bradycardia, headache/confusion o
Labs:hyponatremiaisoftenpronounced,hematuria/proteinuria,hepatitiscanoccurs o
Classicallywithexposuretocontaminatedwater(hospital,hotel,nursinghome,cruiseship) *
Dx: Gram stain often negative with many neutrophils because bug is poorly
staining ?? urine antigen testing for serologic diagnosis * Tx: macrolides (like
azithromycin) or floroquinolones (??-floxacin??) 3267: Trichenellosis (trichenella
roundworm infection) � Ingestion of larvae in undercooked pork (especially outside
the USA) � Presentation o Intestinalstage??diarrhea,nausea,vomitingo Musclestage??
entry/cystformationinthemuscle??Musclepain/weakness,periorbital
edema/redness/bleeding, and subungal hemorrhages � Labs: eosinophilia (typical of
parasite infections) 3246: TB infections (new or re-activated) are VERY common in
HIV/AIDS patients. In fact, any AIDS patient having a PPD test show >5mm induration
should be treated prophylactically immediately. � Tx: Isoniazid (anti-TB) +
pyridoxine (B6 to fight off deficiency) for 9 months 3583: Acute, initial HIV
infection begins as a mono-like disease and should be suspected in higher risk pts:
* Presentation: fever, lymphadenopathy, sore throat, arthralgias, generalized rash,
diarrhea/N/V * Dx: often must be made with high viral load detection (virus isn??t
being attacked by immune system yet) because the anti-HIV abs havn�t been formed.
CD4+ count often normal. * Tx: immediate HAART with partner
notification/prophylaxis 2277: Progressive multifocal leukoencephalopathy (PML) *
Progressive demyelinating disease caused by [JC virus infection +
immunocompromised] * Presentation: any immunocompromised patient getting new onset
of focal neurologic symptoms should immediately be suspected to have PML * Tx: MRI
showing multiple, non-enhancing white matter lesions, typically without mass effect
* Dx: no known treatment, progressively fatal 3172: Parvovirus b19 is a viral
infection usually affecting kids (Fifth??s disease: fever, nausea, slapped cheek
rash!) but classically will affect adults who have exposure to lots of kids
(daycare worker is classic) * Presentation: rash (often bodily), flu symptoms,
systemic polyarthralgia (hands, knees, ankles) o
Aplasticcrisiscanoccurinptswithsicklecelldisease * Dx: B19-antibodies or NAAT (for
immunocompromised typically) * Tx: typically resolves within 6 weeks, no treatment
2845: Epiglottitis can actually be a severe, life-threatening infection as it can
compromise the airway * Presentation: high fever, severe sore throat, drooling,
stridor * Bugs: H.flu or Strep.pyogenes (rare in USA due to vaccinations, but
immigrants may have this) * Dx: clinical scenario with swab and culture * Tx:
immediate airway establishment with emergent treatment to stop asphyxiation ??
treatment of the underlying infection 8866: Remember that floroquinolones (??-
floxacin??) can cause tendonitis/rupture most often in the Achilles � Tx: halt
antibiotic, gentle exercise for the tendon, medical eval to find alternative tx
3263: Erysipelas is infection of the superficial dermis * Presentation: fast-onset
prominent inflammatory rash with sharply demarcated borders, often accompanied by
fever/chills/etc. * Bugs: GAS (most commonly S.pyogenes) * Dx: presentation * Tx:
penicillin (if S.pyogenes) but culture is needed for specific Tx 4656: Secondary
syphilis can be difficult to spot on it??s own, so do you best and always suspect!
* Presentation: rash starting on trunk and spreading out (palms/soles affected) +
generalized lymphadenopathy (the Treponeme can get anywhere!!) and constitutional
symptoms * Dx: RPR/VRDL screen followed by FTA-ABS test * Tx: intramuscular
penicillin G or doxycycline for penicillin allergy o Jarisch-
Herxheimerreaction�hugereleaseofspirocheteantigensfromdestructionby treatment can
cause myalgias, headache, and fever 24hr after treatment starts 3266: Rubella
(German Measles) is a classic viral infection, largely eradicated from vaccination
efforts * Adult presentation: prodrome (fever, lymphadenopathy, malaise) followed
by eruptive macropapular rash that starts on the face/neck and spreads downward
sparing the palms/soles within 24 hrs, with arthralgiaso While rare, post-
infectious encephalitis is a serious complication * Dx: PCR or serology for anti-
rubella IgG/IgM * Tx: supportive therapy o Prevention with rubella vaccine is the
best method of treatment!Note that measles has a similar prodrome (high fevers
though) and rash (more gradual spread) but no arthralgias 3260: Malignant Otitis
externa * Presentation: severe ear pain often radiating to the jaw (TMJ
involvement, exacerbated by chewing), ear discharge, granulation tissue in external
auditory meatus o Pain/infectionwillnotimprovewithtopicalantibiotics * Bugs: 95% of
these are caused by P.aeroginosa (classic if you??re also diabetic!) * Dx: clinical
presentation with swab/culture * Tx: anti-pseudomonals will likely work (pip-tazo
is my go-to) 2262: Two major side effects of isoniazid? B6 (pyridoxine) deficiency
neuropathy and hepatits 2995: If they EVER mention someone is a farmer or country-
man in/around the Mississippi/Ohio River basin, then you MUST consider
Histo/Blasto/Sarcoid. * This pt has signs of non-caseating granulomatous lung
disease and had proper epidemiologic signatures. Initially diagnosed with
sarcoidosis, prednisolone Tx (appropriate for Sarcoid) caused rapid deterioration
due to immune-compromise. This should make you think ??they??re not treating the
correct thing!?? * After that workup for TB/Histo/Blasto should be sought due to
his status from around the Mississippi o Urinary/serum antigen testing is available
for all endemic fungal infectionso Histo:TB-
likesymptoms,pulmonarygranulomas(caseornon-case),mediastinal lymphadenopathy,
arthralgias, or erythema nodosum (bird/bat droppings) o Blasto:TB-
likesymptoms,lesscommon(rottingwood/soil) ?? Disseminated infection hits bones,
skin, and the prostate! 2616: Febrile neutropenia * A medical emergency because of
high susceptibility to overwhelming infection (esp. Pseudomonas). Often caused by
chemotherapy! * Presentation: fever, absolute neutrophils <1500 (<500 is severe!),
but otherwise normal * Dx: clinical presentation; good if you can find a reason for
the neutropenia * Tx: immediate blood/urine cultures + anti-Pseudomonal prophylaxis
(cefepime, pip-tazo, meropenem) 4488: Pelvic Inflammatory Disease * Presentation:
Lower abdominal pain with vaginal discharge and often friable/inflamed cervix on
funduscopic exam; classically infection with either N.gonorrhea or Chlamdyia * Dx:
clinical presentation with gram stain of discharge * Tx: Azithromycin (Chlamydia)
with Ceftriaxone (N.gonorrhea) � always treat the co-infection! o Because of high
morbidity with other STIs pts should be counseled on safe sex, screened for HIV,
syphilis (RPR), HPV cervical cancer (pap smear), HepB (antigen test) o If
concurrent IVDU then Hep C screening is warranted 4476: In chronic liver disease,
no vaccinations are restricted, but the disease puts them at increased risk for
some things that can be vaccinated for: * Normal vaccines:o
Td(once,age18)withTdapevery10years o Flu vaccine once per year * Liver disease
vaccines:o HepA/HepBvaccinesifthey�renotalreadyimmune(checkAbtiters)o PPSV23
immediately in chronic liver disease with PPSV23+PSV13 at age 65 (normal)
2970/3789: Hydatid cyst (Echinococcus granulosus or E.multilocularis) * A
unilocular (E.granulosis) or multilocular (E.multilocularis) cyst that can occur in
any organ; parasite transmitted from close contact with dogs feeding on animal
viscera or sheep (sheep breeders are classic!) where ingestion of eggs results in
hatching and hematogenous spread of parasite. * Presentation: problems caused by
mass effect of cyst are usually being investigated then seen as a cyst with thin
walled ??eggshell calcification?? on imaging (Liver most common, then Lung) * Dx:
Imaging is diagnostic * Tx: Surgical resection with concurrent abendazole o
Drainage can be therapeutic but there??s a huge risk of anaphylaxis due to spillage
4418: Influenza pneumonia * NOT a post-viral pneumonia, but a pneumonia caused by
the influenza virus * Presentation: flu symptoms (abrupt fever, chills, malaise,
myalgias, cough, and coryza), sometimes fever, pulmonary symptoms (wheezes,
crackles, coarse breath sounds) often in winter months o Leukopenia and proteinuria
may be a featureo CXRshowinginterstitialoralveolarpattern * Dx: nasal swab showing
influenza antigens * Tx: Neuramidase inhibitors (oseltamivir/zanamivir) within 48
hours (stops release of progeny virus). Rimantidine and Amantidine can be effective
vs Influenza A 2273/2267: PCP pneumonia (P.jiroveci formerly carinii) * One of the
most common infections for an AIDS patient * Presentation: dry cough, dyspnea,
hypoxia, CXR with bilateral diffuse infiltrate, rarely pleural effusion * Dx:
clinical suspicion + bronchoalveolar lavage showing P.jiroveci (little crushed
ping-pong balls!) * Tx: TMP-SMX + corticosteroids (if poor O2 saturation status;
PaO2 <70 or A-a >35) ?? may show initial worsening of lung function due to death of
bacteria and inflammatory reactions in lung 3261: Lyme disease (Borrelia
Burgdorferi following tick bite) * Early local (days � 1 month): erythema
migrans,fatigue/malaise, mild headache, neck stiffness, myalgias/arthralgias *
Early disseminated (weeks � months): Heart (5%, AV-block, cardiomyopathy); CNS
(15%, uni/bilateral Bell??s palsy, meningitis, encephalitis); Muscle (60%,
migratory arthralgia), Eye (10% conjunctivitis), Skin (multiple erythema migrans!),
regional lymphadenopathy * Late (month � years): Muscle (60%, arthritis), CNS
(encephalomyelitis, peripheral neuropathy) * Tx: doxycycline (1st line);
amoxicillin (pregnant or <8yrs); ceftriaxone can work but IV only (hospitalized) o
IfpresentingwithBell??sPalsy:artificialeyedropsandeyepatchingatnightarerecommended
4417/4012: Nocardiosis (Nocardia spp) * Gram+, partially acid-fast, branching
filamentous rod; disseminated infection in immunocompromised o Endemic in soil;
either inhaled or introduced with traumatic wound * Presentation o Normal:TB-
likesymptoms(weightloss,fever,nightsweats),CXRalveolarinfiltrates+cavitation o
Disseminated: normal with involvement in the brain (often seizures) and skin (rash)
* Dx: presentation with bronchoalveolar lavage growing Nocardia * Tx: TMP-SMX
(first line) with a carbapenem if brain involvement for 6-12 months 3254/9885:
Cryptococcal Meningoencephalitis (Cryptococcus neoformans fungus) * Classically
occurs in pts with immunosuppression (AIDS is classic) * Presentation: fever,
lethargy, headache, altered mental status ?? may progress to coma o
CSF:highopeningpressure,lowWBCs,lowglucose,elevatedprotein o
Papilledema(indicatingincreasedCNSpressure)canbeanimportantsign * Dx: Latex
agglutination (+), cryptococcal antigen (+), India Ink (+), Sabourard Agar growth *
Tx: IV amphotericin B + flucytosine (2 weeks, induction) ?? oral fluconazole (8
weeks) o IntrathecalamphotericinBiffailuretorespondtoIVtreatment o
SeriallumbarpuncturestolimitelevatedCSFpressure 4167: In a patient with spinal
injury needing catheterization (neurogenic bladder), the best practice (lowest
chance of nosocomial UTI) is with intermittent catheterization. The classic
principle is the longer the catheter is in, the high the chance of contamination.
Thus an in-dwelling catheter isn??t the best option here. 2961: Treatment of HepB
infections (evidence of HepB serologically with possible liver damage signs) * Pts
to treat: o Acute liver failure or complications of liver cirrhosis with HepB
serologic evidenceo AdvancedlivercirrhosiswithhighHepBtiterso
NolivercirrhosisbutHepB>20,000copiesorSerumALT>x2normallimito Pts on
chemotherapy/immunosuppression with a history of HBV (present re-activation) * Tx
options:o Interferon�firstlineacutetreatmentinyoungptswithOKliverso Tenofovir or
entacavir � first line in chronic HepB or pts with liver problems 3253/11108:
Kaposi Sarcoma (HHV-8 + AIDS) * Presentation: multiple skin lesions often starting
brownish then becoming purple/red due to increased vascularization of infected
tissue; may accompany other signs of AIDSo
Notethatlesionsmaybequiteimpressiveifinfectionhasbeenpresentforprolongedtime(see
question 11108 for example) * Dx: clinical but biopsy and HIV/AIDS serologic
evidence often used to confirm * Tx: HAART treatment of AIDS will often cause
regression with CD4+ recovery o If refractory, chemotherapy may be used to kill off
the rapidly dividing tissue 3320: Disseminated Gonococcal (N.gonorrhea) infection �
Presentation (two major presentations) o
Jointalone:Purulentarthritiswithoutskininvolvemento
Triad:Tenosynovitis(wrist,ankles,fingers,knees)+pustularrash+migratorypolyarthalgia
without purulence * Dx: blood/joint fluid/pustule/genital cultures (may be negative
due to fastidious growth) or NAAT (better at finding evidence of gonococcus) * Tx:
Drain purulent joints if present + IV ceftriaxone, then PO cefepime (N.gonorrhea) +
empiric azithromycin (chlamydia co-infection) 4470: When testing for TB with a
Tuberculin Skin Test (Mantoux), the size of the induration and the clinical
scenario will guide whether or not you??ll treat: * 5mm: HIV+ or immunosuppressed
(organ transplant), known TB in close contacts, or CXR showing nodular/fibrotic
changes (recently healed TB) * 10mm: recent immigrant (<5yrs), IVDU, high-risk
setting (hospital worker, nursing home, homeless, prison, TB lab personnel),
children <4yrs or with exposure to known cases * >15mm: treat all patients (even
healthy) if this big2916: Remember, that screening for HepC in blood started in
1992, thus if a patient had a blood transfusion before 1992, they should have a
HepC screening. 3103: CMV esophagitis in AIDS pts causes substernal burning/long-
linear ulcers, and biopsy shows intranuclear/intracytoplasmic inclusions (Tx: IV
ganciclovir) 4257: Puncture wound with Pseudomonas osteomyelitis * When you think
of someone stepping on a rusty nail, it??s tempting to go right to C.tetani,
however Pseudomonas can often inhabit the low oxygen environment of a rusty nail
and is a common cause of osteomyelitis after a puncture wound * Presentation: post-
puncture wound local pain, redness, swellingo X-
rayshowssignsofboneinfection(approx.2weeksforprogression) * Dx: culture and x-ray
evidence * Tx: oral or IM floroquinolones (ciprofloxacin would work) 3107:
Bacillary angiomatosis (B.hensliae) * Classically due to a cat scratch *
Presentation: immunosuppressed (AIDS pts most common) with bright red, firm,
friable, exophytic (extends beyond the epithelium) nodules * Tx: oral erythromycin
� 2270: CMV mononucleosis-like syndrome * Presentation: mono symptoms (fever,
fatigue, myalgias, arthalgias), no pharyngitis/cervical lymphadenopathy.o Negative
heterophile antibody (monospot) testo
Atypicallymphocytes(large,basophilic,withvacuolatedappearance) * Dx: clinical
picture
* Tx: ganciclovir 4354/3131/2869: Infectious Mononucleosis (Epstein-Barr virus) �
Presentation: fever, malaise, posterior cervical lymphadenopathy, tonsillar
exudate, and possibly splenomegaly in an otherwise healthy young adulto
InitialHIVinfectioncanlooksimilarbutwillbefever,malaise,lymphadenopathy,diarrhea,an
d rash ?? it??s actually reasonable to test for HIV if monospot is negativeo
Autoimmune hemolytic anemia/thombocytopenia is a complication of EBV-mono from EBV-
antibodies (IgM cold-agglutinin anti-I antibodies) cross-reacting with
RBCs/platelets. Occurs approximately 2-3 weeks post infection * Dx: heterophile
antibody (monospot) test; Anti-EBV antibody test o
Smearshowingvariantlymphocyteswithconvolutenucleiandvacuolatedcytoplasm * Tx: rest
and avoidance of contact sports for >3 weeks if splenomegaly present 3247: Hunman
monocytic Ehrlichiosis (Ehrlichia chaffenesis or E.ewingii) * Endemic to
southeastern/southcentral USA from Lone Star Tick bite * Presentation: acute fever,
malaise, headache, myalgias, altered mental status, no rash o
Leukopenia/thrombocytopenia are often found on CBC o Elevated LFTs and lactate
dehydrogenase found on labs * Dx: often clinical, but definitive with
intracytoplasmic morulae in WBCs or PCR * Tx: Doxycycline (often given empirically)
o Chloramphenicol is second line (can cause blood dyscrasias) 3892: For
smokers/COPD pts, a PPSV23 (S.pneumoniae) vaccine should be given once <65yrs. All
other vaccination guild lines are the same. 3068/3014: Infective endocarditis is
easy to spot on exams but classic bacterial associations must be memorized. *
S.aureus: implanted devices (catheters, valves, defibrillators, etc.) and IVDU *
Viridians Group Strep: dental/respiratory procedures, esp with previously damaged
valve * Coagulase-neg staph: implanted devices (catheters, valves, defibrillators,
etc.) * Enterococci: nosocomial UTIs (classic is after UG procedures) * Strep.
Bovis (gallolyticus): colon carcinoma/IBD 3808: Cysticercosis (T.solium parasite) �
Two major routes of infections with different outcomes: o
Consumptionoflarvaeinmeat:ifanimalseattheeggs,they??llhatch/penetratetheGItractand
larvae will become lodged into the muscles of the animal. If humans eat the meat,
then they??ll get an intestinal infection and shed eggs into feces. o Consumption
of eggs: humans are the definitive hosts for T.solium, thus consumption of the eggs
on any food from feces contamination results in hatch/hematogenous spread into the
brain, muscle, subQ tissue, and eye causing cyst formation � Presentation: multiple
small (<1mm) fluid filled cysts form in their respective tissues with a membranous
wall and invaginated scolex o
Neurocystricosisiswhenitoccursinthebrainandisactuallythemostcommonbrainparasite o
Classically occurs in areas where pigs are raised and sanitation is poor.o
Oftentheseareasymptomatic,andeitherarefoundincidentallyorpresentmuchafter infection
had occurred 3104: Babesiosis (Babesia parasite; Ixodes tick transmission) *
Following the tick bite, the parasite enters the blood where it invades RBCs for
it??s life cycle resulting in hemolytic anemia * Presentation: may be asymptomatic
in healthy patients o
Hemolyticanemia,jaundice,hemoglobinuria,renalfailure,anddeathcanalloccuro
NOrashassociatedwithdisease;maybepurpuricrashifthrombocytopeniaissevere o
Clinicallysignificantillnessinpts>40yr,asplenicpts,andimmunocompromisedpts * Dx:
Giemsa stained thick and thin blood smear for parasite within RBCso
Labs:hemolysis,anemia/thrombocytopenia,elevatedESR,abnormalLFTs,decreasedserum
compliment levels * Tx: [Quinine + clindamycin] or [atovaquone + azithromycin]
3675: Malaria (Plasmodium spp; Anophales mosquito transmission) * Presentation:
cyclical fevers with non-specific symptoms (malaise, headache, N/V, diarrhea,
jaundice, hepatosplenomegaly, myalgia, pallor, anemia, etc.)o
Cyclicfevershavethreestages:cold(chills,shivering;incubation),hot(highfever,withRBC
lysis and spread of parasite); wet (sweating/resolution of fever with re-infection)
* Dx: blood smear showing Plasmodium o Typically,travelerswhodidnotadheretochemo-
prophylaxiswillcontractmalariaevenwith proper protective gear * Tx: anti-malarials
(lots of them!) 4478: Vaccination protocol in HIV/AIDS pts (again!): *
S.pneumoniae: PCV13 (upon dx) ?? PPSV23 (8wks, every 5 yrs) * HepA & B: give upon
dx unless they have documented immunity * Certain live vaccines (if CD4 >200): MMR,
varicella zoster 3013: Broad-spectrum antibiotic treatment for suspected
endocarditis in an IVDU is vancomycin. The most common IE bug for IVDUs is S.aureus
(gram+), thus vanc (with broad spectrum gram+ activity) is a great choice until
specific therapy can be initiated. 2981: Isoniazid (INH) is known for two major
side effects: Vit.B6 deficiency and liver toxicity * LFTs should be regularly
monitored in the pts and most will experience a transient benign hepatic injury
(LFTs <100 IU/L) which does not warrant discontinuation of therapy * Should LFTs
rise above this level, stop the drugs immediately 3674: Cutaneous larva migrans (??
Creeping Eruption??); Ancyclostoma braziliense (??pet hookwork??) * Transmission
occurs with skin contact with infected dog/cat feces containing larvae, classically
in a tropic/subtropic region or Southeastern USA in a sandy beach or sandbox *
Presentation: multiple, itchy, red plaques where the larvae enter the skin, which
track up the arm/leg by a few millimeters per day as the larvae migrate * Dx:
clinical presentation * Tx: anti-hemlithinic agents (abendazole/ivermectin) with
anti-itch creams 2265: Remember! Spirochete visualization on dark-field microscopy
is diagnostic for syphilis! Usually if a person has syphilis, they??ve been
engaging in some risky sexual behavior...thus they should be tested for other STIs,
especially HIV 3422: Don??t forget! Herpes Zoster (shingles) outbreak is treaed
with oral vanacyclovir or acyclovir. Both will work, but valacyclovir has a better
side effect profile! 2292: Aspiration pneumonia (anaerobic organisms) * Should be
suspected in pts with poor dentition (more bacteria in mouth), upper airway
instrumentation, upper GI/nasogastric tube, GERD, dysphagia, alcoholism, or
impaired consciousness * Presentation: fever, chills, cough, leukocytosis, signs of
lung infection (consolidation/crackles/etc.), and foul-smelling sputum (because
anaerobes) * Dx: clinical/radiographic signs with sputum cultures * Tx: clindamycin
(great anaerobe coverage) is first line o Metronidazole+amoxacillin,amoxacillin-
clavuronicacid,oracarbapenem(??-penem??)areall viable alternative options 2239:
Acute epididymitis * Presentation: fever, painful enlargement of testes, and
irritation upon voiding (hurts to pee) o Non-STI: seen in older adults, typically
with a UTI; E.coli and Pseudomonas (GNRs) are common o
STI:seeninyoungeradults,typicallywithanSTI/urethritis(painattipofpenisandurethral
discharge); Chlamydia and N.gonorrhea are common * Dx: clinical presentation with
swabbing of genitals for culture * Tx: treat the appropriate bug 4284: Influenza *
Presentation: rapid onset of fever, headache, myalgia, sore throat, cough, N/V,
etc. o Peaksinwintermonths;FluAandBcausediseasetypically * Dx: throat swab and
culture * Tx: Often self-limited (3-10 days) but early (<48 hr symptom onset)
oseltamivir/zanamivir (neuramidase inhibitors) can help limit duration.o Pt
presenting >48hr after symptoms: symptomatic treatmento
Highriskornonimprovingpts:giveneuramidaseinhibitors/anti-virals ?? Age >65;
pregnant or early post-partum women; pts with chronic organ system illness (e.g.
reno-vasular disease), immunosuppression, morbid obesity, Native Americans, or
nursing home residents 3014: Don??t forget the Viridian�s group Strep spp:
S.sanguins, S.mitis, S.oralis, S.mutans, S.sobrinis, S.milleri 3873: Don??t forget!
If an AIDS pt CD4 count is >200 they can receive the MMR and VSV live virus
vaccines. * MMR is recommended only if pt does not have prior immunization * Should
a pt be diagnosed with HIV and be vaccinated with MMR/VSV before starting HAART,
they should be vaccinated again after HAART initiation 3000: Sporotrichosis
(Sporothrix schenkii; fungus growing on plants/bark/soil ?? rose gardener gets
pricked) * Presentation: Hx of injury in the garden, red nodules that ulcerates at
the side of plant injury with progressive ulcerating lesions tracking up the
extremity as it moves along lymphatics o
Typically,nolymphnodeswelling/systemicsignsofinfection * Dx: clinical diagnosis
with biopsy demonstrating dimorphic fungus * Tx: potassium iodide solution or
itraconazole/fluconazole 3425: Leprosy (Mycobacterium leprae) * Presentation: early
hypo-pigmented plaque; late nerve damage, muscle atrophy, and crippling deformity
(hands, face, ears, wrists, knees, elbows) * Dx: skin biopsy of lesion showing
acid-fast bacilli * Tx: many treatment regimens; [dapsone+rifampicin] is a classic
3245: Bacterial meningitis empiric treatments are often initiated as cultures can
take too long to grow before it??s too late for the patient! Thus it??s important
to treat initially based on demographics: * Age <2: vancomycin +
ceftriaxone/cefotaxime + ampicillin * Age 2-50: vancomycin + ceftriaxone/cefotaxime
* Age 50+: vancomycin + ceftriaxone/cefotaxime + ampicillin (Listeria coverage!) *
Recent Neurosurgery/shunt: vancomycin + cefepime (4th gen cef) * Penetrating injury
to skull: vancomycin + cefepime * Immunocompromised: vancomycin + cefepime +
ampicillin Note that all regimens should also treat with dexamethasone or
methylprednisolone (better outcomes with a steroid for anti-inflammation on board!)
3012: The Modified Duke Criteria are used in diagnosing Infective Endocarditis *
Based of ??major?? and ??minor?? criteria o
DefiniteIE=2majorOR1major+3minorcriteria
o PossibleIE=1maj+1minOR3minoralone * Major criteria: o
Bloodculture(+)fortypicalIEorganisms o Echocardiographic evidence of valvular
vegetation * Minor criteria: o
Predisposingcardiaclesion,IVDU,Temp>38C,embolicphenomena(splinterhemorrhages,
etc.), immunologic phenomena, (+)blood culture of an atypical organism * Clinical
approach: when a patient presents with signs of infective endocarditis you first
draw 3 blood cultures from different venipuncture sites then obtain TTE/TEE to
search for vegetations in the heart o
EmpiricAbxwareinitiatedafterbloodculturesaredrawnordelayeduntilresultsarepresent
2264: Treatment of toxoplamosis * Prophylaxis is TMP-SMX (Bactrim) often for AIDS
or immunosuppressed pts * Tx: empiric sulfadiazine + pyrimethamine if the infection
is actually present; diagnosis may be made if ring-enhancing lesions are seen on
brain imaging with improvement of symptoms with this treatment regimen! 3011: A
clenched fist injury (??fight bite??) is when a person cuts their hand on someone??
s teeth while punching them in the jaw. It can open the fist up to interesting
infections due to the bacteria in the human mouth. * Tx: Amoxicillin-clavuronic
acid is the treatment of choice as these wounds can be infected with multiple
bacteria (gram+/gram-/anaerobes must be covered with broad spectrum) * [Clindamycin
(Gram+/anaerobes) + Ciprofloxacin (Gram+/gram-)] would be an acceptable regimen
should the patient be allergic to penicillins * The regimens would also work well
against dog bites or other suspected polymicrobial infections 11228: Chikungunya
fever (Aedes mosquito Arbovirus; Central/South Americas, Africa coasts, and SE
Asia) * Presentation: high fever, polyarthralgias, headache, myalgia, pink eye,
macropapular rash, peripheral lymphedema, lymphadenopathyo
Labs:lymphopeniaandthrombocytopeniao Usually a person returning from a trip to the
Caribbean * Dx: serologic testing for the virus * Tx: supportive therapy (disease
self-limited) 3742: Toxic Shock Syndrome * Bacterial infection (S.aureus most
common) with Toxic-Shock Toxin-1 (TSST-1), a super-antigen that results in massive
T-cell activation/cytokine release, resulting in loss of intravascular fluids to
the extravascular spaces and shock! * Presentation: rapid development of high
fever, Hypotension (<90 systolic), diffuse red/edematous rash (looks like sunburn),
skin desquamation of palms/soles, multisystem failure o Classically (50%)
associated with a tampon left in post-menstruation, typically arising 2-3 days
after the last menstrual period o Non-menstrualinfectionscanalsocauseit(post-
surgery,sinutitis,etc) * Dx: clinical syndrome with history * Tx: supportive
therapy for shock, removal of foreign materials causing infection, anti-staph
(penicillin + vancomycin) are all part of treatment 3250: Foodborne Illnesses are
wide-ranging with a huge amount of possible presentations. We can narrow down
possible bugs by the symptoms of the patient: * Vomiting predominates: S.aureus,
B.cereus, or Norovirus * Watery diarrhea predominates: C.perfringes, ETEC,
Cryptospoidium, Cyclospora, interinal worms * Inflammatory (bloody) diarrhea
predominates: Salmonella, Campylobacter, EHEC, Shigella, Enterobacter, Vibrio spp,
Yersinia spp. * Non-GI symptoms predominate: you??ll typically know these based on
symptoms/history 3252: Opportunistic infections and primary prophylaxis in HIV/AIDS
* P.jiroveci (PCP) � TMP-SMX (<200) * T.gondii (toxoplasmosis) � TMP-SMX (<100 or
positive IgG for toxo) * Mycobacterium Avium complex � azithromycin/clarithromycin
(<50) * Histoplasmosis � itraconzole (<150 or living in endemic area) * Herpes
simplex virus � acyclovir/valacyclovir (recurrent infections, no CD4 count
specified) * Note that some major HIV related infections are NOT recommended to
have primary prophylaxis o
Candida�Fluconazole:reactivetreatmentisextremelyeffectiveandprophylaxisisexpensive.
Also concerns of resistance with prophylaxis, so we only treat reactively o
Cryptococcus�fluconazole:cost/concernforresistancearesolidreasons,butalsoincidencei
s extremely rare, thus prophylaxis is not administered 2267: Remember! S.pneumoniae
is THE most common cause of pneumonia in HIV/AIDS patients. You might be temped to
think PCP when an AIDS patient has pneumonia, but you better slow your roll: *
S.pneumoniae � unilateral, lobar infiltrate, productive cough, pleural effusions
often occur, >200 CD4 o Remember!
Thisguyisencapsulated,thusevenpeoplewithnormalimmunityhaveaharder time clearing
this infection! * P.jiroveci � bilateral, diffuse infiltrate, dry cough, pleural
effusions rarely occur, <200 CD4 2998: Cocciodomycosis: classic endemic fungal
infection of the American Southwest. * Presentation: fever, fatigue, dry cough,
pleuritic chest pain, erythema multiform/erythema nodosum (?? desert bumps??), and
arthralgias * Dx: lavage showing classic ??crowding spherule?? of cocci * Tx:
itra/ketoconazole for immunocompetent; add amphotericin B for immunocompromised
4669: Miliary Tuberculosis * Hematogenously spreading TB often caused by IVDU.
Associated with incarceration or living in endemic areas/with people infected *
Presentation: subacute/chronic cough, fatigue, intermittent fevers, weight loss.
Organ specific symptoms in the liver, bones, lymph nodes, or CNS can also occur *
Dx: Hx and diffuse reticulonodular pattern (??millet seed??) infiltrate on CXR *
Tx: long-term antitubercular drugs 8880: HACEK group Infective Endocarditis *
Haemophilus aphrophilus, Aggregatibacter actinomycetemcomitans, Cardiobacterium
hominis, Eikinella corrodens, Kingella kingae ?? gram(-) anaerobes of the normal
human flora * Infective endocarditis is RARE, but often occurs in the setting of
poor dentition/periodontal infection where manipulation of the
mucosae/gingiva/teeth/jaw result in systemic seeding GI and Nutrition 2245/2946:
Acalculous Cholecystitis * Acute inflammation of the gallbladder WITHOUT gallstones
typically in critically ill, hospitalized pts resulting in cholestasis/ischemia of
gallbladder ?? 2o infection of gallbladder ?? distention/necrosis * Predisposing
factors: recent surgery, severe trauma, extensive burns, sepsis/shock, prolonged
fasting/TPN, mechanical intubation * Presentation: unexplained fever, leukocytosis,
RUQ abdominal pain/mass, jaundice, abnormal LFTs o
Gallbladderinflammationmaycausegangrene,perforation,oremphysematouscholecystitis
(infection with gas-producing bacteria causing gas in the gallbladder) o Note that
gaseuous distention of the bowel WITHOUT air-fluid levels suggests distention
without obstruction (like with inflammation) o
Highindexofsuspicionshouldbeheldforcriticallyillpatients * Dx: Abdominal ultrasound
is preferred (gallbladder wall thickening, pericholic fluid); CT abdomen or
cholescintigraphy are more sensitive/specific and can be used in unclear ultrasound
* Tx: can be managed medically (abx/anti-inflammatory) or surgically (percutaneous
cholecystectomy with drainage of abscesses) 2585: Lynch Syndrome (Hereditary Non-
polyposis colorectal cancer [HNPCC]) * Two major types: o Lynch syndrome I: only
colon cancer o LynchsyndromeII:colonandextra-
coloniccancer(endometrialcarcinomamostcommon) * Dx: Amsterdam Criteria I o
Atleast3relativeswithcoloncancer(onemustbefirstdegreetotheothertwo) o
Involvementoftwoormoregenerationso Onefamilialcasebeforeage50o Familial Adenomatous
Polyposis excluded (APC gene mutation) * Tx: close watch and removal of any colon
cancers 4389: Suspicion of Colorectal cancer: signs/symptoms � An older man (>60)
with abdominal pain, microcytic anemia, (+)fecal occult blood, and hepatomegaly
with a hard liver edge ?? prompt you to think infiltrative colon cancero Any old
person with microcytic anemia (esp. men) or blood in stool ?? colon cancero
Hepatomegalywithahardliveredge??livercancer(mostoftenfrommetastaticcoloncancer) o
MildlyelevatedAST/ALT/Alk.phosinthissetting??infiltrative/cholestaticdisease(which
metastatic liver cancer would be a part of!)� Dx: because this pt has signs of
colon cancer and liver abnormalities without significant elevations in LFTs, an
abdominal CT should be sought as metastatic malignancy is suspected. 2953/4625:
Management of Hepatic Encephalopathy� Remember that hepatic encephalopathy
classically presents with confusion, high BUN, and ??liver flap?? � Management o 1.
Supportive care (fluids, restraints, correct electrolytes) * ?? �Hypokalemia is
especially important as it will increase renal ammonia production * ?? �Metabolic
alkalosis will cause increased Ammonium ?? ammonia conversion o
2.Adequatenutritionwithoutproteinrestriction ?? Limit proteins makes logical sense
but its been shown not to be beneficial unless the patient cannot tolerate protein
on their own. o 3. Treat precipitating cause o 4. Lower serum ammonia (lactulose +
rifamixin is a classic combo; neomycin can be used as an alternative but has
significant oto/nephrotoxicity, thus isn??t used unless necessary!) 4752/2219:
Hepatorenal Syndrome * Deadly syndrome occurring in end-stage liver disease causing
progressive renal decline in structurally normal kidneys decreased glomerular
filtration in the absence of shock, proteinuria, or other obvious renal
pathology ?? can lead to death via infection/hemorrhage o
Kidneysvasoconstrictinresponsetohypo-perfusion,diminishingrenalbloodflowand
eventually kidney function * Presentation: electrolyte dysregulation, hypotension,
failure to respond to 1.5L saline bolus in the setting of liver failure * Dx:
clinical picture with failure of response to IV saline * Tx: renal transplantation
(no medical treatment with proven benefit) 4635/2936: Chronic Liver Disease
(Cirrhosis) � Presentation: Jaundice, itchiness, GI bleeding, encephalopathy,
decrease in total T3/T4 (free concentration only drops
in severe cases) and gender specific signs due to poor metabolism of estrogens in
liver (increased estrogen in blood) and systemic signs o
Men:hypogonadism(small/firmtestes,decreasedlibido,erectiledysfunction,lossofpuberta
l hair, gynecomastia) o Women:amenorrhea,irregularmenseso
Systemic:telangiectasias,portalHTN,ascites,hepato-splenomegaly,palmarerythema,??
terry nails??, Dupuytren??s contracture, clubbing of fingernails o
Maybetotallyasymptomatic * Dx: clinical picture; may be confirmed with liver biopsy
o Endoscopy to assess for varices as these are treatable complications of liver
disease. Two other complications (hepatic encephalopathy/acites) will be obvious
from clinical exam * Tx: stop damaging behavior/disease; some cirrhotic damage
cannot be undone o Treatmenttopreventcomplications(B-
blockerforvaricies,drainingofascities,etc.)isamajor part of management alongside
treatment of current complications o Cirrhosis in patients without signs/symptoms
(??compensated cirrhosis??) should be monitored for hepatocellular carcinoma
(ultrasound liver/a-fetoprotein screen every 6 months) 2923/2924/2983: Genetic
Diseases of Liver Metabolism * Dubin-Johnson syndrome � conjugated bilirubinemia;
jaundice with body stressors (illness, pregnancy, OCP use) but otherwise no/minor
symptoms (fatigue, abd. pain, weakness) and no hemolysiso MorecommoninSephardicJews
o Clinically normal aside from reactionary jaundice and black liver (epinephrine
metabolites) o Labs:Bilirubin(20-
25mg/dL),normalLFTs,normalcoproporphyrin(predominantlyCoproI) * Rotor syndrome �
Dubin-Johnson syndrome without the black liver * Crigler-Najar syndrome � autosomal
recessive unconjugated bilirubinemia; o
Type1:significantmentalretardation/death;Phototherapy/plasmapheresiscanhelp
conjugate the bilirubin to buy time for curative liver transplant o Type 2: fairly
benign unconjugated bilirubinemia with jaundice; often asymptomatic, but symptoms
(if occuring) can be treated with phenobarbital or clofibrate � Gilbert syndrome �
mild unconjugated bilirubinemia triggered by bodily stressors; very similar to C-N
syndrome II, difference is in the enzyme defect 3588: Dyspepsia * Uncomfortable
feeling of fullness or discomfort after eating; more of a symptom than a disease *
Three major routes to consider based on pt presentation: o
TypicalGERDsymptoms:PPIorH2blockero NSAID/COX-2inh.use:stopusingtheNSAID/COX-2inh.
o Neither of the two above: * ?? �Alarm symptoms (weight loss, GI bleed, anemia,
dysphagia, vomiting, early satiety): upper/lower GI endoscopy * ?? �No alarm
symptoms: * Age >55: Scope * Age <55:o H.Pyloritesting(Breathtestorstoolassay) ??
Treat if positive; PPI trial if negative � If all of that fails, then have the
patient undergo endoscopy 4165: Gastric adenocarcinoma * If you get endoscopic
results of gastric adenocarcinoma, the first thing to do is stage with a CT of the
abdomen and pelvis to check for metastatic disease. If CT is negative, additional
staging procedures (laparoscopy, endoscopic ultrasound, chest CT, and PET/SPECT)
may be necessary. Note that CA-125 is a tumor marker in gastric cancer, but serves
little diagnostic purpose. o Earlystage(limitedtostomach):rare,butagreatprognosis??
surgicalresection o Laterstage(metastatic):commonwithpoorprognosis??
chemo/palliativecare * Don??t get this confused with a MALToma...this is a totally
different cancer! 2596: MALT lymphoma (MALToma) * Gastric cancer often the result
of H.pylori infection; looks like a heaped up ulcer * Dx: endoscopy with biopsy
showing MALT-lymphoma * Tx: o Eradication of H.pylori ([omeprazole, clarithromycin,
amoxicillin] or [bismuth, omeprazole, a tetracycline, an aminoglycoside] o
Chemotherapy ([CHOP] or [CHOP + bleomycin]) can still play a role should H.pylori
eradication fail to cure the cancer 3887: Giardiasis (Giardia Lamblia or
G.intestinalis parasite) * Presentation: profuse, watery, foul-smelling diarrhea
with bloating/abdominal cramps; malabsorbtion/weight loss can occur in more long-
standing infectionso Transmission is classically after a trip abroad/camping trip
through contaminated water/food or fecal-oral route * Dx: Stool-antigen assay
(immunoflourscence or ELISA) for oocysts or trophozoites * Tx: oral Metronidazole
4654: Chronic Hepatitis C and Associated Conditions * Presentation: asymptomatic or
fatigue are the most common; nonspecific symptoms (fever, anorexia, myalgia, weight
loss, etc.) can also occuro Labs:elevatedornormalserumtransaminaseso May progress
to liver cirrhosis (20%) or hepatocellular carcinoma * Associated diseases can clue
you into the HepC infection! o
Essentialmixedcryoglobulinemia(90%ofcaseshaveHepC)�palpablepurpura,arthralgias,
renal complications due to IgM immune complex deposition into medium sized
vessels ?? Low compliment levels are classic for this disease o
Membranoproliferativeglomerulonephritis�willappearasrenaldeclinewithcharacteristic
biopsy histology of the glomeruli o
Porphyriacutaneatarda�fragileskin,photosensitivity,vesicularrash/erosionsondorsumof
the hands o Lichenplanus�itchy,purple,raised,welldemarcatedplaques 3086: Macrocytic
Anemia due to Nutrient Deficiency * Folate: found in leafy green veggies/liver;
destroyed by cooking; depleted within 4-5 months; more common to get through diet *
B12 (cobalamin): found in all animal products (strict vegans); depleted within 3-4
years; typically, this is due to pernicious anemia (anti-parietal antibodies) NOT
diet 4648: Ischemic Hepatic Injury (??Shock Liver??) * Presentation: any form of
shock (septic shock is most common) with rapidly developing AST/ALT elevations
(like in the 1000-2000 range!) and normal total bilirubin/alk.phos * Dx: clinical
syndrome o AcuteHepA/HepBwillquicklyelevateAST/ALT/Bili/Alk.phoso
Cholecystitis/HepatobiliaryobstructionwillelevateBili/Alk.phosmorethanALT/AST o
Other hepatic diseases may raise these levels, but not very high! * Tx: treat the
underlying cause of shock and typically liver enzymes will recover as well!
2627/2935: Hyperbilirubinemia * Unconjugated more elevated: hemolysis
(overproduction), reduced uptake into liver (portosystemic shunt or drug effect),
or conjugation defect (Gilbert??s syndrome or Crigler-Najar) * Conjugated more
elevated: o
AST/ALTelevated:liverdisease/damage(hemochromatosis,hepatitis,cirrhosis,etc)because
hepatocytes are damaged and releasing bilirubin into blod o
NormalAST/ALT/Alk.phos:bilirubinmetabolismdisorder(Dubin-JohnsonorRotorsyndromes)
bilirubin is built up and leaks into blood o
Alk.phoselevated:intrahepaticcholestasisorbiliaryobstruction(gallstones,malignant
obstruction, intrahepatic destruction, etc.) bilirubin is backed up and leaks into
blood Malignant Obstruction of the Hepatobiliary Tree * A classic reason to get
bilirubinemia, typically due to pancreatic adenocarcinoma/cholangiocarinoma *
Presentation: conjugated hyperbilirubinemia with predominantly elevated Alk.phos,
painless jaundice, and fatigue/weakness/weight loss * Dx: Abdominal ultrasound or
CT; retrograde CPG endoscopy if imaging is negative * Tx: Resection or
chemo/radiation therapy 2898/2950: Primary Biliary Cholangitis * Chronic liver
disease characterized by intrahepatic biliary duct destruction by anti-mitochondial
antibodies resulting in cholestasis * Presentation: fatigue, pruritus, jaundice,
hepatomegaly, steatorrhea, portal HTN, xanthalasma, and metabolic bone diseaseo
Labs:elevatedAlk.phos,hyperlipidemia,normalAST/ALTo Classically in middle-aged
women and associated with other autoimmune diseases * Dx: ultrasound to confirm
intrahepatic cholestasis ?? anti-mitochondrial antibodies are diagnostic o
Liverbiopsywouldshowductopenia * Tx: Ursodeoxycholic acid (delays histologic
progression via increased bile transit and possible anti- inflammatory effects o
Livertransplantistheultimatetreatment 4595: Irritable Bowel Syndrome (IBS) * Common
functional GI tract disorder with no identifiable cause. A diagnosis of exclusion *
Presentation: chronic, crampy abdominal pain with alternating episodes of
constipation and diarrhea. Passage of stool relieves the pain. o
Classicallyoccursinyoungwomeno Alarm signs (rectal bleed, severe pain, weight loss,
or abnormal labs) should be investigated further as they point toward something
else, NOT IBD * Dx: Rome III criteria o Recurrentabdominalpainsfor>3dayspermonth o
Twoofthefollowing: * ?? �Symptoms improve with bowel movement * ?? �Changes in
frequency of pooping * ?? �Changes in forms of poop (diarrhea/constipation) * Tx:
treat symptoms (diarrhea = anti-diarrheals; constipation = laxatives) 4612:
Multiple liver masses always suggests metastatic cancer to the liver thus certain
primaries should be ruled out: * 1. Colon cancer: the most common cancer to
metastasize to the liver and should be assessed WHENEVER metastatic liver cancer is
considered ?? colonoscopy * 2. Lung cancer: can metastasize to the liver, albeit
less frequently ?? CXR or CT chest * 3. Breast cancer can metastasize but less
frequently ?? CXR or CT chestNote that alpha-fetoprotein can be a useful marker,
suggesting primary hepatocellular carcinoma, however this is often a slow-growing
solitary liver mass, not multiple! 4919: Chronic Pancreatitis � Presentation: post-
prandial epigastric pain that radiates to the back, steatorrhea (loose, greasy,
smelly stools, hard to flush), fatigue/other constitutional symptomso
Alcoholabuse(mostcommon),cysticfibrosis,orautoimmune/hereditarydisorderareall
possible causeso May result in fat-soluble vitamin (AEDK) deficiencieso Steatorrhea
occurs with 90% loss of pancreatic function * Dx: altered pancreatic function tests
and fecal fat assays (Sudan Stain) * Tx: pancreatic enzyme replacementNote that
there are a LOT of things that can cause steatorrhea, but chronic pancreatic
insufficiency
is a big one 2966: Risk factors for Pancreatic Cancer * Hereditary risk factors:
familial pancreatic cancer, pancreatitis, or genetic disorders * Environmental risk
factors: smoking (#1), chronic pancreatitis, obesity, low-activity level 3732:
Porcelain Gallbladder * Characteristic pathologic deposition of Calcium salts
intra-luminally in the gallbladder; often occurs due to chronic
irritation/inflammation from gallstoneso Appearswitha??bluish??colorand??brittle??
consistencyongrossspecimen o Increased risk of gallbladder adenocarcinoma *
Presentation: RUQ pain with firm, non-tender RUQ masso CXR/CT: hyper-dense rim-like
calcification on the gallbladder * Dx: imaging studies with characteristic findings
* Tx: cholecystectomy (esp. if symptomatic) 4602: New-onset Ascites � � 3918: � �
3603: � � � 3695: � � Enlarged, fluid filled belly, most commonly due to liver
cirrhosis (viral, alcohol, heart failure, etc.) Dx: Paracentesis of fluid with
fluid-analysis AND liver biopsy if liver abnormalities present o
Bothneededtodeterminetheunderlyingcauseoftheasciteso
Majorconcernofabdominalcavityinfection(asceticfluidisessentialbacteriabroth!)
Assessment of a colon polyp (*high yield!) Three major types of colon polyps: o
Hyperplastic:mostcommonnon-neoplasticpolyp;noneedforfurtherworkupo
Hamartomatous:juvenile/Peutz-Jegherpolyps...typicallybenigno
Adenomatous:mostcommonoverallwithpotentialmalignancy??furtherworkup,butless than 1%
of these will actually be malignant!Adenomatous polyps MUST be further assessed as
this will determine its risk for malignancy: o
Morphology:sessile[moremalignant]orpedunculated[morebenign]o Histology: [more
benign] tubular < tubulovillous < villous [more malignant]o Size: [low risk of
invasion] (<1.5cm) < (1.5-2.5cm) < (>2.5cm) [high risk of invasion] Small
Intestinal Bacterial Overgrowth Presentation: persistent bloating, abdominal
discomfort, increased flatulence, watery diarrhea o
Noreliefofsymptomswithbowelmovemento
Possibleweightloss,anemia,nutritionaldeficienciesiflong-standingo
Occurssecondarytosomeotherdisease(changesinGIanatomy,GIsurgery,decreased motility,
or other problems altering the function of the GI tract) Dx: Endoscopy with jejunal
aspirate showing >105 organisms/mL in the gut o Glucose hydrogen breath testing can
be used as well, but less accurateTx: antibiotics (rifamixin), changes in diet,
avoidance of anti-motility agents (opioids), and trial of pro- motility agents
(metoclopramide) Risk factors of the two types of Esophageal Cancer:Squamous cell
carcinoma ?? caustic ingestion (chemicals, hot tea, smoking, alcohol, dietary
deficiencies, etc.) causing mucus producers to become squamous for protection from
ingestion Adenocarcinoma ?? caustic regurgitation (GERD, poor diet, etc.) causing
squamous epithelium to become columnar (mucus-producing) epithelium to protect
itself from stomach contents 4431: Note that the pain from VZV (shingles) re-
activation may precede the rash. Thus any patent with unilateral pain without other
evidence of injury/organ dysfunction should be considered for shingles. *
Classically it arises to bodily stress (infection, chemotherapy, immunosuppression)
but can arise spontaneously in some folks * Will be followed by dermatomal
vesicular rash and sometimes finishes with post-herpetic neuralgia 2213: Diffuse
Esophageal Spasm * Presentation: spontaneous pain/ painful swallowing with hot and
cold food. Does not get provoked by typical angina exacerbants. Relieved by
nitrates/Ca++ channel blockers * Dx: esophageal manometry shows repetitive, non-
peristaltic, high-amplitude contractions * Tx: nitrates/Ca++ channel blockers for
symptomatic treatment 3591: Gastrinoma (Zollinger-Ellison Syndrome) * Gastrin
secreting tumor ?? overwhelming stimulation of parietal cells to secrete
HCl/intrinsic factor * Presentation: dyspepsia, GERD, abdominal pain, weight loss,
diarrhea, frank GI bleeding o
Endoscopy:thickenedgastricfolds,multiplegastriculcers,duodenal/jejunalulcerswhichar
e refractory to PPI use o Oftensporadic(ages20-50)butcanbeassociatedwithMEN-
1syndrome o Mayresultinsteatosisduetoacidicinactivationofpancreaticenzymes� Dx: if
characteristic findings clinically/on upper endoscopy follow this testing algorithm
o Serumgastinlevel:check1weekafterstoppingPPI * ?? �<110 pg/mL = not gastrinoma
* ?? �110-1000 pg/mL = indeterminate, further studies are needed * ?? �>1000 pg/mL
= gastrinoma , confirm with stomach pH testing o
Secretinsecretiontest:atestforindeterminatelevelsofgastrin;secretininhibitsgastrin
producing G-cells, thus if gastrin levels drop, you don�t have a gastrinoma.
Gastinomas are stimulated by secretin, thus a rise means you have gastinoma. * ??
�Calcium infusion study: if a secretin test is negative but clinical suspicion is
still high, the calcium infusion that illicits a rise in serum gastrin points to
gastrinoma * ?? �Chromogranin A: a neuroendocrine tumor marker that??s elevated in
many situations but can be elevated in gastrinoma and helpful if clinical suspicion
is high o
StomachpHtesting:importantconfirmatorytestwithadiagnosticgastrinlevel.Gastrinmaybe
physiologically elevated due to achlorhydria (failure of HCl secretion). * ?? �pH<
4 = gastrinoma * ?? �ph > 4 = not gastrinoma � Tx: surgical resection 2969: Hepatic
Hydrothorax * Presentation: right-sided transudative pleural effusions that occur
in the setting of liver cirrhosis/portal hypertension. The effusion is ascetic
fluid leaking through small defects in the diaphragm * Dx: imaging that indicates
presence of effusion * Tx: o
Besttx:livertransplanttoresolvethecirrhosisandunderlyingproblemo
Typicaltx:therapeuticthoracentesis,salt-restricteddiet,anddiureticso
Refractorytx:transjugularintrahepaticportosystemicshunt(TIPS)toallowforportalsystem
drainage to systemic circuit, giving relief to the portal system; used if typical
Tx isn??t working 2901: Spontaneous Bacterial Peritonitis * Spontaneous growth of
bacteria in peritoneal fluid, typically from direct intestinal gut bacteria
translocation or hematogenous spread * Presentation: Temp >100F (cirrhotic patients
temp runs low), abdominal pain/tenderness, subtle altered mental status (Reitan
Trail Making Test is a classic for subtle mental status change), normal bowel
sounds, no nausea/vomiting o Severe disease = hypothermia, hypotension, and
paralytic ileus o Bugs=GNRs(E.coli,Klebsiella,etc.) * Dx: paracentesis and
examination of ascetic fluid (PMNs >250/mm3 or positive culture) * Tx: 3rd
generation cephalosporins (Tx); floroquinolones (prophylaxis) 2202: Treatment of
C.diff colitis * C.diff causes a diffuse, watery, smelly diarrhea, and unexplainted
WBC elevation; risk factors are recent antibiotic use, advanced age, or
hospitalization * Dx: stool antigen testing * Tx: o Mild-
moderate:WBCs<15,000andcreatinine<1.5xbaseline??oralmetronidazoleo
Severe:WBC>15,000,creatinine>1.5xbaseline,serumalbumin<2.5g/dL??oralvancomycin ??
If ileus is present ?? add oral metronidazole OR rectal vancomycino
Verysevere:severe+toxicmegacolon/severeileus??surgery(colectomyorboweldiversion)
2218: Treatment of Ascites * Ascites is important to treat as is can become
infected! It??s like broth of internal bacteria! * Treatment algorithm ?? advance
to the next level if ascites does not resolve! o 1. Salt/Water restriction (2L/day)
o 2. Add Diuretic therapy with spironolactone (or eplerenone)o
3.AddMoreaggressivediuretictherapywithLasix(furosemide,bumetanide,etc.),butnot more
than 1L/day for feat of hepato-renal syndromeo 4. Add Slow tapping of fluid (2-
4L/day) with/without albumin infusion with close monitoring of renal function;
should function decline, stop this 2943: Post-cholecystectomy syndrome�
Presentation: persistent pain/dyspepsia/nausea/vomiting/pruritis following
cholecystectomy o Canoccurimmediatelymonths,orevenyearspost-operativlyo Thepain??
neverwentaway??,??isnewaftersurgery??,or??hascomeback!??o
Causedbybiliary(retainedstone/sludge/etc,inflammation,dyskinesia)orextra-
biliary(PUD, pancreatitis, coronary artery disease, etc.) * Dx: imaging (endoscopic
ultrasound, endoscopic retrograde cholangiopancreaticography [ERCP], or MRI
cholangiopancreatography) to elucidate the underlying cause * Tx: directed at
underlying cause 2335/4360: Esophageal Perforation * Presentation: chest/abdominal
pain, systemic symptoms, subcutaneous emphysema of the neck which may feature
Hamman�s sign (crepitus upon palpation of the neck)o
Instrumentation(usuallyendoscopy)isthemostcommoncauseo
Boerhaavesyndrome,esophagitis,andesophagealulcerscanallcausethisaswell * Dx: Water-
soluble contrast esophagram is preferred (fast/minimal inflammation) o
Bariumswallowshowsthesamething(moresensitive/specific,BUTinflammationatsite)o
CXR/CTmaybeusefulifsevere,showingwidemediastinum,airinmediastinum/surrounding
tissue, or esophageal thickeningo Drainage of pleural fluid shows exudative yellow
fluid, low pH (acidic), high amylase content � Tx: emergent surgical repair with
subsequent supportive care 2933/2982/4434/2965/2929: Acute Pancreatitis�
Presentation: severe abdominal pain, nausea/vomiting, elevated serum lipase,
sometimes xanthomas o
Alcohol(40%),gallstones(40%),hypertriglyceridemia(classically>1000)arecommono
Drugs(azathioprine,valproicacid,thiazidediuretics),infections,oriatrogeniccauses(cl
assically cholesterol emboli from cardiac catheterization) can also be causes � Dx:
two of the following o Acute epigastric abdominal pain radiating to the backo
Increasedamylaseandlipasex3thenormallimit??typicallythefirststepinworkupo
Diffusepancreaticenlargementwithcontrastenhancement(CT)orhyperechoicity(ultrasound)
and sometimes with fat-stranding; Ultrasound is preferred in patients suspected
with gallstones as underlying cause (fat/40/fertile/female = gallstone)� Tx:
supportive
care (pain control/fluids) as most cases are self-limited (4-7 days) o If caused
by something that can be treated (drug, infection, etc) then treat thato
Ifgallstonessuspected/found,earlycholecystectomyshouldbedoneoncesymtpomsresolve
4603: Severe Acute Pancreatitis * Pancreatitis + evidence of organ failure due to
release of pancreatic enzymes into the vasculature. This causes increased vascular
permeability in/around the pancreas, causing shock! * Presentation: pancreatitis
symptoms with additional ones o
Organdysfunctionduetofluidoverload(dyspnea,tachypnea,abdominalditention,etc.) o
Cullensign:periumbilicalblue-ishcolorationindicatinghemoperitoneumo Grey-Turner
sign: red-brown coloration around the flanks indicating retroperitoneal bleed *
Risk factors: >75yrs, obesity, alcoholism, pulmonary infiltration on X-ray o
Labsat48hrs??CRP>150mg/dL,RisingBUNandCreatinine * Tx: aggressive IV fluid
resuscitation to replace lost volume 3833: Drug induced Acute Pancreatitis � Anti-
seizure (valproate), Diuretics (furosemide, HCTZ), Drugs for IBD (sulfasalazine, 5-
ASA), Immunosuppression agents (azathioprine), HIV-medications (didanosine,
pentamidine), Antibiotics (metronidazole, tetracyclines), and possibly many others!
4303: Elevated BUN:Creatinine ratio may be a sign of upper GI bleeding (abdominal
pain, hematemesis, melena) as the RBC proteins will be broken down increasing
intestinal urea production/absorption. If the kidneys are hypoperfused due to
bleeding, they may reabsorb more urea to increase blood volume. The increased
absorption in both the intestines/kidney raises the BUN increasing the
BUN:Creatinine ratio! 2582/4504: Colorectal Cancer (CRC) Screening in High Risk
Patients: * Family Hx of polyps or CRC: colonoscopy every 2-3 years starting 10
years before first familial diagnosis or age 40 (if the 10 years prior puts you
lower than age 40) * Inflammatory Bowel Disease (Crohn??s or UC): every 1-2 years
starting 8 years post-diagnosis o Canstart12-15yrpost-
diagnosisifdiseaserestrictedtoleftcolon * FAP: colonoscopy every year starting at
age 10 * Lynch syndrome (HNPCC): colonoscopy every 1-2 years starting age 20 3790:
Zinc Deficiency * Zinc typically found in meat, whole grains, beans, and nuts
(Absorbed primarily in the jejunum) * Risk factors: IBD (Crohn??s or UC) or TPN *
Presentation: alopecia, abnormal taste sensation, bullous/pustulous lesions
surrounding mouth/eyes/ extremities, and poor wound healing o
Growthretardationinchildren 3790: Selenium Deficiency * Selenium found in meat,
nuts, and fish * May result from chronic TPN * Presentation: cardiomyopathy 4433:
Biliary colic � Presentation: post-prandial RUQ pain, shoulder/subscapular pain
(referred pain), nausea/vomiting with resolution within 4-6hr after onseto Occurs
due to gallbladder contraction in response to fat in meal. Classically a gallstone
gets stuck in the cystic duct, causing the pain. Resolution is with gallbladder
relaxation. o NO fever, leukocytosis, or abdominal tenderness * Dx: ultrasound
showing gallstones with clinical presentation * Tx: symptomatic treatment or
cholecystectomy 4697: Retroperitoneal Hematoma should be considered for a patient
on Warfarin therapy with risk factors (diabetes, age >60, hypertension, alcoholism,
and supratherapeutic INR). Presents with back pain and isodense mass with organ
displacement on CT scan. 2905: Hepatitis Virus Infection * General symptoms:
Prodromal (fever, nausea, vomiting, anorexia, abdominal pain, and aversion to
smoking), icteric (yellowing of skin and eyes, hepatomegaly, elevated
AST/ALT/bili/Alk.phos, worsening prodromal symptoms), and convalescent (attenuation
and resolution of symptoms) o VirusSpecifics??referto??Hepatitisviruses??writeup *
Dx: clinical presentation and Hepatitis viral antigens * Tx: Depends on specific
virus 3605: Lactose intolerance� Presentation: bloating, cramping, flatulence,
diarrhea after eating lactose containing foods (dairy) due to a lack of lactase
(brush border gut enzyme)o Classically in people of Asian descent, although can
onset in anyone into adulthood o
Mayoccurafterinflammatoryboweldiseases(brushborderdamage)o
Rarely,canoccurwithgeneticlactasedeficiency � Dx:o Lactosehydrogenbreathtest??
ingestionoflactoseresultsinlittlegutabsorptionthus eventual fermentation in the
large intestine, causing H+ productiono Stoolexamination??
lowpH,stoolaniongap,presenceofreducingsubstances � Tx: avoidance of lactose or oral
ingestion of lactase 2203: Mallory-Weiss tear * Presentation: bright-red
hematemesis/epigastric pain following retching/vomiting spells o
Associatedwithalcoholismandhiatalhernia * Dx: endoscopy finding longitudinal tears
in the esophageal mucosa * Tx: often heals spontaneously (90%) although endoscopic
electrocoagulation or epinephrine injection can be used in persistent bleeds 4385:
Indications for RBC transfusion * Hb <7: always indicated * Hb <7-8: heart surgery,
heart failure, or cancer treatment patients * Hb 8-10: any surgery, acute coronary
syndrome, on-going bleeding, symptomatic anemia * Hb >10: rarely indicated 3593:
Factitious Diarrhea (Laxative Abuse) * Presentation: profuse/watery diarrhea,
painful abdominal cramps, 10-20 episodes each day with episodes at night; often
healthcare/upper SES person with multiple admissions for diarrhea * Dx: clinical
presentation and biopsy showing Melanosis Coli (dark brown discolored colon tissue
with pale patches of lymph follicles)o Classicallyoccurswithanthraquinone-
containinglaxative(Biscodyl) * Tx: stop laxative abuse, likely resolves within 4
months 2214/4188: Zenker�s Diverticulum * Abnormal outpouching of esophagus near
the cricopharyngeus muscle (upper esophagus) due to sphincter dysfunction or
esophageal dysmotility * Presentation: dysphagia, regurgitation, halitosis (pooling
of rotting food), sometimes palpable mass off the neck midline that varies in size
with eating/drinking, gurgling in the throato Elderlymenarethemostcommonpatiento
Heightenedriskofaspirationpneumoniaduetoregurgitationortrachealcompression * Dx:
contrast esophagram (barium swallow) is test of choice. Endoscopy could be used but
has much higher risk of complications, so it??s not preferred * Tx: Surgical repair
2914: Never forget [Alcohol + acetaminophen = NAPQI] ?? liver damage or acute liver
failure! 2917: There are MANY toxins that can cause liver failure, thought of as
two major damaging classes: * Direct toxic effects: dose dependent with short
latent periods ?? CCl4, acetaminophen, tetracycline, and the Amanitia phalloides
mushroom * Idiosyncratic reactions: not dose dependent with variable latent periods
?? isoniazid, chlorpromazine, halothane, and HAART drugs * Different histology can
clue you into the type of drug, but honestly you probably won??t remember this, so
don??t even try. However the 5 types are ?? cholestasis, fatty liver, hepatits,
fulminant liver failure, or granulomatous 2904: Acute Cholecystitis � Presentation:
RUQ pain after a fatty meal, referred pain to the shoulder, Murphey??s sign (halt
of inspiration with palpation under right ribcage), fever, nausea/vomiting,
leukocytosiso 90%arecausedbygallstoneimpactioninthecysticduct??
uncomplicated,causesmild elevations of LFTs/bilirubino
Ifgallstonegoesintothecommonbileduct??complicated,icterus&veryhighAlk.phos o
Gangrene,perforation,abscess,orperitonitismaybecomplications * Dx: presentation
with confirmatory imaging * Tx: Supportive care OR laparoscopic cholecystectomy if
complications arise 4386: Management of Bleeding Esophageal Varices * Presents as
hematemesis in the setting of liver disease (Hep C, alcohol, etc.) and portal HTN *
Dx: presentation and endoscopic visualization � Tx: o 1. IV volume resuscitation,
prophylactic antibiotics, and IV octreotide (causes splanchnic vasoconstriction due
to inhibition of vasodilatory substances) o
2.Urgentendoscopywithbandligationorscleropathytostopbleedingo Ifnofurtherbleeding??
B-blockerandremovalofendoscopicband1-2weekslatero Iffurtherbleeding??
repeatbandingorballoontamponadefollowedbyTIPSsurgerytorelieve porto-systemic HTN�
Note that platelet infusion is typically reserved for pts with platelets of <50,000
2921: Management of non-symptomatic Esophageal Varicies� Non-selective beta-
blockers (propranolol/nadolol/others) are recommended as the unopposed a-
adrenergic activity causes constriction of the splanchnic veins ?? shrinking of
varices/slowed progression and decreased risk of bleeding; Ligation of esophageal
varices is also a good option 2198: D-xylose test for Celiac??s Disease * Remember!
Celiac??s disease is an autoimmune disease (anti-gliadin antibodies) causing
atrophy of the small-intestinal brush border with gluten ingestion causing chronic
diarrhea, steatorrhea, and weight loss due to malabsorption * Dx: D-xylose test o
D-xyloseisasugarthatcanbeabsorbedinthesmallintestinewithoutdigestionandwilleasily
be filtered out by the kidney into the urine o Pt drinks 25g of D-xylose and
subsequently has blood/urine sampled to check for levels of D- xylose in each * ??
�Normal or malabsorption from enzyme deficiency = normal D-xylose * ?? �Celiac??s
disease = low D-xylose due to damaged intestinal wall � Tx: avoidance of gluten
containing foods 3585: Diagnosis of Pancreatic Adenocarcinoma * Common symptoms:
Weight loss, gnawing abdominal pain that radiates to the back, worsens with eating,
laying down, or at night * Pancreatic Head symptoms: jaundice and steatorrhea
(obstruction of hepatobiliary secretion) o Abdominal ultrasound is the preferred
technique for diagnosis * Pancreatic Body/Tail symptoms: NO JAUNDICEo Abdominal CT
is preferred technique for diagnosis 3087: Pellagra (??rough skin?? in Italian) *
Lack of niacin or tryptophan (made into niacin) classically in: o People with
primarily
corn in the diet (niacin present, but in a bound, unabsorbable form) o
Impairednutritionalintake(alcoholism,chronicillness,etc.)o Carcinoid syndrome
(tryptophan shunted to make 5-HT and depleted)o
Hartnupdisease(congenitalinabilitytoabsorbsomeAAs,includingtryptophan) o
ProlongedIsoniazidtherapy(interfereswithtryptophanmetabolism) * Presentation: the 3
Ds o Dementia:confusion,memoryloss,psychosiso
Diarrhea:waterywithabdominalpain,nausea,andlackofappetiteo
Dermatitis:sunexposedareasofskinbecomescaly,rough,andhyperpigmented * Dx: clinical
presentation with Hx of niacin/tryptophan depleting situation * Tx: supplement
niacin/tryptophan or treat underlying cause 2212: Dysphagia * Two major types:
Oropharyngeal and Esophageal * Oropharyngeal dysphagia: difficulty in initiating
swallowing, often causing choking, coughing, nasal regurgitation, and aspirationo
Duetosomeweaknessinoropharynx??stroke,dementia,malignancy,muscularproblem,etc. o
Aspiration pneumonia and weight loss are common complicationso Dx: videofloroscopic
modified barium study (can watch the oropharynx in action) * Esophageal dysphagia:
difficulty in peristalsis/passing food down the esophaguso Solids&liquidsatonset??
peristalticdysmotility??bariumswallowwithmanometry o Solidsthenliquids??
mechanicalobstruction?? * ?? �Possible cancer/stricture risk = barium swallow
first, then endoscopy if necessary * ?? �No reason for mechanical obstruction =
upper endoscopy * Dx/Tx based on underlying etiology 2897: Pancreatic Pseudocyst �
Presentation: palpable mass in epigastrum following acute pancreatitis or in
chronic pancreatitis, often with pain radiating to the backo ??Cyst?? actually
lacks a proper epithelium and is covered by a thick, fibrous capsuleo
Filledwithfluid/tissue/debristhatcontainshighlevelsofpancreaticamylase/lipase,thusi
tcan leak into the circulation causing elevation of pancreatic enzymeso If cyst
erodes into a blood vessel, hemorrhage into pseudocyst may occur as an acute
complication, requiring immediate surgical attention * Dx: presentation with
ultrasound visualization * Tx: often symptomatic as cyst will resolve itself o
Drainageindicatedif:persistencefor>6wk,size>5cm,orsecondaryinfection2926: Remember!
If a person is positive for Anti-HBs AND Anti-HBe in a hepatitis B screening,
they??ve been infected but resolved it! The vaccine only contains the surface
antigen, thus vaccinated folks are only anti-HBs positive. If a person had Anti-
HBs/HBc/HBe then they??re recovering from a recent infection! 3581: Tropical Sprue
* Essentially Celiac??s disease presentation but sub-acute onset after a trip for
>1 month to a tropical endemic area (Puerto Rico, Bahamas, etc.) * Presentation:
malabsorbtion (fatty stools, borborygmi, hyperactive bowel sounds, glossitis,
cheilosis, pallor, edema, diarrhea, gas, cramps, fatigue, progressive weight loss)o
ClassicallythiscausesB12/folatemalabsorption??megaloblasticanemia * Dx: Hx and
small intestinal biopsy (villous blunting, lymphocytes, eosinophils, plasma cells)
* Tx: leave the tropical area, should resolve with symptomatic treatment 2773/3602:
Celiac�s Disease (sprue) � Presentation: long-standing bulky/foul/floating
diarrhea, loss of muscle mass/fat, fatigue, and malabsorbtion (may cause specific
symptoms based on what isn??t being absorbed properly)o
DermatitisHerpeteformis�itchy,smallvesicularrashappearingonknees,elbows,forearms,
and buttockso Irondeficiencyanemia�duetopoorintestinalabsorbtiono
Shortstature/weightloss�mayspecificallyoccurinchildren/infantso
Otherautoimmunediseases:thesediseasestendtoruninpacks,andifyouhaveoneyou??re more
likely to have another! * Pathophysiology: Autoimmune disease causing small bowel
destruction in response to gluten ingestion o Anti-gliadin/Anti-
tissuetransglutaminase/Anti-endomysialIgAorIgGantibodies * Dx: IgA serologic
testing, select antibody testing, or intestinal biopsy (villous blunting, chronic
inflammatory cells) o Selective IgA deficiency may actually mask the Anti-IgA
antibodies, this is suspicion is high, but IgA is negative ?? check total IgA for
deficiency and check Anti-IgG antibodies o
Confirmedwithresolutionofsymtpomswithglutenfreediet � Tx: gluten free diet 2581:
Note that IBD (Crohn??s or UC) have a bimodal distribution (20s-30s and 60s) and
both commonly present with neutrophilic crypt abscesses, making the two diseases
hard to distinguish at times. The classic discerning factor is depth of
inflammation; Crohn??s = transmural and UC = mucosal only 4086: Diverticulosis *
Outpouchings of the colon due to weakened areas encountering pressure, thus bulging
out. They??re typically asymptomatic and increase incidence with age, but can cause
complications.o Associated with constipation and oddly enough, may worsen existing
constipation! * Complications: diverticular hemorrhage, diverticulitis,
perforation, abscess formationo
Adequatefruit/vegetablefiberinthedietandphysicalactivitylowerriskofcomplications o
Meat,aspirin/NSAIDs,obesity,andsmokingincreaseriskofcomplications * While these
often pose no problem, it??s important to take steps to limit the risk of
complication in those with diverticulitis with lifestyle changes 2204/3182: Acute
Diverticulitis * Presentation: LLQ abdominal pain, fever, nausea, vomiting,
ileus/urinary urgency and frequency (due to peritoneal irritation in sigmoid colon
affecting the bladder) o Labs:leukocytosis, o
Mayresultinobstruction,fistula,perforation,orabcessformation * Dx: Abdominal CT
w/oral & IV contrast (pericolic fat inflammation, diverticula, bowel wall
thickening, soft tissue masses, abscesses) o Sigmoid/colonoscopy are
contraindicated due to concern of perforation * Tx: o
Uncomplicated:hospitalization,bowelrest,IVAbx,closewatcho Complicated (abscess,
perforation, obstruction, or fistula: treatment based on severity * ?? �Abscess
<3cm diameter � IV abx, bowel rest, close observation * ?? �Abscess >3cm diameter �
CT-guided percutaneous drainage * ?? �Free fluids/feces or failure to improve by
day 5 � surgical drainage, washout, and debridement with possible bowel resection *
d �Pts who cannot tolerate surgery should be treated as ??uncomplicated??
2625/2220: Carcinoid Syndrome � Neuroendocrine tumor of 5-HT (serotonin),
histamine, and vasoactive peptide producing cells o
Primarytumorarisesinsmallintestine,distalcolon,orlung??livermetastasesarecommon! o
Asymptomaticuntilmetastasistotheliver,astheliverwillmetabolizetheneuropeptides,
stopping them from entering circulation. However, within the liver, these cells can
dump the neuropeptides into the body! * Presentation: Episodic
flushing/tachycardia/hypotension, abdominal cramping/diarrhea, telangiectasia,
bronchospasm, and tricuspid regurgitation (neuropeptides blasting against valve ??
damage) with plaque-like fibrous tissue in right side of heart o
Pellagra(niacindeficiency)mayoccurduetotryptophanbeingusedtomake5-HT,depleting the
body??s ability to generate niacin! * Dx: presentation with elevated 24-hr urine 5-
hydroxyindoleacetic acid (5-HIAA), a metabolite of 5-HT o CT/MRI of abdomen for
localization of tumoro Echocardiography if signs of carcinoid heart are present *
Tx: Octreotide pre-treatment for surgery to remove tumors 2948: Stages/Precipitants
of Hepatic Encephalopathy * Hepatic Encephalopathy can be caused by TONS of things
(sedatives, narcotics, hypovolemia, GI bleeding, high-protein diet,
hypokalemia/metabolic acidosis, hypoxia, hypoglycemia, infection, porto- systemic
shunting, and many more!) * The severity is broken down into stages: o
Stage1:hypersomnia/insomnia/invertedsleepcycle,mildconfusion,tremor,asterixiso
Stage2:lethargy/responseslowing,mod.confusion,finemotordysfunction,slurredspeech o
Stage3:severeconfusion,somnolentbutarousableo Stage4:stupor/coma 4321: Non-
alcoholic Fatty Liver Disease � Presentation: wide-ranging symptoms (isolated
steatosis ?? liver cirrhosis/fibrosis) of damage caused by increased Free Fatty
Acids (FFAs) in the liver (cause oxidation/TNF-a damage to hepatocytes) o
Typically,patientshavemetabolicsyndrome(centralobesity,diabetesmellitus,
hyperlipidemia, and hypertension) and no history of alcohol abuse o
Histologically,theliverappearsthesameasalcoholicliverdamage(microvesicularfatty
steatosis with peripheral displacement of hepatic nuclei) * Dx: rule out other
causes of hepatic damage with supporting biopsy * Tx: diet and exercise; if BMI >35
consider bariatric surgery 4624: Vanishing bile duct syndrome is a funky disease of
unknown pathophysiology where the intra-hepatic bile ducts are progressively
destroyed, manifesting in the disease. It??s very much like primary biliary
cirrhosis which causes similar ductopenia through anti-mitochondrial antibodies.
2209: Pancreatic Cancer * Can occur in the head or the body/tail of the pancreas
causing different symptoms! * Head: painless jaundice, ??double duct?? sign,
Courvorsier sign (non-tender, distended gallbladder at right costal margin),
jaundice/pruritis/pale stools/dark urine * Body/Tail: abdominal pain WITHOUT
jaundice/obstruction 2341: Diverticulosis � Presentation: painless, gross rectal
bleeding (much more than just spots on the toilet paper) o
Largevolumemaybeassociatedwithlightheadedness/hemodynamicinstabilityo While
diverticula are classically in the sigmoid colon, diverticular bleeding is more
common in the right colon, causing dark hematochezia * Dx: Colonscopy showing
source of bleed * Tx: Often resolves spontaneously, but may require endoscopic
surgical intervention 2199: Evaluation of Dysphagia to solids and liquids * This
type of dysphagia will be solids and liquids at onset and often shows smooth
tapering down to a smaller point where the blockage is happening. It??s caused by
either achalasia or pseudoachalasia. o
Achalasia�taperingduetoesophagealcontractionwithoutrelaxation
* ?? �Slower onset of symptoms (>5 years until seeking help is average) * ??
�Upper endoscopy shows normal mucosae with smooth taper in diameter with relatively
easy passage of the scope through the contracted sphincter o
Pseudoachalasia�taperingduetoesophagealcancer * ?? �Hx of tobacco/alcohol use;
significant recent weight loss (<6 months); presentation >60yrs, rapid onset of
symptoms * ?? �Upper endoscopy shows malignant growth and often endoscope cannot be
passed through the narrowed portion * Dx: Upper endoscopy confirms etiology of
dysphagia * Tx: Depends on etiology 4626: All patients with chronic liver disease
(viral or otherwise) should be checked for immunity for HepA and HepB. If they are
not already immune, they should be vaccinated as acute-on-chronic liver disease can
cause a huge amount of damage to the liver! * Prednisone can be used to treat
severe alcoholic hepatitis * Lamivudine (3TC) � reverse transcriptase inhibitor;
can be used in HIV or HepB treatment4747: Ascites fluid is an important substance
to analyze in patients with liver failure, thus we??ll talk about it??s
characteristics below. � Color: gives an idea of substances present in the fluid
and etiology o Bloody�trauma,malignancy,TB(rare!)o
Milky�fatty,duetoobstructionoflymphaticvesselso Turbid�possiblyinfectedfluido
Strawcolored�atransudatethat??slikelyduetobenigncauses(increasedpressureinveins) *
Neutrophils: helps indicate/rule out possible infection (peritonitis)o
<250�noperitonitispresento
>250�possibleperitonitis(secondaryorspontaneousbacterialinfection) * Total Protein:
helps establish etiologyo High(>2.5g/dL)�increasedpressure(CHF,Budd-
chiari,etc.)orlunginfections(TB,fungal,etc) o Low (<2.5g/dL) � loss of osmotic
pressure b/c of protein loss (cirrhosis, nephrotic syndrome) * Serum to Albumin
Ascites Gradient (SAAG): differentiates portal from non-portal HTN etiologies o
Calculatedvia:[SerumAlbumin�Peritonealalbumin=SAAG]o Portal(>1.1g/dL):heart-
relatedascites,Budd-chiari,livercirrhosiso
Systemic(<1.1g/dL):TB,pancreaticascites,nephroticsyndrome 3587/3520/2630/3494:
Multiple Endocrine Neoplasia (MEN) � MEN1: o
PrimaryHyperparathyroidism(hypercalcemia,highurinecalcium,highPTH)o
Enteropancreatic tumors (most commonly gastrinoma causing Zollinger-Ellison
syndrome; VIPoma, glucagonoma, and insulinoma all possible)o Pituitary adenomas
(most commonly prolactin secreting) * MEN2a: RET-protooncogene mutationo Medullary
Thyroid Cancer (parafollicular C-cells, produce calcitonin)o Pheochromocytoma
(elevated plasma metanephrines, episodic hypertensive crises), o
ParathyroidHyperplasia * MEN2b: RET-protooncogene mutationo MedullaryThyroidCancero
Pheochromocytomao Mucosal/cutaneousneuromas,Marfanoidhabitus 3178/4462/12142:
Perforated Peptic Ulcer Disease * Presentation: chronic epigastric pain that
suddenly worsens, with rebound tenderness/guarding (peritonitis due to gastric
contents in peritoneal cavity), air under the diaphragm on CXR * Pathophysiology:
chronic NSAID use, Hx of PUD, H.pylori infection, head trauma/severe burns can all
presipose to generating a peptic ulcer * Dx: immediate upright CXR, as diagnosis
and prompt treatment (<12hr) is critical to limit mortality * Tx: immediate
surgical repair via open laparotomy 2900: Acute Liver Failure � Presentation:
nonspecific symptoms (fatigue, anorexia, nausea, etc.), RUQ pain, jaundice,
pruritus, and sometimes hepatic encephalopathy as failure worsens. Labs include:o
^PT/INR(failuretolivertomakecoagulationproteins)o
AST/ALTx10normalwithincreasedbilirubino Progression may show AST/ALT trending down
(liver death is bad that these are being released less and less) and increasing
PT/INR/bilirubin (further loss of liver function; PT is the single most prognostic
factor in Acute Liver Failure) * Dx: clinical presentation with lab values; must
search for underlying cause * Tx: stabilize pt and treat underlying cause once
identified 2930: Gallstone Management * Gallstones without symptoms ?? no treatment
necessary, simply monitor * Gallstones with biliary colic ?? elective laparoscopic
cholecystectomy or ursodeoxycholic acid * Complicated gallstones (acute
cholecystitis, choledocolithiasis, or gallstone pancreatits) ?? cholecystectomy
within 72 hrs (lower rates of complication compared to delayed 7 days) 3467:
Colovesical Fistula * Fistula connecting the colon to the bladder o Caused by:
Diverticular disease (most common, outpouching fuse to bladder), Crohn�s Disease
(full thickness lesions cause inflammation/connection to bladder), Malignancy
(disordered growth bridges to the bladder) * Presentation: Recurrent mixed flora
UTIs, fecaluria (poop out the pee hole), pneumaturia (air in the urine, often
toward the end of the stream) * Dx: abdominal CT with rectal and vesicular contrast
+ colonoscopy (rule out malignancy) * Tx: surgical treatment with treatment of
underlying cause 4362: Chronic Pancreatitis * Etiology: alcoholism (most common
adults), cystic fibrosis (most common kids), duct obstruction (malignancy or
stones), autoimmune * Presentation: chronic epigastric pain radiating to the back,
improved with leaning forward/sitting up (intermittent remission/relapses),
malabsorption (steatorrhea, AEDK deficiency, weight loss), diabetes o
Amylase/lipase may be normal or decreased (??burnt out pancreas)o
CT/MRCPshowingpancreaticcalcifications,dilateducts,enlargedpancreas * Dx: clinical
presentation with radiographic evidence (calcifications are the best thing to see)
* Tx: pain management, alcohol/smoking cessation, frequent small meals, pancreatic
enzyme supplementation during meals 2977: When assessing jaundice, positive urine
bilirubin means conjugated (direct) bilirubinemia * This makes sense, as only
conjugated bilirubin is made to be water soluble, unconjugated (indirect) bilirubin
is inherently not water soluble, thus it cannot be filtered by the kidney into the
urine. * However, a positive urine urobilinogen indicates unconjugated (indirect)
bilirubinemia, as the huge amount of unconjugated bilirubin goes through it??s
normal metabolism in the large intestine, a large amount of urobilinogen (a normal
by-product) will be made. This is NOT the case in a direct bilirubin, as a direct
bilirubinemia is caused by some obstructive process, and it would never make it to
the large intestine to become urobilinogen! 4813: Some Mechanisms for Gallstone
Formation * Total Parenteral Nutrition � without protein/nutrients entering the
duodenum, secretin (which could cause gallbladder contraction) is not released and
gallbladder stasis can result in it??s contents to coalesce into stones! *
Pregnancy/OCPs � estrogen increases cholesterol secretion into the biliary system
and progesterone slows gallbladder emptying. Thus, these two together can cause
cholesterol super-saturation and stasis, resulting in cholesterol stones! *
Partial/Full Bowel resection � results in a decreased ability to absorb/recycle
bile acids. This can occur to a point where the cholesterol:bile acid ratio
increases to the point of cholesterol super-saturation! � Hemolytic anemia � the
huge amount of heme released from massive RBC destruction results in huge amount of
bilirubin to be conjugated in the liver and sent into the bile (heme ?? bilirubin).
Thus bilirubin can become super saturated causing pigmented gallstones. 2907: The
most common causes of liver cirrhosis in the USA are Alcoholism, Hepatitis viruses
(C more than B), and Non-Alcoholic Fatty Liver Disease (NAFLD). But there are a
HUGE amount of reasons why a person may get liver cirrhosis, thus the most common
should be sought out first: � History/physical ?? family history ?? alcohol history
?? HepB/C titers ?? iron studies/HFE protein analysis ?? must make further, rare
inquiries at this point, as commoners are ruled out! 2899: Remember! Hyper-
estrogenism can result from liver cirrhosis, as estrogen is normally broken down in
the liver. Because of cirrhosis, this metabolism is disrupted, resulting in two
major types of effects: * Vasodilitation/angiogenesis ?? spider angiomas & palmar
erythema * Effects on sexual organs ?? gynecomastia, testicular atrophy, decreased
male body hair 2369: Instrumentation of the esophagus is the most common cause of
esophageal perforation. However, other things like Borhaave syndrome can result in
esophageal perforation. The classic thing to look for is air/crepitus in the
mediastinum/neck, as that will clue you into a perforation. Put it together with
the clinical picture to make you diagnosis. 4934: Pill-esophagitis * A classic
problem a persons taking many medications, as damage is the result of direct
effects on the mucosa. It often occurs with certain meds:o
Tetracyclines,alendronate,risendronate,iron(acidicerosion) o
Aspirin,NSAIDs(disruptionofmuscosalbarrier)o Potassium chloride (osmotic damage) *
Presentation: sudden onset painful swallowing/retrosternal pain in the mid-
esophagus (compressed by the aortic arch/left atrium) classically in a person
without esophageal disease * Dx: endoscopic visualization of discrete mucosal
injuries with normal surrounding tissue * Tx: stop offending medication, healing
should occur with time o
Ptsareadvisedtosituprightfor30minutesANDtakepillwithafullglassofwaterin medications
known for this effect 2210: Dr. Jones??s words echoed in Mike??s head, ??An old
person with iron deficiency anemia, especially a man, has a GI bleed until proven
otherwise.?? * The first step is a fecal occult blood test ?? if positive, then
it??ll guide further investigation, but if negative it means NOTHING! * If you have
this clinical scenario and you get a negative FOBT, you then get
endoscopy/colonoscopy on the patient for concern of GI malignancy Note that
radioisotope erythrocyte scintigraphy is only useful in active,
significant bleeding. If it??s a slow or non-active bleed, that test won??t tell
you shit. 2895: Hepatolenticular degeneration (Wilson??s Disease) � Autosomal
recessive disease of copper over-accumulation in the liver and deposition into
various tissues. Initial accumulation is in the liver, which builds up and spills
into the surrounding tissues. o Copper=pro-oxidant??
oxygenfreeradicalformationindepositedtissueso ??Hepato?? (liver) ??lenticular??
(basal ganglia) degeneration * Presentation: a wacky disease that presents with
liver damage (asymptomatic to fulminant hepatitis), neuropsychiatric disease
(Parkinsonism is classic, but personality changes, paranoia, catatonia and much
more are possible), Kayser-Fleicher rings (grey-green corneal rings) o Typically in
younger pts (5-40 years) o
FanconisyndromeandhemolyticanemiaareassociatedwithWilson??sDisease * Dx: o
Typical:lowceruloplasmin(<20mg/dL)+urinarycopperexcretionORKayser-Fleischerrings o
Gold-standard:dryweighthepaticcopperlevelof250mcg/dL * Tx: Decrease copper levels
(d-penicillimine, trientine, oral zinc supplementation), or complete resolution
with liver transplantation 3834/2205: Toxic Megacolon * Presentation: non-
obstructive colon dilatation, severe bloody diarrhea, systemic symptoms (fever,
tachycardia, etc.)o
Causedbyahugenumberofthings:IBD/IBSareclassic,buttherearetonsofreasons * Dx: Plain
abdominal X-ray (colon >6cm, air-fluid levels, thick haustra markings) + 3 of the
following: o Fever(>100.4),pulse>120bpm,WBCs>10,500,oranemia * Tx: IV antibiotics,
IV fluids, bowel rest + IV corticosteroids if caused by IBDo If episode does not
resolve with these, subtotal colectomy surgery is required! 2975: When presented
with a jaundice/direct bilirubinemia, the FIRST thing to do is assess the bile duct
width with RUQ ultrasonography. A dilated biliary tree >3cm suggests extrahepatic
obstructive process. A non-dilated biliary tree (<3cm) suggests an intrahepatic
obstructive process. � ERCP is often performed when dilation >3cm is found as you
must figure out exactly where the obstruction is occurring to uncover etiology
2951/2932: There are really 3 major tumors that happen in the liver. All you need
to do is remember come classic scenarios about them and you should be able to nail
it: * Metastases to the liver: most common by a LONG shot (colonic/lung are
classics). Basically if you find a single OR multiple liver masses, it: s
metastatic until proven otherwise * Hepatic adenoma: the most common benign mass.
Typically occurs in women on OCPs and are not a huge deal. CAN turn malignant or
have hemorrhage into it, thus these must be watched. Are well- demarcated and
hypereichoic on ultrasound * Hepatocellular carcinoma: not very common, but often
occurs in the setting of some chronic liver disease (hepatitis, alcoholism, etc).
Elevated a-fetoprotein is a huge sign of this cancer, thus be acutely aware of it.
4694: Don??t doubt yourself! [Symmetric Esophageal narrowing and dysphagia in the
setting of chronic GERD] is esophageal stricture formation!! Typically this causes
a progressive dysphagia from solids??liquids. � Dx: endoscopy with biopsy (rule out
adenocarcinoma) � Tx: o Ifnomalignancy??esophagealdilatationviaendoscopyo
Ifmalignancy??surgical/chemotherapeutictreatmentstoresolvecancer 2910: Non-
alcoholic Fatty Liver Disease (NAFLD) * Hepatic steatosis occurring WITHOUT alcohol
abuse. Typically occurs in obese patients * Presentation: hepatomegaly, mildly
elevated AST:ALT with ratio <1, * Dx: fatty deposition on imaging/ultrasound/labs
confirmed with liver biopsy * Tx: weight loss/metabolic risk factor control or
bariatric surgery if BMI>35 o Note that statins are considered safe in this disease
2166: The abdominal succession splash (??splashing?? sound heard with belly
auscultation and rocking patient back and forth at the hips) is a physical exam
sign of gastric outlet obstruction. * Gastric contents retained for >3 hours will
make this ??splash?? * Warrants further investigation into suspected gastric outlet
obstruction * Initial workup: nasogastric suction, IV hydration, endoscopy for
definitive diagnosis 3857: Workup of ??Bright Red Blood per Rectum?? � Age <40 Ag
anoscopy (basically a scope of the anus) o
Typicallyyieldshemorrhoids,whichwilloftenresolvewithsymptomatictreatmentorminor
surgery to remove them o If no source sound, do a sigmoid or colonoscopy * Age 40-
49 without red flag signs ?? sigmoidoscopy/colonoscopy * Age >50 or red flags??
colonoscopy * Red flags include: recent bowel habit changes, abdominal pain, weight
loss, anemia, or family history of colon cancer 4085: Angiodysplasia * Dilated
submucosal veins/AVMs commonly occurring in the right colon in people >60yrs old *
Presentation: painless GI bleeding classically presenting with specific co-morbid
conditions: o
Advancedrenaldisease/vonWillendbranddisease�possilbleassociationduetobleeding
tendencies that occur with these diseases o
Aorticstenosis�thoughttobeduetoacquiredvWFdeficiencyfromvWFpeptidesbeing damaged as
the cross the stenotic valve turbulence. The angiodysplasia is actually been shown
to remit with aortic valve replacement * Dx: endoscopy with clean bowel prep.
Because the dilatations may be subtle, they can be easily missed thus a clean bowel
prep is essential to give the best possible chance of visualization. o Note that
other forms of GI bleeding are unlikely to be missed on endoscopy. This is one of
the few situation where bleeding can be very subtle. * Tx: cautery/treatment of
classic underlying associated conditions 3582: Whipple�s Disease (T.whippelii
infection) � Rare multisystemic disease in white men between 40-60 most commonly �
Presentation: o GI:weightloss,abdominalpain,distention,flatulence,steatorrheao
Organsystems:valvulardamage(CHF/regurgitation/chroniccough),migratorypolyarthralgia
o Neurologic (late): dementia, supranuclear opthalmoplegia, myoclonus * Dx: PAS(+)
foamy macrophages in the lamina propria of the small intestine on biopsy * Tx:
antiobiotcs (typically TMP-SMX [Bactrim]) 2950: Elevated Alkaline Phosphatase level
* Remember that Alk.Phos can be elevated from bone, liver, intestinal, or placental
tissue breakdown and we cannot simply see an elevated alk.phos as a sign of liver
damage * When we see elevated alk.phos o CheckGGT??elevated=biliaryorigin|
normal=likelyboneorigin o ^Alk.phos&^GGT??
RUQultrasound(checkbileductdilatation)&anti-mitochondrial antibodies (checking for
primary biliary cirrhosis) * ?? �Bile duct dilatation/AMA normal ?? ERCP to assess
biliary tree * ?? �AMA(+) or abnormal tissue findings ?? liver biopsy * ?? �Both
normal ?? liver biopsy 2920: Primary Sclerosing Cholangitis * Unknown etiology;
inflammation/fibrosis/stricture of the intra/extrahepatic bile ducts o Associated
with IBD (Crohn??s or UC) in 90% of cases * Presentation: typically, asymptomatic
with unexplained LFTs/lab values. Sometimes fatigue and pruritis can occur, but not
classically o
Labs:CholestaticpatternLFTs(ASTandALTelevatedbut<300;severelyelevatedAlk.phosand
bilirubin), hypergammaglobulinemia, elevated IgM, pANCA(+) � Dx: o Ultrasound??
unremarkableandnon-diagnostico Cholangiogram??multifolcalnarrowing/??beading??
ofintra/extrahepaticbileductso Liverbiopsy??ductobliterationwith??onion-skinning??
oflymphaticvessels.Confirmatoryfor diagnosis most times� Tx: liver transplant
within 12 years of diagnosis 4547: Remember that in pts with chronic HepC
infection, titers of HepB/HepA antibodies should be taken and if patient is not
immune, they should be immunized to present acute progression of chronic hepatitis.
2200: Endoscopy??s role in Evaluation of GERD * Basically a person with GERD isn??t
too much of a worry as long as they??re doing OK. However there are certain
situations where further investigation is required * Let??s say you have a patient
with GERD, if: o
Male>50,symptoms>5yrs,cancerrisk(smoking,alcoholism,etc.),alarmsymptomspresent
(dysphagia, odynophagia, weight loss, anemia, GI bleeding, recurrent vomiting) ??
endoscopy o Theydon??thaveanyoftheabovecharacteristics/symptoms??PPItrial2months
* ?? �If symptoms are well controlled ?? stay on that PPI * ?? �If symptoms are
refractory ?? consider switching PPI or increasing dose � If symptoms STILL
refractory ?? endoscopy 2978: Acute Cholangitis * Biliary stasis due to any number
of reasons (commonly gallstone obstruction, malignancy, bile duct stenosis) but all
of them cause backup. The fear is that disruption of the blood-bile barrier could
allow for dissemination of bacteria/toxins * Presentation: [fever, jaundice, RUQ
pain], [confusion, hypotension] (Charcot triad, Reynold??s pentad) o
Labs:neutrophilia,elevatedalk.phos/GGT/AST/ALT/directbilirubin * Dx:
presentation/labs with biliary dilatation (ultrasound FIRST, then CT if not
diagnostic) * Tx: [ERCP with sphincterotomy or percutaneous transhepatic
cholangiography] +[ broad spectrum antibiotics] 4903/2207: Crohn??s Disease can
present with apthous ulcers (small, grey erosions in the oral mucosa) that may show
granulomas if biopsied (30%). These two questions really highlighted the fact that
Crohn�s disease can affect ANY part of the GI tract, from [mouth ?? anus] � Another
fantastic sign that an oral ulcer is due to Crohn??s disease would be signs of
chronic inflammation (^CRP, anemia of chronic disease, or reactive thrombocytosis
>400,000) 2911/4278: Alcoholic Hepatitis� Presentation: signs of hepatitis
(jaundice, RUQ pain, ascites, etc.) and sometimes cirrhosis with history of alcohol
abuse and characteristic labso
Labs:elevatedAST:ALT(2:1,but<300),elevatedGGT/bilirubin/INR/ferritin(acutephase
reactant), neutrophil leukocytosiso Note that AST:ALT ratio is thought to be due to
alcohol depletion of pyridoxyl-5-phosphate, a cofactor needed for ALTo
MayhaveelevatedMCVduetochronicmalnutrition(folateorB12depletion) * Dx: history +
clinical presentation + labso Imaging/biopsy will show fatty liver * Tx:
abstinence/supportive care3926: Although weird, some older patients may have an ??
idiopathic anemia of the elderly??. Classically these patients have multiple
comorbidities (CHF, etc.) that make them poorly tolerant to anemia 11607:
Interestingly prolonged PPI use or H2-blocker use is associated with C.diff
infection. The patient will have a classic presentation (profuse watery diarrhea,
sometimes with occult blood, abdominal pain, low-grade fever) and must be confirmed
with a PCR C.diff Exotoxin A or B assay. � Note prolonged PPI use associated with
decreased Ca2+ absorption and increased bacterial colonization of the upper GI
tract (increased pneumonia risk) 2149: Chronic Mesenteric Ischemia * Impaired blood
flow to the bowel, typically caused by atherosclerosis (smoking/dyslipidemia are
great signs to look for in assessment) * Presentation: intestinal angina (crampy,
post-prandial epigastric pain) leading to food aversion/weight loss. Early satiety,
nausea, and diarrhea all can occur too. o Typically occurs in the celiac or SMA
arterieso Occurs due to shunting of blood away from intestines during eating so it
can go to the stomach. Because the bloodflow is already decreased from narrowing,
there??s REALLY going to be decreased flow and the tissue becomes ischemic and
painfulo Abdominal bruits (50%) and signs of malnutrition are classic signs * Dx:
clinical picture and CT angiography demonstrating stenosiso CT or X-ray may show
vascular calcifications in atherosclerotic plaques BUT are unremarkable for the
most part (helpful for ruling out other diseases) * Tx: risk reduction, nutritional
support, and revascularization surgery Respiratory and Critical Care Medicine 4718:
Oxygen Induced CO2 retention in COPD * In a severe chronic COPD-er, their body is
accustomed to a state of hypoxia, which can be concerning for hospital folks
monitoring their O2 levels. However, rapid resolution of low O2 levels though
oxygen supplementation can result in acute CO2 retention through 3 mechanisms o
V/Qmismatch�normally,COPDcausesVQmismatchthroughalveolardestruction.However, this
is offset through selective vasoconstriction in the lung to only perfuse well
ventilated areas. With the addition of O2, even poorly ventilated areas have
acceptable O2 levels for the body, thus selective vasoconstriction does not occur
AND V/Q mismatch worsens. o
Haldaneeffect�inhypoxemia,deoxyhemoglobin(dHb)servesasabufferforH+ions.With
additional oxygen, these normally dHb will become oxyhemoglobin oHb, releasing
those H+ ions, resulting in [H + HCO3 ?? H2O + CO2], raising CO2 levels o
Decreasedrespiration�thesupplementaloxygenwillcauseincreasedoxygenationinthebody,
which tells the brain to slow down breathing, as it considered O2 levels to be OK.
However, this also will retain CO2. * These three effects together cause increased
CO2 retention and acidosis ?? neural vasodilatation (reflex typically used to
increase bloodflow, but here causes underperfusion) and neurotransmitter changes ??
seizures * As a goal, O2 levels should only be cautiously raised to about 90-93%
for COPD pts 3026: B-2 agonist inhalers (albuterol) are the first line treatment to
induce bronchodilation in an acute asthma attack, however they are not without side
effects: * Low Potassium ?? Muscle weakness, arrhythmias, EKG changes (B-agonism
drives K+ into cells by activating the Na-K-ATPase) * Tremor, headache, and
palpitations may also occur * When this complication occurs ?? check serum
electrolytes to confirm K+ levels 3453/4252/4596: Solitary Pulmonary Nodule * Coin-
like, opaque, lung lesion up to 3cm in diameter surrounded by normal lung tissue
(no edema, atelectasis, adenopathy, or effusion) often found incidentally on
routine chest scans * Typically, benign, but if one is found: o 1. Check for
previous imaging ?? if lesion is stable for >2yrs, no malignancy o
2.Ifgrowingornopreviousimaging??ChestCTforfurtherassessment ?? Benign (<0.8cm,
<40yrs age, never smoked/cessation >15yrs, smooth nodule) � Do serial CTs to
monitor the lesion ?? Intermediate (0.8-2cm, 40-60yrs, current smoker/cessation 5-
15yrs, scalloped nodule) � Biopsy or PET scan for further evaluation ?? Malignant
(>2cm, >60yrs, current smoker/cessation <5yrs, speculated/corona radiata) �
Immediate surgical resection 4210: Pulmonary Aspergillosis * Presentation: chronic
cough in patients with previous TB or from TB endemic area, sometimes with
hemoptysis, dyspnea, chest pain or fevero Immunocompromise and chronic inflammatory
disease (bonus if lung) increase risk * Dx: [(+)IgA for Aspergillosis +
Radiographic evidence] (aspergilloma fungal ball looks like an irregular clearing
in the lung that may move with changes in position. Forms in already made lung
cavities. o Notethattheinfiltratewon??tbesolid(tumor)orhavecleanair-
fluidlevels(abscess) * Tx: surgical resection of aspergilloma +/-
itraconazole/voriconazole/capsofungin 4753/4467: Parapneumonic Effusion * Basically
a transudate or exudate moving form the lung airspace into the lung pleural cavity
* Transudate � the result of increased hydrostatic or decreased oncotic pressure.
Requires no further workup outside of treatment of underlying condition causing the
exudate * Exudate � due to inflammation/irritation of the pleural lining. Defined
by the Light Criteria (having only ONE of these three means its an exudate): o
FluidProtein/Serumproteinratio>0.5??highproteininfluido FluidLDH/SerumLDH>0.6??
highLDHlevelinfluido PleuralLDH>2/3theupperlimitofnormalserumLDH??highLDHinfluido
Note that low glucose (<60mg/dL) is a classic sign of WBCs/bacteria using the
glucose for energy, denoting another sign for exudate. <30mg/dL is highly
suggestive of empyema! � Don??t forget! If the pleural fluid shows exudate, that
often means there??s an infection and local cytokine release has increased
capillary permeability to allow for WBC transit! 4024: Community-Acquired Pneumonia
(CAP) can be treated in any setting, however the first step to deciding treatment
options is to assess patient risk to select appropriate treatment setting. This can
be achieved via the CURB-65 algorithm. * C � Confusion: if confused the patient
gets 1 point * U � Uremia: if BUN >20, the patient gets 1 point * R � Respirations
>30, the patient gets 1 point * B � Blood pressure <90/60 the patient gets 1 point
* 65 � patient >65 yrs old patient gets 1 point Based on this algorithm, we can
approach CAP in the appropriate setting: * 0-1 points � outpatient treatment
(macrolide + doxycycline OR macrolide + floroquinolone) * 2-3 points � inpatient
treatment (floroquinolone OR Beta-lactam + macrolide) * 4-5 points � ICU treatment
(Beta-lactam + floroquinolone or IV macrolide) 11417: Hypothermia� Mild: 90-95F,
tachycardia, tachypnea, ataxia, dysarthria, increased shivering o
Tx:Passiveexternalwarming(removewetclothes&coverwithblankets)� Moderate: 82-90F,
progressive bradycardia, lethargy, hypoventilation, decreased shivering, atrial
arrhythmias (due to poor function of pacemaker cells in cold)o
Tx:activeexternalwarming(warmblankets,heatingpads,warmbaths)o
Notethatthebradycardiaisoftenrefractorytodrug/electricaltreatments(asthepoorly
functioning pacemaker cells cannot respond to the external stimuli), but will
recover with warming.� Severe: <82F, coma, cardiovascular collapse, ventricular
arrythmias o Tx: active internal warming (warm lung irrigation, warm liquids, warm
humidified oxygen) 4520: Spontaneous Pneumothorax from COPD * Presentation: sudden
onset chest/back pain, SOB, reduced breath sounds on affected side, and hyper-
resonanceo Occurs due to chronic alveolar sac destruction forming blebs (seen as
enlarged air sacs on chest CT) that can rupture into the pleural space, compressing
the lungs. * Dx: clinical presentation with Chest CT evidence * Tx: no complete
concensus. Based on clinical scenario and risk stratification. 4489/4663/4413:
Obesity Hypoventilation Syndrome (Pickwickian Syndrome) * Basically these people
are so fat that it??s making chest wall expansion difficult, thus their lungs are
OK but they cannot ventilate properly ?? respiratory acidosiso Long-standing with
metabolic alkalosis compensation blunts the body??s response to increase
respiratory drive, leading to worsening O2 saturation * Presentation: obese patient
with difficulty breathing (SOB, orthopnea) but clear lungs and no overt signs of
heart failure but cor pulmonary/pulmonary HTN can be features o
Labs:hypoxemia,hypercapnia,polycythemia,increasedbicarbonatewithdecreasedCl-o
ObstructiveSleepApnea(apneicevents,difficultysleeping,excessivedaytimesleepiness)ma
y co-exist due to decreased nighttime respiratory drive AND poor chest wall
expansion * Dx: clinical picture * Tx: nocturnal PEEP/BIPaP (first line) + weight
loss + avoidance of sedatives. o Acetazolamide to increase respiratory drive is a
last resort 4201: Rhinitis * Non-allergic Rhinitis o
Nasalcongestion,rhinorrhea,sneezing,post-nasaldrip o Red,boggynasalmucosao No
obvious allergic trigger with symptoms year-round o Typical onset >20y/o o
Tx:intranasalanti-histamineand/orintranasalglucocorticoid * Allergic Rhinitis o
Wateryrhinnorhea,sneezing,witheyesymptoms(red,watery,itchyeyes)o
Pale/bluishnasalmucosao
Obviousallergictriggerorassociatedallergicdisorderwithseasonalpatterns o Typical
onset <20y/o o Tx:intranasalanti-histamineorintranasalglucocorticoid 2615/2632:
Major Primary Cancers of the Lung * Presentation: cough with hemoptysis, chest CT
shows characteristic nodule. May have paraneoplastic syndrome associated with it
Types * Adenocarcinoma: peripherally located solitary nodule, female, non-smokers,
clubbing/osteoarthropathy.
Most common overall regardless of smoking status. * Squamous Cell Carcinoma:
central with necrosis/cavitation, hypercalcemia (PTHrP production: anorexia,
constipation, increased thirst, easy fatigability OR metastases to bone) * Small
Cell Carcinoma: central hilar mass, smokers, paraneoplastic syndromes associated
(Cushing??s from ACTH; Lambert-Eaton from anti-Ca2+channel; SIADH from ADH), often
presenting with metastatic disease. Systemic chemotherapy mainstay of treatment (??
too small to cut out??) * Large Cell Carcinoma: peripheral, associated with
gynecomastia and galactorrhea 3944/4263: The most common side-effect of an ACE-
inhibitor (??-pril??) is chronic dry cough. It??s annoying for the patient and
often a reason to switch from an ACE-inhibitor ?? ARB (??-sartan??) * Due to
accumulation of bradykinin, substance P, thomboxanes/prostaglandins due to ACE
inhibition * Should chronic cough persist after stopping ACE-inhibitor ?? CXR/chest
CT are recommended 3580/3049: Granulomatosis with Polyangiitis (Wegner??s
Granulomatosis) * Small-medium size vasculitis caused most commonly by c-ANCA
(anti-PR3) * Presentation: fever, arthralgia, weight loss, fatigue with organ
specific symptoms: o
Upperrespiratorytract:bloody/purulentdischarge,oral/nasalulcers,sinusitis,hearinglo
ss,or saddle-nose deformity o Lowerrespiratorytract:dyspnea,cough,hemoptysis o
Kidney:glomerulonephritis(hematuria,proteinuria,renaldecline,anemia) * Dx:
presentation, (+)c-ANCA, tissue biopsy showing granulomatous inflammation o
NotethatHIVshouldberuledoutasitcancausefalse(+)ANCAtesting * Tx: High-dose
corticosteroids + immunosuppression 4335: Asthma exacerbation due to GERD �
Presentation: recent worsening of asthma symptoms with normal lung exam. Often sore
throat, morning hoarseness, worsening cough when laying down (at night is common),
need for inhaler following meals, dysphagia, chest pain/heartburn, regurgitation
sensation o Result of microaspirations causing irritation and vagal
hypersensitivity resulting in proclivity to bronchospasm o Often coincides with
weight gain (possibly due to a stomach ulcer!) � Tx: PPI trial 4200/3046:
Sarcoidosis * Should you ever see a patient with dry cough, malaise, and bilateral
lymphadenopathy it??s sarcoid! * Presentation: classically it??s a young, often
black, woman with cough/malaise/bilateral lymphadenopathy on CXR. However, lots of
lovely signs could be present: o Anterior/posterior uveitis (vision loss/pain)o
Peripheral lymphadenopathy/hepatosplenomegaly o Polyarthritis, sometimes with
periosteal bone resorptiono Centraldiabetesinsipidusorhypercalcemiao
Arrhythmias(CompleteAVheartblockmostcommon)�granulomadisruptionofmyocardium ??
Cardiac sarcoidosis should be suspected in any patient <55y/o with unexplained
2nd/3rd degree heart block or with known sarcoidosis o
LofgrenSyndrome:erythemanodosum,hilarlymphadenopathy,migratorypolyarthritis,fever *
Dx: characteristic bilateral lymphadenopathy on CXR with biopsy showing non-
caseating granulomas either from the lung or from peripheral tissue should systemic
involvement be present * Tx: corticosteroids 4665: COPD Physiology � The
hyperinflation and other signs of COPD occur due to two mechanisms: o
Staticalveolardestruction:decreasedelasticityanddestructionoflungparenchymaphysical
ly makes floppy, larger spaces for air fill up. Thus overall you have higher lung
volume at baseline. o Dynamic ??air stacking??: elastic recoil of the alveoli in
the lungs is largely responsible for expiration. Because COPD pts have decreased
elasticity, this expiration is slow. Should a COPD patient need to breath faster
(they go for a run) they??ll start their next inhalation before exhalation is
complete, causing air to ??stack up?? in the lungs causing hyperinflation � The
hyperinflation compresses the diaphragm and gives it less room to contract. Because
the diaphragm is the single most important entity for inhalation, a flattened
diaphragm in COPD results in increased effort on inspiration. 4730/4039/4569/4667:
Acute COPD exacerbation� Presentation: wheezing, tachypnea, prolonged expiration,
and accessory muscle use. Difficulty breathing NOT resolved with albuterol inhaler.
Air trapping with hypoxia, hypercapnia.o
Recentupperrespiratoryinfectionisthemostcommoncauseo Distant heart sounds is a
common finding as heart is displaced downward from lung hyperinflation * Dx:
hyperinflation on CXR & hypoxia/CO2 retention with changes in 1 or more of the
following: o Increasedcoughseverityorfrequencyo Increased volume or change in
character of sputum o Increasedlevelofdyspnea * Tx: supplemental oxygen, inhaled
bronchodilators, systemic corticosteroids (oral prednisone or IV methylprednisone),
or muscarinic antagonists are standard treatment o Antibiotics if suspected
bacterial infectiono Oseltamivir is influenza suspectedo Mechanical ventilation if
failure to resolve event with ventilatory failure 3400: Anaphylactic Shock *
Presentation: sudden onset of symptoms following exposure to possible allergen o
Skin:hives,flushing,itchingo GI:lip/tongueswelling,vomitingo
Respiratory:dyspnea,wheezing,stridor,hypoxiao Cardiovascular:hypotensiono
Mayleadtosuffocation,circulatorycollapse,ordeathifleftuntreated! * Dx: clinical
scenario * Tx: IM epinephrine Txepi-pin?? to the thigh (NOT SUBQ or IV) o Works on
alpha-1/beta-2 receptors to vasoconstrict (increase BP) and bronchodilate
(breathing improvement) and is the best first therapy 4562: When treating patient
with Acute Respiratory Distress Syndrome (ARDS: acute lung injury causing alveolar
collapse and impaired gas exchange), intubation+mechanical ventilation is the
proper first step. * However, a patient may be failing to O2 sat. well; if this is
the case increasing PEEP (open up more alveoli for better lung function) directly
counteracts ARDS mechanism and is a great idea! * Increasing FiO2 to increase
saturation makes sense. However, prolonged high O2 levels are associated with
oxygen toxicity. Often with intubation + mechanical ventilation, the goal is to get
around <60% FiO2 to mitigate this risk. 3029: Recurrent Pneumonia is typically
indicative of some underlying process, with the first main delineating factor being
what lobe it??s occurring in: * Same lung region: Local anatomic obstruction
(neoplasm, foreign body, stenosis, etc.) or recurrent aspiration (alcoholism,
seizure disorder, GERD or other GI regurgitation) o
Firststep=chestCTtoexaminethelungforabnormalities o
Secondstep=bronchoscopyforfurtherevaluationofnegativeCTorforbiopsyofpositiveCT *
Different lung regions: sino-pulmonary disease (Cystic fibrosis, immotile cilia),
non-infectious, or immunodeficiency 3033/4448: Obstructive Sleep Apnea �
Presentation: daytime sleepiness, morning headaches, poor sleep with multiple
awakenings o Labs: erythrocytosis with increased EPO (reaction to hypoxemia)o
Riskfactors:Obesity,tonsillarhypertrophy,excessiveoropharyngealtissue,orshortmandib
le o Sequlae:cor-pulmonale,right-
heartfailure,pulmonary/systemicHTN,depression,daytime accidents due to sleepiness,
impotence * Dx: nocturnal polysomnigraphy ?? >15 apneic or hypopnea events in a
night * Tx: often 1st step is BiPAP, but underlying cause must be addressed 4575:
Ankylosing Spondyloarthritis * Presentation: low back pain/spinal immobility
(bamboo spine) and hip/buttock pain (sacroilitits) in a healthy (often white) male
<40yrs that improves with exercise, worsens with rest, worsens at night. o
Fevers,chills,weightloss,fatigueo Limitedchestwallexpansion??
restrictivepatternofPFTso Inflammation at tendon insertions to bone o
Acuteanterioruveitis(unilateraleyepain,photophobia,blurryvision) o
Inflammatoryboweldiseaseandaorticstenosismayalsooccuro Labs:elevatedESR * Dx:
radiographic evidence of joint changes; HLA-B27 haplotype is contributory * Tx:
symptomatic treatment AND immunosuppression Note the classic patterns of lung
disease based on PFTs: � Obstructive � air is trapped in lung and has difficulty
getting out o FEV1 � <80%o FEV1/FVC�<70%-difficultyingettingthatfirstbitofairout o
FVC�80%orhigher� Restrictive � chest wall expansion is limited due to some
mechanical problem o FEV1 - <80%o FEV1/FVC->70%-restrictedchestwallmakesinitial??
spring??backfasterthannormal o FVC-<80% 10982/4519/8815: Chronic (>8wks) or
subacute (3-8wks) Cough evaluation * There are TONS of reasons to have a chronic
cough, thus evaluation is paramount. * H&P with suspected etiology drives further
testing: o Evaluateandtreatasneededforbelow: * ?? �ACE inhibitor ?? stop the ACE
inhibitor & switch to ARB * ?? �Post-nasal drip (??upper airway cough
syndrome??) ?? 1st gen H1 blocker (anti-histamine) * ?? �Asthma ?? PFTs, 2-4 wk
trial of bronchodilators, or methacholine challenge * ?? �GERD ?? empiric PPI o
Chest X-ray for below: * ?? �Pt does not improve with interventions outlined in
situations above * ?? �Lung parenchymal disease (abscess, interstitial lung
disease, cancer) * ?? �Purulent sputum or immunocompromised state * ?? �No specific
etiology found * Through this method we can cover most (if not all) causes of sub-
acute/chronic cough 4614: The single most important risk factor for TB infection is
being born outside the USA in an endemic area for TB. Typically, a reactivated
latent infection within the first 5 years of moving to the US. � Note that being in
a healthcare field increases the risk, BUT being born in an endemic area abroad is
a far greater risk factor! 3874: Remember that Mitral Stenosis is most often caused
by Rheumatic Fever. However, it can present much later in life with complications
due to the defect due to left atrial enlargement from back pressure: �
Hoarseness/cough (compression of recurrent laryngeal), elevation of left mainstem
bronchus on CXR, and atrial fibrillation (abnormal conduction
through stretch fibers) can all occur, cluing you into previous rheumatic fever!
2602/3776: Pancoast Tumor (superior pulmonary sulcus tumor; typically, non-small
cell carcinoma) � Presentation: o
Ipsilateralshoulderpainradiatingupneckordownarminulnardistribution�T8-12compress o
Horner�ssyndrome(ipsilateralptosis,miosis,anhydrosis)�paravertebralsympatheticchain
o Weakness/atrophy of intrinsic hand muscles � T8-T12 compressiono
Enlargedsupraclavicularnode o Harlequin Sign (sympathetic hyperactivity in
contralateral side with facial flushing/sweating during exercise) * Dx: CXR showing
characteristic apical lung mass * Tx: surgical resection or radiation/chemotherapy
4566/4864: Acute Bronchitis � Presentation: cough from [5 days � 3 weeks]
productive for yellow/green/blood-tinged sputum o
Wheezing/rhonchiwithsorechestwalleasilyresolvedwithcoughing(sputumisgettingout!) o
Nosystemicsymptoms(lackoffever,chills,etc.) o
Classicallyafteraviralupperrespiratoryinfection * Dx: clinical picture; sometimes
CXR used to rule out pneumonia * Tx: NSAIDs/bronchodilators; antibiotics are not
recommended 3050: Exercise Induced Bronchoconstriction *
Bronchoconstriction/difficulty breathing often triggered by high volumes of dry,
cold air. Classically occurs in athletes with current or previous diagnosis of
asthma! * Tx: o Firstline:Albuterol(shortactingB-agonist)inhaler10-20beforeexercise
o Second line: Anti-leukotriene inhaler 15-20 minutes before exercise (cannot
tolerate albuterol!) o Can be combined in high-performance athletes 3038/3474:
Bronchiectasis * Infection/inflammation of bronchial walls some some underlying
condition * Presentation: chronic cough with sputum production, rhinosinusitis,
dyspnea, hemoptysis, pleurisy, wheezing, crackles, or clubbing. Bloody sputum may
occur. * Dx: o
1.ChestCT�demonstratesbronchialdilatation,wallthickening,andlackofairwaytapering o
2.Sputumsamplewithgramstain/cultureo
3.Specifictestedbasedofffindings/suspectedetiology * ?? �localized airway
obstruction ?? broncoscopy * ?? �Diffuse disease ?? evaluation for
systemic/congenital disorders, immunodeficiency * Tx: Coricosteroids/Abx (reduce
inflammation), mucolytics (get sputum up), and treatment of underlying disease when
identified 4115: If you see atypical pneumonia (diffuse interstitial infiltrate,
tachypnea, tachycardia, fever, non- productive cough) in an immunocompromised
(immunosuppressive drugs, chemotherapy, or AIDS) then think PCP pneumonia. If it??s
typical pneumonia ?? S. pneumo. Don??t overthink it hauss. 4048: Theophylline
toxicity * Bronchodilator that??s rarely used due to its narrow therapeutic window
which can be easily thrown off by alterations of the CYP-450 metabolism *
Presentation: CNS stimulation (headache, insomnia, seizure), GI disturbance
(nausea/vomiting), and arrhythmias 4116: Using Diffusion Capacity for Lung Carbon
Monoxide (DLCO) in assessment of lung disease * DLCO is basically how well carbon
monoxide can diffuse across the lung tissue into the blood. o
NormalDLCOis100%ofpredictedvalue * Low DLCO ?? decreased of diffusional capacity,
thickened walls, or low RBCs to accept CO o +obstructive pattern - emphysemao
+restrictivepattern�interstitiallungdisease,asbestosis,sarcoidosis,heartfailure o
+normalspirometry�anemia,pulmonaryembolism,pulmonaryHTN * Normal DLCO ?? nothing??s
wrong with the lung??s ability to diffuse O2o
+obstructivepattern�chronicbronchitis,asthmao
+restrictivepattern�musculoskeletaldeformity,neuromusculardisease * Increased
DLCO ?? retaining air in lungs or huge amount of RBCs for uptakeo +obstructive
pattern - asthmao
+restrictivepattern�morbidobesity(oftenchronichypoxemia=increasedhematocrit) 4040:
1. 2. 3. 4131: � � � � Management of Acute COPD exacerbationInhaled short-acting
bronchodilators, glucocorticoids, and antibiotics with supplemental O2 Non-invasive
positive pressure ventilation � shown to decrease mortality and length of stay in
COPD acute exacerbations, thus it is always the 2nd step unless patient is acute
hypercapnicIntubation with invasive mechanical ventilation � a final effort in
severe situations. Definitely not ideal, and patients face many complications (VAP,
lung perf, broken teeth, etc.) thus is often only used at a final effort.
Indications for Home Oxygen UsePt has typical PaO2 <55mmHg or SaO2 <88% on room air
Pt with cor pulmonale/right heart failure/hematocrit >55 AND Pa02 <59mmHg or SaO2
<89% room air Dosing should be titrated so pt has SaO2 >90% when
sleeping/resting/walkingUse for >15hr a day shown to increase survival o
+normalspirometry�pulmonaryhemorrhage(lotsofRBCexposed),polycythemiavera 4772:
Don??t forget! Pulmonary emboli can be MASSIVE and actually block off much of the
blood flow into the lungs in the pulmonary arteries. This will increase right
atrial/pulmonary artery pressure but can leave normal left atrial pressure. ??
Obstructive shock?? can occur if not enough blood can go through the pulmonary
circuit to even reach the right heart!! 4052: Mediastinal Tumors * Anterior
mediastinal tumors: present with chest heaviness/discomfort. May also feature
Horner??s syndrome, hoarseness, and facial/upper extremity edema with local
invasiono
Thymoma(myastheniagravis&youngageassociation),retrosternalthyroid,teratoma,and
lymphoma * Middle mediastinal tumors: present with vague chest discomfort; seen
with CT scan o
Trachealtumor,bronchiogeniccyst,pericardialcyst,lymphoma,aorticarchaneurysm,or
lymph node enlargement * Posterior mediastinal tumors: neurogenic tumors are ALWAYS
posterior; seen with MRIo
Meningocele,entericcyst,diaphragmatichernia,esophagealtumor,aorticaneurysmor
lymphoma 4208: Typically, in pulmonary embolism poor perfusion causes intense
vasoconstriction in the lung (wheezing) due to V/Q mismatch from poor perfusion of
lunch tissue for gas exchange, resulting in a high-alveolar- arterial O2 gradient
(air gets in but can??t get to blood, as perfusion is limited). Often the lungs
will hyperventilate to try and offset the poor perfusion, leading to a decreased
PaCO2. 8818:resultfrom recurrence of invasive breast cancer) WILL do this.
Normally, lower lobe consolidation (typically from pneumonia) WON??T cause enough
obscuration toin blunting on the costo-vertebral angle. Pleural effusions (this
lady happened to have an effusion likely 3716/3042: The best thing to do to lower
mortality in COPD patients is stop smoking. Long-term oxygen therapy (LTOT) is the
only other thing that has been show to decrease mortality. � Criteria for
initiating LTOT are as follows: o PaO2<55mmHgorSat<88% o
PaO2<59orSat<89%inptwithcorpulmonale,evidenceofHF,orhematocrit>55% 2919/3031:
Alpha-1 Anti-trypsin Deficiency � Presentation: o
Lung:COPD(cough,dyspnea,wheezing,recurrentpulmonaryinfections,mucoidsputum) * ??
�<45 years or with minimal/no smoking history * ?? �Basilar predominant (smoke
rises causing more damage in upper lungs) ?? decreased lung sounds at the base with
bilateral lucency of lung baseso
Liver:mildlyabnormalLFTs,hepatocellularcarcinoma,neonatalhepatitis ?? Family
history/person history of unexplained liver disease o Skin: panniculitis
(inflammation of subcutaneous fat) * Dx: PFTs + serum AAT levels * Tx: human AAT
supplementation + bronchodilators + corticosteroids o Lung/liver transplantation
for severe disease is the definitive treatment 4118/4119: Things predisposing to
Aspiration Pneumonia * Drug intoxication/Alcoholism/Dementia � both cause impaired
cough reflex/glottis closure in swallowing due to altered consciousness *
Neurologic deficits causing dysphagia * Upper GI tract disorders � GERD is classic
for getting stomach contents into the lungs * Nasogastric/endotracheal tubes/large
volume tube feedings in recumbent position � typically if person has these they??re
not swallowing well/have some form of mechanical compromise in their upper airway.
Can allow for secretions to easily get into lungs * Protracted vomiting � if you
throw up a lot, then there??s a higher chance it??ll get in your lung 4664: Chronic
hypoventilation (COPD/obesity hypoventilation syndrome/neuromuscular disease) can
result in CO2 retention ultimately causing a respiratory acidosis. The body takes
two measures to correct this: * The body may try to immediately increase
respiratory rate to blow off some excess CO2, but this may simply not work impaired
respiration is causing the problem in the first place. * Within 48hrs the kidneys
are able to switch gears and increase bicarbonate retention * Both of these
mechanisms will help correct the pH, but even in full force the patient will at
best be slightly acidotic and will never fully correct the acidosis with these
mechanisms 2298: Hypertrophic Pulmonary Osteoarthropathy * Deformity of
hands/joints attributable to underlying lung disease * Presentation: finger
clubbing, wrist/hand joint pain, finger-nail spooning in the setting of lung
disease * Dx: Chest X-ray is best initial study to check for malignancy/other
pathology * Tx: (not specified) likely symptomatic treatment and focus on
underlying cause 8905: Distinguishing Asthma from COPD � Clinically they can both
look similar, especially in an adult patient, but there are two major hallmarks
that can set asthma off from COPD: o Reversibility: FEV1 increase by >12%
demonstrates reversibility ?? asthma. COPD may be partially reversible in early
stages, but never to this degree. o DLCO:normalorincreasedDLCO??
asthma.COPDmaybenormalinearlystages,butnever increased. � Note that adult onset
asthma is harder to treat (more limited response), but is usually the situation
where you??re trying to distinguish it from COPD 4629: Pulmonary Embolism (proximal
artery occlusion � 90%) * Presentation: acute onset SOB, sometimes with unilateral
pleuritic chest pain typically in the setting
of some hypercoagulable state (injury, surgery, immobilization, etc.)o Hypoxemia
(poor perfusion), hypocapnea (hyperventilation), respiratory alkalosis (pH>7.4) *
Dx: clinical picture with signs of clotting (low platelets, D-dimer), or V-Q
mismatch (poor perfusion with normal ventilation of part of the lung) * Tx:
immediate anticoagulation, unless contraindicated (30% mortality) o
Normalrenalfunction:anyanticoagulantwillbefine,factorXainhibitorspreferredo
Poorrenalfunction(GFR<30):limitedtoun-fractionedheparin(untilPTT1.5xnormal)
followed by warfarin. Any inhibition of renal function can cause accumulation of
the really cleared factor Xa inhibitors ?? uncontrolled anticoagulation. 4087:
Malignancy Pleural Effusion * Presentation: progressive SOB with signs of
malignancy (weight loss, fatigue, etc) and consolidation that eliminates the costo-
vertebral angle on CXR o Typically,duetoLungcarcinoma,BreastCarcinoma,orLymphoma *
Dx: diagnostic thoracocentesis with pleural fluid analysis o
Biggestfirststepistransudatevsexudate(Light??sCriteria) o May show malignant cells
indicating underlying cancer * Tx: drainage of fluid with treatment of underlying
cancer 4344/4613: Pulmonary Embolism (peripheral artery occlusion � 10%) *
Presentation: dyspnea, severe unilateral chest pain, worsening with inspiration.
Hemoptysis, tachycardia, tachypnea all possible. History of immobilization (like
long flight) or hypercoagulable state often present o Wells criteria � help
determine what the pre-test probability of PE is present * ?? �+3 � signs of DVT
* ?? �+1.5 � previous PE/DVT | Heart Rate +100 | recent surgery/immobilization * ??
�+1 � hemoptysis | cancero <2 low risk | 2-7 moderate risk | >7 high risk * Dx: CT
pulmonary angiography * Tx: anticoagulation (choose drug depending on renal
function) 3859/4628: Using Modified Well??s Scoring in Treatment of PE � Always
stabilize with O2/fluids then assess contraindications to anticoagulation first o
If patient has no contraindications and PE is likely based on modified well??s
criteria ?? anti- coagulate first, then undergo assessment/testing (unfractioned or
LMW heparin are preferred) o RememberthatPEcanhavea30%mortality!It??
simportanttotreatfirstifpossible o
IfpthasanticoagulationcontraindicationandDOEShaveaPE,consideranIVCfiltertostop
large PEs from causing major damage. * PE unlikely, but symptoms present ?? D-dimer
(sensitive and can rule out PE if low) o <500 PE ruled out o
>500needadditionaltesting * PE likely OR D-dimer >500 with symptoms ?? CT pulmonary
angiogram o Negative=PEruledout o Positive=PEconfirmed 4716/2145/2300: Massive
Pulmonary Embolism (Saddle Embolism) � Presentation: sudden onset chest pain,
dyspnea, hypoxemia, tachycardia, and clear lungs, hypotension, and elevated
JVP/central venous pressure.o
Ofteninthesettingofsomehypercoagulablestate(cancer/surgeryareclassic)o
Maypresentwithrightventriculardysfunctioncausingatrialfibrilaltion,syncope,or
cardiovascular collapse. This occurs because the massive PE blocks off outflow from
the right heart. Back up pressure causes increased tension/O2
demand/ischemia/infarction sometimes presenting with RV hypokinesis with spared
septal function, bowing of the septum into left ventricle, and elevated
BNP/troponins, and new right bundle branch block * Dx: clinical symptoms/signs with
findings on chest echocardiography/CT chest angiography * Tx: surgical
intervention/anticoagulation or placement of IVC filter 4631/4568/4073/4053: Para-
pneumonic Effusions/Empyema * Definition: complications of pneumonia with leakage
of fluid/bacteria into the pleural space, causing a mass to form. Defined by the
fluid analysis from thoracocentesis. * Presentation: severe pneumonia with evidence
of pleural effusion on imaging * Dx/Tx: o Uncomplicatedpara-
pneumoniceffusion�transudatefluidwithminimalbacteria. * ?? �pH >7.2 (typically
around 7.6), normal glucose, LDH ratio >0.6, low protein * ?? �Negative gram stain,
negative bacterial culture * ?? �Tx: antibiotics for pneumonia o Complicatedpara-
pneumoniceffusion�exudativefluidwithbacterialinvasion * ?? �pH<7.2 (fermentation),
low glucose, LDH ratio >0.6, high protein * ?? �Negative gram stain, positive
bacterial culture * ?? �Tx: antibiotics for pneumonia with chest tube drainage o
Empyema�exudativefluidwithfrankpusandbacterialcolonization * ?? �pH<7.2
(fermentation), low glucose, LDH ratio >0.6, high protein * ?? �Positive gram
stain, positive bacterial culture * ?? �Tx: long-term antibiotics with chest tube
drainage 4770: In a lung consolidation (such as pneumonia) ventilation (V) is
diminished as exudate is filling the alveoli in the lungs. However, perfusion (Q)
is intact. Thus, the patient in the question can have better V/Q matching if he??s
laying on the side opposite of his pneumonia (left sided consolidation = right side
gets better O2 sat). Should he lay on his left side, more bloodflow will go toward
the left lung, and the lack of ventilation will result in V/Q of nearly 0 due to
poor ventilation ?? physiologic shunt, thus causing worsening of hypoxemia. 3016:
Bird Fancier�s Lung/Farmer�s Lung * Hypersensitivity pneumonitis resulting from
repeated inhalation of bird antigens, classically from aerosolized bird droppings
(Bird Fancier??s) or molds in hay or other crops (Farmer??s) * Presentation: acute
cough, breathlessness, fever, malaise 4-6 after exposure or chronically fibrosis
and a restrictive pattern of lung damage o CXR:groundglassopacity??haziness??
ofthelowerlunglobes o PFTs:restrictivepatternchanges * Dx: history/symptoms +
antibodies to bird antigens * Tx: avoid exposure to bird antigens (be it full
avoidance or masks to limit exposure) o
Inhaledcorticosteroidarehelpfulinacuteevents,butdon??tchangeprognosis 4521/4447:
Finger Clubbing * Mechanism: disruption of the normal lung capillary beds leads to
passage of un-fractured megakaryocytes, allowing them to enter systemic circulation
and lodge in the capillaries of the distal nail beds (normally they??d be broken up
and be too small to do this). They release PDGF/VEGF resulting in nailbed
connective tissue hypertrophy/increased capillary permeability and vascularity
leading to clubbing o Because the lung capillary beds are disrupted by disease,
it??s associated with chronic hypoxemia, BUT NOT CAUSED BY IT. * Etiology:
Hypertrophic osteoarthopathy, occult lung malignancy, cystic fibrosis, left-to-
right shunt (Osler-Weber-Rendu syndrome) * Dx: Lovibond angle at 180o, seen as
Schamroth??s Sign on exam * Tx: look for underlying cause. Often occult malignancy
is a concern, especially in people that smoke 4105/4706: Acute Asthma Exacerbation
* Presentation: dyspnea, cough, accessory respiratory muscle use, difficulty
speaking, hyperventilation/tachypnea (respiratory alkalosis, low PaCO2), lung
hyperinflation, tachycardia * Dx: clinical signs/symptoms with history of asthma o
NotethatanormalPaCO2onarterialbloodgasisasignofimpendingrespiratorycollapse.
Normally the person will hyperventilate, BUT if they??re so fatigued from the
attack that they??re starting to wear out, they can no longer hyperventilate, PaCO2
will go back to normal and they?? re getting towards the point where they??ll stop
breathing from fatigue. � Tx: SABA (albuterol) ?? +systemic corticosteroid ??
+ipratropium nebulizer ?? +one-time infusion of magnesium sulfate (after 1-hr
without response to other therapies) ?? intubation/mechanical ventilation
4523/4630: Upper Airway Obstruction due to Laryngeal Edema� Presentation: SOB,
dysphagia, stridor/harsh respiratory sounds, no wheezing. Typically, with an
identifiable cause (peanut allergy ate a peanut) and allergy signs (urticaria)o
Note that the lungs are actually fine in this situation. The problem is the
oropharynx/trachea being too swollen to allow for airflow. Thus wheezing is NOT
part of the picture.o
Asthmaexacerbationstypicallycauseairtrappinginthelungsandwillproducewheezing.An
important distinguishing factoro Flow-volume curve shows flattening of inspiration
AND expiration due to impaired flow either way. Kind of looks like a dinner roll! *
Dx: history/presentation * Tx: immediate anti-histamines with life-saving
intubation if severe 3606: Proper anti-coagulation is within an INR range of 2.0-
3.0. Higher than this risks bleeding. The only time you??d want supra-therapeutic
INR (>3.0) is with mechanical heart valve to prevent clot formation on the heart
valve. 2788/4677: Respiratory Acidosis from Alveolar Hypoventilation * For any
reason, if a person is not ventilating enough they??re not going to be able to blow
off enough CO2 to keep blood pH at a normal level. This will result in a
respiratory acidosis. * Some causes of hypoventilation include: o
Pulmonary/thoracicdisease:COPD,sleepapnea,obesityhypoventilation,scoliosiso
Neuromusculardisease:Myastheniagravis,Lambert-Eatonsyndrome,GuillianBarresyndrome o
Drugs:illegalnarcotics(heroin),sedatives,anesthesiao
PrimaryCNShypoventilation:brainstemdamage/stroke,herniation,post-ictalstateseizure
* Classically this presents with acidosis (pH <7.4), hypoxemia (PaO2 <75), and
hypercapnia (PaCO2 >45), especially within the first 48hr before the kidneys can
help compensate 4632: Complications of Endotracheal Tube Placement * Endotracheal
tube placement is ideally 2-6mm above the carina to ensure proper ventilation of
both lungs. Commonly (due to it??s steeper angle), ETTs can slip into the right
main-stem bronchus resulting in over-inflation of the right lung/under-inflation of
the left lung ?? asymmetric chest wall expansion, loss of left sided breath sounds
* Dx: CXR showing deviation of ETT into right bronchus * Tx: repositioning of chest
tube into proper place 2297: Pneumothorax * Puncture of the lung resulting in
airway pressure normalization with atmospheric pressure
within the thoracic cavity ?? collapse of the punctured lung * Presentation:
sudden SOB, hyper-resonance to percussion, absent breath sounds, decreased tactile
fremitus, compression of the mediastinum causing ventricular compression
(hypotension from impaired ventricular filling) and IVC compression (central venous
hypertension from blood backup) o Notethatthemediastinumshiftstowardthenormallungo
This is a classic complication of mechanical ventilation in someone with underlying
lung disease. Increased PEEP can cause hyperinflation and rupture of lung
parenchyma, due to already damaged/fragile lung tissue. * Dx: presentation & CXR
showing lung collapse/tracheal and mediastinal deviation are classic * Tx: chest
tube placement to relieve pressure with surgical repair 3433/3020/2702: Acute
Respiratory Distress Syndrome (ARDS) � Presentation: new/worsening dyspnea within 1
week of some acute insult (many underling etiologies) o Phys: some insult results
in inflammation/cytokine activation in the lungs. This inflammation results in
impaired gas exchange/poor lung compliance/pulmonary HTN o Etio: acute pancreatitis
(pancreatic enzymes leak into blood and enter the lung space through the pulmonary
capillaries causing inflammation and damage ?? diffuse alveolar damage) o Specific
physiologic changes include: * ?? �V-Q mismatch from consolidation/fluid in the
lung lobes * ?? �Decrease in lung compliance (stiff) due to decreased
surfactant/inflammation * ?? �Pulmonary HTN from widespread hypoxic
vasoconstriction/lung parenchyma destruction limiting forward bloodflow in the
lungs * Dx: bilateral lung opacities (pulmonary edema NOT due to CHF/fluid overload
+ PaO2/FiO2 ratio of <300mmgHg * Tx: mechanical ventilation with low Tidal Volume
(6mL/Kg body weight), high PEEP (up to 15-20cm H20 is acceptable to maintain Sats
>88%), with allowance for hypercapnia o This is to minimize risk of alveolar over-
distension thus avoiding barotrauma to alveoli o
Alsonecessarytoprovideadequateoxygenationofalveolibypreventingatelectasis 3775:
Non-Semanomatous Germ Cell Tumor * Presentation: young male patient chest
discomfort/cough/dyspnea/weight loss with large anterior mediastinal mass producing
B-hCG and AFPo Note that semanomatous germ cell tumors only produce B-hCG o
Thesetumorsaremostcommonlyprimary * Dx: clinical presentation, biopsy form
confirmation, ultrasound of testicles to rule out primary tumor causing metastatic
disease * Tx: surgical removal/possible adjuvant treatment 4036: Never forget!
Glucocorticoids greatly raise WBC count� Leukocytosis caused by glucocorticoids
occurs via three mechanisms: o
Mobilizationofmarinatedneutrophils�typicallyneutrophilshangoutinthemarginsofthe
vasculature and are not picked up during routine blood testing. Glucocorticoids
will get these guys off the walls causing and increased amount in the circulating
blood. o
Stimulationofimmatureneutrophilreleasefrombonemarrow�oftenevidencedbyaslight
increase in bands (around 3%) in the WBC differential o
Inhibitionofneutrophilapoptosis� Oddly enough, glucocorticoids also decrease the
number of lymphocytes and eosinophils (increased extravasation, increased
apoptosis, decreased production 4645: Remember that vital capacity in COPD
decreases due to air trapping and obstruction of expiration. * Vital capacity =
amount of air a person can expire with a normal expiration * COPDers trap air in
the lungs due to obstruction/destruction of alveoli, thus they have a harder time
getting the air out! Thus vital capacity deceases greatly 3846: The most common
complication of long term inhaled corticosteroids is thrush (oral candidiasis) as
the local decrease in inflammatory response may predispose to colonization of
Candida. High-dose inhaled corticosteroids have a higher chance for systemization
for further side effect, however this often is dose dependent and does not occur.
4387: For the love of god stop overthinking questions. Here??s some classic breath
sounds for you: � Normal � bronchovesicular/vesicular sound, normal tactile
fremitus, resonant percussion, no shift * Consolidation � increased sound
(crackles, egophony), increased tactile fremitus, dullness to percussion, no
mediastinal shift * Pleural Effusion � decreased/absent breath sounds, decreased
tactile fremitus, dullness to percussion, mediastinal shift away from effusion *
Pneumothroax � decreased/absent breath sounds, decreased tactile fremitus,
hyperresonant to percussion, mediastinal shift away from pneumothorax * Emphysema �
decreased bilateral breath sounds/tactile fremitus, hyperresonance, no shift *
Atelectasis (Mucous plugging) � decreased breath sounds/tactile fremitus, dullness
to percussion with shifting towards the atelectasis 4617/3027: Asthma
Classification and Treatment * Intermittent: daytime symptoms <2x week | nighttime
symptoms <2x month | short-acting B-agonist use <2x week with normal baseline PFTs
and no impairment of function o Tx:PRNalbuterol * Mild Persistent: symptoms >2x
week but NOT daily | nighttime symptoms 3-4x month | normal PFTs baseline with
minor limitations of activitities o Tx:PRNalbuterol,inhaledcorticosteroid *
Moderate Persistent: daily symptoms, weekly nighttime awakenings, moderate
limitation of activites, with FEV1 60-80% predicted valueo
Tx:PRNalbuterol,inhaledcorticosteroid,inhaledLABA * Severe Persistent: symptoms
throughout day, frequent nighttime awakenings, very limited activity, FEV1 <60%
predicted value o Tx:PRNalbuterol,high-doseinhaledcorticosteroid,inhaledLABA,+/-
oralprednisone 4536/3048: Mechanics of Mechanical Ventilation * Often mechanical
ventilation is necessary in acutely ill patient (especially with ARDS) * You
monitor and adjust patients on a vent by certain values: o
[PaO2(O2saturation)�affectedbyFiO2/PEEP].Essentiallyit??stheamountofoxygeninthe
blood influenced by the amount of oxygen in the air/the amount of alveoli open for
gas exchange. Should the PaO2 become too high, turn down the O2 levels. FiO2 <60%
is generally considered safe, and has minimal risk of free radial oxygen
formation/lung damage o
[PaCO2(CO2saturation)�affectedbyminuteventilation/tidalvolume].Essentiallythe
amount of CO2 coming out of the blood is determined by the amount of air that it
can be exchanged for. TV of 6mL/Kg is suggested in ARDS � In assist control mode
when the patient initiates a breath, the machine helps them take that breath. But
if the patient doesn??t take a breath at a pre-determined time (respiratory rate
programmed into the vent) it will initiate one for him. This can lead to
respiratory alkalosis should the rate be set too high! 4863: Differentiating
between Major Lung Diseases with PFTs * Asthma � low FEV1/FVC (obstructive) with
resolution on bronchodilator challenge * COPD � low FEV1/FVC (obstructive) with no
resolution on bronchodilator challenge * Chest Wall Weakness � normal to high
FEV1/FVC (restrictive) with low Vital Capacity + normal DLCO (no difficulty with
air diffusion across lung tissue) * Interstitial Lung Disease � normal to high
FEV1/FVC (restrictive) with low Vital Capacity + low DLCO (trouble with getting gas
across the lung tissue)o Classicislong-tomeasbestosexposurewithlungcalcifications??
pneumoconiosis 3021/3022: Asbestosis� Presentation: progressive dyspnea (months),
bibasilar end-expiratory crackles, clubbing. Cough/sputum/wheezing are NOT
typically present.o
Typicallyarises20+yearsafterexposure(plumber,electrician,carpenter,pipefitter,or
insulation worker, shipbuilder, or plastic manufacturer)o 6x risk for lung
carcinomas and increased risk for mesothelioma (still very rare though!). If
combined with smoking, nearly 59x increased risk!!o Decreased DLCO from fibrosis
and thickening of lung membranes * Dx: CXR (bibasilar reticularnodular infiltrates,
honeycombing, and pleural thickening), high resolution CT (parynchymal
fibrosis/linear densities) + exposure history * Tx: removal of risk factors,
symptomatic treatment4097: The gold standard for diagnosis (and first step) for
classic pneumonia is a chest X-ray. Will show an infiltrate in one/more of the
lobes and helps rule out other causes of presentation like lung malignancy. 11669:
Aspiration (chemical) pneumonitis * Inflammation from chemical damage to lung
parenchyma, classically from aspiration * Presentation: wide ranging symptoms (non-
productive cough ?? respiratory distress/O2 desaturation) within hours of an
aspiration event o CXR:sometimesbilateralinfiltrates * Dx: clinical presentation *
Tx: supportive therapy, will resolve within 24-48 hrs 4177: Primary (Idiopathic)
Pulmonary HTN � Presentation: dyspnea, weakness, fatigue, clear lungs ?? chest
pain, hemoptysis, hoarsness, syncope ?? right ventricular enlargement with right
heart failureo Occursinanormalpersonwhomayhavenoreasonastowhyit�soccuringo
EKG:rightaccessdeviationfromcorpulmonalechangeso
CXR:prominentpulmonaryarterieswithrapidtapering(pruning)andenlargementoftheright
ventricle * Dx: clinical picture with mean pulmonary pressure >25mmHg at rest or
<30mmHg with exercise * Tx: B-blockers or other drugs to lower HTN 4689: Note that
Hodgkin�s Lymphoma classically occurs in young people and is treated with combo
chemotherapy/radiation. Unfortunately, this early treatment puts people at massive
risk for later developing a second malignancy as a result of previous treatment.
3579/2230: Goodpasture�s Syndrome * Autoimmune disease of Anti-a5 chain of Type IV
collagen antibodies typically expressed in renal glomerular basement membrane and
lung elastic fibers * Presentation: weight loss, fever, arthralgias, renal
(nephritic range proteinuria <1.5g/day, acute renal failure, RBC casts with some
bleeding into urine), pulmonary (SOB, cough, hemoptysis)o NotethatAnti-
GBMdiseaseiswhenit�sonlyarenalproblemwithoutlungproblems
* Dx: renal biopsy demonstrating IgG linear deposition of auto-antibodies on GBM *
Tx: IVIG, plasmapheresis, immunosuppression [go through pulmonary section and group
all things with COPD and PE. There??s a ton!] Psychiatry/Behavior/Substance Abuse
8823: Sleep Pattern Disorders * Shift-Work sleep disorder � new onset pattern of
poor sleep due to constant interruptions from shift work. Waking hours are
incongruent with normal circadian rhythm. * Delayed Sleep phase disorder � lifelong
pattern of poor sleep (trouble going/sleepiness when waking up) when needing to
wake up earlier in the day. Often described as ??night owls??. Note that when
allowed to sleep when they??re comfortable, they??re well rested. * Advanced sleep
phase disorder � lifelong pattern of poor sleep when needing to stay up later at
night, classically past 7PM. Often described as ??morning larks?? or ??early
birds??. Well rested when allowed to sleep in preferred pattern. 2661: Alcohol
Withdrawal * Note that ANY patient suspected of alcoholism should be
prophylactically treated with withdrawal * Presentation: CNS rebound hyperactivity
(alcohol is a depressant) with specific timeframes since last drink:o 6-24hr:
anxiety, insomnia, tremors diaphoresiso 24-
48hr:hallucinations(oftenvisual,butcanbetactile/etc.)&seizureso 48-
96hr:DeleriumTremens(HTN,agitation,tachycardia,hallucinations,fever,death) * Dx:
Hx/physical exam * Tx: prophylactic benzodiazepine for CNS depression
(Chlordiazepoxide is a classic) with close watch 11815: Bath Salts intoxication *
Bath salts are cathinone (amphetamine analogues) that increased NE/DA/5-HT. A white
powder labeled as ??bath salts??, ??plant food??, or other substances. They aren??t
used for baths. * Presentation: long lasting (days to weeks), severe agitation,
combativeness, psychosis, delirium, myoclonus, and sometimes seizure o Note that
this looks a lot like PCP, but long-lasting aspect of symptoms is distinguishing o
Normal tox screening DOES NOT look for bath salts, so tox screens may be
unremarkable * Dx: clinical scenario with possibly special screening confirmation *
Tx: hospitalization, benzos, supportive care 2387: Drugs to Aid Smoking Cessation *
Varenicline (Chantix) � the most effective drug on the market today. Partial NACh
receptor agonist * Bupropion (Wellbutrin) � effective anti-depressant drug (NDRI) *
TCAs can be used, but are not FDA approved and are not great due to side effect
profile * The best therapy is a [nicotine patch + one of these drugs] Male
Reproductive Tract 2238: Non-inflammatory Chronic Prostatitis * Presentation:
afebrile with voiding symptoms (urinary frequency/urgency, hesitancy, interruption
of flow) with prostatic secretion showing normal WBC count/negative culture *
Basically this person has symptoms but no overt underlying problem. The question
did not specify a treatment, it just wanted to diagnosis based off the clinical
scenario. 2246: Prostatitis � Acute o Presentation: Fever, chills, malaise,
myalgia, pelvic pain, cloudy urine (resembles febrile UTI) o
Dx:WBCsinurine,tenderprostate,culture(+)forbacteria(E.colimostcommon)with midstream
sample of urine (important for mid-stread clean catch)?? Prostatic massage may be
useful but can cause pain/introduce bacteremia, thus is not indicated unless
necessaryo Tx:TMP-SMXorfluoroquinolonesfor4-6weeks � Chronico
Presentation:Dysuria,^urinaryfrequency,recurrentUTIso Dx:WBCsinurine,+/-
tenderprostate,culture(+)forbacteria(E.colimostcommon) o Tx:floroquinolones(??-
floxacin??)for4-6weeks 2589: Testicular Mass� Presentation: painless, hard mass in
the testicle with evidence on ultrasound * Dx: clinical presentationo Trans-scrotal
biopsy contraindicated due to potential spillage of cells/seeding & spread * Tx:
radical high inguinal orchiectomy (removal of testis AND spermatic cord) with
histologic examination. Depending on history, additional surgery/adjuvant therapy
may be necessary 3369: Infertility due to Anabolic Steroid Use � Presentation:
infertility in an athlete/body builder type young man. Acne, gynecomastia
(testosterone ?? estrone), decreased testicular size, aggressiveness, and psychosis
can all be features.o Labs: normal testosterone (hormone present in steroids is not
differentiated from native testosterone in lab analysis), erythrocytosis (increased
erythropoiesis), elevated Hb, cholestasis, hepatic failure, dyslipidemia, mildly
elevated creatinine (large muscle mass)o Phys:Exogenousandrogens??
feedbackinhibitionofhypothalamus??decreasedLH/FSH?? decreased sperm
production/testosterone production * Dx: history/physical/agreeing labs * Tx:
exogenous steroid taper and discontinuation of anabolic steroid use 3055: Prostate
Specific Antigen � There??s currently a fair amount of controversy with PSA
screening as false positives have been shown in some studies to lead to unnecessary
intervention and ultimately iatrogenic co-morbidities. It??s best to discuss the
problems/benefits of PSA with the patient before doing one. 3916: Causes of
Priapism (prolonged erection) * Sickle cell/leukemia � children and adolescents due
to penile blood outflow obstruction * Perineal/genital trauma causing laceration of
the cavernous artery causing hemorrhage/engorgement * Neurogenic lesions causing
hyperstimulation of penile erection * Medication � trazodone/prazosin are the two
classics to remember Ear, Nose, Throat 11906: Swelling of the Salivary Glands *
Silaladenosis: non-inflammatory, non-tender, bilateral, benign enlargement of the
salivary glands. o
Liverdisease(alcoholic,viral,etc.),diabetes,bulimiaaremajorcauses * Sialadenitis:
inflammatory swelling of salivary glands. Tender, red, and often with fever. o
Sjogren�ssyndromeisaclassicautoimmunecauseofthis * Salivary gland stones: often
unilateral swelling/pain that worsens with meals * Parotitis: painful swelling
that??s typically isolated to the parotids. o
Oftenviral.Mumpsinfectionsareclassicforthis * Pleomorphic adenoma: benign neoplasm.
Firm nodule that??s typically unilateral. 2836: Presbycusis * Sensorineural hearing
loss of aging, typically seen in >60yr old patients * Presentation: high-pitched,
symmetric sensorineural hearing loss. Patients typically complain of trouble
hearing in crowds/noisy environments but do well when things are quiet. * Dx:
clinical picture * Tx: no real treatment. Hearing aid may be useful if loss is
severe/impairing 2844: Leukoplakia � Pre-cancerous squamous epithelial hyperplasia
of the mucosa o Smokelesstobacco/alcoholuseareclassicriskfactorso
Mostlesionsregresswithinafewweeksafterriskfactorcessation o
Mayprogresstosquamouscellcarcinomawithin10years;oftenthisprogressionshowsareas of
induration * Presentation: non-painful white plaque on oral mucosal surface that
cannot be scraped off * Dx: clinical presentation. If ulcer is indurated/changes,
biopsy to rule out cancer is warranted * Tx: cessation of tobacco/alcohol and close
follow-up 4902: Otosclerosis * Abnormal remodeling of the otic capsule (possibly
autoimmune), with fixation of the stapes to the oval window, eliminating its piston
action o Typicallypresentsin20s/30s * Presentation: unilateral conductive hearing
loss without pain or discharge * Dx: documented conductive hearing loss with CT
head showing characteristic changes * Tx: hearing aid or surgical removal of the
stapes 2194: TMJ Dysfunction * Presentation: pain in the region of the TMJ
(sometimes described as ear pain by patients) that??s worse with chewing. May have
crepitus/audible clicks/grinding on palpation. o
Patientsclassicallyhaveahistoryofnocturnalteethgrinding * Dx: clinical presentation
and ruling out of any ear problems * Tx: nighttime bite guard is typical...but
severe cases may warrant surgical intervention 2838: Medication-Induced Hearing
Loss * Bilateral sensorineural hearing loss often with starting a new drug, kidney
disease, or high drug dose * Aminoglycosides, Chemo agents, aspirin (high doses),
and loop diuretics are all known to do this o Note that aspirin can cause tinnitus
at lower doses 2828: Malignant (necrotizing) Otitis Externa * Presentation:
intense, unrelenting ear pain that??s worse at night. Purulent drainage/feeling of
fullness that does not respond to topical medication. Ear canal shows granulation
tissue/edema. May progress to osteomyelitis of the skull base with cranial nerve
involvement (facial droop) or TMJ involvement (pain worsened by chewing) o
Associatedwithpoorlycontrolleddiabetes/immunosuppressioninelderlypatients o
TypicallycausedbyPseudomonasAeruginosa * Dx: clinical presentation with CT/MRI
evidence of infection * Tx: IV ciprofloxacin (first line) o
Fluoroquinoloneresistant:otherIVanti-pseudomonals(Pip-tazo/cefepime/ceftazidime) o
FailuretorespondtoAbx:surgicaldebridement/biopsytoexcludecancer 2839: Serous Otitis
Media * Middle ear effusion resulting in conductive hearing loss without infectious
symptoms. Ear canal shows dull tympanic membrane with hypomobility on pneumatic
otoscopy * The most common middle ear pathology in HIV/AIDS due to lymphadenopathy
obstructing the Eustachian tube 2842/4065: Aspirin-Exacerbated Respiratory Disease
(AERD) � Presentation: asthmatic symptoms (cough, wheezing, chest tightness),
allergic symptoms (chest congestion, rhinorrhea, periorbital edema), and facial
flushing within 30 min � 3hr of NSAID use o
AssociatedwithNasalpolyp,asthma,andchronicrhinosinusitis o Very similar to
allergic/asthmatic flare-up, thus symptoms may not be attributed to NSAIDo Nasal
polyp development can cause bland tasting food (caused by anosmia), recurrent nasal
discharge with grey-glistening mucoid mass in the nasal canal.o Considered a
pseudo-allergic reaction that is not IgE mediated. Instead the aspirin diverts the
arachidonic acid pathway to produce high
amounts of leukotrienes = inflammation * Dx: Clinical scenario * Tx: Surgical
removal of nasal polyp, management of underlying conditions,
avoidance/desensitization of NSAIDs, and sometimes leukotriene inhibitors
(ziletuon/montelukast) 2195: Peritonsilar Abscess * Presentation: fever, chills,
sore throat, muffled voice, uvular deviation, unilateral lymphadenopathy o Airway
obstruction and spread to parapharyngeal space (carotid sheath involvement) * Dx:
clinical scenario with signs on oropharyngeal exam * Tx: immediate abscess drainage
via needle aspiration with culture/empiric antibiotics Allergy/Immunology | Female
Repro | Pregnancy/Childbirth | General Principles 4080: Vaccination with Traveling
* Hepatitis A � Africa or East Asia; the most common preventable traveling virus *
Yellow fever � South America or sub-Saharan Africa; endemic to tropical regions *
Rabies � not needed for any specific region, but considered for visit to developing
countries or places where travelers will spend lots of times outdoors/in rural
areas * N. Meningitis � Sub-Saharan Africa and Asia countries. Legally required for
Hajj to Mecca. 2770: The most common cause of angioedema is an ACE inhibitor. *
Angioedema: swelling of the face, lips, mouth, tongue, glottis, and larynx due to
bradykinin * May be life threatening due to airway obstruction * ACE (aka ??
Kininase??) helps break down bradykinin. [ACE inhibition = ^bradykinin =
angioedema] * May occur at any time on ACE inhibitor therapy and management is
emergent: o
1.Checkairwayforobstructionandvasomotorstability(ABCs)andstopACEinhibitor o
2.AdministerSubQEpinephrine(vasoconstriction)o 3.IffailuretorespondtoEpinephrine??
emergencytracheostomytosecureairway 2386: The two S.pneumoniae vaccines differ in
the way that they induce immune response, giving them characteristics that drive
their immunization protocols. Pneumococcus comes in a HUGE amount of strains, and
infection with one only gives immunity to that strain. Thus high-risk individuals
are vaccinated! � Pneumococcal Polysaccharide vaccine�23 (PPSV23) � contains 23
strains of historically responsible strains for pneumonia. Only contains bacterial
polysaccharides which cannot be presented to T-cells by B-cells, thus the response
is less robust in young/old and has lesser effect, but better coverage o
Giventoalladults<age65(astheoldagewouldmakethisratheruselessfromweak immunogenic
response) o Given to all immunocompromised pts >65 8 weeks after PSV13 and repeated
every 5 years (it won??t give a great response, BUT these people are so at risk
that it may provide benefit) � Pneumococcal Conjugated vaccine�13 (PSV13) �
contains 13 historically responsible strains that are able to be conjugated to
Diptheria toxin protein. This allows B-cell presentation to T-cells giving most
robust responses AND memory of infection, but is limited on coverage. o Given to
all infants and young children (get some coverage that works early on) o Given if
immunocompromised pt hasn??t received it before. 11177: Contact Dermatitis�
Allergic � immunologically mediated Type IV delayed hypersensitivity reaction to an
allergen o Presentation: redness, itching, scaling in well-demarcated patches/lines
of exposed skin. Often acute and does not become chronic due to one-time exposure o
Triggers:poisonivy/oak/sumac,nickel,rubber/latex,leatherdyes,medications o
Dx:clinicalscenariowithallergypatchtestingo Tx:avoidanceofirritant,emollients/anti-
histamines/epi-pinforseverereactions � Irritant � non-immunologically mediated
reaction to some substanceo
Presentation:erythema,itching,dryness,oftenonhands/fingerwebs.Maybeacutebutoften
becomes chronic as irritating is part of some normal behavior.o
Triggers:soaps,detergents,chemicals,protectivegloves,oracids/bases o
Dx:clinicalscenario.Biopsymaybenecessaryifrashdoesn??tclearo Tx:
emollients/protective barriers with avoidance of irritant 3980: Here are some
classic adverse effects of drugs that you simply should memorize. [HIGH YIELD] *
Cyclosporin � IL-2 inhibitor for immunosuppression; mainly suppresses T-cells.
Adverse effects: o Nephrotoxicity�themostcommon.Maybemild(azotemia)orsevere(HUS)o
Gingivalhyperplasiaandhirsutism�aclassicuniquetothisdrugo Hypertension � due to
renal vasoconstriction/Na+ retention. Use Ca2+ blockers to treat. o
Neurotoxicity�wide-rangingeffect.Reversiblewithcessationofdrugo
Glucoseintolerance�common.Maybeseverewithconcomitantglucocorticoiduse. o
Infection/malignancy�partoftheimmunosuppressionpicture * Tacrolimus � macrolide
antibiotic with immunosuppressive properties. Essentially the same as cyclosporine
BUT no gingival hyperplasia or hirsutism. * Azathioprine � purine analogue
converted to 6-MP, inhibiting purine synthesis for cancer treatment o Dose
dependent diarrhea, leukopenia, and hepatotoxicity * Mycophenolate � inosine
monophosphate inhibitor stopping de-novo purine synthesis for cancer Tx o
Severebonemarrowsuppression,oftenusedinbone-marrowtransplantforsuppression 3993:
Selective IgA deficiency * Presentation: often asymptomatic but classically
recurrent sinopulmonary/GI infections due to impaired immunologic IgA barrier on
mucosal surfaceso
Importantlyanybloodtransfusionwillcauseanaphylaxisinthesepatients,astheywillmount
an immune response to IgA present in donor blood. Thus any blood products of a
patient with this disease must be washed for IgA and patients must wear information
bracelets. * Dx: Low IgA with normal other levels of immunoglobulins and B-cells *
Tx: supportive care with medical alert bracelet 11970: Benign Diseases of the
Breast * Breast Cyst � solidary, well circumscribed, nodular mass, +/- breast
tenderness * Fibrocystic Changes � diffusely nodular (cord-like thickening)
multiple masses in the breast, may be tender before menstrual cycle. Occur due to
fluctuations in estrogen/progesterone. NSAIDs and OCPs can give relief to symptoms.
* Fibroadenoma � solitary, well-circumscribed mobile mass that fluctuates with
menstrual cycle in size/tenderness. * Fat necrosis � firm, irregular masses
resulting from post-traumatic/post-surgery changes. Due to damage and calcification
of breast fat. Ecchymosis, skin-retraction, or nipple retraction may be present. *
Breast lipoma � soft, mobile, painless lump on the breast 2605: Breast Cancer
Staging � The #1 prognostic factor for breast cancer patients is TMN staging. o
T=tumorsizeo N = regional lymph node involvement o M=metastases 2256: Anti-
phospholipid Syndrome * Presentation: classically young women with recurrent
miscarriages and a (+)VRDL/(-)FTA-ABS o
Labs:prolongedPTT/thrombocytopenia(beingusedtomakeclots!) * Dx: screening for anti-
phospholipid antibodies * Tx: immediate anticoagulation with LMWH (even before
testing) o Notethatcorticosteroidsarenotthecurrentstandardofcare 4477: Specific
Vaccination/Screening guidelines * Tetanus (Tdap) � initial vaccination preferred
at 11-18 with repeat every 10 years o If >19yrs but not had vaccination previouslyo
Any/allpregnanciesregardlessofvaccinationstatus * Pap Smear � every 3 years
starting at age 21 through age 29o Age30-69:continueevery3years+/-
HPVscreeningevery5yearso Immunocompromised??Papsmearstartingatage21,theneveryyear o
HIV??screenedtwiceinthefirstyearpost-diagnosis,thenannually 2197: Breaking Bad News
Script + SPIKES * Set up situation: get a private room/make eye contact/don??t have
interruptions/make introductions * Perception assessment of disease: ??What do you
think is the cause of __________??? * Invitation from family to known info: ??How
much information do you want to know? * Knowledge/Information passage: Warn of bad
news, speak in straightforward terms, check understanding * Empathetic Statement:
Respond to emotions and be empathetic * Strategy/summary: Summarize / mediate end-
of-life plans if appropriate 3863: Mammography Screening from USPSTF for people
with average risk: * HIV � one-time HIV antibody screen, 15-65 * HTN � Blood
pressure measurement every 2 years for 18+ * Cervical Cancer � pap smear every 2-3
years for women 21-65 * Hyperlipidemia � lipid panel every 5 years for men 35+ *
Breast Cancer � mammogram every 2 years women 50-75 * Osteoporosis � DEXA scan for
women 65+ Hematology/Oncology 4338/4339: Thrombotic Thrombocytopenic Purpura (TTP)
� Autoimmune or hereditary decrease in ADAMTS13 enzyme (cleaves vWF multimers)
resulting in extra- long vWF which promotes intravascular platelet thrombus
formation, which can shear passing RBCs � Presentation: Thombocytopenia,
Microangiopathic hemolytic anemia, renal insufficiency, neurologic changes
(headache, confusion, stroke, coma), and fever. Sometimes scleral icterus. o Labs:
normal PT/PTT (no activation of coagulation cascade!), anemia/thrombocytopenia,
elevated creatinine (kidney damage from clots), o
Smear:fragmentedRBCs(schistocytes) * Dx: presentation with labs/smear * Tx: plasma
exchange (replenishes ADAMTS13/removes possible autoantibody) 3608: DVT complicated
by contraindications � Contraindication to Anticoagulation or Failure of
Anticoagulation o This patient has DVTs but also acute GI bleeding, thus cannot be
anticoagulatedo Best management is placement of a removable IVC filter to prevent
embolization of large DVTs into pulmonary system (prevent massive PE)o Watch for
bleeding or migration/erosion of the filter � Contraindication to Thrombolyticso
Considermechanicalthrombectomy/surgicalthrombectomyorstenting 4348: Pica/Pagophagia
* Pica � appetite for substances other than food (clay, dirt, or paper are common)
o Mayhaveexoticappetite(hair,lightbulbs,etc.)whenassociatedwithpsychiatricdisease *
Pagophagia � appetite for ice * Both classically associated with iron deficiency
anemia and may appear before iron deficiency is present, thus any patient with
these signs/symptoms should
have bloodwork done 4374: Androgen Abuse (Anabolic steroids) * Almost always
present in a young athlete/bodybuilder using either synthetic steroids (nandrolone,
stanozolol), exogenous testosterone, or androgen precursors (DHEA) * Presentation:
o Men:testicularatrophy,lowspermcount,gynecomastia,aggressivebehavior o
Women:acne,hirsutism,deepervoice,irregularmenstrualcycleso
Cardiovascular:LVH,decreasedHDL/increasedLDLo
Heme:polycythemiawithpossiblehypercoagulability * Dx/Tx: presentation or admission
of use with cessation of use 4383/4860: Immune Thrombocytopenia * Platelet
destruction/inhibition of megakaryocyte production by IgG anti-platelet membrane
glycoprotein antibodies * Presentation: asymptomatic petechiae/ecchymosis,
mucutaneous bleeding, possible recent viral inf. o
Labs:isolatedthrombocytopenia(<100,000)o
Smear:megakaryocyteswitnootherabnormalities * Dx: clinical presentation, CBC, Labs
with HIV/HCV testing (may be cause of disease) * Tx: o Kids:Skinonly=observe|
bleeding=IVIGorglucocorticoidso Adults: Plt >30k + no bleed = observe | Plt <30k or
bleed = IVIG or glucocorticoids 4356/4350/3067/3066: Pernicious Anemia � B12
deficiency caused by anti-intrinsic factor antibodies causing destruction of
parietal cells/intrinsic factor resulting in failure of B12 uptake in the terminal
ileum o Note that anemia is due to impaired DNA synthesis of thymidylate and purine
molecules for RBC production (ineffective hematopoiesis) � Presentation: macrocytic
anemia (pale conjunctiva, fatigue, pallor, MCV >100), glossitis (beefy red tongue),
and peripheral neuropathy/loss of lower extremity vibratory sensation (dorsal
column destruction), or cognitive function defects. Sometimes jaundice from
destruction of large RBCs o Smear:mactocyticRBCs,hypersegmentedneutrophilso
Classically associated with atrophic gastritis (parietal cells being attacked as
they make intrinsic factor) increasing the risk for intestininal-type gastric
cancer and gastric carcinoid tumors. * Dx: B12 level, testing for autoantibodies,
Homocysteine level/Methylmalonic acid level to differentiate from folate deficiency
* Tx: B12 injections + periodic stool blood testing for gastric cancer monitoring
4357: Differentiating B12 from Folate deficiency anemia * Both show elevated
homocysteine (both involved with conversion of homocysteine ?? methionine) * Only
B12 def will show elevated methylmalonic acid (conversin of methylmaonyl-CoA ??
succinyl-CoA) * Note that folate deficiency is more common and should be suspected
in any malnutrition picture first as you can become deficiency in 5-10 weeks 4147:
Several drugs can cause megaloblastic anemia due to folate deficiency [HIGH YIELD]
* Anti-epileptics (phenytoin, phenobarbital, primidone) ?? impair folate absorption
in the gut * Bactrim (TMP-SMX) ?? inhibits dihydrofolate reductase, thus decreasing
folate activation * Methotrexate ?? inhibits dihydrofolate reductase (leucovorin
[folinic acid] is indicated as a concurrent supplement when giving methotrexate
because of this) 4416: Hematologic Manifestations of SLE * Note that Lupus can
cause a pancytopenia as a result of multiple mechanisms coming together to cause
destruction of blood cells * Most common: o
Anemia�chronicdisease(ironsequestration),renalinsufficiency(decreasedEPO),GIbleedin
g, or autoimmune hemolysis o Leukopenia�autoimmunedestruction o
Thrombocytopenia�autoimmunedestruction � Less common: o
Anemia�meds,hypersplenism,aplasticanemia o Leukopenia�meds,hypersplenismo
Thrombocytopenia�meds,TTP 3610: Intravascular Hemolytic Anemia (??Macrovascular
Hemolysis??) * Presentation: fatigue, microcytic anemia in the context of heart
valve abnormality o
Labs:elevatedreticulocytect,increasedLDH,decreasedhaptoglobin(highironinblood) o
Smear:schitocyteswithmicrocyticanemiao
Classicallycausedbymechanicalheartvalveorcalcifiedheartvalve * Dx: clinical
presentation/labs * Tx: surgical intervention to decrease harsh valve trauma 2621:
Pain Control Algorithm in Advanced Cancer � It??s often a fear of doctors to use
narcotics/opiates on pts with severe pain, but often advanced cancer patients are
on palliative care, thus every effort to eliminate pain should be sought.
Guidelines include: o 1. Start with NSAIDs to see if it helpso 2.Ifnot??
startwithshort-actingmorphineandtitrateuptoproperpaincontrolo 3. Once at adequate
pain control ?? switch to long acting opiate for long-term control and have short-
acting morphine for break-through pain PRN 2875/2877/4358: Iron Study
Characteristics in Microcytic Anemias * Iron Deficiency: not much iron around, thus
the body is looking to take up as much as possible o
Decreased:MCV,serumiron,ferritin,transferrinsaturation(iron/TIBC) o Increased:TIBC
* Thalassemia: poor production of hemoglobin leaves iron out in the blood o
Decreased:MCV,TIBC o Increased:iron,ferritin,transferrinsaturation * Anemia of
Chronic Disease: the body takes inflammation to mean ??bacterial infection?? and
sequesters iron in hopes that it??ll limit bacterial reproduction. o
Decreased:MCV,iron,TIBC,transferrinsaturationo Increased:ferritino Typically, a
chronic inflammatory disease (autoimmune is classic!) can be noted from vignette.
Treatment is as follows: * ?? �Underlying condition treatment (autoimmune disease
will be immunosuppressed) * ?? �If no improvement ?? administer EPO to stimulate
RBC production * ?? �If no improvement ?? packed RBC transfusion to get RBC count
back up 4331/3609/4347: G6PD deficiency (glucose-6-phosphate dehydrogenase) � � � �
2623: � � � X-linked recessive disorder which can result in acute anemic crises in
response to certain situations. G6PD typically used to generate glutathione to
minimize oxidation damage to RBCs. Should a oxidizing stressor come on, G6PD
deficiency pts are not able to compensate. o Classically triggered by infection,
oxidant drugs (anti-malarials, sulfa drugs, etc.), and fava bean Presentation:
acute hemolytic crisis (fever, jaundice, abdominal pain, dark urine) due to
hemoglobin denaturation and disruption/lysis of RBCs. o
Labs:normalG6PDlevelsaretypical(asthedeficientcellsweredestroyedandnew
reticulocytes have normal G6PD levels) ?? re-test in 3 months after crisis o Smear:
degmocytes (??bite cells??) and Heinz bodies (denatured basophilic hemoglobin) o
Urine may stain with Prussian Blue (+ is presence for iron, thus hemolysis is
occuring Dx: clinical scenario/blood smearTx: supportive care during crisis with
avoidance of precipitating substances Chemotherapy Induced Nausea/VomitingIt??s not
uncommon of chemotherapy to make you sick to your stomach as it??s cellular poison.
This response is typically initiated in the area postrema in the brain which can be
blocked by 5-HT receptor antagonists (specifically ondasetron which targets 5-HT3
receptors)These drugs are well tolerated and often a mainstay for chemotherapy as
prophylaxis and reactive Tx 2646: Cancer-Related Anorexia/Cachexia Syndrome (CACS)
* Hypermetabolic state due to systemic inflammation/hyper-metabolism of cancerous
tissue, and possible side effects (loss of appetite/nausea/etc.) * Presentation:
loss of appetite/extreme weight loss in the setting of malgnancy * Dx: clinical
presentation * Tx: progesterone analogues (megastrol acetate) or corticosteroids �
proven to be more efficacious in malignancy for appetite increase/weight gaino
NOTEcannabinoids(dronabinol)areNOTconsideredefficaciousinthisproblem.They??re
considered great in HIV-related cachexia, but NOT in cancer and are not first-line.
4343/4440: B-Thalassemia Minor * Defect in one of the genes for B-hemoglobin
resulting in reduced hemoglobin production, thus mild chronic anemia refractory to
iron supplementation o ClassicinpeopleofMediterraneanorigin * Presentation:
fatigue/mild microcytic anemia which does NOT response to iron supplementation o
Labs:MCV55-75,Hct28%-40%o Smear:targetcellRBCsandpoikilocytes * Dx: genetic testing
or or elevated HbA2 on electrophoresis * Tx: symptomatic treatment 8894: If there
is a concern of parents a baby with a thalassemia anemia, and they??re not of
African descent a CBC of the mother is the best initial test. Should no abnormality
be found ?? no further testing needed. If there is an anemia with reduced MCV or if
patient is of African descent ?? futher testing is needed. 4160/4671/4672:
Transfusion Reactions and Special Situations with Blood Transfusion * There are
several adverse reactions that can occur with blood transfusion, however more
common ones have fairly specific time frames where they??ll appear, giving you a
clue to the problemo Seconds-Minutes�anaphylacticreactiono
Within1hr�acutehemolyticreaction(poortypematching)o 1-6hrs�Transfusion-
relatedacutelunginjury(TRALI)orFebrileNon-hemolyticreactions o 2-
10days�delayedhemolyticreaction * Anaphylactic reactiono
Rapidshock,angioedema/urticaria,andrespiratorydistresswithinminutesoftransfusion o
CausedbyAnti-IgAantibodiesinrecipientreactingtoIgAinthedonorblood * Acute Hemolytic
Reaction o Occurs due to poor type matching (clerical error) within the 1st hour of
infusion o Presentation:fever,chill,flankpain,hemoglobinuria??DIC/renalfailureo Dx:
(+)direct Coombs test or pink plasma (due to hemolysis)o
Tx:immediatecessationoftransfusionandfluidsforsupportivetherapy � Febrile Non-
Hemolytic Transfusion reactiono Mostcommonadversereactiontoabloodtransfusiono
Because small bits of leukocytes/plasma cells are present even in packed RBC
transfusions, WBCs can release cytokines in storage that will trigger transient
fever, chills, and malaise without hemolysis in responseo
Leukoreductionisnecessarytolimitthesereactions�reducesnumberofWBCsviavarious
methods, decreseing released cytokines AND decreasing cytomegalovirus transmission
(often resides in WBCs)o Tx:Stoptransfusion,administeranti-
pyretics,andonlyuseleukoreducedproductsforfuture
transfusions ?? Premedication with anti-pyretics/anti-histmaines NOT EFFECTIVE *
Transfusion Related Acute Lung Injury (TRALI) o Respiratory distress/non-
cardiogenic pulmonary edema 6 hours after transfusion o Anti-leukocyte antibodyes
in the donor�s serum cause this reaction * Delayed hemolytic reaction o Mild
fever/hemolytic anemia 2-10 days post transfusion caused by amnestic antibody
response (antibody was previously formed, but only in low titers. The transfusion
jacked those titers up) o Dx:(+)directCoombsor(+)newantibodyscreen o
Tx:supportivecare 3508: Superior Vena Cava Syndrome * Presentation: dyspnea, venous
congestion, swelling/plethora of the head/neck/arms but NOT the lower extremities.o
Typically, the result of lung cancer or non-Hodgkin lymphoma compression of the SVC
(>60%) * Dx: chest x-ray (IDs malignancy in chest >80% of cases)o If malignancy
noted, follow-up chest CT with biopsy of lesion * Tx: directed at specific etiology
2894: Chronic Myeloid Leukemia (CML) * Chronic lymphoproliferative disorder,
typically driven by BCR-ABL (9:22 translocation) of a tyrosine kinase to be
constitutively expressed ?? leukemogenesis * Presentation: fatigue, weight loss,
night sweats, splenomegaly (abdominal fullness/early satiety) o Labs: dramatic
leukocytosis (>100,000) o Smear: leukocytosis with basophilia and early WBC
precursors (promyelocytes/myelocytes) * Dx: presentation/smear/genetic studies
showing translocation and fusion * Tx: tyrosine kinase inhibitors (imatinib)
2887/2865: Chronic Lymphocytic Leukemia (CLL) * Chronic monoclonal lymphocyte
proliferation ?? bone marrow destruction o Classically in old folks >70y/o *
Presentation: extreme fatigue, night sweats, fevers, lymphadenopathy (cervical,
supraclavicular, axillary), hepatosplenomegaly, or infection secondary to the
disease process o
Labs:massivelymphocyticleukocytosis(10,000s),withanemia/thrombocytopenia(WBCs
edging the rest out)o Smear:maturelymphocytosiswithsmudgecellso Often asymptomatic
or presents with infection (due to poor function of WBCs) * Dx: flow cytometry
(made with demonstration of lymphocyte monoclonality of mature B cells) o
OftenlymphnodebiopsyisNOTneeded * Tx: chemotherapy regimens (multiple)
4316/4859/4616/2250: Heparin-Induced Thrombocytopenia (HIT) * Type 1 � mild
thrombocytopenia (<100,000) usually within 2 days of starting Heparin o
Doesnotcauseanyilleffects,norwarrantsintervention. o
Notimmunemediatedandwillresolvewithinafewdaysafterstoppingheparin * Type 2 � immune
mediated platelet activation by HIT antibody (IgG against PF4, which is exposed
with platelet exposure to heparin)o Presentation: worsening thrombosis in response
to heparin (usually 5-10 days, may be earlier if prior exposure to heparin), skin
necrosis in injection site (belly, periumbilical) * ?? �Thrombocytopenia �
destruction of platelet-HIT complexes by spleen and on-going thrombus formation
* ?? �Thrombus formation � HIT antibodies activate platelets with promote
aggregation and activation of coagulation cascade, promoting arterial/venous
thrombus formation o
Dx:serotoninreleaseassay(goldstandard)orimmunoassay(onlyhightiters)o Tx: immediate
cessation of heparin with initiation direct thrombin inhibitor (fondiparinux or
argatroban) � start treatment immediately before confirmatory testing 2597:
Waldenstrom�s Macroglobulinemia * Rare, chronic, plasma cell neoplasm marked by
abnormal proliferation and production of IgM antibodies * Presentation: Headache,
dizziness, night sweats, fatigue, bleeding/bruising tendency, pain/numbness in
extremities (demyelination), vision problems, and hepato-splenomegaly with
lymphadenopathy o Typically,bloodishyper-viscouswithvenousengorgement * Dx:
clinical presentation with IgM spike on blood electrophoresis o Multiple myeloma
will typically have an IgA or IgG spike, with no hyperviscosity o
MGUSwillnothaveanysymptomspresentingwithit??sIgspike * Tx: either none, or
chemotherapeutic regimens to decrease plasma cell production 3062/4333: Hereditary
Spherocytosis * Autosomal dominant defect in spectrin or ankyrin RBC structural
proteins resulting in RBC membrane blebbing and eventually deformation into fragile
spheres (instead of bi-concave disks) * Presentation: hemolytic anemia, jaundice,
splenomegaly classically in European-descent folks o
Labs:anemia,inc.MCHC/dec.MCV(smallRBCs)o
Smear:abundantspherocyteswithsomeshearingofRBCso Complications: aplastic anemia in
Parvovirus B19 infection OR pigmented gallstones (increased hemolysis causing
increased bilirubin), overwhelming sepsis from encapsulated organisms if spleen has
been removed. * Dx: Osmotic fragility test (increased fragility), acidified
glycerol lysis test (increased lysis), or abnormal eosin-5-maleimide binding test,
with negative Coomb??s test and blood smear * Tx: splenectomy (stops RBC
destruction), folate supplementation, blood transfusions o Anti-pneumococcus,
Haemophilius, and meningococcus vaccines before splenectomy and daily oral
penicillin for 3-5yrs after surgery due to risk of sepsis post-splenectomy, which
apparently lasts for >30yrs even though our prophylaxis only goes on for about 5
years. [HGH YIELD] 4402/4216: In high volume blood transfusions, the blood is
stored with citrate for anticoagulation. When transfused, the citrate can chelate
Ca2+ resulting in acute hypocalcemia (classically represented by peri-oral
parasthesias, Chvostek sign/Trousseau sign, hyperreflexia, muscle cramps, or
seizures) � Tx: IV calcium gluonate or calcium citrate 2884/2883: Polycythemia Vera
* Uncontrolled hematopoiesis due to JAK2 activating mutation (normally signaled by
EPO) o
Canbeassociatedwithpheochromocytoma,renalcellcarcinoma,hepatocellularcarcinoma, and
hemagioblastoma as a paraneoplastic peoduction of EPO * Presentation: itching after
warm shower, facial plethora, splenomegaly, pan-cythemia, blood hyperviscosity
(HTN, erythromelalgia, transient visual disturbance), gouty arthritis (increased
RBC turnover) o Labs:elevatedHb/Hct,leukocytosis/thrombocytosis o Primary PV = low
EPO | Secondary PV = reactive high EPO * Dx: presentation with JAK2 mutation or
reason for secondary EPO elevation * Tx: periodic phlebotomy or hydroxyurea (worry
of thombus formation) 4013/3943/4466/2864/2889: Multiple Myeloma * A monoclonal
plasma cell proliferation in the bone marrow resulting in monoclonal gammopathy,
massive protein production, and bone/bone marrow destruction * Presentation:
classically an old person (>65) with bone pain (back or chest), bone destruction
(fracture, hypercalcemia??constipation, anemia, leukopenia??recurrent infections),
weight loss, and fatigue o
Labs:normocyticanemia/hypogammaglobulinemia(bonemarrowinvasion),hypercalcemia
(osteoclast activation), elevated creatinine (kidney damage), protein gap (>4g/dL
between total protein and albumin) o Imaging:osteolyticbonelesionsinareasofpaino
Smear: rouleaux formation (due to increased protein) o
MonoclonalIgA/IgGspikeonplasmaelectrophoresis ?? May cause renal insufficiency
(50%; high protein filtrate, bland urinalysis) that can progress to nephrotic
syndrome * Dx: clinical presentation with monoclonal gammopathy and bone marrow
biopsy * Tx: chemotherapeutic regimens to kill of plasma cells 4384: Note that
Hypercoagulability (DVT/PE) in the setting of high homocysteine levels often is
helped via B6 (pyridoxine) and B12 (cobalamin) supplementation to aid conversion of
homocysteine ?? methionine or cysteine. (May help hypercoagulable state, but is not
totally understood!) 4437/2248: Autoimmune Hemolytic Anemia (AIHA) � Warm AIHAo
Hemolysistriggeredbyastressor(abx,infection,etc.)causingIgG/Anti-
C3antibodyformation o
Presentation:normocyticanemia,hemolysis(jaundice,indirectbilirubinemia,inc.serumlac
tate dehydrogenase, decreased serum haptoglobin), splenomegaly * ?? �Smear:
reticulocytes, spherocytes, elliptocytes, and microspherocytes * ?? �Concern of
venous thromboembolic disease o
Dx:directCoombstestdemonstratingspecificantibodiesboundtoRBCs o Tx: high-dose
corticosteroids or splenectomy (if refractory) � Cold AIHA o Hemolysis triggered by
infection (HCV, EBV mono, or Mycoplasma) or in lymphoproliferative disorders
causing IgM/Anti-C3 antibody formation o Presentation: Warm AIHA symptoms + livedo
reticularis/acral cyanosis with cold exposure that disappear with warming ??
Concern of gangrene from cold agglutinin aggregates o Dx:directCoombstest o Tx:
avoid cold temps + rituximab +/- fludaribine 4862: Lead Poisoning in Adults �
Presentation: GI (abdominal pain, constipation, anorexia), neurologic (peripheral
neuropathy/cognitive deficits), anemia (fatigue, etc.) o
Labs:anemia,elevatedleadinblood,elevatedzincprotoporphyrino
Smear:basophilicstipplingofRBCso
Classicallyassociatedwithplumbers,miners,painters,andautorepairmen * Dx: blood lead
levels + x-ray floursecence to measure bone lead levels * Tx: chelation therapy
4037: Sideroblastic Anemia * Anemia resulting from defective heme synthesis from
problem with pyridoxine (Vit B6) dependent synthesis of protoporphyrin. *
Presentation: normocytic to anemia (fatigue, pallor, etc.) o
Labs:increasedironwithdecreasedTIBC(poorRBCfunction,butironisOK) o Smear: dimorphic
RBC population * ?? �Hypochromic population �some bone marrow failing to make
proper proteins * ?? �Normochromic population � some bone marrow that??s still
doing OKo Classically this can happen with tuberculosis treatment with isoniazid,
alcoholism, drugs, etc. * Dx: clinical presentation, can be confirmed with bone
marrow biopsy showing ringed sideroblasts * Tx: pyridoxine (B6) administration
2258: Paroxysmal Nocturnal Hemoglobinuria * Autoimmune disorder resulting in
intravascular/extravascular hemolysis, classically at night due to absent
glycosylphosphatidylinositol anchors (hold
protective proteins CD-55/CD-59 to the surface of RBCs so they won??t be attacked
by the MAC complex) o Occurs at night apparently because decreased respiration
during sleep causes a mild acidosis ?? increased activation of complement ?? mor
MAC complex formation * Presentation: fatigue (hemolysis), cytopenias (impaired
hemopoesis), venous thrombosis (blood sludging/MAC activation of platelets) o
Classically pt will have dark urine in the mornings from nighttime hemolysiso
Labs:cell/marrowdamage(anemia/leukopenia/thrombocytopenia),hemolysis(elevated
lactate dehydrogenase, elevated indirect bilirubin, hemoglobinuria, low
haptoglobin) * Dx: clinical picture and flow cytometry demonstrating no CD-55/CD-59
* Tx: iron/folate supplement (help bone marrow regenerate RBCs) and eculizumab
(inhibits compliment) 4436: Hyposthenuria * Impaired ability to concentrate urine
in the glomerulus often resulting in frequent urination and frequent nocturia seen
in patients with sickle cell traito RBC induced blood thickening within the thin
vasa recta along the glomerulus in the inner medulla (high solute concentration),
causes impaired countercurrent exchange with the glomerulus inhibiting free water
absorption * NOTE that this does not damage this kidney in any way. It??s really a
blood/vascular problem. The kidney is actually functioning just fine! 4861:
Hemophilia * X-linked recessive disorder causing lack of clotting factors (A =
factor VIII def; B = factor IX def) * Presentation: delayed/prolonged bleeding
after minor trauma/procedure o Hemarthroses (bleed into joint), intramuscular
hematomas, GI bleeding, hematuria (without kidney damage), and spontaneous bruising
are all common signs o Labs: Prolonged aPTT with normal platelet count, bleed time,
and PT * Dx: decreased amount of either factor VIII or factor XI * Tx:
Administration of missing factor through injection o Desmopressin can promote
Factor VIII production and be used in mild Hemophilia A 2208: Don??t forget! Cancer
is a hypercoagulable state! If there is no reason as to why someone is having a DVT
age-appropriate cancer screening is the best call as occult malignancy can be the
underlying cause. 2868: Hairy Cell Leukemia * Presentation: fatigue, pallor,
pancytopenia (possible leukocytosis), splenomegaly, bone marrow fibrosis (??dry
tap?? if bone marrow biopsy is attempted) * Dx: demonstration of b-cells with
fine ??hair like projections?? of cytoplasm o Tartrate-resistant acid phosphtase
(TRAP) stain (+) o CD-11c marker on flow cytometry * Tx: Cladribine or Pentostatin
o Cladribine side effects = neurologic/kidney damage 4351: Differentiating Palpable
Lymph Nodes * Normal: soft, ??rubbery??, mobile, <2cm, without systemic symptoms
(often in young/fit people) ?? no big deal, just reassure or observe. * Infection:
painfully enlarged, >2cm, often with concurrent signs of infection ?? workup for
infection * Cancer: firm/hard, immobile, >2cm, systemic symptoms (fever, night
sweats, weight loss, etc.) ?? CBC, inflammation markers, viral titers, biopsy
4349/3978: In chronic kidney disease, anemia can develop as the kidney is
responsible for erythropoietin (EPO) production. The mainstay of anemia with
chronic kidney disease is supplemental EPO + supplemental iron. Iron is
supplemented as EPO will surge RBC production, causing a high need for iron for new
heme. Plus, someone with chronic kidney disease may already be anemic from chronic
inflammation! * Iron supplementation alone should always be tried first before EPO
* Side Effects: BP increase (30%, >10mm diastolic; not well understood), Headaches,
Flu-like syndrome, Red cell aplasia (rare) [HIGH YIELD] 4330: Note that
megaloblastic anemia due to B12 deficiency that??s only treated with folate
supplementation will result in worsening or emergence of neurologic symptoms
associated with B12 deficiency. This id because the folate will aid in RBC
production, which will use up the dwindling B12. Thus megaloblastic anemia should
always be treated with folate AND B12. 4446: Carbon Monoxide Poisoning * Carbon
monoxide has better steric interactions with heme as a molecule. Thus is tightly
binds heme, shifting the oxygen dissociation curve to the left ?? holds on to
oxygen and won??t deliver * Presentation: headache, confusion, malaise/dizziness,
red cheeks ?? syncope, seizure, coma, arythmia/myocardial ischemia. May be
intermittent if patient exposure is intermittent (like works at a traffic stop) o
Labs: secondary polycythemia (reactive EPO production from tissue hypoxia)o Smokers
are more sensitive to external CO as they have a low level (3%) of
carboxyhemoglobin at any given time * Dx: elevated carboxyhemoglobin level on
arterial blood gas o
NotethatpulseoximetrydoesNOTdifferentiatebetweennormal/carboxyhemoglobin * Tx: 100%
oxygen until labs normalize 4647: If ever placed in a situation where a person
needs immediate anticoagulation and has a subtherapeutic INR, never choose warfarin
alone. I know there are emerging studies with not bridging being OK, but on this
test always bridge with some other drug onto Warfarin if you�re going to use it.
This question was kind of weird, but don??t let it bug you man. 2949: Pts with
liver failure can develop life threatening anti-coagulation (low platelets, low
albumin, low Vit. K dependent clotting factor production) which can warrant
immediate attention. Infusion of Fresh Frozen Plasma will allow for immediate
recovery of the clotting factors. 4412: Anti-phospholipid syndrome * Presentation:
typically, a woman with recurrent fetal loss or arterial/venous clots. Elevated PTT
despite hypercoagulable state is due to the responsible antibodies interfering with
lipid components of the PTT test itself. PTT will not correct with 1:1 dilution of
normal plasma. o DilutedRusselvipervenomtestORkaolinclottingtimetestsmayalsobeused
o Occursinapprox.30%ofwomenwithSLE * Dx: must meet 1 clinical criterion and 1 lab
criterion o Clinical: * ?? �Arterial/venous thrombosis * ?? �>3 unexpected fetal
losses before the 10th week gestation * ?? �>1 unexpected fetal loss after the 10th
week gestation * ?? �>1 premature, normal birth before 34 weeks due to pre-
eclampsia, eclampsia, or placental insuffiency o Lab: * ?? �Lupus anticoagulant
(pro-coag in-vivo and anti-coag in-vitro) * ?? �Anti-cardiolipin antibody (IgG or
IgM with medium to high titer) * ?? �Anti-b2GP1 antibody (IgG or IgM with high
titer) 2886/2885: Differentiating a Leukemoid Reaction from CML * Leukemoid: WBC
count >50,000/mm3 due to severe infection, high leukocyte alkaline phosphatase
(LAP), featuring more mature neutrophil precursors, and no basophilia * CML: WBC
count >100,000/mm3 due to BCR-ABL fusion gene, low LAP, less mature neutrophil
precursors, and absolute basophilia 4468: Oddly enough, patients with sickle cell
disease are at higher risk for folate deficiency and megaloblastic anemia. Because
there is chronic hemolysis due to poorly deformable sickle cells, there is high RBC
turnover/production meaning there??s a high demand for folate/B12. These patients
can easily become folate deficient thus ?? a sickle cell patient (or any chromic
hemolytic patient) presenting with macrocytic anemia should first be suspected for
a folate deficiency. � Daily folate supplementation is recommended for any person
with Sickle Cell Disease! 2658/3999/4266: Hereditary Thrombophilias * Any patient
with young age of PE/DVT (<45 y/o), recurrent PE/DVT, or unusual sites of PE/DVT
(cerebral A, mesenteric A, portal veins) should be tested * Types: o
FactorVLeiden�aclassicofwhitewomenandthemostcommonoverall.Autosomaldominant
mutation of the gene for Factor V in coagulation cascade, making it resistant to
Protein C cleavage/inactivation. Thus it induces a hypercoagulable state. o
Prothrombin 20210A � 2nd most common causing increased prothrombin levelso Anti-
thrombindeficiency�decreasedanti-thrombinlevels,oftenacquiredduringDIC, cirrhosis,
or nephrotic syndrome (peeing out all you�re anti-coagulation proteins) o
ProteinC/ProteinSdef.�ifoneisn??tpresent,there??
sdecreasedinactivationofFactorsV/VIII. Protein C deficiency classically causes
Warfarin induced skin necrosis. 3597: DVTs can form in any vein of the leg, but
more proximal veins have higher risk of embolization to the heart/lungs. Thus, when
a thrombus forms in more proximal veins, we??re more concerned about embolization
complicating the picture. * Proximal Veins (90% of PEs): popliteal, femoral, deep
femoral, common femoral, and iliac veins * Distal Veins (10% of PEs):
anterior/posterior tibial veins 4112: Vitamin K Deficiency * Vit K is a critical
co-factor for enzymatic carboxylation of clotting factors II, VII, IX, X. Typically
vitamin K stores can last 30 days but in sick folks only last about 1 week! *
Presentation: bleeding diathesis with evidence of pathologic anticoagulation o
Classicallylackofsupplementationatbirth,malabsorptionforanyreason,orliverdiseasewil
l lead to Vit.K deficiency * Dx: clinical presentation * Tx: Fresh Frozen Plasma
administration with vitamin K injection 3847: Bony metastases from metastatic
prostate cancer post-orchiectomy are best treated with a focused external radiation
beam. Apparently this nails the osteoblastic lesions right where you need it and is
the fastest way to resolve these lesions. � Testosterone inhibitors/GnRH agonists
should have a minimal effect as the testosterone has already been cut down by
cutting the balls out. � 3596: DVT Workup * Presentation: unilateral pain/swelling
of the leg/calf, pitting edema, local tenderness, and prominence of leg veins
especially in the setting of a hypercoagulable state (prolonged immobilization,
recent surgery, etc.) o ModifiedWellsscoreof>2denoteshigh-
riskforDVT(basicallyyouneedtwosymptoms) * Workup/Dx: o Notlikely(Mod.Wells<1)�D-
dimertoruleout;ifpositive,continuewithcompression
ultrasonography of lower extremity o
Likely(Mod.Wells>2)�compressionultrasonographytoconfirmsuspicions.Ifnegativebutstil
l high suspicion, repeat in 5-7 days! � Tx: anticoagulation with heparin+warfarin
or a NOAC drug 4352: Apparently a hard, unilateral, non-tender lymph node in an old
smoker, in the submandibular/cervical region is highly suspicious of squamous cell
carcinoma, a very common head and neck cancer! Immediate biopsy should be performed
for pathology assessment. 4940: Terms for Different modes of Cancer Treatment *
Neoadjuvant � treatment before primary treatment for cancer * Induction � intense
initial primary treatment, aimed at sending pt into remission (<5% tumor burden) *
Adjuvant � therapy in addition to the primary therapy * Maintenance � doses to
continue primary treatment after induction, with the goal of remission *
Consolidation � treatment following achievement of remission to keep patient in
remission * Salvage � secondary treatment used only after primary treatment has
failed 2641: Tumor Lysis Syndrome * Presentation: characteristic lab changes ??
arrhythmias and possibly sudden death o
Labs:hyperphosphatemia/hyperkalemia(intracellularions),uricacidemia(proteinbreakdow
n), and hypocalcemia (binding of calcium from phosphate release) o Classically
associated with poorly differentiated lymphomas and any leukemia * Dx:
characteristic lab changes/status changes in the setting of cancer treatment * Tx:
vigorous hydration and supportive care 2618: Bone Tumors/Disorders of the Knee
Giant Cell Tumor of Bone * Benign, locally aggressive bone tumor classically seen
in young adults * Presentation: pain, swelling, decreased range of motion at site,
sometimes with pathologic fracture o Imaging:??soapbubble??
lesionatepiphysisofboneonx-ray;MRIcanshowbothcysticand hemorrhagic lesions o Biopsy
shows giant cells within the lesion, causing the bone damage * Dx: presentation
with characteristic imaging/x-ray * Tx: surgical resection w/without bone graft
Osgood-Schlatter Disease * Repetitive use injury causing avulsion of tibial
tubercle insertion point, classically in teens going through a growth spurt *
Presentation: pain around the tibial tubercle, especially with use * Dx:
presentation or signs of avulsion at tibial tubercle * Tx: R-I-C-E therapy and rest
with gradual increase in activity Baker??s Cyst (popliteal synovial cyst) * Cystic
swelling behind the knee joint, classically as part of a degenerative joint disease
* Presentation: swelling on posterior-medial popliteal fossa in the gastroc-
semimembranous bursa * Dx: cystic-fluid filled space behind the knee * Tx: incision
and drainage Osteitis Fibrosa Cystica (von Recklinghausen disease of bone) *
Rare ??brown tumor of bone?? caused by hyperparathyroidism due to parathyroid
carcinoma. Osteoclastic activation by PTH results in bone reabsorption and
replacement of brown fibrous tissue * Presentation: bone pain with possible other
signs of malignancy * Dx: bone cysts, ??salt-and-pepper??, and tumors of the long
bones on imaging * Tx: treatment of underlying condition with ablation or surgical
treatment of tumors Osteoid Osteoma � bone tumor appearing as a sclerotic cortical
lesion with a central nidus of lucency. Pain is worse at night and unrelated to
activity with quick response to NSAIDs.3890: This was a bit of a weird question,
but the idea was to recognize the constellation of signs/symptoms of Hereditary
Hemochromatosis * Presentation: Skin (Hyperpigmentation, ??bronze diabetes??), MSK
(arthalgias/arthropathy/chondrocalcinois), GI (elevated LFTs, with hepatomegaly ??
cirrhosis, increased risk of hepatocellular carcinoma), endocrine (diabetes,
hypogonadism/hypothyroidism, diminished libido/erectile dysfunction), cardio
(restrictive cardiomyopathy/abnormal condution), and infections (Listeria, Vibrio,
and Yersinia increased susectibility) * Dx: HFE genetic mutation and elevate iron
studies � Tx: serial phlebotomy (decrease iron store)2872: Note that basophilic
stippling is not as specific as you might think, and that it can occur in
alcoholism (may be part of folate deficiency macrocytic anemia), lead poisoning,
and thalassemia. 2624: Trousseau�s Syndrome (Migratory Superficial
Thrombophlebitis) * Hypercoagulable disorder causing superficial thromboses
typically preceding or concurrent (may occur years in advance) with visceral
malignancy (pancreas most common, lung, prostate, stomach, colon, or leukemia may
also occur) o Occurs due to mucin release from the visceral tumor which react with
platelets to form microthombi ?? thrombophlebitis * Presentation: appearance of
unexplained superficial venous thromboses at unusual sites (upper extremity and
chest are classic) * Dx: clinical presentation * Tx: diagnosis and treatment of
underlying malignancy ?? pt should have a CT abdomen done to assess 2599: Treatment
of Mild Hypercalcemia (<12mg/dL) � Classically due to bone lesions from metastatic
cancer. It does NOT require emergent fluid therapy but initiation of
bisphosphonates helps slow osteoclastic activity and decrease risk of pathologic
fracture/malignant hypercalcemia Renal/Urinary/Electrolytes 3949: Cystinuria [HIGH
YIELD] * A group of autosomal recessive amino acid resorption disorders causing
failure to absorb cysteine, ornithine, lysine, and arginine (COLA). As cysteine is
poorly water-soluble, it forms crystals in the urine * Presentation: flank pain
radiating to the groin, hematuria, often with recurrent stones since childhood or
positive family history of urinary stones * Dx: radiopaque renal stone featuring
hexagonal crystals in urinanalysis or positive cyanide nitroprusside test
confirming presence of cysteine in urine * Tx: hydration, alkalization of urine,
and reduction of protein/salt intake 3942: Nephro/Glomerulosclerosis are classic
renal lesions resulting from long-standing hypertension, ultimately leading to
kidney disease and worsening HTN. * Nephrosclerosis: hypertrophy/fibrosis of renal
arterioles * Glomerulosclerosis: glomerular/peritubular fibrosis with progressive
loss ofglomerular capillary surface area * Presentation: sclerotic shrinking of
kidney with hematuria/proteinuria and decreasing function * Tx: strict control of
HTN to minimize blood vessel damage 3648/2167/4760/4422/4288/8331: Hyperkalemia �
Presentation: confusion, lethargy o EKGchanges:peakedT-
waves,QRSwidening,bradycardia,andventriculararrhythmiaswith sine wave pattern �
Etiologies:o Recent stroke (high neuronal activity means lots of K+ getting into
the blood) o Drugs(non-selectiveB-blockers,ACEinhibitors,ARBs,K-sparingdiuretics
[spirononlactone/eplerenone/amiloride/triamterene], digoxin, NSAIDs, TMP-SMX as it
can block aldostone, apparently) * Dx: high K+ (>5.0) on basic metabolic panel or
fast rise in K level * Tx: o Emergent treatment � Ca2+ carbonate or Ca2+ gluconate
infusion (stabilize cardiac myocyte) o Fast-
actingtreatments�IVinsulin+glucoseAND/ORalbuterolinhalation(activateNa/K+ ATPases
and pull K+ into the cells, lowing blood concentration)o Long-
termtreatments�aimtoreducetotalbodypotassiumafterstabilizationbyothertx * ?? �IV
fluids � dilute blood and promote diuresis for K removal * ?? �Diuretics � promote
diuresis to promote K removal * ?? �Exchange resins (sodium polystyrene sulfonate)
� pull K from the body via the GI tract (takes hours for effect) * ?? �Hemodialysis
� remove K directly via hemodialysis � Note that any of these treatments (esp.
albuterol for bronchodilation) may result in hypokalemia 4432: Anti-Cholinergic
Urinary Retention * Remember that muscarinic (ACh, parasympathetic) influence is
what causes detrusor contraction and internal urethral sphincter relaxation for
urine flow. Elderly people on anti-cholinergic drugs (esp. anti- depressants) are
at high risk for this complication * Presentation: bladder urinary retention with
suprapubic pain * Dx: demonstration of post-void urine volume >50mL (men) or >150mL
(women) * Tx: immediate urinary catheterization with discontinuation of inciting
drug 12033: Types of Urinary Incontinence * Stress incontinence � leakage of urine
with increased intraabdominal pressure (laughing, sneezing, coughing, lifting,
etc.) due to weakness in the pelvic floor o Presentation:(seeabove)o
Dx:clinicalpresentationo Tx: * ?? �Initial: pelvic floor exercises/lifestyle
modifications * ?? �Refectory: pelvic floor surgery * ?? �Surgical
failure/contraindication: pessary placement * ?? �If unipolar depression present:
duloxetine (5-HT, NE reuptake inhibitor) * Urge incontinence � excessive
urgency/need to urinate due to detrusor over-activity o Presentation:
dribbling/leakage of fluid day and night without increased intraabdominal pressure
(laughing, coughing, etc.).o Dx: presentation with post-void residual analysis
(rule out overflow) and urinalysis (rule out infection) o Tx: * ?? �Initial:
bladder training and Kegel exercises to strengthen the pelvic floor * ??
�Refractory: oxybutynin (anti-muscarinic drug to decrease parasympathetic
signaling) to help relax the detrusor. May result in urinary retention and other
anti-muscarinic effects (dry mouth, constipation, blurry vision, etc.) � Overflow
incontinence � constant involuntary dribbling due to incomplete voiding. Bladder
gets overwhelmed by urine pressure and eventually opens non-voluntarily causing
dribbling. May be due to neurogenic bladder (traumatic nerve damage, spinal
compression, diabetic neuropathy) o Presentation:(seeabove) o
Dx:postvoidresidualvolumeshowing>50mL(men)or>150mL(women)withclinical presentation
o Tx:intermittentcatheterizationand/orbethanachol(cholinergicagonisttoincrease
parasympathetic activity) to aid in detrusor contraction 3061/2242: Acute
Interstitial Nephritis * Typically drug-induced damage to interstitial tissue
in the kidney * Presentation: acute renal failure, fever, macropapular rash,
classically following offending drug use (5 days to several weeks following drug),
and sometimes arthralgiao Urinanalysis:Pyuria,hematuria,eosinophiluria,andWBCcasts
o Biopsy:inflammatoryinfiltrationandedema * Dx: clinical presentation with agreeing
labso Drugs:penicillins,TMP-SMX,cephalosporins,rifampin,diuretics,orNSAIDs * Tx:
discontinue offending drug, glucocorticoids, and supportive care 2787: Don??t
forget that pH and PaCO2 are the only two lab values needed to assess acid-base
status! 3336/3481/3477/8929/4615: Benign Prostatic Hypertrophy and Prostate Cancer
* A classic of aging men. It??s said that any man living long enough will have
prostate dysfunction. * Presentation: o
BPH:urinaryurgency,hesitancy,nocturia,andweakurinarystream,sometimeswithbladder
outlet obstruction (pain, renal dysfunction, elevated creatinine) * ?? �Age>50 is
the biggest risk factor * ?? �Note that if a patient has severe pain with Valsalva
and BPH, they may start to have urinary retention, as then need to strain to pee,
but refuse to due to abdominal pain o Prostate cancer: may have signs of BPH with
osteoblastic lesions in spine (if metastatic) ?? Cigarette smoking, African
American race, and age >40 are all risk factors � Dx: Digital rectal exam, renal
ultrasound, BMP, and urinalysis sometimes with cytoscopy o
DRE:distinguishedBPHfromprostatecancermosttimes * ?? �BPH: smooth, symmetric,
centrally enlarged prostate * ?? �Prostate cancer: enlarged, irregular, firm
nodules on the lateral lobes on prostate o
Renalultrasound:canshowhydronephrosisconsistentwithbladderoutletobstructiono
BMP:willshowelectrolyte/creatininechangesifrenaldamageoccuringo Urinanalysis:
checks for renal dysfunction and frank blood (possible cancer indicatoro
Cytoscopy:indicatedforanyonewithunexplainedgrosshematuriaandriskfactorsforbladder
cancero PSA screening isn??t entirely recommended, however, it can be discussed
with the patient and can be used to follow response of diagnosed cancer to therapy
� Tx:o BPH:alphablockers(tamsulosin/doxazosin)or5a-
reductaseinhibitors(finasteride)to shrink/relax prostate. Surgical intervention if
pharmacotherapy does not work. o Prostatecancer:chemotherapeuticregimens 4535: CO2
Narcosis is altered mental status in pts with PaCO2 >60mmHg. Classically this will
occur in the setting of COPD, where CO2 retention is commonplace. It may also
contribute to a respiratory acidosis (increased pH, decreased bicarb) 2235/3693:
Treatment of Different UTIs in non-pregnant women * Uncomplicated Cystitis � UTI in
a relatively healthy person without risk factors, often urinalysis showing pyuria
is enough to treat and a urine culture is only needed in women who don�t respond to
antibiotics o Nitrofurantoin for 5 days (avoid if pyelonephritis or GFR <60) o TMP-
SMX for 3 days (avoid if local resistance >20%)o Fosfomycin single doseo
Floroquinolonesifabovetreatmentscannotbeused * Complicated Cystitis � cystitis in
the setting of co-morbid conditions that increase the risk for treatment failure
(diabetes, CKD, immunocompromised, urinary obstruction, recent instrumentation, or
medical device presence. UA/urine culture needed before treatment. o
Floroquinolones+broadspectrumabx(ampicillin/gentamycin)for5-14days o
Adjustbasedonculturesusceptibilities * Pyelonephritis � UTI that has progressed all
the way up to the kidney. UA/urine culture needed. o
Outpatient:oralfluoroquinoloneso Inpatient:IVfloroquinolonesorIVaminoglycoside+/-
ampicillin o Adjustbasedonculturesusceptibilities * Note that pregnant women should
NEVER receive floroquinolones as they cause birth defects 2803/2820: Salicylate
Intoxication * Presentation: tinnitus, fever, tachypnea, and nausea/vomitingo Anion
gap metabolic acidosis occurs from excessive salicylic acid causing low bicarbo
Respiratory alkalosis via tachypnea in response to acidosis to temper pH/causes low
PaCO2o Often pH will only be slightly acidic (around 7.4) slowing treatment because
of these two things * Dx: presentation with demonstration of excessive salicylates
in blood * Tx: alkalization of blood or dialysis (speed removal of salicylic acid)
4502: Bladder Cancer Screening is not recommended by the USPSTF as bladder cancer
has a low incidence making screening have a poor positive predictive value
regardless of occupational exposure. 4152: Acute rejection of renal transplant
should be treated with immediate anti-rejection therapy (high-dose IV steroids) to
reduce inflammation in hopes of saving the transplant. Surgery is not warranted
until this therapy has failed. 2821: Anion Gap metabolic acidosis following a
Grand-Mal seizure should not immediately be corrected unless pH gets <7.2.
Typically, the intense muscular activity during the seizure produces lactic acid
which will be cleared within 2 hours. Thus re-checking labs after 2 hours is the
proper first step. � If pH <7.2 occurs, gentle bicarbonate infusion should be
given. But full correction of acidosis should NOT be sought, as it is easy to
overshoot your target pH of 7.4. 2229: Myoglobinuria * Acute renal failure
following diffuse muscle damage, classically after a tonic-clonic seizure *
Presentation: acute elevation of creatinine, often with hypertension/tachypnea o
Urinanalysis:largeamountofbloodwithfewRBCsonmicroscopy * Dx: clinical picture with
classic disparity in urinanalysis (RBCs is detection of hemoglobin OR myoglobin
thus, a standard UA will say ??large RBCs amout?? but microscopy will show few
RBCs/hpf) * Tx: hydration and supportive care until return of baseline renal
function 4423/4082: Hypomagnesaemia * Presentation: typically, you can see Mg2+
levels on BMP, but this becomes clinically important as low magnesium is a classic
cause for refractory hypokalemia. Magnesium serves as a cofactor for uptake of
potassium into the cell. Typically, we shoot for a Mg2+ of 2. * Etiology:
alcoholism, diuretic useo
Notethatalcoholismclassicallycauseshypokalemia/magnesemia/phosphatemia *
Hypocalcemia can also be induced by hypomagnesemia. This is because the
hypomagnesemia causes decreased PTH hormone production and decreased PTH
sensitivity. Thus hypocalcemia + hypomagnesemia should always be treated with
repletion of both electrolytes. This problem will also be marked by low-normal
phosphate levels. o Note that primary hypoparathyroidism would have low Ca, low
Mag, and high phosphate 2241: Post-Streptococcal Glomerulonephritis * Autoimmune
disease in response to a streptococcal throat/skin infection occurring 10-20 days
post- infection. Classically happens in kids and young adults. * Presentation:
Fever, rash, arthralgia, periorbital edema, hypertension o
Urine:oliguria,proteinuria,hematuria,sterilepyuria,eosinophiluria,WBCcasts o
Blood:eosinophilia,lowserumC3complimentlevelso Biopsy: sub-epithelial humps due to
complement deposition * Dx: clinical presentation with elevated ASO titer or anti-
DNase B antibodies * Tx: supportive care, should resolve on its own o Prognosis
good in children but very bad in adults often leading to renal failure 2230/10287:
IgA nephropathy * Autoimmune deposition of IgA in the meconium of kidney causing
damage 5 days after URI, classically in young men. Can recur any time after an URI
as it??s the result of over-activation of the normal immune response. Does not
occur with skin infections. o
Themostcommonglomerulonephritisinadults;rememberthatdamageoccursinglomerulus! *
Presentation: recurrent gross hematuria following a URI o Labs: normal serum
compliment levels * Dx: presentation. IgA demonstrated deposition in renal biopsy *
Tx: supportive care (often benign) with close watch for progression 4491: Contrast-
Induced Nephropathy * Renal vasoconstriction/tubular injury due to administration
of IV contrast for imaging procedures * Presentation: spike in creatinine following
contrast administration, with resolution around 5 days later o Pt with impaired
renal function (diabetes, chronic renal insufficiency, etc.) are at high risk * Dx:
clinical presentation * Tx: supportive care for recover, prevention is keyo Pre-
contrast hydration with IV fluids (isotonic bicarb or normal saline) o
Acetylcysteine may be used if concern is high (vasodilation/antioxidant) 2169/2633:
Hypercalcemia * Presentation: confusion, stupor, coma, dehydration (polyuria/poor
oral intake) * Etiology: underlying malignancy, malignancy hyperPTH secretion,
thiazide diruetics * Dx: high Ca2+ on BMP * Tx: o Mild(<12),Moderate(12-
14)orasymptomatic�noimmediatetreatment.Avoid diuretics/lithium and give hydration
to ensure hemoconcentration does not occur o
Severe(>14)orsymptomatic�immediatelygiveIVsaline+calcitoninandstoploopdiuretics
unless pt needs them for CHF. Long-term give bisphosphonates to decrease the amount
of Ca2+ being introduced to the body through bone resorption. 8876: Hypocalcemia�
Presentation: fatigue and weakness o Labs:lowCa2+ � Dx: o Lowmagnesium?
DrugsthatcausehypoCa?RecentBloodtransfusion???correctitifyes. o
Ifno,measurePTHlevel * ?? �Low/normal PTH � surgical damage to parathyroids,
autoimmune destruction of parathyroids, or some infiltrative disease (Wilson??s,
hemochromatosis, etc.) * ?? �High PTH � Vit D deficiency (check 25-Vit D levels),
CKD, sepsis, tumor lysis syndrome 4228: Diabetic autonomic neuropathy can be
extremely wide ranging. So be on the lookout! * Cardiovascular � tachycardia, poor
exercise tolerance, orthostatic hypotension (hard time with autonomic
vasoconstriction to keep BP up when needed) * Peripheral nerves � dry
skin/pruritus/calluses, foot ulcers, poor wound healing, Charcot arthropathy *
Gastrointestinal � gastroparesis/nausea and vomiting from delayed gastric emptying,
esophageal dysmotility/dyspepsia, diarrhea, constipation, or fecal incontinence
* Genitourinary � poor sensation of bladder fullness/neurogenic bladder and
overflow incontinence, recurrent UTI erectile dysfunction/retrograde ejaculation,
dyspareunia 4084: General Dehydration * Presentation: dry oral mucosa, altered
mental status, marginally elevated serum electrolytes and Hct (concentration), with
BUN/creatinine >20 (improper perfusion of kidneys)o Elderly pts are prone to
dehydration, especially after even minor infections or illnesses * Dx: clinical
presentation * Tx: IV crystalloid solutions (sodium solutions) o IV colloid
solutions (albumin) are used in pts with severe burns, as they??ll dehydrate and
lose protein through the burn sites 2958/2232: Cryoglobulinemia secondary to
Hepatitis C infection * Occurs via IgM immune complex deposition causing
inflammation and damage in areas of deposit/vascularture * Presentation:
muscle/joints (arthralgias), skin (palpable purpura, Raynaud??s), liver (elevated
transaminases, ALT>AST), kidney (moderate-to-severe glomerulonephritis), and PNS
(motor-sensory axonopathy) o Labs: decreased compliment levels, cryoglobulins,
serologic evidence of HepC o HxmaysuggestHepCexposure(IVDUisclassic) * Dx: clinical
presentation with agreeing lbs * Tx: plasmapheresis (remove cryoglobulins) and
cyclophosphamide/corticosteroids (immunosupp.) 2183/3986/4515/3902: Signs of
Diabetic Nephropathy * First Sign: hyper-filtration via vascular damage and
increased glomerular pressures o
ACEinhibitorsgoafterthisbydecreasingglomerularhypertension,decreasingdamage * Most
sensitive Early Sign: microalbuminuria (30-300 mg/day) o Must be checked via random
urine microalbumin/creatinine ratios via spot urine or timed urine collections as
urine dipsticks will only detect protein >300 o This is due to glomerular basement
membrane damage from sugar presence. Typically causes thickening of the GBM and
HTN/ o Note that normal protein excretion is <30mg/day) o Adding an ACE inhibitor
or ARB is warranted to slow glomerular damage� Later Signs: macroalbuminuria
(>300mg/day) with possible progression to nephrotic syndrome o Occurs due to damage
to the microvasculature from longstanding (>15yrs) non-enzymatic glycosylation
damages the glomerular capillaries, causing long-lasting damageo
Nodularglomerularsclerosis(Kimmelstein-wilsonnodules)ispathgonomonic 4337: Note
that a BUN:Creatinine >20 indicated Pre-renal azotemia, in that the kidneys are not
being properly perfused for any reason. Thus any sick patient showing this should
receive IV fluids alongside stopping any nephrotoxic drugs (NSAIDs, metformin) �
Metformin can induce a lactic acidosis, thus any patient with acute liver
failure/renal failure/sepsis should have their metformin stopped to decrease the
risk of damage by excessive lactate. 3894: Renal Artery Stenosis/Renovascular
Hypertension * Presentation: resistant HTN (3 drug regimen cannot control),
malignant HTN (end organ damage), new severe HTN (>180/120) after age 55, recurrent
flash pulmonary edemao
Asymmetrickidneysize,abdominalbruits,unexplainedriseincreatinineafterstartingan
ACE/ARB, unexplained atrophic kidney * Dx: clinical presentation with concurrent
findings * Tx: o
Initial:ACE/ARBadministration+additionalagentsifneeded.IfRASisunilateral,the
unaffected kidney is no longer subject to the RAAS activation being set forth by
the stenotic one, and will compensate for proper renal function. If bilateral,
kidney function can worsen o
Refractory:revascularizationorrenalarterystenting.Reservedforthosewhodonottolerate
anti-hypertensives, have flash pulmonary edema, or heart failure due to HTN. 11566:
Cyanide Toxicity * Presentation: CNS (headache, altered mental status, seizure,
coma), cardio (arrhythmias), respiratory (tachypnea turning into respiratory
depression), GI (abdominal pain, nausea, vomiting), renal (metabolic acidosis from
lactic acid, and renal failure) o
Etiology:prolongedsodiumnitroprussideinfusion(metabolizedtoCN-),combustionof
wool/silk (contain CN-), or industrial exposures * Dx: clinical presentation * Tx:
sodium thiosulfate or hydroxycobalamine infusion to remove CN- from blood 3085:
Diuretic Abuse * Presentation: volume depletion/orthostatic hypotension, and often
signs of anorexia (often pts will use diuretics for weight loss, getting them from
a family member) o Labs:hyponatriemia/kalemia/chloremiao
Urine:elevatedsodium/potassiumoutput * Dx: clinical picture with labs * Tx:
rehydration/repletion of electrolytes along with psychiatric counseling 4171: Side
effects of Thiazide diuretics (HCTZ or chlorthalidone) * Glucose intolerance �
worse insulin release from pancreas AND tissue resistance to glucose uptake. Worse
in pt with diabetes or metabolic syndrome * Poor lipid metabolism with increased
LDL/triglycerides � similar to glucose intolerance. Worse in diabetes or metablic
syndrome * Hyponatremia/kalemia/magnesemia and hypercalcemia � based on mechanism
of action. Actually beneficial in staving off osteoporosis * Hyperureciemia and
worsening gout � reduces renal uric acid excretion 3939/4474: Autosomal Dominant
Polycystic Kidney Disease * Genetic defect resulting in adult onset of renal cysts,
ultimately with progressive renal decline * Presentation: hypertension, palpable
bilateral flank masses, microhematuria, with extra-renal manifestations based on
connective tissue weakness: o Berry aneurysms (most common; increased risk for
intracranial bleeding), Hepatic Cysts, Valvular Heart Disease (mitral
prolapse/aortic regurgitation), Colonic Diverticula, and Abdominal/inguinal hernias
o Typically right kidney is palpable which left is not as the right kidney sits
lower in the abdomen and the liver may cystic, pushing the right kidney down
further * Dx: family history or genetic testing * Tx: renal transplant once kidney
function becomes too poor 2180/2181/2636/4642/4643/7722: Syndrome of Inappropriate
ADH (SIADH) * ADH works primarily by increasing free water resorption through
stimulating AQP-2 channels in the collecting duct to concentrate the urine and
retain water. * Presentation: altered mental status, not dehydrated/hypovolemic o
Labs: * o �Low relative plasma osmolality (diluted, <290mOsm/Kg) with high urine
osmolality (concentrated, >100mOsm/Kg) * ?? �Hyponatremia (<130, dilutional) with
high urine sodium (>20mEq/L) * Etiologies: NSAIDs (potentiate ADH), endocrine
dysfunction * Dx: simultaneous measurement of serum osmolality and urine osmolality
o Serumosmolality=[2Na]+[BUN/2.8]+[Glu/18]o
Normalthyroid/adrenalglandfunctionmustbeconfirmedtoconsiderSIADH o
Failuretorepleteserumsodium/increasedurinesodiumwithsalinebolus � Tx:o
Asymptomatic/mild(forgetfulness,unstablegait)�fluidresuscitation+oralsalttablesorlo
op diuretic if urine osmolality x2 higher than serum osmolalityo
Moderate(confusion/lethargy)�hypertonicsalineuntilserumsodium>120mEq/L,thenswitch
to normal saline for further resustitationo
Severe(seizure,coma)�hypertonicsalinebolusesuntilsymptomsresolve+/-vasopressin
receptor antagonists (convaptan) to combat disease provesso Evenifyoucantellit??
sSIADH,ifthepatientisseverelyhyponatremic,treatthatfirst. 2819/4236: Metabolic
Alkalosis from Gastric Contents Loss * Recurrent vomiting (self-induced or
otherwise) or nasogastric suctioning can lead to abrupt losses of stomach HCl,
resulting in an alkalosis. The body responds by taking in K+ into the cells in
exchange for H+ to stave off the alkalosis resulting in hypochloremic, hypokalemic
metabolic alkalosis. * Presentation: dehydration +/- anorexia with concurrent BMP
findings * Dx: presentation with electrolyte findings � Tx: IV isotonic saline with
electrolyte repletion with address of underling causes 4807: Interstitial Cystitis
(Painful Bladder Syndrome) * Poorly understood disorder most commonly in women with
anxiety/pain syndromes * Presentation: suprapublic pain with bladder filling
relieved with voiding, increased urinary frequency/urgency, and dyspareunia/pain
with exercise/pain with alcohol consumption * Dx: bladder pain for >6 weeks without
attributable cause with normal UA * Tx: psychiatric therapy, amitriptyline, and
analgesics for exacerbations 2657: Evaluation of Hyponatremia * Serum osmolality
>290mOsm/Kg? ?? Yes = consider hyperglycemia or advanced renal failure * Urine
osmolality <100mOsm/Kg ?? Yes = consider primary polydipsia or beer drinkers
potomania * Urine sodium <25 mEq/L? o Yes=volumedepletion,CHF,orlivercirrhosiso
No=considerSIADH,adrenalinsufficiency,orhypothyroidism Primary Polydipsia � a
central compulsion to constantly drink water, associated with psychiatric
conditions * Presentation: confusion, lethargy, seizure, coma (due to hyponatremia)
o Thoughttooccurduetosuppressionofthirstreflex,thustheycontinuetodrinkwatereven
though they are diluted eventually overwhelming the kidney�s ability to excrete
water o Labs: severe hyponatremia (in the 110s), low serum osmolality (<290) and
low urine osmolality * Dx: clinical picture with labs * Tx: water restriction and
psychiatric evaluation 2165: Familial Hypocalciuric Hypercalcemia * Benign,
autosomal dominant mutation in the calcium-sensing receptor (CaS-R) of the
parathyroid glands. This causes increased elevation of serum Ca2+ to activate them
to stop PTH secretion. This results in increased Ca2+ resorption in the renal
tubules o Differentiated from primary hyperparathyroidism by calcium urine
excretion * Presentation: asymptomatic with normal renal function o Labs:
hypercalcemia with low urine calcium excretion (<100mg/24hr) * Dx/Tx: lab
abnormalities, no treatment needed in the absence of symptoms 4007/4004: Analgesic
Nephropathy (Tubulointerstitial Nephritis/Papillary necrosis most common) *
Nephropathy due to chronic analgesic use. Be on the lookout when a patient has
inflammatory or joint disease
for years that they said they take NAIDS to help ito Occurs with cumulative
ingestion of 2-3Kg of the index drug * Presentation:o Early: increased urinary with
sterile pyuria/WBC castso
Progression:HTN,mildproteinuria,andworseningrenalurineconcentrationo Late-
stage:nephroticsyndrome,prematureaging,atherosclerosis,andrenalcancers * Dx:
presentation with possible biopsy showing characteristic changes * Tx: stop
analgesic use and proper symptom management 4749: Unilateral Obstructive Uropathy �
An obstructive uropathy, classically cause by renal calculi. This question gave us
an odd situation where the patient only had 1 kidney, and was forming kidney stones
in the other one! o May occur with two kidneys but less common * Presentation:
flank pain (renal capsule distention), poor urine output (outflow obstruction),
intermittent episodes of post-obstructive diuresis (backed up urine coming out
after passing a stone). o
Weaknessandhypokalemiacanoccurwithexcessivediuresisinthiscondition * Dx: clinical
presentation with demonstrable obstructive process * Tx: treatment of underlying
condition 2182/4430/2181/4424: Treatment of Hypernatremia * Euvolemic � supplement
free water (5% dextrose or 0.45% saline) to dilute out the hypernatremia and workup
underlying cause of hyponatremia * Hypovolemic without symptoms � free water
supplement (5% dextrose or 0.45% normal saline) * Hypovolemic + symptoms (dry
mucous membrane/thirst/low BP/etc with low sodium) should first be volume repleted
with normal (0.9% normal saline), then supplement free water (5% dextrose preferred
but 0.45% saline is OK) to dilute out hypernatremia o Note that sodium correction
should be 0.5mEg/dL/hr and never exceed 12mEq/dL/24hr for fear of
demyelination/swelling of the brain causing irreparable damage o
Notethatdifferentcorrectionscausedifferentbrainchanges: * ?? �Hypo??normal = low
Na+ in cells, additional sodium moves water out of the neurons/glia causing
demyelination and damage * ?? �Hyper??normal = high Na+ in cells, additional water
causes cerebral edema from movement of free water into the neurons/glia 2324/4027:
Uric Acid Stones * Presentation: unilateral pain, hematuria, and possible renal
colic (intermittent pain from clogging/unclogging of the ureter)o
Urinalysis:needle-shapedcrystals,frankhematuria,somepyuria * Dx: CT abdomen (best),
abdominal ultrasound, or IV pyelographyo Uric acid stones are radiolucent; thus
they cannot be picked up on abdominal X-ray * Tx: potassium citrate (alkalinize
urine), low purine diet, hydration, and supportive care (stone <1cm) or surgical
removal (stone >1cm) 4026: While cardiovascular disease has been declining in the
general population, it remains the #1 killer in patients on dialysis (50% of
deaths). This is attributed to likely already present risk factors (which likely
got them on dialysis), end stage renal disease, and being on dialysis itself, among
many other risk factors. � Note that cardiovascular disease is a major killer of
renal transplant patients likely for similar reasons. 2798/2793/2799: Approach to
Anion Gap Metabolic Acidosis � Presentation: confusion, disorientation, agitation o
Anion Gap = [Na+ - (Cl- + Bicarb)] ?? anion gap present if >17o
OsmolalGap=measuredserumosmolality�calculatedserumosmolality??osmolalgap present if
>10?? Serum osmolal calculation = [2Na + 18Glucose + BUN/2.8] � Etiologies ??
MUDPILESo Methanol�osmolalgappresent,newonsetblindness o
Uremia�renalfailurewithhighBUNo DKA�hyperglycemia,urine/serumketoneso
Propyleneglycol�osmolalgappresento IsoniazidorIron�recentdrugingestiono
Lacticacid�increasedserumlacticacid o Ethyleneglycol(anti-
freeze)�osmolalgappresent,calciumoxalatecrystals(rectangle envelopes) in urine
sample o Salicylate (aspirin) � recent drug ingestion with early
hyperventilation/near normal pH � Tx: normal saline fluids + antidotes if present
2810: Normal anion-gap metabolic acidosis * Causes: diarrhea, fistulas, CA
inhibitors, renal tubular acidosis, iatrogenic causes * Labs: low bicarbonate, but
no anion gap 4414: Acyclovir Nephrotoxicity * Because acyclovir is principally
excreted in the urine (glomerular filtration and tubular secretion), high doses or
fast infusion can lead to saturation of urine, leading to acyclovir crystal
formation. * The resulting crystaluria can result in renal tubular damage and rapid
decline of renal function * Adequate hydration both prevents and treats this
condition. 3966/2223/3984: Classic Nephrotic Syndrome Diseases and Associations *
Focal Segmental Glomerulosclerosis � Obese Blacks/Hispanics with HIV/Heroin use *
Membranous nephropathy � SLE, HBV, NSAIDS, and adenocarcinoma *
Membranoproliferative glomerulonephritis � HBV/HCV, or lipodystrophy * Minimal
Change Disease � NSAIDs/lymphoma * IgA nephropathy � recent URI Note that often
these will resolve if the underlying cause is fixed! 2228/3435/3895/4058: Calcium
Renal Stones * Calcium oxalate � the most common type of renal stone. Radiopaque.
Small, envelop-shaped crystals are seen on microscopy. Classic risk factors are
small bowel disease, bowel resection, or chronic diarrhea, as they decrease the
absorption of fat in the gut. This is a problem as the fatty acids will chelate
Ca2+, leaving oxalic acid free of Ca2+, so it can be easily absorbed into the body!
* Calcium Phosphate � another radiopaque stone common in primary
hyperparathyroidism or renal tubular acidosis. * Some suggestions to minimize
formation of these stones are: o
Useofthiazidediuretics(passiveincreasedreabosrbtionofCa2+)o
Increasedfluidintake(diluteitouttomakecalciumnotformstones)o Decreased Na+ intake
(increases Na/Ca reabsorbtion, thus decreasing amount in kidney) o NormalCa+
+indiet(poorCa++intakeincreasesoxalateabsorbtion,thuspromotingthe formation of
calcium oxalate stones!)o HighK+diet(decreasesCa++excretion)o
Lowanimalfatdiet(decreasedacidproductiontobefilteredoutbyurine) 4006: Never forget,
rifampin causes red/orange urine discoloration as well as discoloration of tears,
sweat, and saliva. Classically it??s known to stain contact lenses. � It??s
important to do a simple urinalysis to rule out more serious conditions.
2227/11109: Management of Acute Renal Stone * Imaging: abdominal x-ray will often
work, but abdominal CT will pick up even radiolucent stones * Pain control: NSAIDs
preferred in people with normal renal function, but narcotics can be used � Stone
Size: stones <5mm in size should pass spontaneously. Increasing fluid intake to
>2L/day will aid in passing the stone as well as preventing further stone formation
o BMPalongwithurinalysisshouldbeundertakeninanypatientwiththeirfirststoneo
Tamsulosin (a1-blocker) may be used in relax the bladder/ureteral walls to aid in
passing the stone by preventing reflex ureteral spasm� Urology: anuria, urosepsis,
or acute renal failure all warrant immediate urology consult 3997: Amyloidosis is a
classic reason for nephrotic syndrome in adults, typically consisting of enlarged
kidneys with hepatomegaly. Multiple myeloma/Waldenstom??s macoglobulinemia (AL
amyloid), or chronic inflammatory conditions/infections (AA amyloidosis) are
classic causes. � Rheumatoid arthritis is the most common cause of AA amyloidosis
in the UA! 4428: When someone is needing rapid intubation due to respiratory
failure, it??s prudent to use a neuromuscular blocker for easier time placing the
intubation. * Succinylcholine: drug of choice due to rapid onset, however is
contraindicated in pts at risk for hyperkalemia as it may precipitatre worsening of
it. o Crush/burninjuries<8hrold;Guillian-Barresyndrome,andtumorlysissyndrome *
Vcuronium and rocuronium are used if succinylcholine is contraindicated 4733: First
generation H1-receptor antagonists (diphenhydramine, chlorphenhydramine, doxepin,
and hydroxyzine) all have significant anticholinergic effects and may lead to anti-
cholinergic symptoms such as urinary retention (detrusor inactivity), blurry
vision, etc. 2244: In nephrotic syndrome, the body responds to loss of protein
(including anti-thrombin III) via increasing cholesterol/TAG levels in the blood,
which give rise to two major risk factors: * Accelerated atherosclerosis ?? more
cholesterol/TAG * Hypercoagulability ?? loss of AT-III in the urine/??thickening??
of the blood by triglycerides * Aggressive treatment with statins is recommended to
mitigate the increased right for CAD/stroke. 3955: Classic Urine Casts [HIGH YIELD]
* Muddy Brown cast � acute tubular necrosis * RBC cast � glomerulonephritis * WBC
casts � interstitial nephritis or pyelonephritis (inflammation in the kidney) *
Fatty casts � nephrotic syndrome * Broad casts or waxy casts � chronic renal
failure 4701: Post-operative Urinary retention * Presentation: acute abdominal
pain, oliguria (<250mL in 12 hr), increased BUN and Cr in the post- operative
setting o Causedbyanesthesiaresultinginpoordetrusormuscleactivity o More common in
old people, high fluid intake in surgery, and concurrent medications * Dx:
immediate bladder scan (assess volume in urine) * Tx: immediate bladder
catheterization 4211: In end stage renal disease there??s really two options:
dialysis or renal transplant * Renal transplant is associated with better
survival/quality of life than dialysis * Renal transplant of a living, related
donor is the best option, however unrelated and cadaveric transplants are also
possible 2221: Renal Cell carcinoma * Presentation: typically, asymptomatic,
however constitutional symptoms, flank pain, hematuria, palpable renal mass, left
sided varicocele that fails to reduce in the recumbent position are all classic o
Paraneoplastichormoneproduction:EPO(polycythemia),thrombocytosis,fever,cachexia *
Dx: CT abdomen showing renal mass in setting of symptoms * Tx: excision or
chemotherapy 4361: Imaging
for Renal Stones * Renal ultrasound ??stone study?? is best as it is non-invasive,
not toxic, cheap, and can visualize all types and sizes of stones o
Testofchoiceinpregnantwomen * Non-contrast spiral CT can be used as first line, or
after an ultrasound. Due to it??s cost and radiation, it is less preferred, but
necessary sometimes as it??s much higher resolutiono
neverusecontrastinastonestudy,contrastisopaqueandthestoneisopaque...thusyou�re
making it impossible to see the stone * Abdominal X-ray is a decent modality in a
pinch and will visualize 85%, BUT you can only catch radiopaque stones, thus it??s
not preferred. 3951: Uremic coagulopathy is abnormal hemostasis in the setting of
renal failure due to accumulation of platelet toxins (chiefly guanidinouccinic
acid). Typically, PT, aPTT, and TT are normal but the BT is abnormal due to
isolated platelet dysfunction. * Platelet count is typically normal, it??s the
function that??s screwed it * Tx: DDVAP, cryoprecipitate, and conjugated estrogens
are all used, but not entirely understood 2243/4266: Classic complications of
Nephrotic Syndrome * Edema � due to loss of albumin (thus plasma oncotic pressure)
* Increased atheroscloersis/dyslipidemia � due to increased TAGs/LDL in blood in
syndrome * Hypercoagulable state � due to loss of ATIII/protein C/protein S in
urine o This can cause renal vein thrombosis, which is classically seen within the
disease process of membranous glomerulopathy 4379: Some classic UTI antibiotics to
cause acute renal failure are vancomycin (MRSA), amikacin or other aminoglycosides
(GNRs or multi-resistant bugs), and nafcillin (MSSA). In the setting of chronic
renal failure, these guys should be used with caution due to the huge risk of
kidney damage. 10776: Indications for Immediate Dialysis * Acidosis � if metabolic
acidosis with pH <7.1 refractory to therapy * Electrolyte Abnormalities �
symptomatic or severe (>6.5) hyperkalemia * Ingestion � methanol, ethylene glycol,
salicylate, lithium, valproic acid, or carbamazepine * Overload � if volume
overload is refractory to diuretics * Uremia � typically if its symptomatic
(encephalopathy, pericarditis, or bleeding) Endocrine/Diabetes/Metabolism
4324/4588: Evaluation of Hyperthyroidism� Any suspicion of thyroid problems should
begin with TSH/T4 lab values o TSHlow/T4normalwithsignsofhyperthyroid??measureT3
* ?? �Normal T3 ?? subclinical hypothyroid, early pregnancy, non-thyroid problem
* ?? �High T3 ?? If signs of Grave??s disease, it??s Grave??s disease. If no signs,
do a Radioactive Iodine Uptake (RAIU) scano TSHlow/T4highwithsignsofhyperthyroid??
considerprimaryhyperthyroidism ?? If signs of Grave??s Disease, then you??re good;
if not then RAIU scano TSHnormal-high/T4highwithsignsofhyperthyroid??
considersecondaryhyperthyroidism ?? MRI of pituitary for TSH secreting tumor�
Radioactive Iodine Uptake (RAIU) scan performed when hyperthyroid is considered,
but Grave??s disease is not likely due to symptomso Lowuptake??
measurethyroglobulin(Tg)levels * ?? �Low Tg ?? likely exogenous use of thyroid
hormone * ?? �High Tg ?? thyroiditis, extra-glandular production, or iodide
exposure o Highuptakediffuse??Grave??sdiseaseo Highuptakenodular??
Toxicadenoma,ormultinodulargoiter 4324: Central Hyperthyroidism (TSH secreting
adenoma) * Presentation: signs of hyperthyroidism (weight loss, tachycardia,
palpitations, etc) with tumor mass effect signs (headache, visual symptoms,
impaired secretion of other pituitary hormones) * Dx: TSH high with high T4 * Tx:
surgical excision or ablation 4415/3488/4726/4132/2179: Grave??s Disease *
Presentation: hyperthyroidism, exophthalmos, diffusely enlarged thyroid gland o
LowTSHwithhighT3orT4 * Dx: clinical picture with confirmed TSH receptor-antibodies
* Tx: three major options o
Radioiodineablation�basicallygoesinanddestroysthethyroidglandcells.Apparentlythe
point of this treatment is to become euthyroid and complete destruction is NOT
intended. However, pts very often have the side-effect of hypothyroidism. * ??
�Initial worsening of symptoms/exophthalmos (10%) in first week or so due to
release of stored thyroid hormone from cell destruction. Often OK in young, healthy
pts. * ?? �Pre-treatment with glucocorticoids often minimizes treatment symptoms
* ?? �Hypothyroidism (80%) may develop, and is most likely in Grave�s Disease as
the entire thyroid gland is dysfunctional, instead of just part. o
Surgery�removalofthethyroidisalwaysonthetable ?? Risk of damage to recurrent
laryngeal nerve or hypoparathyroidism due to damage or unintentional removal of
parathyroids o
Propylthiouracil(PTU)ormethimazole(MMA)�thioamidesthatblockproductionofT3/T4 * ??
�MMA a teratogen in the 1st trimester, may cause cholestasis * ?? �PTU can cause
hepatic failure and ANCA-associated vasculitis * ?? �Does not permanently cure
disease. Typically used in pts that cannot tolerate other treatments (old people
that cannot handle worsening symptoms or surgery) 3952: Thyrotoxicosis can largely
affect the heart causing changes in rhythm (atrial fibrillation, PACs/PVCs, and
sinus tachy), hemodynamics (increased CO ?? systolic HTN and increased myocardial
O2 demand), heart failure, and angina. 2178/3487: The life-threatening side-effect
of Propylthiouracil/Methimazole is agranulocytosis (0.3%). This classically
presents with fever and sore throat within 90 days of treatment initiation. Should
this occur: 1. Stop PTU/MMA immediately and check WBC levels. 1. WBC >1,500 � PTU
isn??t causing the problem 2. WBC <1000 � PTU should be discontinued for life 2.
Get throat culture, give oral penicillin/acetaminophen, administer broad spectrum
antibiotcs before even knowing the result as lack of immune response could be
fatal. Pseudomonas is especially worrysome in these patients 4307: Hyperthyroid
Bone Disease * Excess thyroid gland activity sitmulate osteoclastic acivity, thus
causing bone resorbtion. The resulting hypercalcemia inhibits PTH production
ultimately leading to hypercalciuria and net calcium wasting. * Brittle bones,
tenendcy toward bone fracture, and decreased bone density are all possible
problems! * Note that a hot nodule (functional, likely toxic goiter) is nearly
NEVER NEOPLASTIC, as it??s an area of isolated hyperacitivty/hypertrophy. A cold
nodule is an area of low activity but growth, which is high suspicious of thyroid
cancer. 3483: Metabolic changes in hypothyroidism include hyperlipidemia (decrease
in LDL receptors), hyponatremia, and asymptomatic elevations of CK (>10x normal). *
Note that hyperlipidemia may persist for months despite adequate replacement
therapy * Statins will increase the chance of hypothyroid myopathy, thus are used
with caution 3878/4382: Hypothyroid Myopathy * Presentation: normal hypothyroidism
signs with elevated CK (mild) to rhabdomyolysis/polymyositis o
CKelevationcanbepresentyearsbeforeclinicalsignsofhypothyroidism o
Typically,normalreflexes * Dx: any pt with unexplained elevatd CK/myositis should
have TSH/T4 checked as this may be the manifestations of hypothyroidism early on.o
Ifnormal,thenmuclebiopsyshouldbeconsidered * Tx: treat underlying cause
4286/10958/11277: Thyroid Storm * Presentation: high fever, cardio (tachycardia,
HTN, CHF, atrial fibrillation), CNS (agitation, delirium, coma), hyperthyroid
(goiter, lid lag, tremor), GI (nausea, vomiting, diarrhea, jaundice)o Typically
caused by: thyroid/non-thyroid surgery, acute illness, childbirth, or acute iodine
load (such as in IV contrast!) * Dx: clinical presentation with precipitating
factor � Tx: propranolol (decrease adrenergic effects), propylthiouracil (decrease
thyroid hormone production), glucocorticoids (suppress TRH/T3??T4 conversion), and
ID trigger to treat/remove 3231/2725/3230/3832/8897: Hyperaldosteronism Primary
Hyperaldosteronism (Conn??s syndrome) * Typically, from an adrenal adenoma or
bilateral adrenal hyperplasia * Presentation: hypertension (increased Na+),
hypokalemia, high aldosterone, low renin, adrenal changes on CT scan, and metabolic
alkalosis (hypoK increases bicarb reabsorption/H+ secretion) * Dx: CT findings +
aldosterone:renin ratio >20 or persistently elevated after oral saline/oral salt
tablet administration (would normally be suppressed by the Na coming in) o Adrenal
venous sampling can distinguish bilateral from unilateral dysfunction o
Bestfirsttestisthealdosterone:reninratio � Tx: o Unilateral:surgicalexcisiono
Bilateralorsurgerynotanoption:aldosteroneantagonists(K-
sparingdiuretics)spironolactone or eplerenone (note that spirono has anti-androgen
effects, but eplerenone will have less of these. Spirono is still the preferred
first-line treatment)� Note that these patients may be on a non-K-sparing diuretic
simply because they seem to have hypertension. But K-wasting due to diuretic use
will not approach the degree that hyperaldosteronism will achieve. Often the two
combined will cause the hypokalemia Secondary Hyperaldosteronism * Typically, from
reno-vascular HTN, malignant HTN, renin-secreting tumor, or diuretic use (basically
the kidney??s normal response to poor perfusion) * Presentation: hypertension
(increase Na+), hypokalemia, high aldosterone, high renin Pseudo-hyperaldosteronism
* What looks like aldo, smells like aldo, but isn??t aldo? Basically things that
increase other ??corticoids?? that aren??t mineralocorticoids...but can act as
mineralocorticoids. CAH, deoxycortisone-secreting tumor, Cushing??s syndrome, or
exogenous mineralocorticoid use * Presentation: hypertension (increase Na+),
hypokalemia, low aldosterone, low renin 3598/2170: Androgen Producing Adrenal Tumor
* Women generate androstenedione (AS)/dehydroepiandrosterone (DHEA)/testosterone
(T) in the adrenals and the ovaries. Dehydroepiandrosteone-sulfate (DHEA-S) is only
produced in
the adrenals, thus elevated DHEA-S is the most specific for an adrenal androgen
producing tumor * Presentation: signs of virilization (pubertal hair, menstrual
suppression, cliteromegaly), negative pregnancy test, and no abnormalities of the
uterus/ovaries * Dx: adrenal tumor on CT scan with presentation * Tx: excision
2171/2184: Diabetic Ketoacidosis (DKA) * Often can be the initial presentation of a
young person with Type I diabetes mellitus. Often pt will have weight
loss/polydipsia and be able to compensate by simply drinking more. However,
anything disrupting oral intake (recent illness) can throw this off and send them
into DKA * Presentation: polydipsia/polyuria, burred vision, weight loss, altered
mentation, hyperventilation, abdominal paino Labs:hyperglycemia(250-
500s),bicarb<18(acidosis),elevatedaniongap,(+)serumketones * Dx: presentation with
specific labs * Tx: High-flow IV fluids, IV insulin, close watch/replacement of
potassium o Note the ketone level (B-hydroxybutryate) or anion gap are the best
methods by which you track response to treatment 4247/4514: Hyperkalemia in DKA
[HIGH YIELD] * When DKA occurs, pts often show paradoxical hyperkalemia due to
1extra-cellular shift of K in exchange for H+ ions to limit the acidosis and
2impaired K+ entry into cells due to low insulin levels (insulin helps K+ enter
into cells o Called??paradoxical??
becausethebodyisactuallywastingK+,andoveralllevelsarelow, however serum
concerntration is high due to extracellular shift * Thus pts in DKA should be given
supplemental K+, insulin, and IV fluids because once insulin is on board, the K+
level can tank quickly, unless it??s very high 2186: Hyperosmolar Hyperglycemic
State (HHS) � Presentation: old person with type II diabetes; confusion/lethargy,
fever, dehydration, gradual onset of hyperglycemia symptoms (polyuria, polydipsia,
etc.)o
Labs:electrolyteabnormalities,glucose>1000,pHaroundnormal(7.4ish),normalbicarb,
negative serum ketones, serum osmolality >320o Pts often have paradoxical
hyperkalemia driven by insulin deficiency/hyperosmolality resulting in severe
diuresis. The K+ moves out and is peed out. * Dx: clinical picture with normal pH
and severely high glucose (>1000) * Tx: aggressive normal saline hydration (switch
to 0.45% if sodium replete), potassium supplementation, IV insulin NOT SUB-Q
INSULIN DAMMIT and close moitoring o
Useketoneleveloraniongaptotrackresponsetotreatment 3800/3795: Diabetic Neuropathy *
Typically, this occurs in a stocking-glove pattern. Two major manifestations of
diabetic neuropathy: o Small fiber disease: pain/allodynia predominate with less
sensory/reflexive loss o
Largefiberdisease:numbnessandlossofsensation,oftenwithlossofdistalreflexes * Tx:
many options available and are listed in terms of desire: o First line: TCAs
(amitriptyline, desipramine, nortriptyline); good but may cause worsening urinary
symptoms and autonomic hypotension o
Secondline:Gabapentin;bestusedwhenTCAsideeffectscannotbetolerated(elderly,pre-
existing heart condition, renal dysfunction) o
Thirdline:NSAIDs(ketorolac,etc.);mayworsenrenalfunctions,thusnotasdesired 3797:
Gastroparesis due to Diabetic Autonomic Neuropathy * Presentation: decreased
appetite, nausea, abdominal bloating, and early satiety after meals in the setting
of long-standing diabetes mellitus II * Dx: clinical presentation, possibly gastric
emptying study showing gastroparesis * Tx: drugs (below) with small, more frequent
meals o Metoclopramide:prokinetic/antiemetic;riskoftardivedyskinesiao
Erythromycin:helpswithGIkineticactivation;bestusedIVinacuteexacerbations o
Cisapride: typically, not used for risk of cardiac arrhythmias/death 2810: Renal
Tubular Acidosis in Diabetes Mellitus * Classically Type 4 RTA (retention of K+/H+
by kidney resorption) occurs in poorly controlled DM * This results in preserved
kidney function, with non-anion gap metabolic acidosis o
Labs:mildhyperkalemia,mildacidosis,diminishedGFR,noaniongap 11367: Tight glycemic
control in Diabetes Mellitus� While glycemic control goals are between 6-7%, it
doesn??t decrease all the complications of DM: o
Macrovascularcomplications(stroke,atherosclerosis,etc.)don�tchangewithtightcontrol
o Microvascular complications (nephropathy, retinopathy) decrease with tight
controlo All-case Mortality is not changed with tight control, but goes up with
poor control 2910/3902: Tight Blood Pressure Control in Diabetes Mellitus * All
diabetes patients should be treated to keep blood pressure around 140/90 * Pts with
diabetic nephropathy should have more intese blood pressure control of 130/80 to
limit the effects of nephrotic syndrome. Typically, careful administration of an
ACE or ARB are warranted. This has been proven to decrase end-organ damage and
should be initiated at the first signs of diabetic nephropathy (microalbuminuria)
3807: Screening for Diabetes Mellitus * Available Tests: Fasting Plasma glucose
(>126), Random glucose (>200), HbA1c (>6.5), or oral glucose tolerance test (>200)
� the values indicate a diagnosis of diabetes mellitus * All tests should be
repeated to confirm diagnosis * USPSTF � screen all patients with sustained BP
>135/80 * ADA � screen all patients >45y/o with risk factors for DM 3729/3899:
Diabetes Insipidus * Presentation: increased thirst, need to urinate, normal
fasting glucose * Dx: o
Waterdeprivationtest�serialmeasureofurinevolume/osmolalityuntillevelsarestableon
approximately 2-3hrs of testing * ?? �Diabetes Insipidus � urine will continue to
be dilute, while serum will be concentrated * ?? �Primary Polydipsia � urine will
concentrate (>600mOsm) o
VasopressinChallenge�givevasopressin(ADH)toseeifurineconcentrates * ?? �Central DI
� urine successfully becomes concentrated (kidneys can respond) * ?? �Nephrogenic
DI � urine fails to concentrate � Tx:o CentralDI�intranasaldemopressin(ADHanalogue)
o NephrogenicDI�supportivecareandHCTZorotherdiuretics ?? Discontinue offending
drugs lithium, demeclocycline, foscarnate, cidofovir amphotericin B 2645:
Glucagonoma� Glucagon secreting tumor. Crazy rare, but hey, this is the USMLE we??
re taking! � Presentation: o Necrolytic migratory erythema: erythematous
papules/plaques on face, perineum, extremities; lesions enlarge/coalesce over 1-2
weeks ?? central clearing, blistering, crusting/scaling border o Diabetes mellitus:
mild, only requiring diet control/oral agentso
GIsymptoms:diarrhea,anorexia,abdominalpain,constipationo
Heme:normocyticanemia(chronicdiseaseORglucagoneffectsonerythropoiesis) o
Other:weightloss,venousthrombosis,andneuropsychiatric(ataxia,dementia,etc.) * Dx:
hyperglycemia with glucagon >500 pg/mL, or demonstration of tumor on abdominal
imaging * Tx: tumor excision with diabetes control 3996/2414: Polycystic Ovarian
Syndrome (PCOS) * Presentation: classically overweight female with menstrual
irregularities and signs of virilization * Dx: based on [2 out of 3 diagnostic
criteria + rule out other hyper-androgenic conditions] o
Androgenexcess:maybebiochemicalorphysicalsignsofexcesso Oligo/anovulationo
Polycystic ovaries on ultrasound (>12 developed follicles and >10mL volume) * Tx:o
First Line: Weight loss + oral contraceptiveo
Ifwantingtobecomepregnant:clomipheneforovulationinductiono
PtsshouldbescreenforDMII;AddmetforminifcoexistingDiabetesTypeII 3860/4161: Remember
that in initial evaluation of erectile dysfunction, one must differentiate organic
(bloodflow) problems from psychogenic problems. Nocturnal/early morning tumescence
(erections at night) is a good screening tool, as it will occur normally if the
penis is functionally OK. � Typically, if pelvic trauma/surgery or catheterization
has occurred and person has organic ED, there??s a good chance that nerve damage is
the reason for the dysfunction 4308/4134/4309/3102: Evaluation of Hypercalcemia *
Step 1: Confirm hypercalcemia (repeat Ca2+ level/measure serum albumin to correct
for it) * Step 2: Determine the source (measure PTH) o
High/normalPTH:PTHdependenthypercalcemia ?? Primary hyperparathyroidism, familial
hypocalciuric hypercalcemia, or lithium o LowPTH:PTHindependenthypercalcemia * ??
�Malignancy (Ca >15) from bone mets, PTHrP production (suppression of PTH),
increased 1-25 Vit.D production (lymphoma), or IL-6 prodcution (Multiple Myeloma) *
?? �Vit D toxicity (too much Ca++ retaining), granulomatous diseases (makes Vit.
D), thiazide toxicity (Ca+ resorbtion), milk-akali syndrome (over ingestion of Ca+
+), thyrotoxicosis (increased bone resorbtion), Vit. A toxicity (direct osteoclast
simulation in high doses), prolonged immobilization (increased osteoclastic
activity without matching osteoblastic activity) � often more mild elevations
3634/4323: Acromegaly � Presentation: enlarging hands/feet/head circumference with
coarsening of the facial features o
HTNandheartenlargement(symetricleftventricularhypertrophy)o Due to abnormal
production of GH causing elevated IGF-1 (often pituitary adenoma) causing excessive
growtho
Majorcauseofdeathiscongestiveheartfailureduetosizeexpansion.CAD,arrhythmias,
cardiomyopathy, respiratory failure, strokes, adrenal failure, colon cancer, and
adrenal failure are all possible complications * Dx: clinical features with
demonstrated IGF-1 excess (not GH levels, as they fluctuate) * Tx:
octreotide/lanreotide for GH suppression or surgical removal 2174: Addison�s
Disease (Adrenal Insufficiency) * Presentation: constitutional (fatigue, weight
loss, weakness), GI (N/V, diarrhea, decreased appetite), aldosterone deficiency
(volume depletion, hyperkalemia, hyponatremia, hypotension/syncope, increased ADH),
skin (vitiligo or hyperpigmentation) * Dx: 8AM serum cortisol + plasma ACTH or ACTH
stimulation test (250mcg cosyntropin) o Low cort + high ACTH or poor response =
primary adrenal adrenal insufficiency
?? Loss of aldosteroneo Low cort + low ACTH or poor response = secondary or
tertiary adrenal insufficiency ?? Aldoerstone intacto Low cort + Normal ACTH or
normal response = likely something else, keep investigating � Tx: depends on
underlying cause 3100: Because much of serum calcium is bound to albumin,
hypoalbuminemia can result in alteration of measured serum levels. Thus, something
like proteinuria can easily cause hypoalbuminemia, leading to falsely decreased
serum calcium levels. � Correction to assess ionized (unbound, active) serum
calcium is necessary in these situations: o
CorrectedCa=Serumcalcium+0.8(4.0�serumalbumin) 4318: Toxic Adenoma * Presentation:
thyrotoxicosis with single hot thyroid nodule on exam * Dx: demonstration of
single, hot nodule on radioactive iodine scan o Note that toxic multinodular goiter
would have a patchy distribution on RI scan * Tx: ablation or removal
3498/3499/3497: Classes of Thyroid Malignancy * Papillary � epithelial origin,
unencapsulated, most common, best prognosis o Typically metastasizes to the lymph
nodeso Increasedriskfromfamilyhistoryandchildhoodradiationofhead/necko FNA often
reveals large cells with pale, grooved nucleio Often demonstrates Psamomma bodies
and may demonstrate Hurthle cells * Follicular - epithelial origin, encapsulated,
decent prognosis o Early hematogenous spread (lung/brain/bone) and invasion of
thyroid capsuleo
FNAoftenshowsnormallookingfollicularcells.Invasionthroughcapsule/hemotgenous spread
is necessary for diagnosis of carcinoma (vs adenoma) o May demonstrate Hurthle
Cells * Medullary � parafollicular c-cell origin, good prognosis, produces
calcitonin, 80% are sporatic o
AssociatedwithMEN2a/MEN2b;screeningforthesediseasesisrecommended * Anaplastic �
epithelial origin, rare, classically in old people o
Poorprognosis,deathwithin6monthstypicallyo May involve other adjacent structures
(trachea/esophagus/etc.) due to rapidly enlarging thyroid mass� Primary Thyroid
lymphoma � rare, typically in the setting of Hashimoto�s thyroiditis o Has rapidly
enlarging thyroid gland but good prognosiso Pemberton sign (plethora of the face
when arms extended above head) is the result of retrosternal extention of the
tumor, resulting in compression of the subclavians 2176/4304: Primary
Hyperparathyroidism� Presentation: typically, asymptomatic, but may present with
fatigue, constipation, abdominal pain, renal stones, bone pain, or neuropsychiatric
symptoms o Labs: hypercalcemia, elevated PTH, elevated urinary calcium excretion o
NotethatMEN1aisassociatedwithparathyroidadenoma! * Etiology: parathyroid adenoma
(or other tumor), parathyroid hyperplasia * Dx: diagnostic labs with clinical
picture * Tx: can be treated medically or surgically via parathyroidectomy if
symptomatic (osteoporosis, renal manifestations), age <50, or extremely high serum
(>1g) or urine (>400g) calcium 3496: Thyroiditis Hashimoto�s Thyroiditis *
Presentation: predominantly hypothyroid symptoms with non-tender diffuse goiter *
Dx: Anti-thyroid peroxidase (TPO) or anti-thyroglobulin antibodies in high-titer o
Note that nearly 10% of the normal population is (+) for anti-TPO antibodies o Note
that high Anti-TPO antibodies are associated with recurrent miscarriage Silent
(painless) Thyroiditis * Presentation: variant of Hashimoto??s with a mild, brief
hyperthyroid phase (destruction and releae of T3/T4), with a small, non-tender
goiter and slowly going back to euthyroid * Dx: Anti-TPO antibodies and low radio-
iodine uptake Subacute (DeQuervain�s) thyroiditis * Presentation: post-viral
inflammatory disease causing prominent fever / hyperthyroidism with painful/tender
goiter * Dx: presentation with elevated ESR/CRP and low radioiodine uptake 2191:
Struma Ovarii � Rare thyroid hormone producing ovarian teratoma. Classically in
women over age 40 with pelvic mass, ascites, and abdominal pain
2173/2592/4721/4419: Cushing�s Syndrome� Presentation: central obesity, buffalo
hump, moon facies, skin atrophy with purple striae, proximal muscle weakness,
hypertension (mineralocorticoids), glucose intolerance, skin hyperpigmentation,
eccymoses/easy bruising, women may have hirsutism/menstrual irregularities o
Maycausemyopathy/muscleweaknessfrommusclewastingviacatabolismofmuscletissue from
excessive cortisol production (painless + normal CK/normal ESR) o
Labs:hyperglycemia,hypokalemia * Etiology: exogenous corticosteroid administration
(most common), ACTH-producing tumor (Cushing??s disease), ectopic ACTH-production
(small-cell lung cancer), or primary adrenal disease * Dx: o
Establishhypercortisolismwithsalivarycortisolassay,24-hrfreeurinecortisol,andlow-
dose dexamethasone suppression test (2/3 must be positive) o If hypercorticolism
present ?? ACTH level measurement (see if process is ACTH dependent or independent)
o IfACTHiselevated??high-dosedexamethasonesuppressiontesttodetermineifsourceof ACTH
is pituitary (will be suppressed) or ectopic (won??t be suppressed, likely lung
cancer) � Tx: aimed at underlying cause 4164: Metabolic Syndrome [HIGH YIELD] *
Syndrome characterized by the following parameters: o
Abdominalobesity(men>40inchwaist,women>35inchwaist) o Elevated fasting glucose
(>100-110 mg/dL)o Mild hypertension (>130/80)o Elevatedtriglycerides(>150mg/dL) o
LowHDLcholesterol(Men<40,women<50) * Insulin resistance is central to the
pathogenesis AND chronically high insulin levels has huge effects on the body as a
whole, which is thought to be the major cause of these symptoms. 3594: Testicular
Germ Cell Tumors * Leydig Cell Tumor � the most common testicular sex cord tumor.
Can produce testosterone (normal cell function) and estrogen (due to increased
aromatase expression). Classicaly high sex hormones with FSH/LH suppression.
Gynecomastia (adult men) or precocious puperty (boys) are classic. *
Choreocarcinoma � germ cell tumor that produces beta-HCG * Seminoma � tumor of
syncytiotrophoblasts, typically with normal serum markers, but sometimes elevated
beta-HCG * Yolk Sac Tumor (endodermal sinus tumor) � germ cell tumor with increased
serum AFP * Teratoma � multiple early tissue tumor that can elevate beta-HCG or AFP
likely due to multiple tissue types present within the tumor 3976: Pheochromocytoma
* Neuroendocrine tumor of chromaffin cells producing catacholamines (typically
epi/norepi) o Association with MEN2a/MEN2b * Presentation: episodic hypertension,
palpitations, sweating, pallor classically with increase intraabdominal pressure
(urination, palpation, positional change) or anesthesia/surgery o Beta blockers
alone will cause hypertensive crisis (5-HT activates a-receptors)o Mustgivea-
blockersbeforesurgicalremoval(phenoxybenzamine) * Dx: clinical presentation
demonstration of mass on imaging * Tx: pre-treatment of phenoxybenzamine and
surgical removal 3494/3493/3595: Prolactinoma * A classic pituitary tumor that
produces prolactin o ProlactinwillsuppressGnRH/LH??
sexhormonesandissuppressedbyDopamine * Presentation: o Men: erectile dysfunction,
decreased libido, impotence, gynecomastiao
Women:lowestrogen(vaginaldryness,amenorrhea,hotflashes,decreasedbonedensity),high
prolactin (breast tenderness, swelling, and galactorrhea), if large bitemporal
hemianopsia o Labs:prolactinemia(>200ng/mL)o
Imaging:smallorlargemasswithinthepituitaryvault * Dx: clinical presentation with
labs/imaging * Tx: treatment only sought with symptoms present or large size o
Firstline:dopamineagonists(bromocriptineorcabergoline)tosuppressprolactinandpossibl
y shrink the tumor (DA is a feedback hormone against prolactin) o Second line:
surgical resection if >3cm OR if increase with size upon treatment 8918: Note that
non-functioning pituitary adenomas can often cause mild elevations of prolactin due
to disruption of DA pathways around the pituitary (mass effect) which feedback
inhibit prolactin. 2649: VIPoma (??pancreatic cholera??)� Presentation: intense
watery diarrhea, hypo/achlorhydria (decreased HCl secretion), flushing, nausea,
vomiting, muscle weakness/cramps (hypokalemia)o Labs: hypokalemia (increased K+
secretion in gut), hypercalcemia, hyperglycemia, Vasoactive intestinal peptide
(VIP) >75 pg/mLo Stoolstudy:secretorywithincreasedstoolNa+andosmolalgap<50mOsm/kg o
ClassicallyassociatedwithMEN1(GItumors) * Dx: presentation/labs and abdominal
CT/MRI showing pancreatic mass (typically in the tail) o Often metastasize to liver
by presentation * Tx: surgical resection 3495: Euthyroid Sick Syndrome (??Low T3
syndrome??) � Presentation: acute, severe illness accompanied by abnormal thyroid
function tests o Labs:lowT3withnormalT4andTSHo Result of of decreased deiodination
of T4 from caloric deprivation, glucocorticoids, and acute phase reactants * Dx:
typically thought to be hypothyroidism, but often thyroid levels are unreliable in
acute illness * Tx: treatment of underlying disease should resolve the abnormal
tests 2188: Select Odd Reasons of Hypoglycemia * Insulinoma (Beta-cell tumor) �
pancreatic tumor of beta-cells (produce insulin). You will see low glucose, with
high insulin, and high C-peptide/pro-insulin (>5pg.mL), without the presence of a
sulfonylurea. * Non-beta cell tumor � a larger pancreatic tumor that actually can
produce hypoglycemia through IGF-II production which mimics insulin for this
effect. Oddly, this hypoglycemia is insulin independent. * Sulfonylura overuse �
presentation identical to insulinoma, however sulfonylurea levels in blood will be
obviously elevated. * Insulin overuse � high insulin, low C-peptide/pro-insulin
3490/3489: Osteomalacia � Failure of mineralization of bone matrix, classically
from Vitamin D deficiency in adults. Bascially the lack of vitamin D results in
excessive PTH with bone wasting (due to phosphorus loss) and bone resorption. o
RememberthatVit.Ddeficiencyinkidsleadstoricketso
Note that procedures/diseases that may produce malabsorbtion (bowel resection,
Chrohn??s dx) can contribute to Vit.D deficiency, resulting in osteomalacia *
Presentation: bone pain, muscle weakness/cramping, trouble walking/waddling gait o
Labs: * ?? �Elevated: Alk.Phos (bone destruction), PTH, urinary phosphorus * ??
�Decreased: serum Ca++, Phosphorus, urinary calcium, 25-Vit-D levels o Imaging:
reduced bone density, thinning of cortex, pseudofractures * Dx: presentation with
low Vit D levels and radiologic evidence * Tx: supplement Vit D 4154: Oddly enough,
oral estrogen replacement therapy will increase Thyroid Binding Globulin (TBG)
levels due to decreased breakdown of TBG in the liver. * Pts with a normal thyroid
function will make more and compensate without trouble. * Pts on levothyroxine for
hypothyroidism will have to increase the dose (as the TBG increase will mean less
free T4 present). The increased dose will saturate the increased TBG, and restore
euthyroidism. * *transdermal estrogen does not have this effect as it bypasses the
liver 3781: Monofillament testing is a pressure test where a single filament is
placed at the sole of the foot and 10Gs of pressure is applied. The patient is
asked about their ability to sense the filament, giving a more objective measure
for peripheral neuropathy, especially in diabetic neuropathy to assess risk of foot
ulceration. Other sensory modalities can be tested to help understand losses. 3099:
Calcium binding dynamics in blood pH changes: * Don??t forget! Ca2+ exists in
ionized, albumin-bound, and inorganic/organic ion bound forms * Acidosis: serum
albumin will have more H+ ions bound to it simply due to more H+ present in the
blood, meaning it kicks off Ca2+, leading to more ionized Ca2+ in blood *
Alkalosis: less H+, thus more spots for Ca2+, thus more Ca2+ bound to albumin.
Oddly enough, a longstanding respiratory alkalosis can result in signs of
hypocalcemia due to this effect. 2192: Anti-Diabetes Drugs * Metformin (1-2% drop)
� typically first agent in DM control. Weight neutral/low risk of hypoglycemia.
Life threatening lactic acidosis is the major side effect. * Sulfonylureas (1-2%
drop) � typically added with metformin monotherapy failure. Weight gain and
hypoglycemia are major side effects. * Thiazoliadones (??-glitazone??; 1-1.5% drop)
� low risk of hypoglycemia, but weight gain, edema, CHF, bone fracture are all
possible. Can be used in renal insufficiency. * DPP-4 inhibitors (??-gliptin??;
0.5% drop) � low risk of hypoglycemia, weight neural, can be used in renal
insufficiency * GLP-1 agonists (??-tide??; 0.5-1% drop) � low hypoglycemia risk,
may aid in weight loss. Can cause acute pancreatitis 3083: DON??T FORGET!!!
THIAZIDE DIURETIC HYPECALCEMIA IS MILD AND WON??T CAUSE SYMPTOMS. 3083: Milk-
Alkalai syndrome * Occurs due to over-supplementation with calcium and absorbable
alkalai. Essentially you take too much result in renal vasoconstriction, decrease
in GFR, Na/K/2Cl inhibition (diuresis) * Presentation: N/V, constipation,
polyuria/polydipsia, AKI, suppressed PTH in the setting of calcium supplementation
(this patient was taking supplements for osteoporosis)o
Labs:hypercalcemia,hypomagnesiemia,hypophosphatemia,metabolicalkalosis * Dx:
clinical presentation * Tx: discontinue supplementation with IV fluids/furosemide
to flush out the kidneys Dermatology10152: Hidradenitis supuritiva (??acne
inversa??) * Chronic inflammatory occlusion of folliculopilosebaceous units which
stops proper shedding of keratinocytes off to the surface, and accumulation under
the skin. * Presentation: initially solitary, painful inflamed nodules in the
axilla, groin, or perineal areas. Can progress to abcesses with open drainage and
sinus tracts/comedones/scarring. * Dx: clinical based on appearance 2751: Bullous
Pemphigoid * Separation of epidermis from dermis due to IgG/C3 againt
hemidesmosomes connecting epi/dermis junction basement membrane * Presentation:
tense bullae with an inflammated base with severe pruritis rarely involving the
mucus membranes. Sometimes presents with pre-bullous prodome of
urticarial/eczematous lesions * Dx: skin biopsy showing subepidermal cleavage &
immunofluorescence showing linear IgG/C3 dep. * Tx: clobetasol (high potency
topical steroid), systemic steroids are not very effective 10298: Urticaria * Mast
cell activation in the superficial dermis due to many possible etiologies *
Presentation: well-circumscribed raised erythematous plaques with cental pallor
with intense pruritis (often at night), often arising quickly and resolving within
24hrs, sometimes with deeper swelling causing angioedema o
Acutelastsfor<6weeks&chroniclasts>6weeks * Etiology: idiopathic (50%), NSAIDs, bug
bites, direct mast cell activation, IgE activation, infection, etc. * Dx: clinical
* Tx: address underlying cause 2746: Tinea Corporis (Ring-Worm) * Infection with
any dermatophyte, however Trychophyton rubrum is classic * Presentation: ring-
shaped patches with central clearing with intense itching and well demarcated
border * Dx: KOH scraping/prep showing hyphae * Tx: 2% antifungal lotion/cr�me
(terbinafine) or systemic griseofulvin if extensive o
Notethatextensiveinfectionshouldpromptsearchforimmunosupperativedisease 2747: Tinea
Versicolor (pityriasis versicolor) * Skin infection with Malassezia globose
classically in hot/humid weather * Presentation: hypopigmented area noticed during
summer months or vacation (infected skin fails to tan due to acid production from
the fungus), may also feature fine scale or pruritis * Dx: KOH scrape/prep showing
hyphae & yeast cells (spaghetti and meatballs appearance) * Tx: topical
ketoconazole, topical terbinafine, or selenium sulfide (selsun blue) 2762/2603:
Basal Cell Carcinoma * Most common, often an excellent prognosis. Correlates with
cumulative sun exposure * Presentation: pearly/rolled edge nodule with keratinized
or ulcerated center. Sometimes featuring spider angiomata on the lesion, oozing or
crusting * Dx: clinical picture and biopsy * Tx: o
Superficial�electrodessicationorcryotherapy o Deep�MOHSsurgery 2604/4033/4319:
Squamous Cell Carcinoma * Intermediate incidence with intermediate prognosis,
typically not metastatic when found, but will invade if left untreated. Correlates
with # of severe sun exposure events (burns, tanning beds, etc.) * Presentation:
rough scaly plaque/nodule with possible hyperkeratosis/ulceration/bleeding.
Classically can cause neurologic damage due to perineural invasion
(numbness/parastheisa) o
Sunburns,radiation,immunosuppression,burns,scars,andwartsareallriskfactorso Note
that if you??ve a lesion on the lower lip (more sunlight exposure) is SCCo Note
that a Marjolin ulcer is an SCC arising from the site of a scar/burn/previous
injury and has an increased risk of metastases * Dx: skin biopsy that includes the
deep reticular dermis (assess depth of invasion) showing dysplastic/anaplastic
keratinocytes/keratin pearls * Tx:o
Lowrisk:excisionorlocaldestruction(cryotherapy/electrodessication) o
Highriskorcosmeticareas:Mohsmicrographicsurgery 2767/2765/4312: Malignant Melanoma
* Least common skin cancer, but most deadly * Presentation: new or existing
melanotic skin lesion demonstrating the ABCDEs (Asymmetry, Raggy Border, verigated
Color, Diameter >6mm, Enlargemnt or new symptoms) o
Consideredthemostcommonmalignancyofwomenage25-29 o Women typically get it on the
legs while men get it on the back * Dx: excisional biopsy to show depth of invasion
* Tx: surgical excision with wide (1cm) margins o We actually wait for this as the
wide excision may disrupt lymphatic flow 2764: Seborrheic Keratoses * Benign lesion
that tends to favor the face/trunk/old people and is often consider unsightly o May
be indicative of underlying GI malignancy as the Sign of Leser-Tr�lat where many of
these lesions appear rapidly. * Presentation: waxy/greasy, ??stuck-on??, well
circumscribed lesion that may be flat or raised with normal surrounding skin. Can
vary from pink/white to pale to brown/black. Typically, slowly enlarging. * Dx:
clinical * Tx: none needed except for cosmetic reasons 4410: Actinic Keratosis *
Presentation: hyperkeratosis causing ??sand-paper like?? papules in areas of sun
exposure. Often begin small/flat but may accumulate becoming ??cutaneous horns??.
Pre-malignant for SCC * Dx: shave biopsy with light microscopy showing
characteristic cell proliferation * Tx: electrodessication or cryotherapy 4151:
Graft vs Host disease occurs up to 50% of the time in bone marrow transplants
typically targeting the skin (macropapular rash of palms/soles/face), intestines
(bloody diarrhea), and liver (abnormal LFTs and jaundice). It??s the result of
graft T-lymphocyte activation targeting the host??s tissues. 4693: Herpes Zoster
Flair (Shingles) * Flair of varicella zoster virus often associated with aging,
stress, and emotions. Typically VZV will lay dormant in nerve roots (esp the
trigeminal nerve!) and reactivate at that nerve??s distribution * Presentation: may
begin with pain/no rash, progressing to pain with vesicular rash across 1-2
dermatomes and NOT crossing the midline, then post-herpetic neuralgia may persist
for weeks later o Rash crossing the midline should prompt investigation for
HIV/immunosuppressiono Immunosuppressive therapy (TNF-a inhibitors) may resut in a
flair * Dx: clinical * Tx: oral acyclovir, famcyclovir, or valacyclovir can all
work to resolve flair and diminish post-herpetic neuralgia 4076/4091: Treatment of
Acne VulgarisComedonal Acne � closed/open comedones which may progress to pustules
� Topical retinoids or mild acid treatments (salicyclic, glycolic, etc.)
Inflammatory Acne � inflamed papules/pustules (<5mm) with erythma * Mild � topical
retinoids + benzoyl peroxide
* Moderate � add topical antibiotics (erythromycin or clindamycin) * Severe � add
oral antibiotics Nodular (cystic) Acne - >5mm inflamed nodules/pustules, appear
cystic * Moderate/Severe � same as inflammatory acne * Unresponsive � Oral
isotretinoin (??renin A??) 4812: Apparently taking chronic oral steroids can result
in ??steroid acne??, a chronic inflammatory folliculitis consisting of monomorphous
pink papules, NOT COMEDOMES Case 1 � Adult Male Health Maintenance Cardiovascular
Diseases * ?? �Hypertensiono Men 18-39 � Office BP measurement every 3-5 years if
within normal rangeo Men 40+ � Office BP measurement every year if within normal
rangeo If abnormal range � confirm with Ambulatory or Home Blood Pressure
Measurement * ?? �Lipid Disorderso Men 20-34 � Fasting HDL/Total Cholesterol or
Fasting HDL/LDL/Lipid panel if increased risk o Men 35-45 � Fasting HDL/Total
Cholesterol or Fasting HDL/LDL/Lipid panel every year * ?? �Abdominal Aortic
Aneurysmo Men 65-75 & Ever Smoked � one-time abdominal ultrasound to rule in/outo
Men 65-75 & Never Smoked � may consider abdominal ultrasound, but not necessary
* ?? �Coronary Artery Diseaseo Screening in asymptomatic adults with EKG, CT, or
stress testing NOT recommended * ?? �Peripheral Artery Diseaseo
ScreeninginasymptomaticadultsNOTrecommended Cancer * ?? �Colorectal Cancer o Men
50-75 � colonoscopy every 10yr �OR� FOBT or Flexible Sigmoidoscopy every 3-5yr o
Men 76-85 � if never screened or if clinically indicated, pt may benefit * ??
�Prostate Cancer o Men Any Age - may be benefit for detection with Digital Exam or
PSA, however, outcomes are not shown to be consistently improved, thus screening is
NOT recommended * ?? �Lung Cancero Men 55-80 with 30+ smoking Hx OR quit within
last 15yr � annual screening with low dose CT scan of chest/abdomen/pelvis * ??
�Bladder, Testicular, or pancreatic cancers o Insufficient or not recommended to
screen for any of these in an asymptomatic adult Other Health Concerns * ??
�Obesityo All Adults BMI 30+ - intensive counselling/behavioral intervention to
promote weight loss * ?? �Type II DM o All adults 40-70 overweight or obese � blood
glucose screening at annual visitso Initiate earlier screening if: HTN,
hyperlipidemia, family Hx DM, Hx of gestational DM, Hx of PCOS, or if
Black/Hispanic/Pacific Islander/Native American * ?? �Depression o Use of a
standard depression questionnaire in any patients who have not been screened or
suspected of depression. * ?? �Tobacco Useo Clinical History that shows any tobacco
use warrants counselling and treatment for cessation * ?? �Alcohol Useo Use of
standard alcohol abuse screenings (AUDIT or AUDIT-C) who have not been screened or
if suspected of alcohol abuse Adult Immunizations/Lifestyle Interventions (from CDC
recommendations) * ?? �Influenza � every year around October regardless of health
status * ?? �Td/Tdap � Td booster every 10 years with a single Tdap in adult life;
pregnant women need Tdap with every pregnancy to protect the baby regarless of
health status * ?? �Varicella (Shingles) � one dose at age 60+, even if you�ve had
the shingles before o Contraindicated in pregnancy, immunodeficiency, or HIV with
CD4 <200 * ?? �Pneumococcal o PSV13 � single dose at age 65+ or under certain
medical conditions (weak immune system, if HIV+ regardless of CD4+, poor kidney
function, or asplenia) o PPSV23 � single dose at age 65+ or under certain medical
conditions (weak immune system, if HIV+ regardless of CD4+, poor kidney function,
asplenia, chronic liver/heart/lung disease, alcoholism, or diabetes I or II) o Pts
with risk factor diseases should receive at age 50+ and then either again 5 yrs
later or at age 65yr, whichever is later * ?? �Meningococcal Disease � recommended
for high risk groups (college dorm or military recruits), asplenia, or certain
compliment deficiencies * ?? �MMR � <60yr and not previously receivedo
Contraindicated in pregnancy, immunodeficiency, or HIV with CD4 <200 * ?? �HPV �
women age 19-26 OR men age 19-21 who haven�t gotten it already * ?? �Varicella
(Chickenpox) � any age if not previously received o Contraindicated in pregnancy,
immunodeficiency, or HIV with CD4 <200 * ?? �Hepatitis A � give if not received as
a child o Give if pt has chronic liver disease * ?? �Hepatitis B � give if not
received as a child o Give if pt has chronic liver disease, HIV+, poor kidney
function, or Diabetes I or II * ?? �Haemophilus influenza (Hib) � give if pt
asplenic, sickle cell disease, or had a bone marrow transplant Lifestyle
Interventions ?? Exercise, Healthy Diet, Safe Sex, and Seat Belt Use should be
encouraged at all visits however mixed results have been shown as to the level of
motivation counselling confers Case 2 � Chronic Obstructive Pulmonary Disease
(COPD)COPD is a spectrum of disease encompassing for Chronic Bronchitis and
Emphysema * ?? �Chronic Bronchitis � cough/sputum production most days for at least
3mo during 2yrs consecutively * ?? �Emphysema � SOB caused by enlargement of
bronchioles and alveoli due to lung tissue destruction The most common etiology of
COPD is cigarette smoke exposure (90%; primary, second-hand smoke, or
environmental) but young/non-smokers may contract it due to rare a1-antitrypsin
deficiency * ?? �Pathologic changes: Mucous gland hypertrophy/hypersecretion,
ciliary dysfunction/destruction, lung tissue destruction, and airway remodeling
* ?? �Pathologic consequences: fixed airway obstruction, poor mucous clearance,
cough, wheezing, dyspnea * ?? �Presentation: cough (intermittent ???constant),
thick/white mucus production, dyspnea, �barrel chest�, distant heart sounds,
expiratory wheezes or distant breath sounds, accessory muscle use in respiration,
signs of cyanosis o CXR: normal until advanced stage disease; may show lung
hyperinflation, increased AP diameter, flattening of diaphragm, and lung bullae
formation o Spirometry: FVC/FEV1 are both decreased and ratio is <0.7 without
albuterol reversibility (gain of 12% function or 200mL) and decreasing FEV1 with
progression Dx: clinical symptoms and spirometry Tx: depends on severity of disease
* ?? �Stage 0 � early with cough/sputum but normal spirometry??smoking cessation
(reduce rate of pulmonary function decline to non-smoker rate), vaccination to
pneumococcus and influenza (prevent exacerbations) * ?? �Stage 1 � FEV/FVC <0.7 |
FEV1 >80% | +/- symptoms??add SABA (albuterol or ipratropium) * ?? �Stage 2 �
FEV/FVC <0.7 | FEV1 50-80% | +/- symptoms??add LABA (salmetrol, tiotropium) * ??
�Stage 3 � FEV/FVC <0.7 | FEV1 30-50% | +/- symptoms??add Inhaled corticosteroid
(fluticasone/triamcinolone) will aid in decreasing exacerbations * ?? �Stage 4 �
FEV/FVC <0.7 | FEV1 <30% or <50% with symptoms??add O2 supplementation 15hr/day
Case 2.5 � Uworld Tips about COPD 4665: COPD Physiology ?? The hyperinflation and
other signs of COPD occur due to two mechanisms:o Static alveolar destruction:
decreased elasticity and destruction of lung parenchyma physically makes floppy,
larger spaces for air fill up. Thus overall you have higher lung volume at
baseline. o Dynamic �air stacking�: elastic recoil of the alveoli in the lungs is
largely responsible for expiration. Because COPD pts have decreased elasticity,
this expiration is slow. Should a COPD patient need to breath faster (they go for a
run) they�ll start their next inhalation before exhalation is complete, causing air
to �stack up� in the lungs causing hyperinflation ?? The hyperinflation compresses
the diaphragm and gives it less room to contract. Because the diaphragm is the
single most important entity for inhalation, a flattened diaphragm in COPD results
in increased effort on inspiration. 4645: Remember that vital capacity in COPD
decreases due to air trapping and obstruction of expiration. * ?? �Vital capacity =
amount of air a person can expire with a normal expiration * ? �COPDers trap air in
the lungs due to obstruction/destruction of alveoli, thus they have a harder time
getting the air out! Thus vital capacity deceases greatly 4718: Oxygen Induced CO2
retention in COPD * ?? �In a severe chronic COPD-er, their body is accustomed to a
state of hypoxia, which can be concerning for hospital folks monitoring their O2
levels. However, rapid resolution of low O2 levels though oxygen supplementation
can result in acute CO2 retention through 3 mechanisms o V/Q mismatch � normally,
COPD causes VQ mismatch through alveolar destruction. However, this is offset
through selective vasoconstriction in the lung to only perfuse well ventilated
areas. With the addition of O2, even poorly ventilated areas have acceptable O2
levels for the body, thus selective vasoconstriction does not occur AND V/Q
mismatch worsens. o Haldane effect � in hypoxemia, deoxyhemoglobin (dHb) serves as
a buffer for H+ ions. With additional oxygen, these normally dHb will become
oxyhemoglobin oHb, releasing those H+ ions, resulting in [H + HCO3??H2O + CO2],
raising CO2 levels o Decreased respiration � the supplemental oxygen will cause
increased oxygenation in the body, which tells the brain to slow down breathing, as
it considered O2 levels to be OK. However, this also will retain CO2. * ?? �These
three effects together cause increased CO2 retention and acidosis ???neural
vasodilatation (reflex typically used to increase bloodflow, but here causes
underperfusion) and neurotransmitter changes ???seizures * ?? �As a goal, O2 levels
should only be cautiously raised to about 90-93% for COPD pts 4535: CO2 Narcosis is
altered mental status in pts with PaCO2 >60mmHg. Classically this will occur in the
setting of COPD, where CO2 retention is commonplace. It may also contribute to a
respiratory acidosis (increased pH, decreased bicarb) 8905: Distinguishing Asthma
from COPD ?? Clinically they
can both look similar, especially in an adult patient, but there are two major
hallmarks that can set asthma off from COPD:o Reversibility: FEV1 increase by >12%
demonstrates reversibility??asthma. COPD may be partially reversible in early
stages, but never to this degree.o DLCO: normal or increased DLCO??asthma. COPD may
be normal in early stages, but never increased.?? Note that adult onset asthma is
harder to treat (more limited response), but is usually the situation where you�re
trying to distinguish it from COPD 4730/4039/4569/4667: Acute COPD exacerbation
* ?? �Presentation: wheezing, tachypnea, prolonged expiration, and accessory muscle
use. Difficulty breathing NOT resolved with albuterol inhaler. Air trapping with
hypoxia, hypercapnia. Classically change in sputum from white??yellow/greeno Recent
upper respiratory infection is the most common causeo Distant heart sounds: common
finding as heart is displaced downward from lung hyperinflation * ?? �Dx:
hyperinflation on CXR & hypoxia/CO2 retention with changes in 1 or more of the
following: o Increased cough severity or frequencyo Increased volume or change in
character of sputumo Increased level of dyspnea * ?? �Tx: supplemental oxygen,
inhaled bronchodilators, systemic corticosteroids (oral prednisone or IV
methylprednisone), or muscarinic antagonists are standard treatment o Antibiotics
if suspected bacterial infectiono Oseltamivir is influenza suspectedo Mechanical
ventilation if failure to resolve event with ventilatorary failure 2919/3031:
Alpha-1 Anti-trypsin Deficiency ?? Presentation: o Lung: COPD (cough, dyspnea,
wheezing, recurrent pulmonary infections, mucoid sputum)???<45 years or with
minimal/no smoking history???Basilar predominant (smoke rises causing more damage
in upper lungs)??decreased lung sounds at the base with bilateral lucency of lung
baseso Liver: mildly abnormal LFTs, hepatocellular carcinoma, neonatal hepatitis
???Family history/person history of unexplained liver disease o Skin: panniculitis
(inflammation of subcutaneous fat) * ?? �Dx: PFTs + serum AAT levels * ?? �Tx:
human AAT supplementation + bronchodilators + corticosteroids o Lung/liver
transplantation for severe disease is the definitive treatment 4520: Spontaneous
Pneumothorax from COPD * ?? �Presentation: sudden onset chest/back pain, SOB,
reduced breath sounds on affected side, and hyper- resonanceo Occurs due to chronic
alveolar sac destruction forming blebs (seen as enlarged air sacs on chest CT) that
can rupture into the pleural space, compressing the lungs. * ?? �Dx: clinical
presentation with Chest CT evidence * ?? �Tx: no complete concensus. Based on
clinical scenario and risk stratification. 3716/3042: The best thing to do to lower
mortality in COPD patients is stop smoking. Long-term oxygen therapy (LTOT) is the
only other thing that has been show to decrease mortality. ?? Criteria for
initiating LTOT are as follows:o PaO2 <55mmHg or Sat <88%o PaO2 <59 or Sat <89% in
pt with cor pulmonale, evidence of HF, or hematocrit >55% 4593/4297: Cor pulmonale:
process of increased lung-vascular pressure. Untreated, causes right heart failure.
* ?? �Etiology: COPD (most common), idiopathic pulmonary HTN, interstitial lung
disease, obstructive sleep apnea. Note that LVF causing RVF is NOT cor pulmonale. *
?? �Dx: o Sym: Dyspnea, syncope, or angina on exertiono Sign: Peripheral edema,
increased JVD, hepatojugular reflex, pulsatile liver, edema, ascities, etc. o
Imaging: EKG or echo can be used but right heart catheterization with elevated
pulmonary artery systolic pressure >25mmHg is confirmatory ?? Tx:
vasodilators/anti-HTN drugs Case 3 � Joint PainIf a patient presents with a non-
traumatic mono-articular joint swelling, it�s important to examine the joint for
swelling, redness, warmth, or other signs of disease. Should these signs be present
aspiration of the joint with analysis of the joint fluid is the first step.
Possible etiologies include: ?? Septic Joint � very limited ROM (pain), joint
effusion, fever. The ROM is very telling as cellulitis, bursitis, and osteomyelitis
will often still retain joint mobility o Monoarticular joint infection is 90% of
the time bacterialo Chronic joint infection may be fungal or mycobacterialo Acute
polyarticular infection may be due to seeding from endocarditis or H.gonorrhea o
Aspiration will often have a positive culture, classically with S.aureus and WBCs
around 100,000 (mainly neutrophils); in fact, these are more common in patients
with rheumatoid arthritis as the chronic inflammation and use of steroids
predispose to infectiono HIV(+) pts may have N.gonorrhea, Salmonella, or H.flu
infectionso IVDU pts may have odd organsisms like Strep spp., Staph spp., Gram(-)
bugs, or Pseudomonas o Tx: drainage and IV antibiotic treatment of infection ??
Gouty Arthritis � classically of the first metatarsophalangeal joint (podagral) but
can happen at any joint. Often monoarticular. o Aspiration yields Monosodium Urate
crystals (needles, negative birefringence) with high WBC content (2000 � 60,000) o
Classically occurs with trauma, surgery, heavy meals (wine/cheese; high purine
foods), and thiazide diuretic use (reduces renal uric acid excretion) o Tx: NSAIDs
with avoidance of triggers; possibly others if recurrent * ?? �Pseudogout � similar
to gout but aspiration will yield calcium oxalate, positively birefringent,
rhomboid crystals. Classically this can occur in pts with kidney disease (poor
oxalate excretion) o Tx: NSAIDs with treatment of underlying condition * ??
�Osteoarthritis � classically in older adults due to repetitive use of joint,
trauma, or obesity causing cartilage destruction and bone-to-bone contact/ligament
damage o Pain gradually onsets with dull/deep ache that worsens at the end of
day/improves with rest and may become constant at later stages. o Crepitus, joint
instability, effusion??joint deformity and limited ROMo Typically, X-rays are
normal at first with development of bony sclerosis, subchondral cysts, and
osteophytes occuring as disease progresseso Tx: NSAIDs with physical therapy and
possibly joint injections ?? Rheumatoid Arthritis � classically affecting women in
their 30-50s, it�s an autoimmune disease that attacks the joints, causing damage
and destruction o Often worse in the morning and improves with movement; with
classic deformities to the hands/fingers and possibly signs of other autoimmune
disease o (+)Rheumatoid factor & (+)anti-cyclic citrullinated protein (CCP) are
classic immunologic correlates; other autoimmune diseases may be positive (more
common if you have one!) o Elevated ESR, CRP, anemia, thrombocytosis, and low
albumin can all be signs of chronic inflammation o Tx: Physical therapy + DMARD
(Sulfasalazine/Methotrexate/Infliximab/Etanercept) Case 4 � Prenatal Care[Ch.6 Pre-
conception and Antepartum Care � Topic 9 & 10]All health encounters during
reproductive years should include counseling about proper medical care to have the
best possible pregnancy outcomes. This is especially emphasized with pre-conception
care! It is known that good preconception counselling and antepartum care increase
the likelihood of a healthy baby! Preconception Counselling Vaccinations * ?? �All
women should receive these if planning a pregnancy: rubella, varicella zoster,
pertussis, and hepatitis B vaccines should be given, unless already immune. An HIV
test should also be given unless the patient specifically declines it. o Pregnancy
should be delayed 1 month after receiving any live vaccine * ?? �If woman is at
risk, screen for: STD, TB (Mantoux test), any other worrisome disease * ?? �Some
genetic testing can be offered based on race: sickle cell (AA), B-thalassemia
(Mediterranean, southeast Asians), a-thalassemia (Mediterranean, southeast Asians),
Tay-Sachs (Ashkenazi Jews), Canavan disease (Ashkenazi Jews), Cystic Fibrosis
(White people and Ashkenazi Jews), anything indicated with family history Health
Maintenance * ?? �Make sure pre-existing conditions are well controlled (HTN,
diabetes, thyroid disorders, seizures, etc.) * ?? �Folate supplementation (0.4mg
normally or 4mg in moms with Hx of NTDs) * ?? �Lifestyle adjustments: Work to
achieve proper weight, abstaining from alcohol/tobacco/drugs, advising on certain
foods to avoid (soft cheese, deli meats, etc.), exercise, etc. Diagnosis of
Pregnancy ?? Presentation: one/more missed periods following sexual activity
without proper contraception o
Symptoms:Breasttenderness,fatigue,nausea/vomitingarecommono Early Signs: Uterine
enlargement (apparent around 6wk), Chadwick sign (bluish vaginal discoloration),
Hegar sign (softening of the cervix)o Late signs: quickening (perception of fetal
movement, 16wk), hyperpigmentation of skin/linea alba (increased a-MSH)?? Dx: urine
b-hCG detection/serum b-hCG quantitative testing/ultrasonographic detection of
fetal heart o Best performed early in the morning when hCG levels are highest.o
Home pregnancy tests are designed for specificity (low false positive rate, high
false negative) o B-hCG levels should double every 48hrs, but at minimum must
increase 53% in that time. Initial Prenatal Visit * ?? �Full history/physical with
a pelvic exam to assess 1dimentions of the bony pelvis, 2cervical length/
consistency/shape/mobility/dilation * ?? �History/physical should focus on risks
that they can give to the pregnancy (smoking, alcohol, seat belt use, etc.), then
focused testing or intervention to minimize these risks should be undertaken
Assessment of Gestational Age/Estimated Date of Delivery ?? Gestational age �
number of weeks elapsed since the first day of LMP and the date of delivery o
Naegele rule (LMP + 7 days � 3 months) is used to quickly calculate estimated date
of delivery (EDD) from LMP o These are useful but can
be flawed, as an exact date of the LMP and a normal uterine cycle must be present
for it to work o Ultrasound measurement gestational age is much more accurate; best
at 18-20wk gestation Subsequent Antenatal Visits * ?? �Typically, you schedule a
visit [once every 4 weeks from week 1-28], then [once every 2 weeks from week 29-
36], then [weekly visits thereafter] * ?? �More frequent visits may be scheduled
for patients at risk for complications! * ?? �In these visits you: o
Askaboutproblems(bleeding,nausea/vomiting,dysuria,vaginaldischarge) o
Askifmomcontinuestofeelregularfetalmovementso Measure blood pressure, weight,
fundal height, and fetal heart tones ???Fundal height approximates the #of weeks
gestation until 36 weeks; after 36, the baby�s head engages and the uterus begins
to shrink as it moves into the pelvis ???Fetal heart rate should be approx. 110-
160bpm; deviation should be assessed o Palpate the uterus for presentation (95% are
ultimately �vertex�) * ?? �Note that recommended maternal weight gain is adjusted
for starting weight: o Underweight � gain 28-40lbs (1lb per week)o Normal weight �
gain 25-35lbs (1lb per week)o Overweight � gain 15-25lbs (0.6lb per week) o Obese �
gain 11-20lbs (0.5lb per week) Common Screening Tests * ?? �First Trimester (10-
13wk) � pregnancy-associated plasma protein A (PAPP-A), B-hCG, and ultrasound
assessment of nuchal translucency * ?? �Second Trimester (15-20wk) � triple (MS-
AFP, estriol, B-hCG) or quad (triple + inhibin A) screening or other genetic
screenings (cell-free DNA), without an ultrasound exam for signs of trisomies/NTDs
* ?? �Third Trimester (20+wk) - glucose challenge test (24-28wk normally, first
trimester if obese or diabetic) with subsequent glucose tolerance test if abnormal.
GBS swab (35-37wk) is also done universally. Hemoglobin, hematocrit, HIV, and Rh-
factor repeat are also done. Fetal Assessment Techniques ?? Fetal growth is best
charted via ultrasoundo Early: crown-rump length correlates closely with
gestational ageo Later: skull circumference/diameter, abdominal circumference,
femur length, and cerebellar diameter are used to assess gestational age and fetal
weight ?? Fetal Well-being is assessed via many techniques o Kick Counting �
common, indirect measurement that mom can do! Mom should feel approximately 10
fetal movements every 2 hours o Non-stress test (NST) � mom�s intrauterine pressure
and baby�s heart rate are monitored via external monitoring. Baby�s line hopefully
shows variability, accelerations, or late decelerations in correspondence with
increased maternal pressure. Non-reactive, early decelerations, variable
decelerations, or other abnormal findings should be followed up. o Contraction or
Oxytocin Stress Test � basically an NST but baby�s heart rate is looked at during a
contraction or mom is given oxytocin for a contraction to see how it reacts. High
false positive rate, thus multiple tests must be interpreted collectively to give a
proper picture. o Biophysical Profile (BPP) � typically these are undertaken when
non-reassuring NST is seen. It is an ultrasonographic evaluation of 5 parameters,
lasting 30 minutes. 8/10 or 10/10 is good. ???Non-stress test � if reactive, +2???
Fetal Breathing � >1 episode of diaphragm movement for >30sec, +2???Fetal Movement
� >3 discrete arm/leg/back/finger movements, +2???Fetal Tone � >1
extremity/back/hand extension with return to flexion, +2 ???Amniotic Fluid volume �
a single pocket >1x2cm, +2 o Modified BPP � only a non-stress test (reactive is
good) and amniotic fluid index (AFI; assessment of 4 quadrants of amniotic fluid;
>5 is good). Typically used as it�s easier and similarly predictive as the full BPP
o Ultrasonography of the umbilical artery bloodflow � a technique to assess forward
flow through the artery, typically using a systolic/diastolic ratio to assess how
well flow occurs. Placental insufficiency can lead to significant morbidity/fetal
death, and if the placenta is �pushing back� less diastolic flow will occur. Thus
increased sys/diastolic ratio quantifies worsening placental blood flow and can
even forewarn of impending fetal demise. Typically end systolic reverse flow is an
indication for induction/C-section. ?? Fetal Maturity is assessed through lung
development, as it�s one of the last systems to fully mature o Surfactant/albumin
ratio (via amniocentesis) � high means higher surfactant productiono
Lecithin/Sphingomyelin ratio � higher means more lecithin (a component of
surfactant)o Phosphatidylglycerol � present with complete fetal lung maturity,
approx. 35wk o These techniques are important in assessment, as immature lung
function increases the risk for respiratory distress syndrome (collapse of airway
due to lack of surfactant) ???Should a neonate need to delivered early, balancing
risk of RDS vs continuing pregnancy must be assessed ???Antenatal corticosteroids,
post-natal ventilation/close monitoring are mainstays Antepartum Patient Education
* ?? �Employment � you can keep working; look into your job�s maternity leave
policies * ?? �Exercise � 30min of moderate exercise per day is good. Avoid supine
exercises. Don�t go too hard. Don�t get into a sauna or hot tub afterwards.
Remember your balance will change, increased fall risk * ?? �Nutrition/Weight gain
� iron and folate supplementation is good. You may get pica (sign of anemia).
Follow the BMI-based guidelines on how much weight you should gain. You�re not
eating for two. * ?? �Breastfeeding � it�s really good for baby (immunity, good
nutrients, bonding) and you (weight loss, bonding), just make sure to supplement
Vit.D (or sunshine) and don�t deny the Vit.K shot. * ?? �Sexual activity � OK
unless contraindication (placenta previa, PPROM, or preterm labour). * ?? �Travel �
OK. Make sure your properly immunized for where you�re going. Get a record of your
gyn care in case you go into labour. Don�t sit around too much (increased risk of
DVT, walk every 1-2hr). It�s recommended NOT to travel after 36wk...you may go into
labour away from your normal healthcare. Wear a seatbelt every time. * ??
�Teratogens � timing, dose, and susceptibility will determine the effects of a
teratogen o Medications: Short list of teratogens. Refer to pg. 75-76 for good
summarieso Ionizing radiation: <5 rads is fine. Usually concern with therapeutic
range radiation doses (think chemotherapy). Most imaging techniques are specialized
in pregnancy to give a low rad dose. o Methyl mercury: Large fish (tuna, shark,
king mackerel) have higher mercury content because they eat smaller fish, and
should be avoided in pregnancy. Shrimp, canned light tuna (not white albacore)
salmon, pollock, and catfish are all low and are fine to eat (approx. 2x week) o
Herbal remedies: don�t take these. They don�t work and could cause harmo Alcohol �
don�t drink it. The #1 most common preventable cause of mental retardation,
developmental delay, and birth defects. o Smoking/Drugs � don�t do it. Common
Pregnancy symptoms?? Headache (normal; if not relieved by Tylenol then call the
doc); Edema (normal; should resolve with sitting down/going to bed);
Nausea/Vomiting (normal in 1st trimester, hyperemesis gravidarum is rare but will
be much worse); Heartburn; Constipation (physiologic; docusate/psyllium can help);
Fatigue (typically restricted to 1st trimester) Leg Cramps/Back Pain/Round Ligament
Pain (all from bodily adjustments you�re making to accommodate baby); Varicose
Veins/Hemorrhoids; Vaginal Discharge Risk Factors for Genetic Disorders * ??
�Advanced maternal age - increases the risk for trisomy 21/all chromosomal
abnormalities (increasing risk with increasing age), however the majority of tri-21
cases occur in women younger than 35 * ?? �Previous chromosomal abnormality �
basically if you�ve had one previously, it increases the chance (1.6-8.2 x maternal
age risk) of having another depending on various factors)o Type of trisomy,
spontaneous abortion or no, maternal age at previous affected pregnancies, current
maternal age * ?? �Hx of early pregnancy loss � 50% of first-trimester losses are
due to chromosomal abnormalities. The most common is monosomy X, however others all
can have this effect * ?? �Advanced paternal age � fathers >50yrs significantly
increase the risk of X-linked recessive and autosomal dominant disorders due to
increased risk of mutation * ?? �Ethnicity � blacks (sickle cell), whites (cystic
fibrosis), and Ashkenazi Jews (Tay-Sachs, Gaucher, Niemann-Pick diseases),
Mediterraneans (B-thalassemia), and Asians (a-thalassemia) are mentioned in the
text, however this is simply to highlight that certain races have certain
predilections for disease Prenatal Screening (finding someone at heightened-risk in
a low-risk population) ?? First-Trimester Screening (1-13wk) � Trisomy 21, Trisomy
18, Trisomy 13 o hCG, PAPP-A are both measured in the first trimestero Advantage is
that decisions about continuation of pregnancy can be made at this time o Trisomy
21 * ???�Associated with elevated hCG and decreased PAPP-A * ???�Combined with
ultrasonographic imaging for nuchal transparency (fluid collection at the fetal
neck; an early sign of trisomy 21) * ???�When noting these markers, genetic
council, 2nd trimester CVS/amnio are offered o Any major/minor structural
malformations increase the risk of aneuploidy and should warrant a karyotyping of
mom/genetic testing of fetus ?? Second Trimester Screening (14-27wk)o Triple screen
(AFP, B-hCG, unconjugated estriol) or quadruple screen (+ inhibin A) are used in
detection of Trisomy 21, as well as other chromosomal disorders ???Trisomy 21 * ??
�Decreased � AFP, unconjugated estriol * ?? �Increased � B-hCG, Inhibin A ???
Trisomy 18 � all levels decreased o Ultrasound � cardiac defects and �soft markers�
(nuchal fold, ventriculomegaly,
echogenic bowel, shortened femur/humerus, absent nasal bone, pyelectasis) increase
risk of Down syn. ???Finding abnormalities on ultrasound??genetic counseling and
further testingo Screening for Neural Tube Defects (NTDs) � elevated maternal serum
AFP indicated increased risk for NTDs. If a mom has elevated AFP??ultrasound exam
for abnormalities should be done. * ???�All women should have 0.4mg folic acid
prior to conception as most women will not know their child has a NTD until it is
too late to correct it. * ???�Women with a previous NTD pregnancy should have 4mg
daily folic acid ?? Integrated Screeningo Using both first-trimester AND second-
trimester testing together, gives a 85-88% detection rate of serum-detectable
abnormalities Questions from This Section * ?? �The most accurate week for
ultrasound is between week 14.0 � 15.6 * ?? �While PAPP-A/Nuchal translucency/free
B-hCG is a fine first trimester screening test for Down�s Syndrome, the most
accurate test is the maternal cell-free DNA test. It will detect 99% of Down�s
syndrome cases, and can be used as early at 9wks. * ?? �When a pregnant patient
fails with 1-hr and 3-hr oral glucose tolerance test the first change is to
educate/initiate glucose monitoring + diabetic diet. If this fails to put person in
normal glucose ranges, then insulin or an oral hypoglycemic agent may be initiated.
Further oral glucose challenges are likely not necessary. * ?? �Shoulder dystocia,
metabolic disturbances, preeclampsia, polyhydramnios and fetal macrosomia are all
associated risks of gestational diabetes. Apparently intrauterine growth
restriction (IUGR) is a complication associated with pre-existing diabetes in
pregnancy. * ?? �According to ACOG, the recommended dose for patients not at risk
for NTDs is at least 0.6 mg/day. However, other organizations may suggest
0.4mg/day. Regardless, women at increased risk should take 4mg/day, switching to
0.6 mg/day after the first trimester. * ?? �Valproic acid use during pregnancy is
associated with a 1 to 2% incidence of neural tube defects, specifically lumbar
meningomyelocele. Fetal ultrasound examination at approximately 16 to 18 weeks
gestation is recommended to detect neural tube defects. * ?? �In an apparently
malnourished patient, folic acid supplementation, as well as evaluation for
deficiencies in her iron, protein and other nutrient stores should occur. In
general, a patient needs approximately 70 grams of protein a day, along with her
other nutrients. Pts should never lose weight in pregnancy, but should adjust
weight gain based on BMI. * ?? �Incorrect dating, specifically under-estimation of
gestational age, is the most common explanation for an elevated MSAFP. 90-95% of
cases of elevated MSAFP are caused by conditions other than NTDs including under-
estimation of gestational age, fetal demise, multiple gestation, ventral wall
defects and a tumor or liver disease in the patient. Next appropriate step in the
management of this patient is to obtain an ultrasound to assess the gestational
age, viability, rule out multiple gestation as well as a fetal structural
abnormality. * ?? �While Cell-free DNA screening can detect 99% of Down�s syndrome
cases, it should not be used as a rule-out for chromosomal abnormalities.
Amniocentesis or Chorionic Villus Sampling would be better choices (although the
question doesn�t explain why). The fetus in this case had a thickened NT, this
patient should be scheduled to have a detailed fetal ultrasound and echocardiogram
at 18-20 weeks to rule out anomalies. However, it is not possible to diagnose a
chromosomal abnormality with an ultrasound. Similarly, although genetic sonograms
(targeted sonogram) focus on markers associated with Down syndrome, they are not
diagnostic. * ?? �Ibuprofen is safe to take until around 32 weeks gestation, when
premature closure of the ductus arteriosis is a risk. While heparin is safe during
pregnancy, warfarin has known teratogenic effects and should not be given. If
continued anticoagulation is necessary, low molecular weight heparin is the drug of
choice. [Ch.7 Genetics and Genetic Disorders in OBGYN � Topic 9 and Topic 32]
Prenatal Diagnosis of Genetic Disorders * ?? �Essentially you have someone in a
high risk group (Ashkanazi Jews) or you�ve identified someone via pre-natal
screening tests and diagnosis is being sought * ?? �Carrier testing o Testing to
see if mom or dad carry a certain disease; typically one parent is tested first,
then the other if their test comes back positiveo Direct testing � blood/saliva
sample is taken and the DNA in those cells is tested fro specific mutations or
sequences that have been shown to cause disease. This will only work with diseases
that have an already-identified genetic basiso Indirect testing � same process, but
the test is looking for DNA sequences that are often linked to mutations that cause
disease called restriction fragment length polymorphisms. This is used in diseases
that do not have a specific mutation to test for yet. ?? Fetal Diagnostic
Procedures o Amniocentesis � taking some fluid under ultrasound guided needle
extraction for gene analysis ???Early (11-13wk) � heightened risk for
complications/fetal demise, not recommended???Midtrimester (15-20wk) � >99%
diagnostic accuracy and a <1% risk for complications o Chorionic Villus Sampling
(CVS) � using ultrasound guided needle to sample part of the chorion (immature
placenta) * ???�Before 10 weeks � increased risk of limb/oro-facial abnormalities,
not recommended * ???�Transabdominal CVS After 10 weeks � similar risk profile to
midtrimester amniocentesis, thus thought to be relatively safe, and able to be used
earlier o Percutaneous Umbilical Blood Sampling (PUBS; �cordocentesis�) � sampling
of the fetal blood via the umbilical cord after 20 weeks gestation???Benefit of
rapid karyotyping (18-24hrs), but not as useful nowadays ?? Genetic Counseling �
typically referral to a medical geneticist who will council the patient using the
key elements of accurate diagnosis, communication, and non-directive presentation
of options o The whole point is to inform the patients as much as possible for them
to make an informed decision as to the options that are available Questions form
This Section?? Serum Screening Tests in order of sensitivity o Triple Screen (69%),
Quad Screen (81%), 1st trimester combined screen (PAPP-A, hCG, nuchal translucency;
85%), Integrated screen (if nuchal translucency not obtained, 85-88%), Sequential
Screen (1st trimester combined + 2nd trimester quad; 93%), and Cell-Free DNA (>99%)
Case 4.5 � Antepartum Care Tips from UWorld 2404: Routine Prenatal Visit Labs * ??
�First visit: Blood Type/Rh-D type/antibody screen (Lewis, Duffy, Kell);
Hb/Hct/MCV, diseases (HIV, VRDL/RPR, HBsAg, Chlamydia PCR), Rubella/varicella
immunity, urine culture, urine protein * ?? �24-28wk: Hb/Hct, Antibody screen with
RhoGAM admin (If RhD-), and 50g 1-hour glucose challenge * ?? �35-37wk: GBS swab
and culture 10441: If there�s any question that wants you to do screening for the
baby and �cell free DNA testing� is an answer choice...just choose that one.
Although it isn�t diagnostic (you�ll need a CVS or amniocentesis for that) you can
get great screening results to guide further testing. 2569: 2nd trimester Quadruple
Screening Classic Findings:?? Trisomy 21: MS-AFP low; B-hCG low; Estriol low;
normal inhibin A * ?? �Trisomy 18: MS-AFP low; B-hCG high; estriol low; inhibin A
high * ?? �NTDs or abdominal wall defect: MS-AFP high; all other normal o The most
likely cause of an elevated MS-AFP is fetal abdominal wall defect (gastroschesis or
omphalocele); but NTDs and multiple gestations can do it as well o AFP is like the
albumin of the fetus, thus if the gut is open to the amniotic fluid, AFP riseso
Note that elevated AFP warrants careful ultrasound evaluation for structural
abnormalities 2568: In a patient with abnormal triple/quad screening results; the
next best step for assessment is an ultrasound. While you may be temped to go
straight to CVS/amniocentesis, the ultrasound can be used to check for anatomic
abnormalities associated with congenital defects as well as guide you for the best
place to do the amniocentesis. CVS/amnio will get done, they�ll simply need an
ultrasound first. Case 5 � Well-Child Exam Pediatric History * ??
�Prenatal/Perinatal History � Duration of pregnancy, complications, birth weight,
type of birth, medications given, and any records from the hospital pertaining to
the child�s birth * ?? �Family History � any diseases, problems, or abnormal growth
patterns * ?? �Social history � parental education, religion, smoking/drinking/drug
use, etc. Growth * ?? �Height/weight should be taken and plotted against a standard
growth chart * ?? �Head circumference should be taken in children <3yr of age * ??
�Blood pressure taken in children starting at 3yr of age Development � typically
plotted against standard things that a child should do at that age Age Motor
Language Social Other 1 mo Reacts to pain Responds to noise Eye contact/notes the
human face 2 mo Eyes follow object to midline/head up prone Vocalizes Social smile/
recognizes parent 4 mo Eye follow object past midline/rolls over Laugh/squeal Note
hands 6 mo Sits unsupported/ transfers objects between hands / rolls prone to
supine Babbles Recognizes strangers 9 mo Pincer grasp/ crawls/ cruises �Mama�,
�Dada�, �bye-bye� Explores 1 yr Walks/ throws objects 1-3 words; follows 1 step
commands Stranger anxiety/ separation anxiety �1 word at 1� 2 yr Traverses stairs/
copies a line/ runs/ kicks ball 2-3 word phrases, refers to self as name, pronouns
Parallel play 3 yr Copies a circle, pedals a tricycle, bridge of 3 cubes, repeats 3
numbers Sentences, recognizes 3 colors Group
play, simple games, knows gender, knows 1st/last name Tricycle, 3 cubes, 3 colors,
3 kids in a group 4 yr Knows body parts, copies a cross, Copies a square, hops on
one foot, throws overhand Speech is understood by all, tells a story Plays with
kids, social interaction 5 yr Copies a triangle, catches a ball, partially dresses
self Writes name, counts 10 objects 6 yr Draws a person with 6 parts, ties shows,
skips Knows right form left Screening Tests * ?? �2 weeks or younger � PKU,
congenital hypothyroidism, hemoglobinopathies, galactosemia, and in-born errors of
metabolism are all screened for in early life * ?? �Lead poisoning � more rare
nowadays, but 1yr and 2yr should be screened * ?? �Iron deficiency � usually taken
between 6mo � 1yr, often iron deficiency is the most common cause of anemia in
children. Often empiric treatment with iron supplementation is done * ??
�Hearing/Vision screening � often done in the newborn nursery. o Hearing typically
done by snapping finger and noting a responseo Vision tested by looking for the red
reflex (present is NORMAL)o Strabismus should be referred to pediatric opthamology
as soon as noted * ?? �TB in high risk children (often in immigrants or with family
that has known Hx of TB) * ?? �Lipid panel between ages 2-10yr to rule out
congenital lipid disorder Guidance * ?? �Includes guidance on injury prevention,
nutrition, discipline, exercise, mental health, and healthcare * ??
�Accident/injuries are the leading cause of death in children >1yr old * ?? �Car
seats should be a mainstay o <20lbs � rear facing car-seato 20-40lbs � forward
facing car seato >40lbs � booster seat until about 4�9� (can sit with back against
the seat rest with legs bent) * ?? �Sudden Infant Death Syndrome (SIDS) � sudden,
unanticipated death of a child during sleep. Thought to be due to shutting down of
the brainstem during REM and suffocation. Parents should have children sleep on
their backs on a firm mattress in the crib, with nothing else in the crib with them
* ?? �Food o Breast feeding is the best initial nutrition for the infanto
Cereal/other baby food/water introduced at 4-6mo of ageo Whole cow�s milk
introduced at 12mo and continued until 2yrs, then switch to skim Immunizations from
Age 0-18yr Immunization Dose 1 Dose 2 Dose 3 Dose 4 Hepatitis B Birth 1-2 months 6-
18 months Rotavirus 2 months 4 months DTaP 2 months 4 months 6 months 15 month + 4-
6yr H.flu (Hib) 2 months 4 months 12-15 months 12-15 months Pneumonia (PCV13) 2
months 4 months 6 months 12-15 months Polio (Inactivated) 2 months 4 months 6-18
months 4-6yr Influenza Start at 6months (annual Vaccine) MMR 12-15 months 4-6yr
Varicella 12-15 months 4-6yr Hepatitis A 12-23 months 12-23 months Meningococcal
11-12 yr TDap 11-12 yr HPV >11yr >11yr >11yr Meningococcus B 16-18yr Pneumonia
PPSV23 High-risk only By age: * ?? �0mo�HepB * ?? �2mo � HepB, Rota, DTaP, H.flu,
PCV13, Polio * ?? �4mo � * ?? �6mo � Hep B, * ?? �12mo � * ?? �6yr � * ?? �12yr � *
?? �18yr � Rota, DTaP, H.flu, PCV13, Polio DtaP, DtaP, PCV13, polio, Flu H.flu,
PCV13, MMR, Varicella, HepA MMR, Varicella Meningococcal, TDaP, HPV Meningococcus B
Case 6 � Allergic DisordersAllergic Rhinitis � inflammation of the nasal mucous
membranes due to allergy exposure ?? Presentation: sneezing, nasal
congestion/itching, rhinorrhea, anosmia, post-nasal drip, headache, ear- ache,
watery/itchy/red eyes, or drowsiness. Sinuses are often inflamed with blue-grey
coloration (venodilation). o The result of IgE-response to allergen, which allow
activation of mast-cell degranulation when allergen is present in the body after
sensitization o Mast cell degranulation results in histamine, tryptase, chymase,
kinase, leukotriene, and prostaglandin D2 release to mediate inflammation, mucous
production, and nerve sensitization o
Neutrophil/eosinophil/leukocyte/macrophagerecruitmentoccurstocontinueinflammation
and may result in systemic effects (malaise, fatigue, sleepiness) ?? Physical Exam:
allergic shiners (dark circles under eyes), small horizontal crease on nose bride
(�allergic crease�) caused by rubbing the nose (�allergic salute�); boggy, pale
blue-grey sinuses producing clear, thin mucus. o Nose: palpation of sinuses,
Inspection for nasal polyps, tumors, septal deviationo Ear: tympanic membrane
retraction, air-fluid levels, or bubbles behind the eardrum or loss of tympanic
mobility may all occur with Eustachian tube involvemento Eyes:
injection/swelling/tear production; sometimes with circles/lines o Throat:
erythema, �cobblestoning�, or tonsillar hypertrophy * ?? �Dx: presentation with
search for possible triggers * ?? �Tx: o Education and avoidance of allergen are
primary modalitieso 1st gen antihistamines (diphenhydramine) � cheap, but often
sedating & anticholinergic effects (dry mouth, blurry vision, urinary retention,
esp in elderly)o 2nd gen antihistamines (loratidine/cetirizine) � more expensive,
but non-sedating due to poor CNS penetration and less anti-cholinergic size effect.
Often onset 15-30min after taking, thus best used intermittently for flare-upso
Decongestants (pseudoephedrine) � a-agonist given intranasal that causes
vasoconstriction. Best used very short term for administration of other drugs as
rebound-hyperemia will ensure that the pt will never stop using the spray.o
Corticosteroid Spray � very effective for long-term control or persistent
allergies; often working within 2-4wk. Nosebleeds, pharyngitis, and URIs can all
occur more often.o Leukotriene inhibitors (montelukast or zileuton) � used best in
pts with allergies + asthma as they can treat both conditions; however, not more
effective than corticosteroids o Oral Corticosteroids � only to be used with
severe, unresponsive allergieso Desensitization therapy � used in pts who fail to
respond to treatments ???1. Spot testing to ID specific allergens???2. Injections
of highly diluted allergens with progressive increasing increments, eventually
reducing antigen inflammatory response (weekly/biweekly) ???note that anaphylactic
reactions may occur Anaphylaxis � widespread, severe allergic reaction due to
systemic response to allergen * ?? �Presentation: rapid onset dyspnea/bronchospasm,
viscera edema, hypotension, GI/uterine contraction, urticarial and angioedema after
allergen exposure * ?? �Dx: clinical * ?? �Tx: immediate administration of 1:1000
dose aqueous epinephrine (epi-pin) with repeated injections every 15-30min as
necessary. If hospitalized, IV fluids should be started and intubation should be
undertaken if necessary with monitoring for the next 24hr Conjunctivitis �
infection of the conjunctiva (the most common eye disease) * ?? �Presentation:
redness, discomfort, and sometimes crusting of one/both eyes, photophobia; NO
blurring or loss in vision should occur in this disease * ?? �Dx/Tx: based on
swab/culture for bacterial or virus analysis o Bacterial � Staph, Strep,
Haemophilus, Moraxella, or Pseudomonas could all occur; often unilateral but may
become bilateral; sulfonamide eye drops should clear the infection o Viral � most
commonly Adnovirus; often less crusting and more watery discharge and often
bilateral; weak topical steroids used to control inflammation with resolution in
approx. 2wk o Allergic � will occur with other allergy symptoms and resolve with
treatmento Chemical � result of damage to eye; immediate flushing and normal care
should resolve Case 7 � Tobacco CessationTobacco use is the single greatest cause
of preventable death and it�s been shown that physician intervention at patient
encounters increases tobacco cessation rate. Discussion should involve the Five As:
* ?? �Asking about current level of tobacco use * ?? �Advising to quit through
specific messages for the patient * ?? �Assess willingness to quit and proceed when
patient would like to proceed * ?? �Assist Quitting via help groups, encouragement,
and pharmacologic intervention * ?? �Arrange for follow-up and support! Drug
Therapy ?? Nicotine Replacement � gives the addictive substance with gentle
decrease in amount until no nicotine is being used. May result in replacing smoking
with a new nicotine habit (inhaler with highest potential) o All Category D drugs;
thus cannot be used in pregnancyo Nicotine gum should be chewed then placed in
cheek (like chewing tobacco); continuous chewing actually decreases efficacy??
Zyban (long acting Bupropion) � NE/DA blocker which is thought to remove the
�reward� gain by smoking, thus making smoking less enjoyable, thus easier to quito
Begin 1-2wk before quit date with 150mg for 3 days, then 150mg BID for 4 days for
7-12wk; may be used in conjunction with nicotine replacement therapyo Adverse
effects � dry mouth, insomniao Contraindication � Eating disorders, on MAO-
inhibitors within last 2wks, or seizure disorders o Category C-drug, thus not known
what it does in pregnancy, but relatively safe ?? Chantix (Varenicline) � partial
nicotine agonist reducing cravings, withdrawal symptoms, and may decrease smoking�s
�reward� via blocking endogenous nicotine agonism o Begin 1wk before quit ate with
0.5mg for 3 days, then 0.5mg BID for 4days, then 1mg/day for the rest of the 6mo
treatment; may be used with nicotine replacement therapy o Adverse effects �
nausea, insomnia, vivid dreams, psychiatric effects (behavior changes, agitation,
depression, suicidal ideation) o Drug must be used in reduced dosages in pt with
renal clearance <30 mL/min o Category C-drug, thus not known what it does in
pregnancy, but relatively safe?? Women who smoke should be encouraged to quit
without the use of pharmacotherapy; but Zyban and Chantix are NOT contraindicated.
While benefits are best if smoking ceases before;
occurring with cessation at ANY time during pregnancy. Case 8 � Ethics in Medicine
This case addresses a teenager with an issue that they want to keep private from
their parents; while autonomy, beneficence, nonmaleficence, and justice should all
be followed, there are situations where a patient�s wishes may not be followed:
* ?? �Suicidal or homicidal ideation � pt is a danger to themselves or others and
this must be reported * ?? �Serious chemical/drug dependence � pt is in danger of
death due to overdose * ?? �Abuse � pt is in danger from their abuser and must be
protected Some situations may happen where a minor is considered able to receive
care without parental consent: * ?? �Judicial bypass � a state law that can allow a
minor to be deemed �mature� thus allowing them to undergo medical treatments under
their own will * ?? �Emancipation � a minor is of certain age, lives apart from
parents, and is self-sufficient. May also occur if patient is married, pregnant/has
children, in military, or simply declared emancipated by the law. * ?? �Type of
healthcare sought � maternity services, contraception, STI dx/tx, reportable
disease dx/tx, treatment of drug/alcohol related problems, sexual assault
treatment, or mental health treatment Reportable diseases: confidentiality is often
requested, but some diseases are legally required to be reported * ?? �This varies
by state but often includes STIs, HIV, and other serious infectious diseases * ??
�Pt�s partners and parents may be informed through the state department * ?? �It�s
best to inform the patient that their disease MUST be reported, and the health
department will inform partners/parents without the patient�s consent if they do
not go themselves. Pregnancy/abortion services availability to teenagers vary by
state law. It�s best to simply look up where your state laws stand with these
situations. Case 9 � Anemia in the Geriatric PopulationPresentation: weakness,
fatigue, conjunctival/buccal/palmar pallor with additional signs pointing to cause
of the anemia * ?? �Microcytic/normocytic � iron deficiency, thalassemias, anemia
of chronic disease, anemia of elderly, sideroblastic (B6 deficiency), acute or
chronic hemorrhage, RBC hemolysis * ?? �Macrocytic � folate deficiency, b12
deficiency Case 9.5 � Anemia Tips From UWorld4358/2877: Iron Study Characteristics
in Microcytic Anemias o ?? �Iron Deficiency: not much iron around, thus the body is
looking to take up as much as possible o Decreased: MCV, serum iron, ferritin,
transferrin saturation (iron/TIBC)o Increased:TIBC o ?? �Thalassemia: poor
production of hemoglobin leaves iron out in the blood o Decreased: MCV, TIBC o
Increased: iron, ferritin, transferrin saturation o ?? �Anemia of Chronic Disease:
the body takes inflammation to mean �bacterial infection� and sequesters iron in
hopes that it�ll limit bacterial reproduction. o Decreased: MCV, iron, TIBC,
transferrin saturationo Increased:ferritino Typically, a chronic inflammatory
disease (autoimmune is classic!) can be noted from vignette. Treatment is as
follows: ???Underlying condition treatment (autoimmune disease will be
immunosuppressed) ???If no improvement??administer EPO to stimulate RBC production
???If no improvement??packed RBC transfusion to get RBC count back up 4389:
Suspicion of Colorectal cancer: signs/symptoms?? An older man (>60) with abdominal
pain, microcytic anemia, (+)fecal occult blood, and hepatomegaly with a hard liver
edge??prompt you to think infiltrative colon cancero Any old person with microcytic
anemia (esp. men) or blood in stool??colon cancero Hepatomegaly with a hard liver
edge??liver cancer (most often from metastatic colon cancer) o Mildly elevated
AST/ALT/Alk.phos in this setting??infiltrative/cholestatic disease (which
metastatic liver cancer would be a part of!)?? Dx: because this pt has signs of
colon cancer and liver abnormalities without significant elevations in LFTs, an
abdominal CT should be sought as metastatic malignancy is suspected. 2210: Dr.
Jones�s words echoed in Mike�s head, �An old person with iron deficiency anemia,
especially a man, has a GI bleed until proven otherwise.� * ?? �The first step is a
fecal occult blood test??if positive, then it�ll guide further investigation, but
if negative it means NOTHING! * ?? �If you have this clinical scenario and you get
a negative FOBT, you then get endoscopy/colonoscopy on the patient for concern of
GI malignancy Note that radioisotope erythrocyte scintigraphy is only useful in
active, significant bleeding. If it�s a slow or non-active bleed, that test won�t
tell you shit. 3926: Although weird, some older patients may have an �idiopathic
anemia of the elderly�. Classically these patients have multiple comorbidities
(CHF, etc.) that make them poorly tolerant to anemia 4348: Pica/Pagophagia ?? Pica
� appetite for substances other than food (clay, dirt, or paper are common) o May
have exotic appetite (hair, light bulbs, etc.) when associated with psychiatric
disease * ?? �Pagophagia � appetite for ice * ?? �Both classically associated with
iron deficiency anemia and may appear before iron deficiency is present, thus any
patient with these signs/symptoms should have bloodwork done 4356/4350/3067/3066:
Pernicious Anemia * ?? �B12 deficiency caused by anti-intrinsic factor antibodies
causing destruction of parietal cells/intrinsic factor resulting in failure of B12
uptake in the terminal ileumo Note that anemia is due to impaired DNA synthesis of
thymidylate and purine molecules for RBC production (ineffective hematopoiesis)
* ?? �Presentation: macrocytic anemia (pale conjunctiva, fatigue, pallor, MCV
>100), glossitis (beefy red tongue), and peripheral neuropathy/loss of lower
extremity vibratory sensation (dorsal column destruction), or cognitive function
defects. Sometimes jaundice from destruction of large RBCs o Smear: mactocytic
RBCs, hypersegmented neutrophilso Classically associated with atrophic gastritis
(parietal cells being attacked as they make intrinsic factor) increasing the risk
for intestininal-type gastric cancer and gastric carcinoid tumors. * ?? �Dx: B12
level, testing for autoantibodies, Homocysteine level/Methylmalonic acid level to
differentiate from folate deficiency * ?? �Tx: B12 injections + periodic stool
blood testing for gastric cancer monitoring 4357: Differentiating B12 from Folate
deficiency anemia * ?? �Both show elevated homocysteine (both involved with
conversion of homocysteine??methionine) * ?? �Only B12 def will show elevated
methylmalonic acid (conversion of methylmaonyl-CoA??succinyl-CoA) * ?? �Note that
folate deficiency is more common and should be suspected in any malnutrition
picture first as you can become deficiency in 5-10 weeks 4147: Several drugs can
cause megaloblastic anemia due to folate deficiency [HIGH YIELD] * ?? �Anti-
epileptics (phenytoin, phenobarbital, primidone)??impair folate absorption in the
gut * ?? �Bactrim (TMP-SMX)??inhibits dihydrofolate reductase, thus decreasing
folate activation * ?? �Methotrexate??inhibits dihydrofolate reductase (leucovorin
[folinic acid] is indicated as a concurrent supplement when giving methotrexate
because of this) 3086: Macrocytic Anemia due to Nutrient Deficiency * ?? �Folate:
found in leafy green veggies/liver; destroyed by cooking; depleted within 4-5
months; more common to get through diet * ?? �B12 (cobalamin): found in all animal
products (strict vegans); depleted within 3-4 years; typically, this is due to
pernicious anemia (anti-parietal antibodies) NOT diet2872: Note that basophilic
stippling is not as specific as you might think, and that it can occur in
alcoholism (may be part of folate deficiency macrocytic anemia), lead poisoning,
and thalassemia. 4330: Note that megaloblastic anemia due to B12 deficiency that�s
only treated with folate supplementation will result in worsening or emergence of
neurologic symptoms associated with B12 deficiency. This id because the folate will
aid in RBC production, which will use up the dwindling B12. Thus megaloblastic
anemia should always be treated with folate AND B12. 4468: Oddly enough, patients
with sickle cell disease are at higher risk for folate deficiency and megaloblastic
anemia. Because there is chronic hemolysis due to poorly deformable sickle cells,
there is high RBC turnover/production meaning there�s a high demand for folate/B12.
These patients can easily become folate deficient thus??a sickle cell patient (or
any chromic hemolytic patient) presenting with macrocytic anemia should first be
suspected for a folate deficiency. ?? Daily folate supplementation is recommended
for any person with Sickle Cell Disease! 4037: Sideroblastic Anemia * ?? �Anemia
resulting from defective heme synthesis from problem with pyridoxine (Vit B6)
dependent synthesis of protoporphyrin. * ?? �Presentation: normocytic to anemia
(fatigue, pallor, etc.) o Labs: increased iron with decreased TIBC (poor RBC
function, but iron is OK) o Smear: dimorphic RBC population ???Hypochromic
population �some bone marrow failing to make proper proteins ???Normochromic
population � some bone marrow that�s still doing OKo Classically this can happen
with tuberculosis treatment with isoniazid, alcoholism, drugs, etc. * ?? �Dx:
clinical presentation, can be confirmed with bone marrow biopsy showing ringed
sideroblasts * ?? �Tx: pyridoxine (B6) administration 4349/3978: In chronic kidney
disease, anemia can develop as the kidney is responsible for erythropoietin (EPO)
production. The mainstay of anemia with chronic kidney disease is supplemental EPO
+ supplemental iron. Iron is supplemented as EPO will surge RBC production, causing
a high need for iron for new heme. Plus, someone with chronic kidney disease may
already be anemic from chronic inflammation! * ?? �Iron
supplementation alone should always be tried first before EPO * ?? �Side Effects:
BP increase (30%, >10mm diastolic; not well understood), Headaches, Flu-like
syndrome, Red cell aplasia (rare) [HIGH YIELD] * ?? �Note that the goal of EPO
administration during dialysis is to get Hb to 10-12 g/dL; higher than this has
been found to have worse outcomes (increased cardiovascular death) 4385:
Indications for RBC transfusion * ?? �Hb <7: always indicated * ?? �Hb <7-8: heart
surgery, heart failure, or cancer treatment patients * ?? �Hb 8-10: any surgery,
acute coronary syndrome, on-going bleeding, symptomatic anemia * ?? �Hb >10: rarely
indicated Case 10 � Acute Diarrhea Definitions * ?? �Acute Diarrhea � persists for
<2wk duration * ?? �Subacute Diarrhea � persists between 2-4wk duration * ??
�Chronic Diarrhea � persists for >4wk duration Presentation: diarrhea and/or
vomiting, sometimes with fever, and abdominal pain * ?? �Determine volume status -
membranes moist or dry, skin turgor, or capillary refill time * ?? �Determine Oral
intake ability � are they vomiting too much to keep anything down? * ?? �Get
history � changes in stool, sick contacts, other symptoms, recent travel, recent
meals, etc. Dx: clinical presentation * ?? �Lab: stool sample for leukocytes,
culture, ova/parasites, or C.diff toxin * ?? �Note that most acute diarrhea is
viral and does not need further workup, only supportive care Tx: typically consists
of re-hydration, anti-secretory therapy, and antibiotics or probiotics if necessary
* ?? �Mild: often can tolerate oral intake; if not able to drink, then pt should be
hospitalized for IV fluids * ?? �Severe: profuse/blood diarrhea, severe pain,
fever, children/elderly/immunocompromised should all be hospitalized for supportive
care and treatment Quick Tips * ?? �Anti-secretory drugs aid symptoms but do NOT
speed length of recovery time * ?? �Best prevention of viral diarrhea is hand
washing and staying home from school for recovery * ?? �Serve food immediately from
refrigerator or after cooking; room temp = bacterial growth * ?? �Note that
clindamycin is classically associated with C.diff development and pseudomembranous
colitis; however any antibiotic may be associated with this development Traveler�s
Diarrhea * ?? �E.coli is the most common etiology (classic Hx of trip to Mexico)
* ?? �Best to avoid local water/ice cubes/raw fruits and vegetables * ??
�Prophylaxis is typically ciprofloxacin 500mg BID for 1-3 days * ?? �If a pregnant
woman or child: azithromycin 1000mg one-time (adult) or 10mg/kg for 3 days (child)
as floroquinolones may damage development of fetal/child bones and connective
tissue * ?? �Rifamixin 200mg TID for three days may also be used, although less
effective * ?? �Classically bismuth subsalicylate has been used as prophylaxis, BUT
the large quantities needed predispose to salicylism, thus should be avoided. Case
10.5 � Diarrhea Tips from UWorld3917/3590: Diarrhea in HIV/AIDS typically occurs
with different etiologies based on CD4+ count * ?? �Cryptosporidium (<180) � severe
watery diarrhea, wt loss, fevero Classically from animal contact, water, or person-
persono Dx: modified acid-fast stain shows cryptosporidial oocytes (4-6mcg) o Tx:
anti-retroviral therapy (resolves with CD4 receovery) * ?? �Microsporidium or
isosporidium (<100) � watery diarrhea, wt loss, cramps, no fever * ??
�Mycobacterium Avium Complex (<50) � watery diarrhea, wt loss, high fever (>102F) *
?? �CMV (<50) � bloody/small volume diarrhea, abdominal pain, wt loss, fever o Dx:
colonoscopy with biopsy � intracytoplasmic eosinophilic/basophilic inclusions o Tx:
gancicloviro Must examine eyes to rule out CMV retinitis 2269: Profuse watery
diarrhea in HIV/AIDS patients is typically from a opportunistic infection (bloody
would be more high infectious things). ?? First step in diagnosing what is causing
the diarrhea is stool examination for ova/parasites as often parasitic infections
will be the cause here! 3613: Typically, if a post-transplant pt shows lung
problems (cough, dyspnea, CXR infiltrates) and GI problems (abdominal pain,
dysphagia, diarrhea) you should immediately consider CMV infection. * ?? �Bone
marrow suppression (fatigue, cytopenias), and myalgias are other possible
manifestation * ?? �Dx: bronchoalveolar lavage with PCR for CMV * ?? �Tx: IV
acyclovir 3249: Traveler�s diarrhea is not uncommon, however it often lasts a <1
week and remits. If it lasts >2 weeks parasitic infections should be considered:
* ?? �Cryptosporidium, Cystoisospora, Giardia or microsporidia spp are major
parasites to be considered. * ?? �Dx: stool examination should reveal parasites
3248: In normal, healthy folks, there are TONS of reasons why you�d get GI problems
and the specific organism is based off the symptoms and cultures (often USMLE wants
to diagnose based off scenario!) So here�s some classics to remember: * ??
�B.cereus??diarrhea within 6 hours of eating re-heated rice * ?? �S.aureus??rapid
onset of vomiting (within 6hr) and sometimes diarrhea; classically from mayonnaise
* ?? �C.difficile??post-antibiotic Tx with diffuse, watery stools * ??
�C.perfringens??brief cramps, fever, diarrhea associated with unrefridgerated food
* ?? �V.vulnificus ???raw/undercooked shellfish causing vomiting/cramp/diarrhea o
May be life-threatening with invasive infection in immunocompromised! * ??
�E.coli??watery or bloody (shiga-toxin) diarrhea typically from undercooked
hamburger beef * ?? �Shigella??bloody diarrhea/bacteremia classically with travel
outside the US or undercooked chicken * ?? �Salmonella ???someone who ate
undercooked chicken or mayonnaise * ?? �Campylobacter??bloody diarrhea, can cause
Guillian-Barre * ?? �Rotavirus??classically diarrhea in the winter and exposure to
kids (often daycare workers) 3250: Foodborne Illnesses are wide-ranging with a huge
amount of possible presentations. We can narrow down possible bugs by the symptoms
of the patient: ?? Vomiting predominates: S.aureus, B.cereus, or Norovirus * ??
�Watery diarrhea predominates: C.perfringes, ETEC, Cryptospoidium, Cyclospora,
interinal worms * ?? �Inflammatory (bloody) diarrhea predominates: Salmonella,
Campylobacter, EHEC, Shigella, Enterobacter, Vibrio spp, Yersinia spp. * ?? �Non-GI
symptoms predominate: you�ll typically know these based on symptoms/history 3887:
Giardiasis (Giardia Lamblia or G.intestinalis parasite) * ?? �Presentation:
profuse, watery, foul-smelling diarrhea with bloating/abdominal cramps;
malabsorbtion/weight loss can occur in more long-standing infectionso Transmission
is classically after a trip abroad/camping trip through contaminated water/food or
fecal-oral route * ?? �Dx: Stool-antigen assay (immunoflourscence or ELISA) for
oocysts or trophozoites * ? �Tx: oral Metronidazole Case 11 � Adult Female Health
Maintenance[Ch.2 The OBGYN Role in Screening/Preventative Care � Topics 3 & 7]The
HPV vaccine is nearly 100% effective in prevention of HPV strains it�s against * ??
�Vaccination age range is 13-26 for females AND males * ?? �Best if given before
sexual activity, but sexually active people can still benefit * ?? �Do not give
vaccine during pregnancy * ?? �Do give vaccine during breastfeeding The Pap smear
(cervical cancer) and mammography (breast cancer) are the only acceptable screening
tests for gynecologic cancers * ?? �Note that there�s no acceptable screening test
for ovarian, endometrial, vaginal, or vulvar cancers and a biopsy of the region is
NOT considered a screening test * ?? �Leading causes of cancer death in women:
1Lung, 2Breast, 3Coleorectal Breast Cancer * ?? �Clinical breast exams and
screening mammography are effective screening tools * ?? ��Breast self-awareness�
should be emphasized; shown to increase detection rates of breast problems * ??
�Regular self breast exams are NOT recommended anymore * ?? �ACOG recommendations:
o Age 20-39: clinical breast exam every 1-3yrso Age 20-39 (high risk): consider
annual clinical breast examso Age 40+: annual clinical breast exam + annual
screening mammography o Age 40+ (high risk): regular recs + annual MRI of breast
tissue Cervical Cancer * ?? �Cervical Intraepithelial Neoplasia (CIN) is the
precursor to cervical cancer. CIN 1 often spontaneously resolves, but CIN 2 or CIN
3 will progress to cervical cancer and must be treated. * ?? �Pap Smear
(exfoliative cytology + papanicolaou test) recommendations: o Age <21: no screening
(regardless of sexual activity)o Age 21-29: screening with cytology every 3 yearso
Age 30-65: screening/cytology + HPV co-testing every 5yr (preferred) �OR�
screening/cytology every 3 yro Age 65+: no screening if >3 consecutive negative
tests + no hx of CIN 2 o Special Situations: ???Hysterectomy with removal of
cervix: no screening if removal was for benign reasons and no Hx of CIN 2 or
greater ???Hx of CIN 2 or greater: screening continues 20yrs after regression, then
resume normal screening guidelines ???HPV vaccination: follow normal guidelines
Colorectal Cancer?? Screening recommendations: o Age 50: colonoscopy every 10 years
o Alternativestocolonoscopy: ???Annual Fecal Occult Blood test or Fecal
Immunochemical testing ???Flexibal Sigmoidoscopy, Barium Enema, or CT colonography
every 5 years Sexually Transmitted Diseases (STDs) * ?? �HIVo All women should be
screened at least once for HIVo Women with the following risk factors should be
offered annual testing/repeat testing: ???IV drug users, have partners who are IDVU
or are HIV infected, exchange sex for drugs/money, have had an STD in the past
year, have had a new sexual partner o ELISA blood screening is the most common
screen o Abnormal ELISA testing should be followed with a confirmatory Western Blot
* ?? �Chlamydia o The most commonly reported STD in the USA o
Typically asymptomatico Screeningguidelines: ???Age <25 and sexually active:
annual screen (NAAT of endocervical/vaginal swab/urine) ???Age >26 and at risk:
annual screen (NAAT of endocervical/vaginal swab/urine) * ?? �Gonorrhea � Same
screening as Chlamydia applies here * ?? �Syphilis o All �at risk� women should be
screened annually o All pregnant women should be screened: ???During gestation as
early as possible (so intervention can occur) ???Again during 3rd trimester if from
high-risk population???Again during delivery o Screen is the VDRL or RPR with
confirmatory FTA-ABS or other testing Metabolic/Cardiovascular Diseases ??
Osteoporosis o Screeningguidelines * ???�DEXA scan with BMD/FRAX at age 65 * ???
�Testing at younger age if at increased risk for fracture (alcoholism, smoking, hx
of fragility fracture, body weight less than 127lb, medical cause of bone loss,
rheumatoid arthritis) o Bone Mineral Density (BMD) � an indirect measure of bone
fragility assessed with a DEXA scan. Basically a person�s BMD is charted against
population data to find the T-score/Z-score ???T-score BMD � based on young,
healthy adult population???Z-score BMD � based on reference population that patient
fits within???Normal BMD is > -1 ???Osteopenia BMD is between -2.5 and -1 ???
Osteoporosis BMD is < -2.5o Fracture risk assessment tool (FRAX) � assessment tool
used to determine the risk of a women >40 with low BMD�s risk of a bone fracture in
the next decadeo Preventative measures include, Ca2+/Vit.D consumption, regular
weight-bearing exercise, smoking cessation, decreasing alcohol intake, and
prevention of falls * ?? �Thyroid Diseaseo TSH at age 50, with repeat every 5 years
(may present as dementia in older adults!) o Earlier if risk factors or clinical
signs of hypothyroidism * ?? �Diabetes Mellitus � Screening fasting blood glucose
at age 45, with repeat every 3 years * ?? �Hypertension � screen with blood
pressure reading annually in all women >13 years * ?? �Lipid Disorders � screen
with lipid profile starting age 65, with repeat every 5 years * ?? �Obesity �
measurement of height/weight with BMI calculation should be with any physical exam
Case 12 � Minor Sprains and Strains Basic ?? ?? ?? ?? ?? ?? Ankle ?? ?? ?? Knee ??
Principles of Musculoskeletal Injury EvaluationInspection (swelling, bruising,
deformity, use of support devices, mobility of joint)Palpation (pain localization,
muscle tightness, swelling, sensation, temperature, pulses, capillary refill)
Passive Range of Motion (mobility of the joint/joint damage)Active Range of Motion
(muscle/tendon function, neurovascular function)Specific Testing (depends on joint,
listed at end of section)Imaging (X-ray is first choice, & MRI used for soft tissue
damage) Presentation: pain, swelling, redness, warmth, or loss of range of motion,
typically following injury o Classically the lateral ankle is weaker and more
susceptible to injury (Anterior talofibular ligament [ATFL] > calcaneofibular
ligament > posterior talofibular ligament) o The medial ankle is much more durable
due to the deltoid ligament Dx: clinical, but requires staging and possibly imaging
o Staging: 1 (stretching of ATFL) 2 (partial tear ATFL, sprain CFL) and 3 (complete
tear ATFL/CFL) o Ottawa Ankle Rules: nearly 100% sensitive in ruling out
malleolar/midfoot fractures. If any of these conditions are present, then a plain
X-ray should be undertaken.???Bony tenderness of posterior edge or tip of medial or
lateral malleolus ???Inability to bear weight on affected ankle for 4 steps???
Tenderness to palpation of the navicular bone or base of 5th metatarsal Tx: PRICE
(Protect, Rest, Ice, Compress, Elevate) + NSAIDs or Acetaminophen + Physical
Therapy o PT should be initiated 48-72hr following the injury at tolerated. The
biggest thing causing lasting mobility problems is not initiating PT early enough!
Ottawa Knee Rules: strong sensitivity/specificity; imaging should occur if any of
these apply: o Pt age 55yr or oldero Isolatedpatellartendernesso
Tendernessattheheadofthefibula o Inabilitytoflextheankleto90o o Inability to bear
weight on affected knee for 4 consecutive steps (even if there�s a limp) Specific
Rotator Cuff Testing * ?? �Empty Can Test (supraspinatus) � outstretched �thumbs
down�, don�t let doc press hands down * ?? �Lift-Off test (subscapularis) � dorsum
of hand on lower back, lift off from back * ?? �Internal Rotation (subscapularis) �
elbows at 90o, rotate hands toward stomach * ?? �External Rotation
(infraspinatus/teres minor) � same at internal but rotate outward * ?? �Hawkins
Impingement (subacromial impingement of supraspinatus tendon) � shoulder and elbow
flexed. Then internal rotation of the shoulder in that position * ?? �Drop-arm test
(large rotator cuff tear) � lift arm into air and slowly adduct the arm Specific
Ankle Testing ?? Anterior drawer (ATFL) � stabilize shin and pull ankle anteriorly
* ?? �Inversion stress test (CFL) � stabilize shin and invert the ankle * ??
�Squeeze test (syndesmosis; high ankle sprain) � squeeze tibia/fibular at midcalf
Knee * ?? �Lachman test (ACL) � knee at 20o, pull forward to attempt to mobilize
the knee * ?? �Anterior Drawer (ACL) � knee at 90o, pull forward to attempt to
mobilize the knee * ?? �Posterior Drawer (PCL) � knee at 90o, push backwards to
attempt to mobilize the knee * ?? �Valgus Strain (Medial Collateral [MCL]) �
stabilize shin 30o flexion and apply force to left side of knee * ?? �Varus Strain
(Lateral Collateral [LCL]) � stabilize shin 30o flexion and apply force to right
side of knee Case 13 � Evaluation of a Nevus + Tips from UWorld 2762/2603: Basal
Cell Carcinoma * ?? �Most common, often an excellent prognosis. Correlates with
cumulative sun exposure * ?? �Presentation: pearly/rolled edge nodule with
keratinized or ulcerated center. Sometimes featuring spider angiomata on the
lesion, oozing or crusting * ?? �Dx: clinical picture and biopsy * ?? �Tx: o
Superficial � electrodessication or cryotherapy o Deep � MOHS surgery
2604/4033/4319: Squamous Cell Carcinoma * ?? �Intermediate incidence with
intermediate prognosis, typically not metastatic when found, but will invade if
left untreated. Correlates with # of severe sun exposure events (burns, tanning
beds, etc.) * ?? �Presentation: rough scaly plaque/nodule with possible
hyperkeratosis/ulceration/bleeding. Classically can cause neurologic damage due to
perineural invasion (numbness/parastheisa) o Sunburns, radiation,
immunosuppression, burns, scars, and warts are all risk factorso Note that if
you�ve a lesion on the lower lip (more sunlight exposure) is SCCo Note that a
Marjolin ulcer is an SCC arising from the site of a scar/burn/previous injury and
has an increased risk of metastases * ?? �Dx: skin biopsy that includes the deep
reticular dermis (assess depth of invasion) showing dysplastic/anaplastic
keratinocytes/keratin pearls * ?? �Tx:o Low risk: excision or local destruction
(cryotherapy/electrodessication) o High risk or cosmetic areas: Mohs micrographic
surgery 2767/2765/4312: Malignant Melanoma ?? Least common skin cancer, but most
deadly o Superficial Spreading � most common type; shallow penetration with spread
radially in superficial skin layers. Often raised with brown/pink/white-grey/pink.
Common in both sexes, but men get it on their back) and women get in on their legs
o Lentigo Maligna � least common subtype. A tan-brown lesion with very irregular
borders. Classically on the elderly (most commonly diagnosed in the 7th decade of
life) o Acral Lentiginous � flat irregular brown-black lesions on the palms of the
hand or under the nailbed. Most common in Black and Asian people. o Nodular
Melanoma � most aggressive and often invasive at time of diagnosis. Brown-black
with nodular appearance; often grow from existing nevi. ?? Presentation: new or
existing melanotic skin lesion demonstrating the ABCDEs (Asymmetry, Raggy Border,
verigated Color, Diameter >6mm, Elevation/Evolution) o Considered the most common
malignancy of women age 25-29 o Women typically get it on the legs while men get it
on the back * ?? �Dx: excisional biopsy to show depth of invasion (most important
diagnostic factor) o Rarely malignant with <1mm depth of invasion * ?? �Tx:
surgical excision with wide (1cm) margins o We actually wait for this as the wide
excision may disrupt lymphatic flow 2764: Seborrheic Keratoses * ?? �Benign lesion
that tends to favor the face/trunk/old people and is often consider unsightly o May
be indicative of underlying GI malignancy as the Sign of Leser-Tr�lat where many of
these lesions appear rapidly. * ?? �Presentation: waxy/greasy, �stuck-on�, well
circumscribed lesion that may be flat or raised with normal surrounding skin. Can
vary from pink/white to pale to brown/black. Typically, slowly enlarging. * ?? �Dx:
clinical * ?? �Tx: none needed except for cosmetic reasons 4410: Actinic Keratosis
* ?? �Presentation: hyperkeratosis causing �sand-paper like� papules in areas of
sun exposure. Often begin small/flat but may accumulate becoming �cutaneous horns�.
Pre-malignant for SCC * ?? �Dx: shave biopsy with light microscopy showing
characteristic cell proliferation * ?? �Tx: electrodessication or cryotherapy Case
14 � Asymptomatic Hematuria + Tips From UWorldHematuria found on routine urinalysis
can be a sign of something further and needs to be investigated. A short list of
things that could cause hematuria includes: * ?? �Recent UG/genital trauma, urinary
infection, renal disease/tumors/calculi, BPH, exercise, menses, etc * ??
�Presentation: laboratory finding of 3 or more RBCs should prompt proper work-up o
Gross hematuria (specimen is visibly discolored from blood) or microscopic
hematuria (gross sample looks normal, but RBCs detected on analysis) o
Eosinophiluria
is classically due to Acute Interstitial Nephritis (drug-induced) * ?? �Risk
factors for intrinsic kidney disease are: smoking, occupational hazards
(benzenes/aromatics), age >40, Hx of gross hematuria/urologic disease/UTI/analgesic
abuse/pelvic irradiation * ?? �Dx: First step: Repeat urinanalysis; if persistent,
then proceed with further workup o Basic labs (CBC and BMP including serum
creatinine)o Microscopic evaluation of sample/urinary sedimento Cytology and
culture of urine sampleo Imaging (often CT abdomen & pelvis) of upper and lower
urogenital tracts; IVP, retrograde pyelogram, ultrasound, CT, CT urography, and
cystoscopy are all options for imaging???Note that if giving any IV contrast; renal
function needs to be assessed PRIOR to administration with proper hydration +/- N-
acetylcysteine or IV sodium bicarb ?? Tx: depends on etiology of hematuria o If
urine culture if positive; give antibiotic treatment; no need for further follow-up
if hematuria resolves with Abx o Exercise induced microscopic hematuria should
resolve within 72hrso If workup if unrevealing, then follow-up blood pressure,
urinalysis, and urine cytology at 6, 12, 24, and 36 months should be undertaken. If
these are normal, then no further follow-up is needed.Note that gross hematuria
always deserves a full workup! Even in a bodybuilder who has been working out.
3955: Classic Urine Casts [HIGH YIELD] * ?? �Muddy Brown cast � acute tubular
necrosis * ?? �RBC cast � glomerulonephritis * ?? �WBC casts � interstitial
nephritis or pyelonephritis (inflammation in the kidney) * ?? �Fatty casts �
nephrotic syndrome * ?? �Broad casts or waxy casts � chronic renal failure 4491:
Contrast-Induced Nephropathy * ?? �Renal vasoconstriction/tubular injury due to
administration of IV contrast for imaging procedures * ?? �Presentation: spike in
creatinine following contrast administration, with resolution around 5 days later o
Pt with impaired renal function (diabetes, chronic renal insufficiency, etc.) are
at high risk * ?? �Dx: clinical presentation * ?? �Tx: supportive care for recover,
prevention is keyo Pre-contrast hydration with IV fluids (isotonic bicarb or normal
saline)o N-Acetylcysteine may be used if concern is high (vasodilation/antioxidant)
3061/2242: Acute Interstitial Nephritis * ?? �Typically drug-induced damage to
interstitial tissue in the kidney * ?? �Presentation: acute renal failure, fever,
macropapular rash, classically following offending drug use (5 days to several
weeks following drug), and sometimes arthralgiao Urinanalysis: Pyuria, hematuria,
eosinophiluria, and WBC casts o Biopsy: inflammatory infiltration and edema * ??
�Dx: clinical presentation with agreeing labs o Drugs: penicillins, TMP-SMX,
cephalosporins, rifampin, diuretics, or NSAIDs ?? Tx: discontinue offending drug,
glucocorticoids, and supportive care 4807: Chronic Interstitial Cystitis (Painful
Bladder Syndrome) * ?? �Poorly understood disorder most commonly in women with
anxiety/pain syndromes * ?? �Presentation: suprapublic pain with bladder filling
relieved with voiding, increased urinary frequency/urgency, and dyspareunia/pain
with exercise/pain with alcohol consumption * ?? �Dx: bladder pain for >6 weeks
without attributable cause with normal UA * ?? �Tx: psychiatric therapy,
amitriptyline, and analgesics for exacerbations 2241: Post-Streptococcal
Glomerulonephritis o ?? �Autoimmune disease in response to a streptococcal
throat/skin infection occurring 10-20 days post- infection. Classically happens in
kids and young adults. o ?? �Presentation: Fever, rash, arthralgia, periorbital
edema, hypertension o Urine: oliguria, proteinuria, hematuria, sterile pyuria,
eosinophiluria, WBC casts o Blood: eosinophilia, low serum C3 compliment levelso
Biopsy: sub-epithelial humps due to complement deposition o ?? �Dx: clinical
presentation with elevated ASO titer or anti-DNase B antibodies o ?? �Tx:
supportive care, should resolve on its own o Prognosis good in children but very
bad in adults often leading to renal failure 2230/10287: IgA nephropathy * ??
�Autoimmune deposition of IgA in the meconium of kidney causing damage 5 days after
URI, classically in young men. Can recur any time after an URI as it�s the result
of over-activation of the normal immune response. Does not occur with skin
infections. o The most common glomerulonephritis in adults; remember that damage
occurs in glomerulus! * ?? �Presentation: recurrent gross hematuria following a URI
o Labs: normal serum compliment levels * ?? �Dx: presentation. IgA demonstrated
deposition in renal biopsy * ?? �Tx: supportive care (often benign) with close
watch for progression 2229: Myoglobinuria * ?? �Acute renal failure following
diffuse muscle damage, classically after a tonic-clonic seizure * ?? �Presentation:
acute elevation of creatinine, often with hypertension/tachypnea o Urinanalysis:
large amount of blood with few RBCs on microscopy * ?? �Dx: clinical picture with
classic disparity in urinanalysis (RBCs is detection of hemoglobin OR myoglobin
thus, a standard UA will say �large RBCs amount� but microscopy will show few
RBCs/hpf) * ?? �Tx: hydration and supportive care until return of baseline renal
function 4006: Never forget, rifampin causes red/orange urine discoloration as well
as discoloration of tears, sweat, and saliva. Classically it�s known to stain
contact lenses. ?? It�s important to do a simple urinalysis to rule out more
serious conditions. Case 15 � Thyroid Disease + Tips from UWorld Hyperthyroidism
* ?? �Signs: progressive nervousness, difficulty concentrating, palpitations,
weight loss, moist skin, fine resting tremor, dyspnea on exertion, diarrhea, and
heat intolerance * ?? �Symptoms: Rapid pulse, elevated BP (systolic > diastolic),
and rarely atrial fibrillation Hypothyroidism * ?? �Signs: lethargy, depressed
affect, sluggish mentation, forgetfulness, weight gain, dry skin, constipation,
cold intolerance; may be confused with depression (women) or dementia (elderly) o
1o hypothyroidism will show an high TSH but low T3/T4 (poor thyroid function) o 2o
hypothyroidism will show a low TSH??TRH administration is used ???A normally
functioning pituitary will respond and TSH will rise. If it doesn�t then there�s
something wrong with the pituitary (get imaging of the pituitary) ???If the
pituitary responds then there may be something wrong with the hypothalamus (not
making TRH, thus no TSH production) * ?? �Symptoms: low blood pressure,
bradycardia, non-pitting edema, hair loss, dry/cracked skin, slowly relaxing
reflexes, and rarely myoedema * ?? �Tx: thyroid hormone replacement (typically 1.7
mcg/kg daily)o Children (use a lot for growth) and pregnant women (increased TBG)
may need increased doses o Elderly (decreased TBG) may need decreased doseso TSH is
regular follow-up for adequate response 4 weeks after any changes in dose
4324/4588: Evaluation of Hyperthyroidism ?? Any suspicion of thyroid problems
should begin with TSH/T4 lab values o TSH low/T4 normal with signs of
hyperthyroid??measure T3???Normal T3??subclinical hypothyroid, early pregnancy,
non-thyroid problem ???High T3??If signs of Grave�s disease, it�s Grave�s disease.
If no signs, do a Radioactive Iodine Uptake (RAIU) scan o TSH low/T4 high with
signs of hyperthyroid??consider primary hyperthyroidism ???If signs of Grave�s
Disease, then you�re good; if not then RAIU scan o TSH normal - high/T4 high with
signs of hyperthyroid??consider secondary hyperthyroidism ???MRI of pituitary for
TSH secreting tumor ?? Radioactive Iodine Uptake (RAIU) scan performed when
hyperthyroid is considered, but Grave�s disease is not likely due to symptoms o Low
uptake??measure thyroglobulin (Tg) levels???Low Tg??likely exogenous use of thyroid
hormone???High Tg??thyroiditis, extra-glandular production, or iodide exposure o
High uptake diffuse??Grave�s diseaseo High uptake nodular??Toxic adenoma, or
multinodular goiter 4324: Central Hyperthyroidism (TSH secreting adenoma) * ??
�Presentation: signs of hyperthyroidism (weight loss, tachycardia, palpitations,
etc) with tumor mass effect signs (headache, visual symptoms, impaired secretion of
other pituitary hormones) * ?? �Dx: TSH high with high T4 * ?? �Tx: surgical
excision or ablation 4415/3488/4726/4132/2179: Grave�s Disease * ?? �Presentation:
hyperthyroidism, exophthalmos, diffusely enlarged thyroid gland o Low TSH with high
T3 or T4 * ?? �Dx: clinical picture with confirmed TSH receptor-antibodies * ??
�Tx: three major options o Radioiodine ablation � basically goes in and destroys
the thyroid gland cells. Apparently the point of this treatment is to become
euthyroid and complete destruction is NOT intended. However, pts very often have
the side-effect of hypothyroidism. * ???�Initial worsening of symptoms/exophthalmos
(10%) in first week or so due to release of stored thyroid hormone from cell
destruction. Often OK in young, healthy pts. * ???�Pre-treatment with
glucocorticoids often minimizes treatment symptoms * ???�Hypothyroidism (80%) may
develop, and is most likely in Grave�s Disease as the entire thyroid gland is
dysfunctional, instead of just part. o Surgery � removal of the thyroid is always
on the table ???Risk of damage to recurrent laryngeal nerve or hypoparathyroidism
due to damage or unintentional removal of parathyroids o Propylthiouracil (PTU) or
methimazole (MMA) � thioamides that block production of T3/T4 * ???�MMA a teratogen
in the 1st trimester, may cause cholestasis * ???�PTU can cause hepatic failure,
ANCA-associated vasculitis, and agranulocytosis * ???�Does not permanently cure
disease. Typically used in pts that cannot tolerate other treatments (old people
that cannot handle worsening symptoms or surgery) 2178/3487: The life-threatening
side-effect of Propylthiouracil/Methimazole
is agranulocytosis (0.3%). This classically presents with fever and sore throat
within 90 days of treatment initiation. Should this occur: 1. Stop PTU/MMA
immediately and check WBC levels. 1. WBC >1,500 � PTU isn�t causing the problem 2.
WBC <1000 � PTU should be discontinued for life 2. Get throat culture, give oral
penicillin/acetaminophen, administer broad spectrum antibiotcs before even knowing
the result as lack of immune response could be fatal. Pseudomonas is especially
worrysome in these patients 3952: Thyrotoxicosis can largely affect the heart
causing changes in rhythm (atrial fibrillation, PACs/PVCs, and sinus tachy),
hemodynamics (increased CO??systolic HTN and increased myocardial O2 demand), heart
failure, and angina. 4307: Hyperthyroid Bone Disease * ?? �Excess thyroid gland
activity stimulate osteoclast activity, thus causing bone resorption. The resulting
hypercalcemia inhibits PTH production ultimately leading to hypercalciuria and net
calcium wasting. * ?? �Brittle bones, tendency toward bone fracture, and decreased
bone density are all possible problems! * ?? �Note that a hot nodule (functional,
likely toxic goiter) is nearly NEVER NEOPLASTIC, as it�s an area of isolated
hyperacitivty/hypertrophy. A cold nodule is an area of low activity but growth,
which is high suspicious of thyroid cancer. 4286/10958/11277: Thyroid Storm * ??
�Presentation: high fever, cardio (tachycardia, HTN, CHF, atrial fibrillation), CNS
(agitation, delirium, coma), hyperthyroid (goiter, lid lag, tremor), GI (nausea,
vomiting, diarrhea, jaundice)o Typically caused by: thyroid/non-thyroid surgery,
acute illness, childbirth, or acute iodine load (such as in IV contrast!) * ?? �Dx:
clinical presentation with precipitating factor * ?? �Tx: propranolol (decrease
adrenergic effects), propylthiouracil (decrease thyroid hormone production),
glucocorticoids (suppress TRH/T3??T4 conversion), and ID trigger to treat/remove
3483: Metabolic changes in hypothyroidism include hyperlipidemia (decrease in LDL
receptors), hyponatremia, and asymptomatic elevations of CK (>10x normal). * ??
�Note that hyperlipidemia may persist for months despite adequate replacement
therapy * ?? �Statins will increase the chance of hypothyroid myopathy, thus are
used with caution 3878/4382: Hypothyroid Myopathy * ?? �Presentation: normal
hypothyroidism signs with elevated CK (mild) to rhabdomyolysis/polymyositis o CK
elevation can be present years before clinical signs of hypothyroidism o Typically,
normal reflexes * ?? �Dx: any pt with unexplained elevated CK/myositis should have
TSH/T4 checked as this may be the manifestations of hypothyroidism early on.o If
normal, then muscle biopsy should be considered * ?? �Tx: treat underlying cause
3495: Euthyroid Sick Syndrome (�Low T3 syndrome�) ?? Presentation: acute, severe
illness accompanied by abnormal thyroid function tests o Labs: low T3 with normal
T4 and TSHo Result of of decreased deiodination of T4 from caloric deprivation,
glucocorticoids, and acute phase reactants * ?? �Dx: typically thought to be
hypothyroidism, but often thyroid levels are unreliable in acute illness * ?? �Tx:
treatment of underlying disease should resolve the abnormal tests 3496: Thyroiditis
Hashimoto�s Thyroiditis * ?? �Presentation: predominantly hypothyroid symptoms with
non-tender diffuse goiter * ?? �Dx: Anti-thyroid peroxidase (TPO) or anti-
thyroglobulin antibodies in high-titer o Note that nearly 10% of the normal
population is (+) for anti-TPO antibodies o The most common cause of hypothyroidism
is the USA Silent (painless) Thyroiditis * ?? �Presentation: variant of Hashimoto�s
with a mild, brief hyperthyroid phase (destruction and release of T3/T4), with a
small, non-tender goiter and slowly going back to euthyroid * ?? �Dx: Anti-TPO
antibodies and low radio-iodine uptake Subacute (DeQuervain�s) thyroiditis * ??
�Presentation: post-viral inflammatory disease causing prominent fever /
hyperthyroidism with painful/tender goiter * ?? �Dx: presentation with elevated
ESR/CRP and low radioiodine uptake 2191: Struma Ovarii ?? Rare thyroid hormone
producing ovarian teratoma. Classically in women over age 40 with pelvic mass,
ascites, and abdominal pain 4318: Toxic Adenoma * ?? �Presentation: thyrotoxicosis
with single hot thyroid nodule on exam * ?? �Pathophys: activating mutatinos in the
TSH receptor (auto-activation) * ?? �Dx: demonstration of single, hot nodule on
radioactive iodine scan o Note that toxic multinodular goiter would have a patchy
distribution on RI scan * ?? �Tx: ablation or removal 3498/3499/3497: Classes of
Thyroid Malignancy * ?? �Papillary � epithelial origin, unencapsulated, most
common, best prognosis o Typically metastasizes to the lymph nodeso Increased risk
from family history and childhood radiation of head/necko FNA often reveals large
cells with pale, grooved nucleio Often demonstrates Psamomma bodies and may
demonstrate Hurthle cells * ?? �Follicular - epithelial origin, encapsulated,
decent prognosis o Early hematogenous spread (lung/brain/bone) and invasion of
thyroid capsuleo FNA often shows normal looking follicular cells. Invasion through
capsule/hemotgenous spread is necessary for diagnosis of carcinoma (vs adenoma),
thus surgical diagnosis must be made to see if invasion outside the capsule occurs
o May demonstrate Hurthle Cells * ?? �Medullary � parafollicular c-cell origin,
good prognosis, produces calcitonin, 80% are sporatic o Associated with
MEN2a/MEN2b; screening for these diseases is recommended * ?? �Anaplastic �
epithelial origin, rare, classically in old people o
Poorprognosis,deathwithin6monthstypicallyo May involve other adjacent structures
(trachea/esophagus/etc.) due to rapidly enlarging thyroid mass * ?? �Primary
Thyroid lymphoma � rare, typically in the setting of Hashimoto�s thyroiditis o Has
rapidly enlarging thyroid gland but good prognosis * ?? �Note that because thyroid
cancers are often indolent, it can be prudent to wait till after pregnancy to
evaluate and treat the problem in a pregnant woman 4154: Oddly enough, oral
estrogen replacement therapy will increase Thyroid Binding Globulin (TBG) levels
due to decreased breakdown of TBG in the liver. * ?? �Pts with a normal thyroid
function will make more and compensate without trouble. * ?? �Pts on levothyroxine
for hypothyroidism will have to increase the dose (as the TBG increase will mean
less free T4 present). The increased dose will saturate the increased TBG, and
restore euthyroidism. * ?? �*transdermal estrogen does not have this effect as it
bypasses the liver Case 16 � Labor and Delivery/ROM [Chapter 8: Intrapartum Care �
Topic 11] Early Signs of Labour ?? Uterine contractions � frequent (occur every 3-
5min) and uncomfortable transitioning in to painful with cervical dilation are
characteristic. Often pain radiates to the lower back/abdomen o Braxton-Hicks
contractions (false labour) are more sporadic and are not associated with labour.
These are less intense and can be relieved by hydration/ambulation/analgesia.
Sometimes, these can be distinguished from true contraction by being able to
palpate through the uterus. True uterine contractions make this palpation more
difficult. * ?? ��Lightening� � a sensation of the baby feeling lighter due to
engagement of the baby�s head with the pelvis. Mom may feel the baby is �dropping�
and she can breathe more easily. * ?? ��Bloody show� � with the loss of the mucus
plus from cervical dilation, blood-tinged mucus will come out of the vagina. This
is a common sign that labour is occurring. Evaluating for Labour * ?? �Moms should
be instructed to immediately contact their healthcare provider for four major
reasons: o Contractionsoccurevery5minutesforatleast1hour(correspondswithlabour) o
Sudden gush of fluid from the vagina (corresponds with ROM)o Significant vaginal
bleeding (many reasons, often not good)o Significant decrease in fetal movement
(concern for fetal demise) * ?? �Abdominal Examination should be done with the
Leopold Maneuvers o Fundal Determination � palpate the fundus (top) of the uterus
on the belly to find either the head (breech lie), or lower extremities (vertex
lie) if the baby is laying longitudinalo Locating the Small Parts � palpate down
the uterus to either feel the spine or the hands/feet o Identifying the Presenting
Part � palpate suprapubically to find the presenting part. Then manipulate the
part. If the entire body moves, then it�s a breech; if only the presenting part
moves, it�s likely the more mobile head.o Identifying the Cephalic Prominence � If
this is palpable, the fetus is likely above the 0 station. * ?? �Vaginal
Examination � digital examination for effacement and dilation are periodically done
to chart the process of labour. The presenting part may also be palpated. * ??
�Fetal Station � Ranges from �3 to +3 with 0 being the fetal head being at the
level of the ischial spines. When the baby�s head is at 0 station, it�s indicative
that labour is progressing properly. Stages of Labour * ?? �First Stage � onset of
labour??full cervical dilation (10cm); mom may feel the urge to push but should be
discouraged as the cervix may not be fully dilatedo Latent Phase � cervical
effacement and early dilationo Active Phase � more rapid dilation, typically
starting around 4cm * ?? �Second Stage � full cervical dilation??delivery of the
infant; pushing is now encouraged. Molding or caput succedaneum can occur, giving a
false sense of descent. o Episotomy MAY be used in certain situations but is not
routinely recommended as there is increased risk of 3rd/4th degree laceration o
Excessive traction should not be placed on the fetus for fear of brachial plexus
injury * ?? �Third Stage � delivery of the infant??delivery of the placenta;
typically
indicated by 1rising of the uterus, 2change of uterus to a more globular shape,
3lengthening of the visible umbilical cord, and 4a gush of blood. Traction should
be light for fear of uterine inversion. 30 minutes allotted for this stage. * ??
�Fourth Stage � after the delivery of the placenta when mom is undergoing
physiologic adjustment; this is the time where mom is at greatest risk for post-
partum complications (esp. bleeding) Mechanisms of Labour (�Fetal Cardinal
Movements�) ?? Engagement (descent of the fetal head into 0 station; nulliparous
women typically have this days to weeks before active labour, multiparous women
typically have this with active labour)??Flexion (fetal head flexes to move into
mom�s pelvis)??Descent (movement into the birth canal; fastest rate occurs in the
active stage 1 of labour and stage 2)??Internal rotation (allows passage of baby�s
head through mom�s pelvis)??Extension (baby�s neck extends as it reaches the
introitus)??External Rotation (�restitution�; delivery of the head results in
further head rotation into a �face forward� position) ???Expulsion (rapid delivery
of the body; this is why �catching a baby� is a thing) Induction of Labour * ??
�Oxytocin � helps stimulatie uterine contractions * ?? �Cervical ripening � aiding
in dilation of the cervix, especially if induction is not favorable o Oxytocin or
Prostaglandin E2 � vaginally administered, these medications help with dilation and
contraction of the uterus. May cause hyperstimulation if both are administered.
Dual administration is contraindicated in pts with prior c-section or uterine
surgery due to increase risk of uterine rupture o Laminaria japonica rods �
hygroscopic rods are inserted into the uterus and swell with absorption of fluids,
helping slow dilate the cervix. Not often used. o 30mL foley catheter � works
similarly to the L.japonicum rods?? Membrane Manipulation � �stripping� or
�sweeping� the amniotic membranes. Not routinely recommended as it increases the
risk for infection as well as bleeding if an undiagnosed placenta previa is present
[UWise Chapter 8 Questions] * ?? �Braxton Hicks Contractions � irregular,
uncomfortable contractions in the lower pelvis/groin without cervical dilation or
effacement. Can happen at any time in pregnancy (even at term!) * ?? �Group B
strep. recto-vaginal swab/culture is typically performed at 35-37wk and if
positive, women should be treated prophylactically during labour (GBS is fast
growing; could grow back within 1 week!) o If a woman has GBS bacteuria in
pregnancy??no need to swab, just give Abx intra-partumo If a woman has Hx of GBS
infection in prior pregnancy??no swab, just give Abx intra-partum o GBS prophylaxis
does not need to be given if a C-section is done before membranes rupture * ??
�Upon presentation to the hospital in labor, first steps are: review of the
prenatal records with special focus on the antenatal complications and dating
criteria, a focused history and a targeted physical examination to include maternal
vital signs and fetal heart rate, and abdominal and pelvic examination. o Other
tests may be needed (nitrazine test, ultrasound, etc.) but these would be indicated
by the clinical scenario and are not routine * ?? �Remember! Fetal Heart tones MUST
be assessed during placement of an epidural (fear of fetal bradycardia). If a pt
cannot sit still for Doppler readings to be assessed during placement, a fetal
scalp electrode monitor is the way to go. Mom can move all she wants and you can
still get proper readings on baby to ensure epidural placement is OK.?? In this
question, pt was presenting in labor with the fetus at +2. While initially, heart
rates were fine, the latest reading was that baby�s heart rate was in the 60s. In
this situation:o Measure mom�s heart rate to make sure Dopplers aren�t measuring
hero Encourage mom to push to try and finish the 2nd stage of deliveryo IF mom
cannot complete delivery of the baby�s head within 1-2 pushes, opt for operative
forceps or vacuum-assisted delivery to expedite the process of labor?? In this
question, you were trying to place an intra-uterine pressure catheter (IUPC) and
300cc of frank blood/amiotic fluid came out! The next best thing to do is to
confirm baby is OK, thus withdraw the IUPC and check fetal heart tracings. o If
reassuring??attempt to place the IUPC again o If non-reassuring??consider placental
abruption/uterine damage and go to C-section * ?? �Some classic fetal heart tracing
changes: o Variable decelerations � umbilical cord compressiono Late decelerations
� placental insufficiencyo Fetal head compression � early decelerationso Sustained
fetal bradycardia � umbilical cord prolapse or tachysystole o Sustained fetal
tachycardia � Maternal fever/chorioamnionitis o Loss of fetal variability � opiate
drugs taken/administered to the mom o Sinusoidal wave patterns � fetal acidosis,
anemia, or hypoxemia * ?? �When umbilical cord prolapse is diagnosed (typically
through palpation of cord in the vaginal vault) the two things to do are
1manipulate the fetus to minimize cord compression, and 2call for assistance for
immediate C-sectiono Replacement of the cord, continuation of labor, and surgical-
assisted delivery are not indicated as fetal status can quickly deteriorate or
rupture of the cord can occur. * ?? �Performance of a median episiotomy is the
single greatest risk factor for third- or fourth-degree lacerations and more highly
associated with anal incontinence [Chapter 9: Abnormal Labour and Intrapartum Fetal
Surveillance � Topics 22 & 26] Abnormal Labour (dystocia) is any form of abnormal
progression of labour ?? Three Major Factors that can lead to dystocia (�The Three
Ps�)o Uterine Contractions (�Power�) � if you�re not contracting properly, then
you�re not having proper labour. Typically monitored with external tocodynamometry
OR IUPCs. �Adequate� contractions measure >200 Montevideo units over a 10-minute
period. �Too frequent� contractions are not optimal as relaxation between
contractions allows for bloodflow to baby. o Fetal Factors (�Passenger�) � if baby
is big/presenting poorly then it�ll be harder to squeeze through the pelvis!
Estimated weight of >4000-4500g (9-10lbs) increases risk of getting stuck. Poor
presentation (brow, face, mentum anterior face, occipitoposterior, or compound
presentations) can make the fetal diameter larger than if in other presentations.
Fetal anomalies (hydrocephaly, soft tissue tumors, etc.) may play a role as well! o
Maternal Factors (�Parent�) � if mom�s pelvis is too small or if she has some soft
tissue growth that could impede the birth canal, you could have trouble passing
baby. However, clinical pelvemitry, CT, or radiographic analysis of the pelvis is a
poor predictor of maternal vaginal delivery success, barring very small diameters.
?? Risks of abnormal Labour � several risks are increased with dystocia, mainly
infection (esp. with ruptured membranes) causing sickness to mom and baby. ??
Diagnosis/Management � basically there�s two major types, Protraction (slow labour)
or arrest (halted labour). These are usually called based on mom�s measurements
compared to the Friedmann Curve. o First Stage Disorders include Prolonged Latent
Phase (lasts >20hrs in nulliparous, or >14hrs in multiparous) or Prolonged Active
Phase (dilation <1cm/hr in nulliparous, or <1.2cm/hr in multiparous). Management
options are: * ???�Observation � just watch mom and see if she begins progressing
more normally * ???�Augmentation � consider this if mom�s contractions are
inadequate (<3 contractions/10min, or contractions <25mmHg above baseline. May be
achieved by amniotomy (artificial ROM) +/- oxytocin (stimulates uterine
contractions). If mom doesn�t enter the active phase after amiotomy, consider
adding oxytocin. * ???�Continuous Labour Support � basically support from
family/friends/midwife. o Second Stage Disorders � considered with 2nd stage
1lasting >3hr with anesthesia, 2>2hr without anesthesia, or 3if pushing has lasted
>1hr * ???�Prolonged 2nd stage of labour is NOT an indication for operative
delivery as long as baby and mom are doing well under surveillance. Labour should
be continued with efforts to increase pressure to expel baby and open mom�s pelvic
canal * ???�Operative or cesarean delivery are considered if surveillance shows
distress Operative Delivery ?? Types � basically different conditions warrant
different naming/set of risks o Outlet operative vaginal delivery � scalp is
visible without separating the labia, fetal skull has reached the pelvic floor,
sagittal suture is anteriorposterior or right/left occiput, fetal head is at the
perineum, and rotation does not exceed 45o o Low operative vaginal delivery � fetal
station at +2 or lower o Medpelvis operative vaginal delivery � fetal station is
above +2 * ?? �Indications � no absolute indications but prolonged/arrested 2nd
stage of labour, fetal compromise, or benefit to mom by shortening labour are all
indications * ?? �Contraindications � 1if <34wk, no vacuum deliveries (inc. risk of
hemorrhage); 2if the fetus as a bone defect, bleeding diathesis, or is unemerged
(inc. risk of hemorrhage) * ?? �Forceps � Foreceps are applied to baby�s head/neck;
indicated to aid mom�s efforts if they�re inadequate. There are risks to mom
(trauma, hematoma, pelvic flood injury) and baby (brain/spine injury, cornea
abrasion, and shoulder dystocia if >4000g). * ?? �Vacuum Extraction � application
of a soft, mechanical vacuum on baby�s scalp. Typically less trauma to mom but baby
has major risks (intracranial hemorrhage, subgaleal hematoma, scalp lacerations,
hyperbilirubinemia, retinal hemorrhage, or separation of the scalp causing
cephalohematoma; 5% risk). Breech Presentation � there are three types of breech
(Frank, complete, or footling),
all of which increase fetal/maternal risks as opposed to cephalic presentation.
* ?? �External Cephalic Version (ECV) � manual rotation of baby to achieve a vertex
lie. 50% success rate. Best done around 36wk gestation as spontaneous cephalic
version likely would occur before this time. Note that the fetus must have
reassuring heart tones, adequate amniotic fluid, and the presenting part must NOT
be in the pelvis. Tocolytic agents MAY be used to relax the uterus to aid version.
* ?? �If a baby cannot be verted, C-section is preferred as most physicians lack
experience in breech deliveries. Make sure to inform mom if risks if attempting a
breech delivery and get C-section consent. Shoulder Dystocia � basically baby�s
shoulders get stuck in mom�s pelvis. The turtle sign (emergence and retraction of
the head in a contraction) is a classic sign of shoulder dystocia * ?? �McRoberts
Maneuver � hyperflexion of mom�s hips (open up pelvis/sacrum) and applied
suprapubic pressure (angle shoulders to make diameter smaller) is a common first
step * ?? �Zavanelli maneuver � flexion of the head with re-insertion of baby into
mom�s uterus to re-establish bloodflow for a C-section. This is a last resort kind
of maneuver. * ?? �Episiotomy is typically NOT indicated as it�s the bony tissue
that baby is stuck on * ?? �Incidence of brachial plexus injury is 4-40% BUT <10%
of these injuries are persistent. Typically mom can be re-assured that baby will be
OK with shoulder massage. Intrapartum Fetal Surveillance * ?? �Pathophysiology �
the uteroplacental unit is the source of oxygen/nutrients/waste removal for the
fetus. If it is interrupted, it leads to hypoxia/shunting of blood to baby�s
brain/heart/adrenals. If this hypoxia goes uncorrected, anaerobic metabolism will
occur and lactic acid buildup will begin, causing progressive damage to the fetal
organs. * ?? �Intrapartum Fetal Heart Rate Monitors � This is basically all the
things you know about fetal heart monitoring. If you want a refresher, go to
pgs.114-117 * ?? �Ancillary Testing � because false-positive rates of fetal
distress can be high, other tests can be used to confirm worries with a non-
reassuring FHR tracing. o Fetal stimulation � scalp sampling, allis clamp scalp
stimulation, digital scalp stimulation, or vibroacoustic stimulation are all
methods. Basically you�re looking for accelerations with any of these applied on
the fetal heart monitor. o Fetal blood pH or lactate � blood sample is taken from
the scalp. If pH is decreased, its bad o Pulse oximetry � not useful, don�t use it
?? Diagnosis of Non-Reassuring Fetal Heart Tones � don�t forget your Stage I, Stage
II, and Stage III criteria o Turning mom on her left side, applying oxygen,
correction of hypotension, and discontinuation of oxytocin are all reasonable first
steps to correct fetal hypoxia. o If acidosis or persistent fetal hypoxia are
present, then C-section is warrantedMeconium � thick, tarry poo that�s present in
the fetal gut in-utero/at birth. If the baby is stressed in-utero then it may poop
out some of this meconium into the amniotic fluid, staining it dark green/black. ??
Meconium aspiration syndrome � fetal inhalation of meconium-stained amniotic fluid
causing pneumonitis, pneumothorax, or pulmonary HTN. If this occurs, the infant
should be intubated if not vigorous/thick meconium is present. If the baby is
vigorous, then it�s likely OK. [Chapter 9 Questions] * ?? �A patient failing to
dilate further during active labour (like they�ve been stuck at 5cm for 8 hours)
should warrant suspicion arrest of dilation. Interventions are as follows: o
Oxytocin infusion (increase contraction frequency/strength; promote dilation)o If
not adequate: place an IUPC and see if contractions are adequate (>200 MVU/10min) o
If not adequate: Consider C-sectiono Note that ambulation DOES NOT aid in
progressing delivery * ?? �In the question, a patient is at term (40wk) and in
severe back pain, desiring induction of labour. She�s closed and 20% effaced. The
suggested course of action: o Give Misoprostol (cytotec) for �ripening� of the
cervix, then induction with oxytocin (Pitocin) can be initiated once a more
favorable cervix is achieved o Note that waiting till 42 weeks in this setting
severe back pain is not appropriate. The patient is at term and extremely
uncomfortable, thus ripening and induction are reasonable. Plus, going to the
absolute maximum of 42wk is associated with problems (macrosomia, oligohydramnios,
uteroplacenta insufficiency, etc.) * ?? �Prematurity, multiple gestation, genetic
disorders, polyhydramnios, hydrocephaly, anencephaly, placenta previa, uterine
anomalies and uterine fibroids are all associated with breech presentation. * ??
�Note that prolonged latent phase is defined as >20 hours for nulliparas and >14
hours for multiparas, and may be treated with rest or augmentation of labor.
Artificial rupture of membranes is not recommended in the latent phase as it places
the patient at increased risk of infection * ?? �Never forget! Gestational diabetes
is the biggest risk factor for macrosomia. Maternal obesity, diabetes mellitus,
postterm pregnancy, a prior delivery complicated by a shoulder dystocia, and a
prolonged second stage of labor are all associated. * ?? �Secondary arrest of
dilation: lack of cervical change in the active phase for over four hours.
Management includes: o Amniotomy (artificial ROM) as first stepo If still
inadequate: Careful observation and oxytocin admin to increase contractions o If
still inadequate or fetus is non-reassuring: consider C-section * ?? �Don�t forget!
Prolonged 2nd stage (active) labour alone is NOT an indication for operative
delivery or C-section. Fetal macrosomia, feto-pelvic disproportion, or
materal/fetal distress would all give indication for them, but not prolongation
alone! * ?? �Any Category III fetal heart tracing warrants immediate C-section.
* ?? �Frank breech is the most common type of breech presentation, occurring in 48-
73% of cases and the buttocks are the presenting part. * ?? �First Stage Labour
(Active) arrest of dilation should be assessed with the following: o Place IUPC to
check if contractions are adequate (>200MVU/10min)o If not adequate??consider
oxytocin administrationo If still not adequate??consider operative-assisted
delivery or C-section * ?? �Note that misoprostol (Prostaglandin E1) and cervadil
(Prostaglandin E2) are contraindicated in VBAC. However, operative assisted
delivery is OK TO USE in VBAC. * ?? �Don�t forget! Amnioinfusion may be used for
repetitive variable decelerations; not for recurrent lates. * ?? �Initial measures
to evaluate and treat fetal hypoperfusion (occasional late decelerations): o Change
in maternal position to left lateral position which increases perfusion to the
uterus o Maternalsupplementaloxygenationo Treatment of maternal hypotensiono
Discontinue oxytocin o Consider intrauterine resuscitation with tocolytics and
intravenous fluids, fetal acid-base assessment with fetal scalp capillary blood gas
or pH measurement Case 17 � Hypercalcemia + Tips from UWorldCalcium physiology:
there are really 3 ways that calcium is controlled in the body: * ?? �Bones �
release via osteoclasts or sequestration via osteoblasts/mineralization * ??
�Intestines � increased/decreased absorption from the gut * ?? �Kidneys �
increased/decreased excretion in to the urine There are two major hormones that
control Ca2+: PTH and calcitonin * ?? �PTH � raises blood calcium levels via
activating osteoclasts (bone breakdown) & kidney resorption of Calcium/excretion of
phosphate, stimulates kidney 1a-hydroxylase mediated conversion of 25-OH VitD ??1,
25-OH VitD (stimulates many things, but importantly kidney Ca/phosphate
reabsorbtion) * ?? �Calcitonin � decreases blood calcium via deactivating
osteoclasts, increasing kidney Calcium excretion, and limiting activation of
Vitamin DEtiology of Hypercalcemia: extremely variable, but some common threads can
be found based on phys. * ?? �Thyrotoxicosis (most common) � hypermetabolic state
causing increased bone breakdown * ?? �Primary hyperparathyroidism � results in too
much PTH secretion (familial, sporatic, or in MEN 1 or 2) * ?? �Malignancy (2nd
most common) o PTH-rP secretion � effectively too much PTH secretion (lung,
head&neck, renal cancers)o Direct osteolysis � cancer spreads to the bone causing
breakdown (breast, multiple myloma, prostate cancer) * ?? �Hypervitaminosis A �
works on RAR or RXR receptors to stimulate osteoclasts/inhibit osteoblasts,
resulting in increased bone turnover (vitamin A over-supplementation or Analogue
acne treatments) * ?? �Immobilization � poorly understood, but thought to be a lack
of osteoblast activation due to poor bone stimulation without loss of osteoclast
activation. (post-surgery, elderly, paralyzed for any reason) * ??
�Hypervitaminosis D � increased absorption of Ca2+ (over-supplementation) * ??
�Granulomaous Disease (Sarcoid, TB, Hodgkins disease) � epitheliod
histiocytes/granulomas can convert 25-OH VitD??1,25-OH VitD * ?? �Milk-alkali
syndrome � calcium over-supplementation (Ca-antacids or osteoporosis supplements)
causing hypercalcemia, metabolic alkalosis, & renal insufficiency * ?? �Mediations
o Thiazides (HCTZ or chlorthalidone) � decreased calcium excretion based on
mechanism o Lithium � poorly understood, but may affect both the kidney and
parathyroids * ?? �Rhabdomyolysis � massive myocyte hemolysis causing Ca2+ release
into blood * ?? �Adrenal Insufficiency � poorly understood; possibly from
hemoconcentration secondary to loss of aldosterone production and diuresis
Hyperparathyroidism is a common cause, especially on tests; so let�s examine how it
happens: * ?? �1o � typically parathyroid adenoma (one dominant thyroid gland with
other atrophy) o Constitutional
PTH overproduction; kidney responds to it o Hyper-calcemia, hypo-phosphatemia,
high PTH * ?? �2o � hypocalcemia or low Vit.D; classically from early renal
failure; parathyroid glands are normal sized o PTH overproduction via physiologic
response to low Ca2+; kidney responds poorly o Normal/hypo-calcemia&hyper-
phosphatemia,highPTH * ?? �3o � long-standing renal failure resulting in
constitutional parathyroid hyperplasia even with renal transplant or regular
dialysis o Long-standing PTH production able raise Ca2+, but kidney is still
failing o Hyper-calcemia, hyper-phosphatemia, high PTH 2169/2633: Hypercalcemia
* ?? �Presentation: stones (renal calculi), bones (arthritis, osteoporosis),
abdominal moans (abdominal pain, constipation, N/V, pancreatitis, anorexia),
psychiatric overtones (confusion, stupor, coma) and others dehydration
(polyuria/poor oral intake) & cardiac problems (shortening QT/arrhythmias) * ??
�Etiology: underlying malignancy, malignancy hyperPTH secretion, thiazide
diuretics, others * ?? �Dx: high Ca2+ on BMP * ?? �Tx: o Mild (<12), Moderate (12-
14) or asymptomatic � no immediate treatment. Avoid diuretics/lithium and give
hydration to ensure hemoconcentration does not occur o Severe (>14) or symptomatic
� immediately give IV saline + calcitonin and stop loop diuretics unless pt needs
them for CHF. Long-term give bisphosphonates to decrease the amount of Ca2+ being
introduced to the body through bone resorption. 4308/4134/4309/3102: Evaluation of
Hypercalcemia * ?? �Step 1: confirm hypercalcemia (repeat Ca2+ level/measure serum
albumin to correct for it) * ?? �Step 2: Determine the source (measure PTH) o
High/normal PTH: PTH dependent hypercalcemia???Primary hyperparathyroidism,
familial hypocalciuric hypercalcemia, or lithium o Low PTH: PTH independent
hypercalcemia???Malignancy (Ca >15) from bone mets or PTHrP production (suppression
of PTH) ???Vit D toxicity (too much Ca++ retaining), granulomatous diseases (makes
Vit. D), thiazide toxicity (Ca+ resorbtion), milk-akali syndrome (over ingestion of
Ca++), thyrotoxicosis (increased bone resorbtion), Vit. A toxicity (direct
osteoclast simulation in high doses), prolonged immobilization (increased
osteoclastic activity without matching osteoblastic activity) � often more mild
elevations 2599: Treatment of Mild Hypercalcemia (<12mg/dL)?? Classically due to
bone lesions from metastatic cancer. It does NOT require emergent fluid therapy but
initiation of bisphosphonates helps slow osteoclastic activity and decrease risk of
pathologic fracture/malignant hypercalcemia 8876: Hypocalcemia?? Presentation:
fatigue and weakness o Labs: low Ca2+ ?? Dx: o Low magnesium? Drugs that cause
hypoCa? Recent Blood transfusion (citrate sequestration)? ??correct it if yes. o If
no, measure PTH level???Low/normal PTH � surgical damage to parathyroids,
autoimmune destruction of parathyroids, or some infiltrative disease (Wilson�s,
hemochromatosis, etc.)???High PTH � Vit D deficiency (check 25-Vit D levels), CKD,
sepsis, tumor lysis syndrome 4722: Primary hyperparathyroidism is a classic cause
of secondary hypertension, typically due to a parathyroid adenoma (80% of cases).
The PTH causes excessive Vit D activation, leading to renal calcium resorption, GI
absorption, and bone breakdown * ?? ��Stones, bones, abdominal groans, psychiatric
overtones� * ?? �Hypercalciuria (renal stones), bone pain (resorption of calcium
from bone), GI upset/constipation (intense absorption) and
confusion/depression/psychosis (not sure!) * ?? �It�s actually NOT entirely clear
how PHPT causes hypertension, but significant HTN may be related to
pheochromocytoma in the context of MEN 2A. 2176/4304: Primary Hyperparathyroidism *
?? �Presentation: typically, asymptomatic, but may present with fatigue,
constipation, abdominal pain, renal stones, bone pain, or neuropsychiatric symptoms
o Labs: hypercalcemia, elevated PTH, elevated urinary calcium excretion o Note that
MEN1a is associated with parathyroid adenoma! * ?? �Etiology: parathyroid adenoma
(or other tumor), parathyroid hyperplasia * ?? �Dx: diagnostic labs with clinical
picture * ?? �Tx: can be treated medically or surgically via parathyroidectomy if
symptomatic (osteoporosis, renal manifestations), age <50, or extremely high serum
(>1g) or urine (>400g) calcium 2165: Familial Hypocalciuric Hypercalcemia ??
Benign, autosomal dominant mutation in the calcium-sensing receptor (CaS-R) of the
parathyroid glands. This causes increased elevation of serum Ca2+ to activate them
to stop PTH secretion. This results in increased Ca2+ resorption in the renal
tubules o Differentiated from primary hyperparathyroidism by calcium urine
excretion (low in 1ohyper- parathyoidism, as the kidney is trying to resorb the
Ca2+) ?? Presentation: asymptomatic with normal renal function o Labs:
hypercalcemia with low urine calcium excretion (<100mg/24hr) ?? Dx/Tx: lab
abnormalities, no treatment needed in the absence of symptoms 2228/3435/3895/4058:
Calcium Renal Stones * ?? �Calcium oxalate � the most common type of renal stone.
Radiopaque. Small, envelop-shaped crystals are seen on microscopy. Classic risk
factors are small bowel disease, bowel resection, or chronic diarrhea, as they
decrease the absorption of fat in the gut. This is a problem as the fatty acids
will chelate Ca2+, leaving oxalic acid free of Ca2+, so it can be easily absorbed
into the body! * ?? �Calcium Phosphate � another radiopaque stone common in primary
hyperparathyroidism or renal tubular acidosis. * ?? �Some suggestions to minimize
formation of these stones are: o Use of thiazide diuretics (passive increased
reabosrbtion of Ca2+)o Increased fluid intake (dilute it out to make calcium not
form stones)o Decreased Na+ intake (increases Na/Ca reabsorbtion, thus decreasing
amount in kidney) o Normal Ca++ in diet (poor Ca++ intake increases oxalate
absorbtion, thus promoting the formation of calcium oxalate stones!)o High K+ diet
(decreases Ca++ excretion)o Low animal fat diet (decreased acid production to be
filtered out by urine) 2227/11109: Management of Acute Renal Stone * ?? �Imaging:
abdominal x-ray will often work, but abdominal CT will pick up even radiolucent
stones * ?? �Pain control: NSAIDs preferred in people with normal renal function,
but narcotics can be used * ?? �Stone Size: stones <5mm in size should pass
spontaneously. Increasing fluid intake to >2L/day will aid in passing the stone as
well as preventing further stone formationo BMP along with urinalysis should be
undertaken in any patient with their first stoneo Tamsulosin (a1-blocker) may be
used in relax the bladder/ureteral walls to aid in passing the stone by preventing
reflex ureteral spasm * ?? �Urology: anuria, urosepsis, or acute renal failure all
warrant immediate urology consult 4361: Imaging for Renal Stones * ?? �Renal
ultrasound �stone study� is best as it is non-invasive, not toxic, cheap, and can
visualize all types and sizes of stoneso Test of choice in pregnant women * ??
�Non-contrast spiral CT can be used as first line, or after an ultrasound. Due to
it�s cost and radiation, it is less preferred, but necessary sometimes as it�s much
higher resolution o never use contrast in a stone study, contrast is opaque and the
stone is opaque...thus you�re making it impossible to see the stone * ?? �Abdominal
X-ray is a decent modality in a pinch and will visualize 85%, BUT you can only
catch radiopaque stones, thus it�s not preferred. 3083: Milk-Alkalai syndrome * ??
�Occurs due to over-supplementation with calcium and absorbable alkalai.
Essentially you take too much result in renal vasoconstriction, decrease in GFR,
Na/K/2Cl inhibition (diuresis) * ?? �Presentation: N/V, constipation,
polyuria/polydipsia, AKI, suppressed PTH in the setting of calcium supplementation
(this patient was taking supplements for osteoporosis)o Labs: hypercalcemia,
hypomagnesiemia, hypophosphatemia, metabolic alkalosis * ?? �Dx: clinical
presentation * ?? �Tx: discontinue supplementation with IV fluids/furosemide to
flush out the kidneys 4171: Side effects of Thiazide diuretics (HCTZ or
chlorthalidone) * ?? �Glucose intolerance � worse insulin release from pancreas AND
tissue resistance to glucose uptake. Worse in pt with diabetes or metabolic
syndrome * ?? �Poor lipid metabolism with increased LDL/triglycerides � similar to
glucose intolerance. Worse in diabetes or metabolic syndrome * ??
�Hyponatremia/kalemia/magnesemia and hypercalcemia � based on mechanism of action.
Actually beneficial in staving off osteoporosis * ?? �Hyperureciemia and worsening
gout � reduces renal uric acid excretion 3083: DON�T FORGET!!! THIAZIDE DIURETIC
HYPECALCEMIA IS MILD AND WON�T CAUSE SYMPTOMS. 3100: Because much of serum calcium
is bound to albumin, hypoalbuminemia can result in alteration of measured serum
levels. Thus, something like proteinuria can easily cause hypoalbuminemia, leading
to falsely decreased serum calcium levels. ?? Correction to assess ionized
(unbound, active) serum calcium is necessary in these situations: o Corrected Ca =
Serum calcium + 0.8(4.0 � serum albumin) 3587/3520/2630/3494: Multiple Endocrine
Neoplasia (MEN) ?? MEN1: o Primary Hyperparathyroidism (hypercalcemia, high urine
calcium, high PTH)o Enteropancreatic tumors (most commonly gastrinoma causing
Zollinger-Ellison syndrome; VIPoma, glucagonoma, and insulinoma all possible)o
Pituitary adenomas (most commonly prolactin secreting) * ?? �MEN2a: RET-
protooncogene mutationo Medullary Thyroid Cancer (parafollicular C-cells, produce
calcitonin)o Pheochromocytoma (elevated plasma metanephrines, episodic hypertensive
crises), o ParathyroidHyperplasia * ?? �MEN2b: RET-protooncogene mutationo
Medullary Thyroid Cancero Pheochromocytomao Mucosal/cutaneous neuromas, Marfanoid
habitus 2615/2632: Major Primary Cancers of the Lung * ?? �Presentation: cough
with hemoptysis, chest CT shows characteristic nodule. May have paraneoplastic
syndrome associated with it Types * ?? �Adenocarcinoma: peripherally located
solitary nodule, female, non-smokers, clubbing/osteoarthropathy. Most common
overall regardless of smoking status. * ?? �Squamous Cell Carcinoma: central with
necrosis/cavitation, hypercalcemia (PTHrP production: anorexia, constipation,
increased thirst, easy fatigability OR metastases to bone) o Will cause suppression
of PTH with elevated calcium??always considered malignancy * ?? �Small Cell
Carcinoma: central hilar mass, smokers, paraneoplastic syndromes associated
(Cushing�s from ACTH; Lambert-Eaton from anti-Ca2+channel; SIADH from ADH), often
presenting with metastatic disease. Systemic chemotherapy mainstay of treatment
(�too small to cut out�) * ?? �Large Cell Carcinoma: peripheral, associated with
gynecomastia and galactorrhea 4200/3046: Sarcoidosis * ?? �Should you ever see a
patient with dry cough, malaise, and bilateral lymphadenopathy it�s sarcoid! * ??
�Presentation: classically it�s a young, often black, woman with
cough/malaise/bilateral lymphadenopathy on CXR. However, lots of lovely signs could
be present: o Anterior/posterior uveitis (vision loss/pain)o
Peripherallymphadenopathy/hepatosplenomegalyo Polyarthritis, sometimes with
periosteal bone resorption o Central diabetes insipidus or hypercalcemia
(hypervitaminosis D)o Arrhythmias (Complete AV heart block most common) � granuloma
disruption of myocardium ???Cardiac sarcoidosis should be suspected in any patient
<55y/o with unexplained 2nd/3rd degree heart block or with known sarcoidosis o
Lofgren Syndrome: erythema nodosum, hilar lymphadenopathy, migratory polyarthritis,
fever * ?? �Dx: characteristic bilateral lymphadenopathy on CXR with biopsy showing
non-caseating granulomas either from the lung or from peripheral tissue should
systemic involvement be present * ?? �Tx: corticosteroids Case 18 � Health
Maintenance in the Elderly + Tips from UWorldFunctional Assessment � old people
aren�t great at doing stuff. It can cause a huge drop in quality of life if they
cannot perform proper activities of daily living, thus, IADLs and ADLs should be
monitored * ?? �Activity of Daily Living (ADL) � bathing, dressing, eating,
toileting, grooming, movement/transfers * ?? �Instrumental ADL � driving, shopping,
cooking, money management, cleaning, laundry, etc. * ?? �Pts who cannot perform
IADLs independently have a greatly increased risk of dementia Vision Screening �
most sensitive screening is a vision test with a Snellen or Jaeger card, although
referral for ophthalmologic examination is a prudent idea if feasible * ?? �Age-
related Macular Degeneration � the leading cause of severe vision loss in the
elderly. o Atrophy of cells in the central macula of the retina (loss of central
vision) * ?? �Glaucoma � elevated intraocular pressure that causes optic
neuropathy, thus vision loss * ?? �Cataract Disease � the most common cause of
blindness worldwide o Opacification of the lens due to changes in lens proteins
* ?? �Diabetic Retinopathy � leading cause of blindness in adults in the USA
Hearing Screening � correlated with social isolation/depression, hearing loss is
common and best assessed with a whispered voice test or Hearing Handicap Inventory
(HHIE-S), although audiometry is most accurate * ?? �Presbycusis � hearing loss of
the elderly, classically with difficulty hearing with background noise, but none in
a quiet or silent room. Selective high-frequency loss and difficulty with voice
discrimination. Not associated with complete hearing loss * ?? �Noise-induced
hearing loss � wear and tear hearing loss from noise exposure. Can occur at any
age; difficulty with voice discrimination, hearing over background noise, and
tinnitus * ?? �Cerumen impaction � reversible transient conductive hearing loss;
lovely to clear out * ?? �Otosclerosis � autosomal dominant disorder of the inner
ear bones causing hearing loss onset from age 20-40yr. Oddly, speech discrimination
is well preserved. * ?? �Central auditory processing disorder � CNS dysfunction
causing hearing loss Fall Assessment � the leading cause of non-fatal injury in the
elder is a fall; and often falls can cause hip fracture leading to significant
functional impairment a loss of quality of life. ?? Always ask about falls,
dizziness, and assess gait in old peopleCognitive Screening � dementia rate doubles
every 5 years after age 60; thus we should screen for it * ?? �Typically, a clock-
draw and a three item recall are easy, reliable tests to screen for dementia * ??
�A positive screening should be followed by Mini-mental status exam for more
complete assessment Incontinence Screening � they happen; ask about the poops
Depression Screening � often treatable and can vastly improve quality of life if
treated; may also present as pseudodementia, blurring the line between cognitive
and emotional dysfunction * ?? �Asking Have you felt down/depressed/hopeless in the
last 2 wk? and Have you felt little interest/pleasure in doing things? Is a solid
screening (high sensitivity) * ?? �Geriatric Depression Scale should be done on any
elderly patient screening positiveNutrition Screening � serial weight
measurement/questioning about about appetite are often good screens * ?? �Daily
multivitamin supplementation is recommended for all elderly patients * ?? �Protein
malnutrition is common in nursing homes and associated with increased infection
risk, anemia, orthostatic hypotension, and decubitus ulcersHypertension Screening �
heart disease and CVA are the leading causes of death in the elderly. Thus, BP
screening should always be part of assessment. Thiazides are commonly used in
elderly patientsStroke Prevention � risk doubles with every 10yr increase in age
* ?? �HTN � keep within normal range with diet/exercise/medication * ?? �Atrial
fibrillation � worry of mural thrombus/embolization; anticoagulation should be
undergone Cancer Screening � often regular screening can be stopped when life
expectancy is below 5-10yrs Osteoporosis Screening � DEXA scan at 60; make sure to
supplement Ca2+/VitDImmunization � follow normal guidelines; specific elderly
considerations include: flu shot each year, Tdap at age 60, Shingles vaccine at age
60, and Pneumovax at age 65. End of Life Issues * ?? �Advance Directives � prior
oral/written statements to guide care if pt is incompetent. These statements trump
any and all other input as they are the pt�s exact wishes * ?? �Durable Power of
Attorney � appointment of a surrogate decision-maker to make the decisions that the
patient is assumed to have wanted based on their experiences with the patient * ??
�DNR � only 15% of CPR interventions are successful with significant risk for
injury (rib fracture, laceration, neurologic damage). These decision should be
about how a patient will die, rather than if they�ll live or not as the outcomes
are often poor. 2836: Presbycusis * ?? �Sensorineural hearing loss of aging,
typically seen in >60yr old patients * ?? �Presentation: high-pitched, symmetric
sensorineural hearing loss. Patients typically complain of trouble hearing in
crowds/noisy environments but do well when things are quiet. * ?? �Dx: clinical
picture * ?? �Tx: no real treatment. Hearing aid may be useful if loss is
severe/impairing Case 19 � URI and Sinus Infections 4566/4864: Acute Bronchitis
* ?? �Presentation: cough from [5 days � 3 weeks] productive for
yellow/green/blood-tinged sputum however, the cough alone may last for months o
Wheezing/rhonchi with sore chest wall easily resolved with coughing (sputum is
getting out!) o No systemic symptoms (lack of fever, chills, etc.)o Classically
after a viral URI (influenza, parainfluenza, adnovirus, rhinovirus, etc.)o Note
that production of yellow-green sputum does NOT indicate bacterial infection here *
?? �Dx: clinical picture; CXR used to rule out pneumonia (fever, consolidation, Hx
of lung dx, or elderly) * ?? �Tx: NSAIDs/bronchodilators; antibiotics are not
recommended 4201: Rhinitis * ?? �Non-allergic Rhinitis o Nasal congestion,
rhinorrhea, sneezing, post-nasal drip o Red, boggy nasal mucosao No obvious
allergic trigger with symptoms year-round o Typical onset >20y/o o Tx: intranasal
anti-histamine and/or intranasal glucocorticoid * ?? �Allergic Rhinitis o Watery
rhinnorhea, sneezing, with eye symptoms (red, watery, itchy eyes)o
Pale/bluishnasalmucosao Obvious allergic trigger or associated allergic disorder
with seasonal patterns o Typical onset <20y/o o Tx: intranasal glucocorticoid 3285:
Rhinosinusitis * ?? �Presentation: purulent nasal discharge, maxillary tooth pain,
facial pain, maxillary sinus pain/tenderness, and non-specific URI symptoms lasting
>7 days o Micro: S.pneumo and H.flu are most common organisms * ?? �Dx: clinical
presentation, sometimes with naso-pharyngeal swab evidence of infection * ?? �Tx:
antibiotics, short course (<3 days) decongestants, and NSAIDs/Acetaminophen o 1st
line � amoxicillin or TMP-SMXo 2nd line � amoxicillin-clavulonic acid, 3rd gen
cephalosporins, floroquinolones, or macrolides Pharyngitis * ?? �Presentation: non-
specific o Micro: typically, viral (mycoplasma, chlamydia pneumoniae,
Arcanobacterium haemolyticus) o Examination to rule out more serious causes
(Epiglotitis, Peritonsilar abscesss, Group A strep) * ?? �Dx: clinical presentation
with ruling out of more serious problems * ?? �Tx: supportive treatment; should
resolve with time 2195/2847: Peritonsilar Abscess (�Quinsy�) * ?? �Presentation:
fever, chills, sore throat, muffled �hot potato� voice, uvular deviation,
unilateral lymphadenopathy, pooling of saliva, and trismus (unable to open jaw)
from muscle spasmo Airway obstruction and spread to parapharyngeal space (carotid
sheath involvement) * ?? �Dx: clinical scenario with signs on oropharyngeal exam
* ?? �Tx: immediate abscess drainage via needle aspiration with culture/empiric
antibiotics o GAS and respiratory organsisms should be covered 2845: Epiglottitis
can actually be a severe, life-threatening infection as it can compromise the
airway * ?? �Presentation: high fever, severe sore throat, drooling, stridor,
�tripod position� to breathe * ?? �Bugs: H.flu or Strep.pyogenes (rare in USA due
to vaccinations, but immigrants may have this) * ?? �Dx: clinical scenario with
swab and culture * ?? �Tx: immediate airway establishment (intubation or
cricothyroidotomy) with emergent treatment to stop asphyxiation??treatment of the
underlying infection Group A Strep (S.pyogenes) * ?? �Possible GAS manifestations
(Rheumatic fever, Post-strep glomerulonephritis, Toxic shock syndrome.
Peritonsillar abscess, Meningitis, Bacteremia) * ?? �Dx: rapid antigen test
(faster) or throat culture (gold standard) * ?? �Tx: oral or IM penicillin; if
allergy cephalosporins or macrolides can work well Rheumatic Fever * ?? �Occurs a
few weeks after a GAS strep throat * ?? �Antibodies formed from infection cross-
react with host antigens (notably in the valves of the heart) due to molecular
mimicry * ?? �Dx: JONES criteria o J � joint pain from migratory polyarthritiso ? �
pancarditis initially with mitral/aortic valve damage over years o N � nodules in
the skin (often firm, but painless)o E � erythema marginatum (rash with a distinct
red border)o S � Syndenham�s chorea (neurologic problem)o An ASO titer being high
can also be helpful to confirm diagnosis * ?? �Tx: full treatment for GAS to
eliminate ANY bacteria possibly there, then prevention via antibiotic prophylaxis
for years 2241: Post-Streptococcal Glomerulonephritis o ?? �Autoimmune disease in
response to a GAS throat/skin infection occurring 10-20 days post-infection.
Classically happens in kids and young adults. o ?? �Present: Fever, rash,
arthralgia, periorbital edema, hypertension, �tea-colored urine�, Hx sore throat o
Urine: oliguria, proteinuria, hematuria, sterile pyuria, eosinophiluria, WBC casts
o Blood: eosinophilia, low serum C3 compliment levelso Biopsy: sub-epithelial humps
due to complement deposition o ?? �Dx: clinical presentation with elevated ASO
titer or anti-DNase B antibodies o ?? �Tx: supportive care, should resolve on its
own o Prognosis good in children but very bad in adults often leading to renal
failure 3742: Toxic Shock Syndrome * ?? �Bacterial infection (S.aureus most common)
with Toxic-Shock Toxin-1 (TSST-1), a super-antigen that results in massive T-cell
activation/cytokine release, resulting in loss of intravascular fluids to the
extravascular spaces and shock! * ?? �Presentation: rapid development of high
fever, Hypotension (<90 systolic), diffuse red/edematous rash (looks like sunburn),
skin desquamation of palms/soles, multisystem failure o Classically (50%)
associated with a tampon left in post-menstruation, typically arising 2-3 days
after the last menstrual period o Non-menstrual infections can also cause it (post-
surgery, sinutitis, etc) * ?? �Dx: clinical syndrome with history * ?? �Tx:
supportive therapy for shock, removal of foreign materials causing infection, anti-
staph (penicillin + vancomycin) are all part of treatment 3263: Erysipelas is
infection of the superficial dermis * ?? �Presentation: fast-onset prominent
inflammatory rash with sharply demarcated borders, often accompanied by
fever/chills/etc. * ?? �Bugs: GAS (most commonly S.pyogenes) * ?? �Dx: presentation
* ?? �Tx: penicillin (if S.pyogenes) but culture is needed for specific Tx
4354/3131/2869: Infectious Mononucleosis (Epstein-Barr virus) ?? Presentation:
fever, malaise, posterior cervical lymphadenopathy, tonsillar exudate, and possibly
splenomegaly in an otherwise healthy young adulto Initial HIV infection can look
similar but will be fever, malaise, lymphadenopathy, diarrhea, and rash??it�s
actually reasonable to test for HIV if monospot is negativeo Autoimmune hemolytic
anemia/thombocytopenia is a complication of EBV-mono from EBV- antibodies (IgM
cold-agglutinin anti-I antibodies) cross-reacting with RBCs/platelets. Occurs
approximately 2-3 weeks post infection * ?? �Dx: heterophile antibody (monospot)
test; Anti-EBV antibody test o Smear showing variant lymphocytes with convolute
nuclei and vacuolated cytoplasm * ?? �Tx: rest and avoidance of contact sports for
>3 weeks if splenomegaly present 3007: Infectious mononucleosis (Epstein-Barr virus
infection): fever, lymphadenopathy (tonsillitis, swollen cervical lymph nodes,
swollen eyelids), exhaustion, +/- hepato-splenomegaly * ?? �Dx: Positive Monospot
(25% false negative on first week), atypical lymphocytosis, transient hepatitis
* ?? �Tx: rest and avoidance of strenuous activities for >3weeks after onset (risk
of splenic rupture) o Splenic rupture: abdominal pain and anemia Otitis Externa
* ?? �Presentation: ear pain/itching worse with manipulation, sometimes with
inflamed/swollen external ear canal with drainage and discharge.o Micro: Staph,
Strep, and rarely Pseudomonas (swimmer�s ear; most common in diabetics) * ?? �Dx:
clinical presentation * ?? �Tx: irrigation, debridement, and antibiotics (IV for 4-
6wk if bones involved) 2828: Malignant (necrotizing) Otitis Externa * ??
�Presentation: intense, unrelenting ear pain that�s worse at night. Purulent
drainage/feeling of fullness that does not respond to topical medication. Ear canal
shows granulation tissue/edema. May progress to osteomyelitis of the skull base
with cranial nerve involvement (facial droop) or TMJ involvement (pain worsened by
chewing) o Associated with poorly controlled diabetes/immunosuppression in elderly
patients o Typically caused by Pseudomonas Aeruginosa * ?? �Dx: clinical
presentation with CT/MRI evidence of infection * ?? �Tx: IV ciprofloxacin (first
line) o Fluoroquinoloneresistant:otherIVanti-pseudomonals(Pip-
tazo/cefepime/ceftazidime) o
FailuretorespondtoAbx:surgicaldebridement/biopsytoexcludecancer 3260: Malignant
Otitis externa * ?? �Presentation: severe ear pain often radiating to the jaw (TMJ
involvement, exacerbated by chewing), ear discharge, granulation tissue in external
auditory meatus o Pain/infection will not improve with topical antibiotics * ??
�Bugs: 95% of these are caused by P.aeroginosa (classic if you�re also diabetic!) *
?? �Dx: clinical presentation with swab/culture * ?? �Tx: anti-pseudomonals will
likely work (pip-tazo is my go-to) 2839: Serous Otitis Media ?? Presentation:
Middle ear effusion resulting in conductive hearing loss without infectious
symptoms. Ear canal shows dull tympanic membrane with hypomobility on pneumatic
otoscopy and inflammation o The most common middle ear pathology in HIV/AIDS due to
lymphadenopathy obstructing the Eustachian tubeo Micro: typically, viral (URI
pathogens) but may become bacterial (superimposed) o Complications (rare) �
mastoiditis, meningitis, brain abscess, subdural empyema * ?? �Dx: clinical
presentation, sometimes with ear swab and culture * ?? �Tx: often resolves
spontaneously, but amoxicillin is first line Case 20 � Chest PainInitial Management
of Chest Pain??should be done within 10 minutes of presentation * ?? �There�s a
HUGE differential for chest pain, but we need to rule out things that will kill the
pt * ?? �Best to get an H&P to see if you can determine etiology o First priority:
12-lead EKG & CXR??if cardiac etiology then treat immediately! o Next priority:
Place two IVs and draw labs (CBC, CMP, BUN, PT/PTT/INR, CK/CK-MB/Troponins) * ??
�EKG considerations o Angina: ST-elevation/depression or T-wave inversiono MI:
signs of angina with elevated CK/CK-MB/Troponinso Don�t forget that not all
myocardial infarctions have pathologic signs and clinical picture should drive
interventions. If there�s high suspicion of MI, then interventions may still be
sought Myocardial Infarction * ?? �Presentation: �crushing� sub-sternal, central
chest pain sometimes radiating to the jaw, shoulder, arm or hand (often on left
side), nausea/vomiting, persisting >20-30min with decreased exertion o Angina alone
should subside with decreased exertiono Risk factors for CAD: male, age >40yr, HTN,
tobacco use, DMo Risk factors for MI: all CAD risks, cocaine use, dyslipidemia,
LVH, Hx of CAD * ?? �Dx: clinical suspicion with EKG + cardiac enzyme findings * ??
�Tx: MONA = morphine, O2 (2-4 L/min), nitroglycerine (sublingual), Aspirin (325mg
chewed) o Primary Tx: MONA therapy + B-blocker + GP IIb/IIIa blockers???Cath lab
for PCI if within 90min of MI???ACE inhibitor if within 24hr of MI???Magnesium
infusion if Mg2+ becomes low (decrease risk of Torsades) ???Ca2+ channel blockers
have shown NO benefit in clinical trials o Secondary Tx: modification of risk
factors/exercise program + Aspirin/nitrates/B-blocker/Statin 2732: Post-MI
remodeling is part of the normal healing process in the heart and will result in a
white scar. However, ventricular dilatation can be significant and actually change
the ventricle so much that it can result in eventual CHF. * ?? �Ventricle will be
dilated, globular, and thinned with scarring * ?? �Tx: ACE inhibitor treatment
within 24hrs of MI has been shown to limit this dilatation/remodeling and reduces
the incidence of remodeling-induced CHF [Differential Dx for Chest Pain]4127:
Stable angina pectoris is predictable chest discomfort occurring with exertion and
relieves with rest in <30 minutes due to insufficiency of coronary bloodflow during
increased myocardial oxygen demand. * ?? �EKG, CXR, and cardiac enzymes should be
used to rule out MI if this presents * ?? �1st line: beta blockers??avoided
in low BP/bradycardia, or if side effects aren�t tolerated well; work well as they
decreased blood pressure and contractility of the heart * ?? �2nd line: Ca++
channel blockers (-�dipines�) or long acting nitrates??used after B-blockers fail
2722/2723: Variant (Prinzmetal) Angina: a vasospatic angina that typically occurs
in young women without cardiovascular risk factors, onset in the middle of the
night, and often exacerbated by smoking. * ?? �May be precipitated by exercise,
hyperventilation, emotion, cold exposure, cocaine abuse; but will not be
consistently exacerbated with exercise like Typical Angina * ?? �EKG can show
transient ST elevation with complete return to baseline after ischemic vasospasm
* ?? �May be associated with other vasospastic disorders (such as migraines or
Raynaud�s phenomenon) * ?? �Tx: Cessation of smoking + nitrates or Ca++ channel
blockers (vasodilation) ---------------3521: Pericarditis: sharp, stabbing chest
pain that�s worse with inspiration (more preload = more stretching of pericardium)
and better with leaning forward; classically occurs with a friction rub * ??
�Characteristic EKG: diffuse ST elevation with depression in aVR * ?? �Post-MI
Acute pericarditis: occurs a few days after MI * ?? �Dressler�s syndrome: an
immunologic pericarditis against heart tissue that occurs a few weeks after a heart
attack (takes time for the titers to rise to do damage)o
Fever/malaise/elevatedESRareallsignstolookoutfor o Tx: NSAIDs or Corticosteroids
for refractory cases 3635: Constrictive Pericarditis: occurs when the pericardium
is damaged, loses elasticity, and becomes fibrous resulting in altered heart
function * ?? �Etiology: idiopathic, viral, cardiac surgery,
radiation/chemotherapy, or tuberculosis * ?? �Presentation: fatigue/dyspnea on
exertion with peripheral edema/ascites, and increased JVP with sharp X/Y waves
(forward flow compromise) o Pulsus paradoxus/abnormal septal movement: systolic BP
drops upon inspiration; heart can�t distend well and when you breathe in, more
blood flows into the right ventricle...so the septum compensates moving into the
left ventricle, diminishing outflowo Calcifications on X-ray of the pericardiumo
Kussmaul�s sign: failure of central venous BP decrease on inspiration ?? Tx:
Diuretics (temporary relief) with pericardiectomy (definitive Tx) 10764:
Constrictive pericarditis: pathologic thickening of the pericardium which results
in heart constriction and ultimately failure of diastolic function * ?? �Dx: signs
of right heart failure (fatigue/dyspnea, elevated JVP, cardiac cirrhosis/nutmeg
liver); Kussmaul�s sign (lack of JVP decrease on inspiration), pericardial
calcifications, or midsystolic pericardial knock (like the beat is knocking against
something hard) * ?? �Etiology: idiopathic, viral, cardiac surgery, prior chest
radiation, TB (endemic) * ?? �Tx: if new and not severe??anti-inflammatory drugs
followed by pericardectomy; if severe then immediate pericardectomy * ?? �Note that
normal JVP is <8cm H20) 3979: Uremic pericarditis is pericardial inflammation due
to high blood nitrogen (BUN) levels. * ?? �Typical signs of pericarditis (chest
pain, friction rub, better with leaning forward) * ?? �Elevated BUN (>60 is
classic) with elevated creatinine will clue you into renal failure * ?? �Does not
present with typical EKG findings due to a lack of inflammatory penetration with
this one * ?? �Tx: hemodialysis (gets rid of the nitrogen waste and will eventually
resolve the pericarditis) 2224: Uremic pericarditis: in the setting of renal
failure, a BUN >60 mg/dL can result in pericardial sac inflammation and ultimately
a pericarditis (friction rub, chest pain relieved by leaning forward). * ?? �May
have abnormal, but not classic EKG due to only low level of inflammation * ?? �Tx:
immediate dialysis (typically yields quick recovery from symptoms) ---------------
4720: Acute aortic dissection is a life-threatening, terrifying tearing of the
aortic lumen media layer ?? Signs/symptoms: tearing chest pain radiating to the
back, hypotension, but other signs can result from involvement of arteries coming
off the aorta getting involvedo Pericardium: pericardial effusion??cardiac
tamponade/pulsus paradoxuso Aorta:aorticregurgitationo Carotid/subclavian As:
pronounced hypotension in heat/limb their feeding (blood pressure in the left arm <
right arm)o Renal artery: stenosis/compression??renal hypoperfusion ?? Dx: clinical
signs + radiologic evidence of tear (possibly chest CT) 3956: If you see a person
with emergent aortic dissection and you need to confirm the diagnosis you: * ??
�Order a CXR??if suggestive of something else, treat that * ?? �If not, get a serum
creatinine and check for contrast allergy o If normal Cr/no allergy??get chest CT
with contrast o If Cr^/allergy??get Transesophageal echocardiography * ?? �MRI may
be used if it�s a non-emergent situation 3056: Recognizing aortic dissection can be
as easy as seeing a false lumen on a chest CT scan. * ?? �Hypertension is a
necessary feature to cause tearing and dissection o Stanford A: goes back toward
the heart??B-blocker with surgical treatment o Stanford B: goes down the descending
aorta??B-blocker and follow-up * ?? �Tx: Labetalol (or possibly another b-
blocker)??these will decrease BP and heart rate reducing stress on the aortic wall
quickly 4380: Remember! Aortic dissection can go proximal toward the heart and rip
the aorta causing blood to flood into the pericardium??cardiac tamponade! * ??
�Increased pericardial pressure??diastolic failure??decreased preload and heart
failure * ?? �Dx: hypotension, tachycardia, distended JVs, pulsus paradoxus * ??
�Tx: emergency pericariocentesis to drain fluid with surgical repair of dissection
11104: Sudden onset chest discomfort with mediastinal widening and pericardial
effusion should prompt you to think �proximal aortic dissection�. This is a
surgical emergency and needs to be rapidly assessed with trans- esophageal
ultrasonography (better picture for better Dx) 4484: Marfan�s syndrome (fibrillin-1
mutation) can have major cardiac implications due to weakened elastic tissue in the
aorta! * ?? �Aortic dissection: painful tearing sensation, radiating toward the
back. Uneven BP in the left vs right arm. Aortic root dilatation causing aortic
regurgitation (decrescendo diastolic murmur) * ?? �Mitral valve prolapse may also
occur causing backflow into the pulmonary circuit. --------------- 2297:
Pneumothorax * ?? �Puncture of the lung resulting in airway pressure normalization
with atmospheric pressure within the thoracic cavity??collapse of the punctured
lung * ?? �Presentation: sudden SOB, hyper-resonance to percussion, absent breath
sounds, decreased tactile fremitus, compression of the mediastinum causing
ventricular compression (hypotension from impaired ventricular filling) and IVC
compression (central venous hypertension from blood backup) o Note that the
mediastinum shifts toward the normal lungo This is a classic complication of
mechanical ventilation in someone with underlying lung disease. Increased PEEP can
cause hyperinflation and rupture of lung parenchyma, due to already damaged/fragile
lung tissue. * ?? �Dx: presentation & CXR showing lung collapse/tracheal and
mediastinal deviation are classic * ?? �Tx: chest tube placement to relieve
pressure with surgical repair 4520: Spontaneous Pneumothorax from COPD * ??
�Presentation: sudden onset chest/back pain, SOB, reduced breath sounds on affected
side, and hyper- resonanceo Occurs due to chronic alveolar sac destruction forming
blebs (seen as enlarged air sacs on chest CT) that can rupture into the pleural
space, compressing the lungs. * ?? �Dx: clinical presentation with Chest CT
evidence * ?? �Tx: no complete concensus. Based on clinical scenario and risk
stratification. ---------------11126: Remember how we made fun of people for
misdiagnosing heart attacks for GERD? Well that shit is real because GERD can sound
a whole lot like coronary artery disease! A patient with GERD might come
complaining of chest pain with radiation!! Note the characteristic GERD signs: * ??
�Prolonged pain >1hr, post-prandial symptoms, heartburn/dysphagia, relief with
anti-reflux drugs * ?? �Often cardiovascular workup is necessary in these patients,
but will remain unremarkable 4346: Note that chronic GERD patients may have chronic
cough (stomach HCl into lungs) or hoarseness (HCl into the larynx) as part of their
clinical picture. 4335: Asthma exacerbation due to GERD ?? Presentation: recent
worsening of asthma symptoms with normal lung exam. Often sore throat, morning
hoarseness, worsening cough when laying down (at night is common), need for inhaler
following meals, dysphagia, chest pain/heartburn, regurgitation sensation o Result
of microaspirations causing irritation and vagal hypersensitivity resulting in
proclivity to bronchospasm o Often coincides with weight gain (possibly due to a
stomach ulcer!) ?? Tx: PPI trial 2200: Endoscopy�s role in Evaluation of GERD * ??
�Basically a person with GERD isn�t too much of a worry as long as they�re doing
OK. However there are certain situations where further investigation is required
* ?? �Let�s say you have a patient with GERD, if: o
Male>50,symptoms>5yrs,cancerrisk(smoking,alcoholism,etc.),alarmsymptomspresent
(dysphagia, odynophagia, weight loss, anemia, GI bleeding, recurrent vomiting)??
endoscopy o They don�t have any of the above characteristics/symptoms??PPI trial 2
months ???If symptoms are well controlled??stay on that PPI???If symptoms are
refractory??consider switching PPI or increasing dose ?? If symptoms STILL
refractory??endoscopy ---------------3178: Perforated Peptic Ulcer Disease * ??
�Presentation: chronic epigastric pain that suddenly worsens, with rebound
tenderness/guarding
(peritonitis due to gastric contents in peritoneal cavity), air under the
diaphragm on CXR * ?? �Dx: immediate CXR, as diagnosis and prompt treatment (<12hr)
is critical to limit mortality * ?? �Tx: immediate surgical repair ---------------
2982/4434/2965/2929: Acute Pancreatitis ?? Presentation: severe abdominal pain,
nausea/vomiting, elevated serum lipase, sometimes xanthomas o Alcohol (40%),
gallstones (40%), hypertriglyceridemia (classically >1000) are commono Drugs
(azathioprine, valproic acid, thiazide diuretics), infections, or iatrogenic causes
(classically cholesterol emboli from cardiac catheterization) can also be causes ??
Dx: two of the following o Acute epigastric abdominal pain radiating to the backo
Increased amylase and lipase x3 the normal limit??typically the first step in
workupo Diffuse pancreatic enlargement with contrast enhancement (CT) or
hyperechoicity (ultrasound) and sometimes with fat-stranding; Ultrasound is
preferred in patients suspected with gallstones as underlying cause
(fat/40/fertile/female = gallstone)?? Tx: supportive care (pain control/fluids) as
most cases are self-limited (4-7 days) o If caused by something that can be treated
(drug, infection, etc) then treat that 4603: Severe Acute Pancreatitis * ??
�Pancreatitis + evidence of organ failure due to release of pancreatic enzymes into
the vasculature. This causes increased vascular permeability in/around the
pancreas, causing shock! * ?? �Presentation: pancreatitis symptoms with additional
ones o Organ dysfunction due to fluid overload (dyspnea, tachypnea, abdominal
ditention, etc.) o Cullen sign: periumbilical blue-ish coloration indicating
hemoperitoneumo Grey-Turner sign: red-brown coloration around the flanks indicating
retroperitoneal bleed * ?? �Risk factors: >75yrs, obesity, alcoholism, pulmonary
infiltration on X-ray o Labs at 48 hrs??CRP >150mg/dL, Rising BUN and Creatinine
* ?? �Tx: aggressive IV fluid resuscitation to replace lost volume 3833: Drug
induced Acute Pancreatitis ?? Anti-seizure (valproate), Diuretics (furosemide,
HCTZ), Drugs for IBD (sulfasalazine, 5-ASA), Immunosuppression agents
(azathioprine), HIV-medications (didanosine, pentamidine), Antibiotics
(metronidazole, tetracyclines), and possibly many others! 4919: Chronic
Pancreatitis?? Presentation: post-prandial epigastric pain that radiates to the
back, steatorrhea (loose, greasy, smelly stools, hard to flush), fatigue/other
constitutional symptomso Alcohol abuse (most common), cystic fibrosis, or
autoimmune/hereditary disorder are all possible causeso May result in fat-soluble
vitamin (AEDK) deficiencieso Steatorrhea occurs with 90% loss of pancreatic
function * ?? �Dx: altered pancreatic function tests and fecal fat assays (Sudan
Stain) * ?? �Tx: pancreatic enzyme replacement --------------- 2213: Diffuse
Esophageal Spasm * ?? �Presentation: spontaneous pain/ painful swallowing with hot
and cold food. Does not get provoked by typical angina exacerbants. Relieved by
nitrates/Ca++ channel blockers * ?? �Dx: esophageal manometry shows repetitive,
non-peristaltic, high-amplitude contractions * ?? �Tx: nitrates/Ca++ channel
blockers for symptomatic treatment ---------------4650: Costochondritis is an
important cause of chest pain that�s sharp, non-radiating, lasts for hours, worsens
with inspiration/movements, and importantly REPRODUCABLE WITH PALPATION. It�s not a
heart problem, it�s a joint tenderness problem.---------------4334: First thing: if
a patient has a history of panic attack and is having chest pain YOU CANNOT GO
THINKING IT�S AN ANXIETY EXACERBATION UNLESS YOU GET A NORMAL ECG TO RULE OUT ACS.
* ?? �If a patient presents with chest pain??get a focused H&P, vitals, and venous
access o If unstable??check ABCs, stabilize, and assess for underlying causeso If
stable??ECG + CXR + aspirin if the chance of aortic dissection is low ???If ECG is
weird then assess for STEMI/NSTEMI ???If ECG is not weird look at the CXR o ?? �If
CXR is diagnostic??treat whatever it is o ?? �If CXR is NOT diagnostic??look for
underlying causes * ?? �If you went through all that crap and they don�t have any
cardiopulmonary problems or GERD...then maybe (MAYBE) you can give them some benzos
for their panic attack. --------------- 4042: Any person (especially younger)
presenting with agitation, dilated pupils, atrophic nasal mucosa, HTN, and acute
myocardial ischemia should be suspected for cocaine abuse! * ?? �a/B adrenergic
stimulation = HTN/pupil dilatation/agitation/ischemia * ?? �cocaine also
potentiates thrombus formation * ?? �Tx: immediate benzodiazepines/O2 + aspirin,
nitrates, calcium channel blockers * ?? �NEVER GIVE A B-BLOCKER: it will cause
unopposed a-adrenergic activity and HTN crisis! 3188: If a patient comes in with
signs of heart attack, dilated pupils, and blood in the nose consider cocaine abuse
induced MI. ?? Tx: (same as normal MI) cardiac catheterization/thrombolysis with
aspirin/clopidogrel/nitrates/Ca++ channel blockers or a-blockers/morphine. DO NOT
USE A B-blocker as it will cause hypotensive crisis due to cocaine + B-blockade =
unopposed a-activity ---------------4693: Herpes Zoster Flair (Shingles) ?? Flair
of varicella zoster virus often associated with aging, stress, and emotions.
Typically VZV will lay dormant in nerve roots (esp the trigeminal nerve!) and
reactivate at that nerve�s distribution * ?? �Presentation: may begin with pain/no
rash, progressing to pain with vesicular rash across 1-2 dermatomes and NOT
crossing the midline, then post-herpetic neuralgia may persist for weeks later o
Rash crossing the midline should prompt investigation for HIV/immunosuppression o
Immunosuppressive therapy (TNF-a inhibitors) may result in a flair * ?? �Dx:
clinical * ?? �Tx: acyclovir, famcyclovir, or valacyclovir can all work to resolve
flair and diminish post-herpetic neuralgia 4431: Note that the pain from VZV
(shingles) re-activation may precede the rash. Thus any patent with unilateral pain
without other evidence of injury/organ dysfunction should be considered for
shingles. * ?? �Classically it arises to bodily stress (infection, chemotherapy,
immunosuppression) but can arise spontaneously in some folks * ?? �Will be followed
by dermatomal vesicular rash and sometimes finishes with post-herpetic neuralgia
3422: Don�t forget! Herpes Zoster (shingles) outbreak is treaed with oral
vanacyclovir or acyclovir. Both will work, but valacyclovir has a better side
effect profile! Case 21 � Chronic Kidney DiseaseCommon Risk Factors: Diabetes
(leading cause!), hypertension, and glomerulonephritis Stages of CKD are determined
by estimated GFR * ?? �Normal Kidney function??GFR between 90-120 mL/min * ?? �1??
GFR>90 mL/min + signs of kidney disease * ?? �2??GFR 60-89 mL/min * ?? �3??GFR 30-
59 mL/min * ?? �4??GFR 15-29 mL/min * ?? �5??GFR <15 mL/minPresentation � decreased
urination, change in appearance of urine, low volume status (poor skin turgor, dry
mucous membranes, orthostatic hypotension, dizziness, tachycardia) or fluid
retention (pulmonary & LE edema, SOB, JVD, rales), occasional emesis * ?? �Labs �
elevated creatinine, hyperkalemia, elevated uric acid, metabolic acidosis, anemia,
proteinuria or microalbuminuria, signs of uncontrolled diabetes * ?? �Imaging �
asymmetric or bilaterally shrunken kidneysDx � based on presentation. Work-up
should include CBC, CMP, LFTs, urinalysis, C3/C4 test, hepatitis panel, HIV test,
HbA1c/fasting serum glucose. ?? Imaging or renal biopsy may be necessary depending
on suspected etiology Tx � treatment aimed at underlying problem and reversing
possible etiologies * ?? �Trial of fluids ???help hypovolemia, hypotension, and
sometimes infection * ?? �Achieve blood pressure control at 130/80 with
ACE/ARB/diuretic ???help alleviate HTN disease * ?? �Phosphate restriction/oral
phosphate binders ???used in stage 3-5 to limit hyperphosphatemia * ?? �Low
potassium diet/potassium binders??used if K+ levels become elevated * ?? �EPO
administration??aids in reversing/staving off anemia due to kidney disease * ??
�Urinary tract obstruction ???seen on imaging, often surgical resolution * ??
�Reno-vascular occlusion??seen on imaging, often surgical resolution * ?? �Referral
to a nephrologist should be sought in women with Cr >1.2mg/dL and men with Cr
>1.5mg/dL 4349/3978: In chronic kidney disease, anemia can develop as the kidney is
responsible for erythropoietin (EPO) production. The mainstay of anemia with
chronic kidney disease is supplemental EPO + supplemental iron. Iron is
supplemented as EPO will surge RBC production, causing a high need for iron for new
heme. Plus, someone with chronic kidney disease may already be anemic from chronic
inflammation! * ?? �Iron supplementation alone should always be tried first before
EPO * ?? �Side Effects: BP increase (30%, >10mm diastolic; not well understood),
Headaches, Flu-like syndrome, Red cell aplasia (rare) [HIGH YIELD] Case 22 �
Vaginal Disease[Chapter 28: Vulvovaginitis � Topic 35] Normal Vaginal Secretions
* ?? �Presentation: asymptomatic, with small amount of clear/white/flocculant
discharge; pH 3.8-4.2; Whiff test (-); Microscopic slide: squamous epithelium with
numerous lactobacilli * ?? �Dx: clinical * ?? �Tx: none needed Bacterial Vaginosis
* ?? �Polybacterial overgrowth (Gardnerella Vaginalis) in vagina replacing normal
lactobacilli * ?? �Presentation: Increased thin/homogenous/white-grey/sticky
discharge that worsens after sex; pH >4.5 o Whiff test (+; fishy) o Microscopic
slide: increased WBCs, decreased lactobacilli, clue cells present * ?? �Dx: 3 out
of 4 present: Abnormal grey discharge, pH >4.5, (+) whiff test, or clue cells or
Gram stain (+) * ?? �Tx: metronidazole (oral or intravaginal) or clindamycin (oral
or intravaginal) o Treatment of sexual partners
does NOT help prevent recurrence Vaginal Candidiasis (�yeast infection�) * ??
�Overgrowth of Candida spp. typically from air-born sources; requires estrogenized
tissue * ?? �Presentation: increased thick/white/�cottage-cheese like� discharge
with itching and burning that often �cannot be reached�; normal vaginal pH; o Whiff
test (-)o Microscopicslide:hyphae/budspresent * ?? �Dx: Visualization (+) on slide
or culture (+); clinical evaluation is not reliableo Latex agglutination testing is
useful for non-C.albicans Candida as they do not show hyphae * ?? �Tx: intravaginal
nystatin or oral fluconazole (150mg)o Intravaginal botic acid capsules or gentian
violet will treat C.Glabrata as it resists azoles o Sexual partners are NOT
treated, as it is not considered an STD Trichomoniasis * ?? �Growth of a protozoan
that only lives within the human urogenital tract * ?? �Presentation: increased
yellow-green/grey/frothy/sticky discharge with dysuria, dyspareunia,
itching/burning; pH >4.5; strawberry cervix with punctate hemorrhageso Whiff test
(+/-; fishy)o Microscopic slide: normal epithelial cells, increased WBCs, motile
Trichomonads * ?? �Dx: visualization on microscopic slide * ?? �Tx: metronidazole
(oral; don�t forget disulfiram-like rxns) or tinidazole (oral) o Screening for
other STDs should be undertaken with women infected o Sexual partners also need to
be treated Atrophic Vaginitis may also present with similar complaints (itching,
burning, dyspareunia) typically occuring in older women; usually does NOT involve
vaginal discharge; pH often >4.2; improved with vaginal lubricant * ?? �Urinary
tract may have similar changes causing increased urinary frequency/increased UTIs *
?? �Tx: vaginal lubricant and topic/oral estrogen replacement therapyDesquamative
inflammatory Vulvo-vaginitis typically occurs in post-menopausal women with
purulent discharge, exfoliation of epithelium, vulvar burning/erythema, few
lactobacilli. * ?? �Often caused by overgrowth of Gram (+) bugs affecting both
vaginal and vulva * ?? �Tx: clincamycin cream (2%) for 14 days[Chapter 29: Sexually
Transmitted Diseases � Topic 36] Screening * ?? �When one STD is present, other
should be tested for. Because the patient is engaging in risky enough sexual
activity to contract one, they can likely contract more than one. * ?? �Regular
Screening based on age should be part of a normal visito Sexually active <25yr:
regular screening for chlamydia and gonorrheao Developmentally Disabled women: one
panel of common STDs at least onceo All sexually active women: HIV test at least
onceo Women with cervicitis: screen for PIDo Women with PID (salpingitis): screen
for chlamydia, gonorrhea, BV, and trichomonas Prevention * ?? �Education, limiting
of sexual partners, and condom use are all cornerstones of prevention * ??
�Immunization of HPV and HepB are important to prevent transmission * ?? �Use of
expedited therapy and health department reporting with chlamydia, gonorrhea, and
syphilis o Expedited therapy is the treatment of a patient�s sexual partner when
the patient is diagnosed with certain STDs (trichomonas, chlam, gono, syph, etc.)
without testing o The laws of expedited therapy and reporting differ by state so
read up son! Chlamydia trachmomatis * ?? �Presentation: abnormal vaginal bleeding,
cervicitis/salpingitis, mucopurulent discharge, etc * ?? �Dx: NAAT for Chlamydia of
endocervical swab * ?? �Tx: azithromycin (1g) or doxycycline (100mg BID Q7) with
acute repeat testing 3-4wk after initial treatment is completed and at 3mo post-
treatment Neisseria gonorrhea * ?? �Presentation: mucopurulent green/yellow
discharge from penis/vagina; may be mild and overlooked o Increased rates of PID
compared to other STDs, as well as increased risk for HIV w/ infection o Micro:
gram(-) diplococcuso Risk Factors: highest rate of infection in teens/young adults
* ?? �Dx: swab with culture/gram stain/NAAT * ?? �Tx: ceftriaxone IM (250mg) + oral
azithromycin (1g) or doxycycline (100mg BID Q7) o Testing for chlamydia, HIV, and
syphilis are indicated Pelvic Inflammatory Disease (Salpingitis) ?? Presentation:
cervical motion/adnexal/uterine tenderness, abdominal pain fever, mucopurulent
discharge, vaginal bleeding, sometime in the setting of previous STD diagnosiso
Micro: Chlamydia or Gonorrhea infection most commono Labs: leukocytosis, elevated
CRPo Risk Factors: pt with prior PID, adolescence, multiple sexual partnerso Fitz-
Hugh-Curtis syndrome (perihepatitis): ascending infection up the right paracolic
gutter resulting in local fibrosis/scarring between the liver and anterior
abdominal wall. o Tubo-ovarian abscess (TOA) � localized form of infection
resulting from STD infection often with high fever, tachycardia, severe pelvic
pain, and N/V; rupture may result in septic shock * ?? �Dx: clinical based on
symptoms * ?? �Tx: treat for gonorrhea/chlamydia with possible hospitalization if
complicated (acute emergency, pregnancy, severe illness, TOA development Genital
Herpes (Herpes Simplex Virus-1 or 2) ?? Presentation: flu-like illness/neurologic
symptoms on initial infection followed by eruption of painful �dew drop on rose
petal� vesicular lesion. Often lesions will lyse leaving a yellowish crust. Dysuria
and rarely aseptic meningitis may occur! o Secondary infection are less severe and
are triggered by activation of virus from the Dorsal Root Ganglion at site of
infection; often preceded by tinging/burning with subsequent eruption o HSV-1 (cold
sores) and HSV-2 (genital lesions) are typically �above� and �below� the belt
respectively, but may go ether way * ?? �Dx: viral culture with PCR for viral DNA *
?? �Tx: although it cannot be eradicated from the DRG, oral acyclovir, famciclovir,
or valacyclovir for 7-10 days are all viable options o Typically used as episodic
therapy to help shorten flair courseo Can be used as suppressive therapy in pts
with frequent recurrences /decrease transmission to sexual partners and to fetus if
pregnanto If pt has an active flair during labor c-section is indicated to limit
vertical transmission Human Papilloma Virus * ?? �Presentation: condyloma
accuminata (low risk; wartly like, mounded up lesions; think that they �accumulate�
just like we can accumulate many types of HPV!) or cervical dysplasia (high risk)o
Micro: Low risk (6,11) and High Risk (16, 18, 31, 33, 45) are the ones we really
care about * ?? �Dx: physical exam or biopsy showing cellular changes * ?? �Tx:
condyloma acuminatata are treated with cautery/removal; cervical dysplasia is
treated based on cervical cancer algoithmso Gardasil (HPV 6, 11, 16, 18) vaccine is
important to give to boys/girls ages 9-26 to help decrease the chance of the most
common types of HPV infection Syphilis (Treponema Pallidum) * ?? �Honestly I think
this topic has been bludgeoned to death by our studies, thus a review of symptoms
should be sufficient. * ?? �Primary � painless, firm, �punched out�, excoriated
chancre appearing 10-60 days after infection. Local adenopathy should be present.
Resolution occurs spontaneously within 3-6wk * ?? �Secondary � 4-8wks post-
infection; rough/red-brown rash starting on palms/soles, lymphadenopathy, fever,
headache, weight loss, fatigue, muscle aches, and patchy hair loss. Condyloma lata
(flattened, more �raw� looking warts). * ?? �Latent � occurs after secondary stage;
no symptoms but (+)testing; symptoms may recur or pt may progress to tertiary
stages * ?? �Tertiary � CNS damage (tabes dorsalis), heart damage (vasa vasorum
infection/aortic aneurysm), ophthalmic (Marcus-Gunn pupil), and painful gumma
formation can all occur HIV/AIDS � I�m comfy with this disease; there�s not much
written in the text anyway Other STDs * ?? �Lymphogranuloma venereum (LGV;
C.trachomatis L1,L2,L3) � inguinal/femoral lymphadenopathy (vaginal) or
bleeding/purulent anal discharge, constipation, anal spasm (anal) * ?? �Granuloma
inguinale (Donovanosis; Calymmatobacterium granulomatis) � ulcerative lesions which
easily bleed; typically acquired in New Guinea, Austrailia, India, or West Africa *
?? �Chancroid (Haemophilus ducreyi) � painful �raggy� ulcers with grey/yellowish
base and sharp borders * ?? �Molluscum contagiosum � highly contagious through any
skin contact; pox virus causing small, painless, itchy papules with �umbilicated�
tops; often scratched off appearing as ulcers with crust * ?? �Pubic Lice/Scabies �
they can get on pubes; �nuff said. [Chapter 28: Vulvovaginitis � Topic 35
(QUESTIONS)] * ?? �Tx for BV is either Metronidazole 500 mg orally BID for seven
days, or vaginal Metronidazole 0.75% gel QHS for five days. * ?? �Phimosis is
resorption of the clitoris * ?? �Trich. treatment is metronidazole 2 grams orally
in a single dose or metronidazole 500mg orally twice daily for seven days with
empiric treatment of sexual partner * ?? �Treatment for uncomplicated vulvo-vaginal
Candidiasis consists of short-course topical Azole formulations (1-3 days), which
results in relief of symptoms and negative cultures in 80%-90% of patients who
complete therapy. * ?? �Vestibulodynia (formally vulvar vestibulitis) syndrome
consists of a constellation of symptoms and findings limited to the vulvar
vestibuleo Presentation: abrupt onset severe, �sharp/burning/raw� pain on
vestibular touch or attempted vaginal entry, tenderness to pressure, erythema???
Symptoms can occur with tampon insertion, tight clothing, or sex ???Typically, a
primary inciting event cannot be identified o Dx: clinical presentation o Tx: ???
Medical: Tricyclic antidepressants to block sympathetic afferent pain loops, pelvic
floor rehabilitation, biofeedback, and topical anesthetics. ???Surgical:
vestibulectomy is reserved for patients who do not respond to standard therapies
and are unable to tolerate intercourse. *
?? �Treatment of Gonorrhea/Chlamydia mucopurulent cervicitis is ceftriaxone +
azithromycin * ?? �If you get an elderly (>55 y/o) woman with a vulvar lesion
causing her pain, the next step is to perform a biopsy to evaluate for vulvar
cancer. * ?? �Detrusor instability o Presentation: urinary frequency/incontinence
with negative UTI/STD workup and normal post- void residual volume ???Inability for
the detrusor muscle to relax to allow for bladder filling???Parasympathetic system
stimulation via muscarinic ACh receptors allows for normal bladder emptying o Dx:
clinical presentation o Tx: anti-cholinergic drug administration (e.g. oxybutynin);
note that TCAs are anticholinergics but are really dirty drugs and not really the
best first line Tx [Ch. 29 STDs/Ch. 30 Pelvic Support Defects, Incontinence, UTIs �
Topic 36, 37 (QUESTIONS)] * ?? �Don�t forget! Herpes (HSV) can begin with a
prodrome of viral/flu-like illness followed by onset of vaginal itching/burning
before the onset of vesicular rash. While HIV can also have a flu-like illness
associated with initial infection, there�s rarely vulvar-vaginal itching and
burning. * ?? �Hep B transmission is through sexual contact in 38% of infections;
if exposed, PEP should be administered as soon as possible but no later than 7 days
if blood exposure and 14 days if sexual o Source HepB (+) � give immediate HBIG +
HepB vaccine serieso Source HepB(-) or unknown � only give HepB vaccine serieso If
inoculated is HepB immune � no further treatment needed * ?? �In treating STDs/PID
adolescents have no better outcomes from inpatient vs outpatient therapy, but
hospitalization ensures compliance and aggressive treatment may prevent UG tract
scarring. The recommended regimen for inpatient IV treatment for
gonorrhea/chlamydia is either [cefotetan or cefoxitin + doxycycline or clindamycin
+ gentamicin.] * ?? �The rate of tubal infertility has been reported as 12% after
one episode of PID, 25% after 2 episodes and 50% after three episodes. Recurrent
STDs or PID can result in significant long-term sequelae, such as chronic pelvic
pain, hydrosalpinx, tubal scarring and ectopic pregnancy. * ?? �When assessing
urinary incontinence, a normal post-void residual (PVR) is 50-60 cc. An elevated
PVR, usually >300 cc, is found in overflow incontinence. * ?? �Apparently, women
with a family history of POP have up to a 2.5 fold increase in prolapse and it�s a
huge risk factor for development. o Although hysterectomy is associated with an
increased risk of apical prolapse, studies show mixed results on in the development
of prolapse. The risk of future prolapse may be highest when hysterectomy is
performed in women with existing prolapse, while the risk in women with normal
pelvic support is less clear. ?? In comparing surgical procedures for stress
incontinence due to urethral hypermobility or intrinsic sphincter deficiency (ISD):
o Retropubic urethropexy such as tension-free vaginal tape and other sling
procedures have the best five-year success rates for patients with stress
incontinence due to hypermobility. o Urethral bulking procedures are best for ISD
with little to no mobility of the urethra. These are minimally invasive and have
80% success rate. o Needle suspensions and anterior repairs have lower five-year
success rates for GSI. o Colpocleisis is one option to treat uterine prolapse, and
is not indicated for urinary incontinence. * ?? �A �drain-pipe urethra� is simply
another name for intrinsic sphincter deficiency (ISD). The resemblance is that a
drain pipe is very wide at the top, then narrows, just as the widened proximal
portion of the urethra looks with ISD. * ?? �Oxybutynin apparently is the classic
anti-cholinergic drug to give for urge urinary incontinence * ?? �Often when a
pelvic organ prolapse occurs, the prolapsing organ is affixed to abdominal fascia:
o Central and lateral cystoceles are repaired by fixing defects in the pubocervical
fascia or reattaching it to the sidewall, if separated from the linea alba. o
Defects in the rectovaginal fascia are repaired in rectoceles.o Enteroceles are
repaired by either vaginal or abdominal enterocele repairs.o Vaginal vault prolapse
is treated either by supporting the vaginal cuff to the uterosacral or sacrospinous
ligaments, or by sacrocolpopexy * ?? �Don�t forget! If the patient has pelvic organ
prolapse but isn�t symptomatic...intervention is NOT necessary at this point. * ??
�In a patient with high surgical mortality risk (this lady was 90y/o with heart
disease and diabetes) colpocleisis is a good option; it�s a procedure where the
vagina is surgically obliterated and can be performed quickly without the need for
general anesthesia. o Sacrospinous fixation (cuff to sacrospinous-coccygeus
complex) or sacrocolpopexy (cuff to sacral promontory using interposed mesh)
require regional or general anesthesia and is not the best option for this patient
with high surgical morbidity. Case 23 � Lower GI BleedingBasically if a patient
comes in with complaint of changes in stools, get a guiac-stool test; if positive
or negative, whatever, it�s likely you�ll have to snag a colonoscopy or some
sigmoid/anoscopy to assess for bleeding depending on the clinical presentation.
3857: Workup of �Bright Red Blood per Rectum�?? Age <40??anoscopy (basically a
scope of the anus) o Typically yields hemorrhoids, which will often resolve with
symptomatic treatment or minor surgery to remove them o If no source found, do a
sigmoid or colonoscopy * ?? �Age 40-49 without red flag signs ???
sigmoidoscopy/colonoscopy * ?? �Age >50 or red flags???colonoscopy * ?? �Red flags
include: recent bowel habit changes, abdominal pain, weight loss, anemia, or family
history of colon cancer 4303: Elevated BUN:Creatinine ratio may be a sign of upper
GI bleeding (abdominal pain, hematemesis, melena) as the RBC proteins will be
broken down increasing intestinal urea production/absorption. If the kidneys are
hypoperfused due to bleeding, they may reabsorb more urea to increase blood volume.
The increased absorption in both the intestines/kidney raises the BUN increasing
the BUN:Creatinine ratio! Hemorrhoids ?? Presentation: hematochezia with defecation
sometimes with pain/irritation/palpable lump in anus from engorged peri-anal veinso
Risk factors: chronic constipation, liver/heart disease, pregnancy, & prolonged
sitting o Internal: above the dentate line and NOT painfulo External: below dentate
line and very painful; often palpable * ?? �Dx: presentation * ?? �Tx: high-fiber
diet, stool softener, cessation of straining; surgical removal may be necessary
2341: Diverticulosis ?? Presentation: painless, gross rectal bleeding (much more
than just spots on the toilet paper) o Large volume may be associated with
lightheadedness/hemodynamic instabilityo While diverticula are classically in the
sigmoid colon, diverticular bleeding is more common in the right colon, causing
dark hematochezia * ?? �Dx: Colonoscopy showing source of bleed * ?? �Tx: Often
resolves spontaneously, but may require endoscopic surgical intervention 4086:
Diverticulosis * ?? �Outpouchings of the colon due to weakened areas encountering
pressure, thus bulging out. They�re typically asymptomatic and increase incidence
with age, but can cause complications.o Associated with constipation and oddly
enough, may worsen existing constipation! * ?? �Complications: diverticular
hemorrhage, diverticulitis, perforation, abscess formationo Adequate
fruit/vegetable fiber in the diet and physical activity lower risk of complications
o Meat, aspirin/NSAIDs, obesity, and smoking increase risk of complications ??
While these often pose no problem, it�s important to take steps to limit the risk
of complication in those with diverticulitis with lifestyle changes 2204: Acute
Diverticulitis * ?? �Presentation: LLQ abdominal pain, fever, nausea, vomiting,
ileus/urinary urgency and frequency (due to peritoneal irritation in sigmoid colon
affecting the bladder)o Labs: leukocytosis,o May result in obstruction, fistula,
perforation, or abscess formation * ?? �Dx: Abdominal CT w/oral & IV contrast
(pericolic fat inflammation, diverticula, bowel wall thickening, soft tissue
masses, abscesses) o Sigmoid/colonoscopy are contraindicated due to concern of
perforation * ?? �Tx: bowel rest and Abx 3467: Colovesical Fistula * ?? �Fistula
connecting the colon to the bladder o Caused by: Diverticular disease (most common,
outpouching fuse to bladder), Crohn�s Disease (full thickness lesions cause
inflammation/connection to bladder), Malignancy (disordered growth bridges to the
bladder) * ?? �Presentation: Recurrent mixed flora UTIs, fecaluria (poop out the
pee hole), pneumaturia (air in the urine, often toward the end of the stream) * ??
�Dx: abdominal CT with rectal and vesicular contrast + colonoscopy (rule out
malignancy) * ?? �Tx: surgical treatment with treatment of underlying cause
--------------- Ulcerative colitis??if relapsing/poor response to treatment; look
for CMV (owl eye) * ?? �Mucosal/sub-mucosal inflammation * ?? �Always begins in
rectum and moves its way up; never goes past the cecum, but involves a variable
amount of the colon; continuous (absence of �skip lesions�) * ?? �Presentation: LLQ
pain (rectum) with bloody diarrhea * ?? �Histology o Neutrophils with crypt
abscesses and crypt ruptureo Architectural disarray indicates longstanding
inflammation; restricted to the superficial mucosa o NO GRANULOMAS (Th2-mediated) *
?? �Endoscopy: �loss� of vasculature due to inflammation * ?? �Gross: friable
mucosal �pseudopolyps�, loss of haustra causing �lead pipe appearance� on imaging *
?? �Complications o Toxic megacolon � stricture and buildup of feces; may result in
ruptureo Carcinoma � chronic inflammation predisposes to cancer; risk increases
with increasing involvement and duration of disease (>10 years) � colonoscopy
screening every 2-3 years is standard * ?? �Extra-intestinal Manifestationso
Primary sclerosing cholangitiso p-ANCA positivity � think the neutrophil invasion!
* ?? �Smoking protects against ulcerative colitis Crohn�s Disease??24 yo woman,
weight loss 12lbs, appears pale, non-bloody diarrhea up to 6 stools a day,
tenderness in RLQ going on for months (NOT IBS, it�s likely Crohn�s because damage
to the terminal ileum is causing obstruction/destruction, resulting in the pain in
a specific region). May have palpable mass in RLQ. * ?? �Full thickness
inflammation with �knife-like� lesions * ?? �Can occur anywhere from esophagus to
rectum; not continuous (�skip lesions�) o Most common place: terminal ileum o Least
common place: rectum * ?? �Presentation: RLQ pain (terminal ileum) with non-bloody
diarrhea * ?? �Histology: lymphoid aggregates/non-caseating granulomas (Th-1
mediated) * ?? �Gross o Cobblestone mucosa � healing of the knife-lesionso Creeping
fat � contraction of mesenteric fat by granulation tissue contractiono Strictures
(�string-sign� or �air in the ileum� on imaging) � fibrosis/granulation tissue
narrowing the lumen gauge * ?? �Complications: o Malabsorbtion with nutritional
deficiency � destruction of mucosao Calcium oxalate nephrolithiasis � greater
oxalic acid permeability; accumulation in kidney o Fistula formation � perforation
and insertion into a nearby bowel segmento Carcinoma (if colonic disease present) *
?? �Extra-intestinal manifestations o Ankylosing spondylitis � spine/sacroiliac
joints; low back pain (�bamboo spine�, stiffness in back) often in young men; HLA-
B27 associationo Sacroitilitis � inflammation of sacroiliac jointso Migratory
polyarthritis � joint pain, moving between joints, usually larger joints/unilateral
o Erythema nodosum � inflammation of fat cells, often seen as red lumps on the legs
o Uveitis � inflammation of uvea (pigmented area on the eye) ?? Smoking increases
risk for Crohn�s disease 2581: Note that IBD (Crohn�s or UC) have a bimodal
distribution (20s-30s and 60s) and both commonly present with neutrophilic crypt
abscesses, making the two diseases hard to distinguish at times. The classic
discerning factor is depth of inflammation; Crohn�s = transmural and UC = mucosal
only 4903/2207: Crohn�s Disease can present with apthous ulcers (small, grey
erosions in the oral mucosa) down to anal fissures that may show granulomas if
biopsied (30%). These two questions really highlighted the fact that Crohn�s
disease can affect ANY part of the GI tract, from [mouth??anus] ?? Another
fantastic sign that an oral ulcer is due to Crohn�s disease would be signs of
chronic inflammation (^CRP, anemia of chronic disease, or reactive thrombocytosis
>400,000) 3790: Zinc Deficiency * ?? �Zinc typically found in meat, whole grains,
beans, and nuts (Absorbed primarily in the jejunum) * ?? �Risk factors: IBD
(Crohn�s or UC) or TPN * ?? �Presentation: alopecia, abnormal taste sensation,
bullous/pustulous lesions surrounding mouth/eyes/ extremities, and poor wound
healing o Growth retardation in children 2920: Primary Sclerosing Cholangitis ??
Unknown etiology; inflammation/fibrosis/stricture of the intra/extrahepatic bile
ducts o Associated with IBD (Crohn�s or UC) in 90% of cases ?? Presentation:
typically, asymptomatic with unexplained LFTs/lab values. Sometimes fatigue and
pruritis can occur, but not classically o Labs: Cholestatic pattern LFTs (AST and
ALT elevated but <300; severely elevated Alk.phos and bilirubin),
hypergammaglobulinemia, elevated IgM, pANCA(+) ?? Dx:o Ultrasound??unremarkable and
non-diagnostico Cholangiogram??multifolcal narrowing/�beading� of
intra/extrahepatic bile ductso Liver biopsy??duct obliteration with �onion-
skinning� of lymphatic vessels. Confirmatory for diagnosis most times?? Tx: liver
transplant within 12 years of diagnosis ---------------4389: Suspicion of
Colorectal cancer: signs/symptoms ?? An older man (>60) with abdominal pain,
microcytic anemia, (+)fecal occult blood, and hepatomegaly with a hard liver edge??
prompt you to think infiltrative colon cancer o Any old person with microcytic
anemia (esp. men) or blood in stool??colon cancero Hepatomegaly with a hard liver
edge??liver cancer (most often from metastatic colon cancer) o Mildly elevated
AST/ALT/Alk.phos in this setting??infiltrative/cholestatic disease (which
metastatic liver cancer would be a part of!)?? Dx: because this pt has signs of
colon cancer and liver abnormalities without significant elevations in LFTs, an
abdominal CT should be sought as metastatic malignancy is suspected. 2582/4504:
Colorectal Cancer (CRC) Screening in High Risk Patients: * ?? �Family Hx of polyps
or CRC: colonoscopy every 2-3 years starting 10 years before first familial
diagnosis or age 40 (if the 10 years prior puts you lower than age 40) * ??
�Inflammatory Bowel Disease (Crohn�s or UC): every 1-2 years starting 8 years post-
diagnosis o Can start 12-15yr post-diagnosis if disease restricted to left colon
* ?? �FAP: colonoscopy every year starting at age 10 * ?? �Lynch syndrome (HNPCC):
colonoscopy every 1-2 years starting age 20 3918: Assessment of a colon polyp [HIGH
YIELD] ?? Three major types of colon polyps: o Hyperplastic: most common non-
neoplastic polyp; no need for further workupo Hamartomatous: juvenile/Peutz-Jegher
polyps...typically benigno Adenomatous: most common overall with potential
malignancy??further workup, but less than 1% of these will actually be malignant!??
Adenomatous polyps MUST be further assessed as this will determine its risk for
malignancy: o Morphology: sessile [more malignant] or pedunculated [more benign]o
Histology: [more benign] tubular < tubulovillous < villous [more malignant]o Size:
[low risk of invasion] (<1.5cm) < (1.5-2.5cm) < (>2.5cm) [high risk of invasion]
2210: Dr. Jones�s words echoed in Mike�s head, �An old person with iron deficiency
anemia, especially a man, has a GI bleed until proven otherwise.� * ?? �The first
step is a fecal occult blood test??if positive, then it�ll guide further
investigation, but if negative it means NOTHING! * ?? �If you have this clinical
scenario and you get a negative FOBT, you then get endoscopy/colonoscopy on the
patient for concern of GI malignancy Note that radioisotope erythrocyte
scintigraphy is only useful in active, significant bleeding. If it�s a slow or non-
active bleed, that test won�t tell you shit. Case 24 � Pneumonia Pneumoniao
Presentation: productive cough, fever, pleuritic chest pain, dyspnea, tachypnea
(children), altered mental status/confusion (elderly), and some specific signs can
give specific types (discussed below) o Ronchi, rales, egophany (E??A), percussive
consolidation may all occur o Broad Sub-types:o Community Acquired (CAP) � the
classics like S.pneumo (rust-color sputum) or H.flu (COPD) o Atypical Pneumonia �
more common in teens and young adultso Hospital Acquired (HCAP) � occurs in
hospitals, nursing homes or other healthcare facilities; CAP organisms are still
king here, but S.aureus and drug resistant bugs are possible o Ventilator Acquired
(VAP) � occurs on ventilator patients; this is a bad time o Dx:o Clinical
presentation o CXR: shows lobar consolidation (classic) or diffuse interstitial
markings (atypical) o Labs: CBC, BMP, and sputum culture o Tx: o Often directed at
severity of presentation and suspected source (shown below) 4024: Community-
Acquired Pneumonia (CAP) can be treated in any setting, however the first step to
deciding treatment options is to assess patient risk to select appropriate
treatment setting. This can be achieved via the CURB-65 algorithm. * ?? �C �
Confusion: if confused the patient gets 1 point * ?? �U � Uremia: if BUN >20, the
patient gets 1 point * ?? �R � Respirations >30, the patient gets 1 point * ?? �B �
Blood pressure <90/60 the patient gets 1 point * ?? �65 � patient >65 yrs old
patient gets 1 point Based on this algorithm, we can approach CAP in the
appropriate setting: * ?? �0-1 points � outpatient treatment (macrolide +
doxycycline OR macrolide + floroquinolone) * ?? �2-3 points � inpatient treatment
(floroquinolone OR Beta-lactam + macrolide) * ?? �4-5 points � ICU treatment (Beta-
lactam + floroquinolone or IV macrolide) 4097: The gold standard for diagnosis (and
first step) for classic pneumonia is a chest X-ray. Will show an infiltrate in
one/more of the lobes and helps rule out other causes of presentation like lung
malignancy. 8818: Normally, lower lobe consolidation (typically from pneumonia)
WON�T cause enough obscuration to result in blunting on the costo-vertebral angle.
Pleural effusions (this lady happened to have an effusion likely from recurrence of
invasive breast cancer) WILL do this. 4166/3892: S.pneumoniae is THE most common
cause of CAP/HCAP/HAP (not VAP but hey whatever) ?? S.pneumoniae (pneumococcus)
vaccine o PCV-13�givetoall>65,followedbyPPSV-236-12monthslaterorinhighriskgroups o
PPSV-23 alone � give to pts <65 with chronic medical conditions, then give normal
vaccines once they hit 65 o For smokers/COPD pts: a PPSV23 (S.pneumoniae) vaccine
should be given once <65yrs. All other vaccination guild lines are the same. o For
HIV/AIDS pts: S.pneumoniae: PCV13 (upon dx)??PPSV23 (8wks, every 5 yrs) 2386: The
two S.pneumoniae vaccines differ in the way that they induce immune response,
giving them characteristics that drive their immunization protocols. Pneumococcus
comes in a HUGE amount of strains, and infection with one only gives immunity to
that strain. Thus high-risk individuals are vaccinated! ?? Pneumococcal
Polysaccharide vaccine�23 (PPSV23) � contains 23 strains of historically
responsible strains for pneumonia. Only contains bacterial polysaccharides
which cannot be presented to T-cells by B-cells, thus the response is less robust
in young/old and has lesser effect, but better coverage o Given to all adults <age
65 (as the old age would make this rather useless from weak immunogenic response) o
Given to all immunocompromised pts >65 8 weeks after PSV13 and repeated every 5
years (it won�t give a great response, BUT these people are so at risk that it may
provide benefit) ?? Pneumococcal Conjugated vaccine�13 (PSV13) � contains 13
historically responsible strains that are able to be conjugated to Diptheria toxin
protein. This allows B-cell presentation to T-cells giving most robust responses
AND memory of infection, but is limited on coverage. o Given to all infants and
young children (get some coverage that works early on) o Given if immunocompromised
pt hasn�t received it before. 2267: Remember! S.pneumoniae is THE most common cause
of pneumonia in HIV/AIDS patients. You might be temped to think PCP when an AIDS
patient has pneumonia, but you better slow your roll: * ?? �S.pneumoniae �
unilateral, lobar infiltrate, productive cough, pleural effusions often occur, >200
CD4 o Remember! This guy is encapsulated, thus even people with normal immunity
have a harder time clearing this infection! * ?? �P.jiroveci � bilateral, diffuse
infiltrate, dry cough, pleural effusions rarely occur, <200 CD4 2273/2267: PCP
pneumonia (P.jiroveci formerly carinii) * ?? �One of the most common infections for
an AIDS patient * ?? �Presentation: dry cough, dyspnea, hypoxia, CXR with bilateral
diffuse infiltrate, rarely pleural effusion * ?? �Dx: clinical suspicion +
bronchoalveolar lavage showing P.jiroveci (little crushed ping-pong balls!) * ??
�Tx: TMP-SMX + corticosteroids (if poor O2 saturation status; PaO2 <70 or A-a
>35)??may show initial worsening of lung function due to death of bacteria and
inflammatory reactions in lung 3938: PCP pneumonia is one of the most common
infections in AIDS patients * ?? �Sym: dry cough, fever, exertional dyspnea (out of
proportion to CXR findings) * ?? �Signs: CXR (bilateral interstitial infiltrates),
elevated lactate dehydrogenase * ?? �Dx: bronchioalveolar lavage demonstrating
P.jiroveci * ?? �Tx: TMP-SMX (Bactrim) for 21 days + corticosteroids (PaO2 <70) o
IV pentamidine is an alternative for those that cannot take TMP-SMX but it has a
lot of side effects (damage to kidney, liver, heart, etc.) 4115: If you see
atypical pneumonia (diffuse interstitial infiltrate, tachypnea, tachycardia, fever,
non- productive cough) in an immunocompromised (immunosuppressive drugs,
chemotherapy, or AIDS) then think PCP pneumonia. If it�s typical pneumonia??S.
pneumo. Don�t overthink it hauss. 4071: Ventillatory Associated Pneumonia (VAP) is
typically arise 48hr after being intubated/on a ventilator. * ?? �Presentation:
fever, purulent secretions, poor ventilation, leukocytosis * ?? �Typical
infections: o Gram+ cocci (MRSA, streptococcus) o Gram- rods (Pseudomonas, E.coli,
Klebsiella) * ?? �Approach: CXR??If abnormal get sputum samples for culture &
empiric abx 4418: Influenza pneumonia * ?? �NOT a post-viral pneumonia, but a
pneumonia caused by the influenza virus * ?? �Presentation: flu symptoms (abrupt
fever, chills, malaise, myalgias, cough, and coryza), sometimes fever, pulmonary
symptoms (wheezes, crackles, coarse breath sounds) often in winter months o
Leukopenia and proteinuria may be a featureo CXR showing interstitial or alveolar
pattern * ?? �Dx: nasal swab showing influenza antigens * ?? �Tx: Neuramidase
inhibitors (oseltamivir/zanamivir) within 48 hours (stops release of progeny
virus). Rimantidine and Amantidine can be effective vs Influenza A 4867/4517:
S.aureus typically does NOT cause pneumonia, however it often affects certain
subgroups: hospitalized patients, nursing home residents, IV drug users, cystic
fibrosis pts and pts with recent influenza infection. Typically these pts will have
the flu (fever, myalgia, N/V, etc.), get treated and recover, only to find they get
pneumonia (this is prominent in older adults). Some other classic pneumonias: * ??
�Pneumocystis jiroveci (PCP) � HIV pts * ?? �Klebsiella pneumoniae � diabetics,
alcoholics (aspiration), and nosocomial; classically has the �currant jelly
sputum�, cavitation, and empyema. * ?? �Pseudomonas aeruginosa � cystic
fibrosis/bronchiectasis (poor sputum release) * ?? �Mycoplasma pneumoniae �
�atypical pneumonia� (productive cough, headache, rash; often better in morning and
worse in evening) * ?? �Anaerobic infection pneumonia � aspiration (often pts have
poor dentition from vomiting) and typically features lung abscess! 3054/4233:
Legionnaire�s Disease (L.pneumophilia; lives in water inside protozoa) * ??
�Presentation: pneumonia, watery diarrhea, high fever with bradycardia,
headache/confusion o Labs: hyponatremia is often pronounced, hematuria/proteinuria,
hepatitis can occurs o Classically with exposure to contaminated water (hospital,
hotel, nursing home, cruise ship) * ?? �Dx: Gram stain often negative with many
neutrophils because bug is poorly staining??urine antigen testing for serologic
diagnosis * ?? �Tx: macrolides (like azithromycin) or floroquinolones (�-floxacin�)
2292: Aspiration pneumonia (anaerobic organisms) * ?? �Should be suspected in pts
with poor dentition (more bacteria in mouth), upper airway instrumentation, upper
GI/nasogastric tube, GERD, dysphagia, alcoholism, or impaired consciousness * ??
�Presentation: fever, chills, cough, leukocytosis, signs of lung infection
(consolidation/crackles/etc.), and foul-smelling sputum (because anaerobes) * ??
�Dx: clinical/radiographic signs with sputum cultures * ?? �Tx: clindamycin (great
anaerobe coverage) is first line o Metronidazole+amoxacillin, amoxacillin-
clavuronic acid, or a carbapenem (�-penem�) are all viable alternative options
4118/4119: Things predisposing to Aspiration Pneumonia * ?? �Drug
intoxication/Alcoholism/Dementia � both cause impaired cough reflex/glottis closure
in swallowing due to altered consciousness * ?? �Neurologic deficits causing
dysphagia * ?? �Upper GI tract disorders � GERD is classic for getting stomach
contents into the lungs * ?? �Nasogastric/endotracheal tubes/large volume tube
feedings in recumbent position � typically if person has these they�re not
swallowing well/have some form of mechanical compromise in their upper airway. Can
allow for secretions to easily get into lungs * ?? �Protracted vomiting � if you
throw up a lot, then there�s a higher chance it�ll get in your lung 3029: Recurrent
Pneumonia is typically indicative of some underlying process, with the first main
delineating factor being what lobe it�s occurring in: * ?? �Same lung region: Local
anatomic obstruction (neoplasm, foreign body, stenosis, etc.) or recurrent
aspiration (alcoholism, seizure disorder, GERD or other GI regurgitation) o First
step = chest CT to examine the lung for abnormalities o Second step = bronchoscopy
for further evaluation of negative CT or for biopsy of positive CT * ?? �Different
lung regions: sino-pulmonary disease (Cystic fibrosis, immotile cilia), non-
infectious, or immunodeficiency 4753/4467: Pneumonia featuring Parapneumonic
Effusion * ?? �Basically a transudate or exudate moving form the lung airspace into
the lung pleural cavity * ?? �Transudate � the result of increased hydrostatic or
decreased oncotic pressure. Requires no further workup outside of treatment of
underlying condition causing the exudate * ?? �Exudate � due to
inflammation/irritation of the pleural lining. Defined by the Light Criteria
(having only ONE of these three means its an exudate): o Fluid Protein/Serum
protein ratio >0.5??high protein in fluido Fluid LDH/Serum LDH >0.6??high LDH level
in fluido Pleural LDH >2/3 the upper limit of normal serum LDH??high LDH in fluido
Note that low glucose (<60mg/dL) is a classic sign of WBCs/bacteria using the
glucose for energy, denoting another sign for exudate. <30mg/dL is highly
suggestive of empyema! ?? Don�t forget! If the pleural fluid shows exudate, that
often means there�s an infection and local cytokine release has increased capillary
permeability to allow for WBC transit! 4631/4568/4073/4053: Para-pneumonic
Effusions/Empyema * ?? �Definition: complications of pneumonia with leakage of
fluid/bacteria into the pleural space, causing a mass to form. Defined by the fluid
analysis from thoracocentesis. * ?? �Presentation: severe pneumonia with evidence
of pleural effusion on imaging ?? Dx/Tx: o Uncomplicated para-pneumonic effusion �
transudate fluid with minimal bacteria. ???pH >7.2 (typically around 7.6), normal
glucose, LDH ratio >0.6, low protein ???Negative gram stain, negative bacterial
culture???Tx: antibiotics for pneumonia o Complicated para-pneumonic effusion �
exudative fluid with bacterial invasion ???pH<7.2 (fermentation), low glucose, LDH
ratio >0.6, high protein???Negative gram stain, positive bacterial culture???Tx:
antibiotics for pneumonia with chest tube drainage o Empyema � exudative fluid with
frank pus and bacterial colonization???pH<7.2 (fermentation), low glucose, LDH
ratio >0.6, high protein ???Positive gram stain, positive bacterial culture ???Tx:
long-term antibiotics with chest tube drainage Case 25 � Depression and Mood
Disorders Persistent Depressive Disorder (Dysthymia) ?? o o ???o ??????Depression *
?? �Risk factors o o o o o ?? o o o o o * ?? �DSM-5 Criteria: o
???????????????????????????* ?? �Dx: DSM-5 criteria o o o * ?? �Tx:o First line:
Therapy + anti-depressant is most efficacious DSM-5 Criteria Depressed mood for
majority of the time on most days for at least 2 years in adults (1 year in
children/teens) Two or more of the following: Poor concentration/trouble making
decisions; Feelings of hopelessness; Poor
appetite or overeating; Insomnia or hypersomnia; Low energy or fatigue; Low self-
esteem In the 2-year period of depressed mood: Person has not been free of symptoms
for >2 months for the 2 year period Dx: DSM-5 criteria Patient never had a manic
episode Tx: anti-depressant + therapy is most efficacious ?? ?? High cortisol
associated with HPA-axis disorder associated with depression Hypothyroidism is a
classic medical reason for signs of MDD Adverse life experiences (esp. in
childhood); especially loss of parent before age 11 If you have a first degree
relative with MDD Pancreatic cancer (like from poor prognosis) increases risk
Changes in sleep patterns Multiple nighttime awakenings, fracturing sleep
initial/terminal insomnia (trouble falling asleep and waking up extremely early)
'Leaden paralysis' upon waking: feels like limbs are extremely heavy Earlier
entry/greater duration of REM sleep with decreased Stage 3/Stage 4 sleep Atypically
hypersomnia can occur Must have 5 of the following symptoms for >2 weeks Depressed
mood most of the time Anhedonia Change in appetite or weight (increase or decrease)
Change in sleeping pattern (Insomnia or hypersomnia) Feelings of worthlessness or
guilt Diminished concentration Change in psychomotor activity (agitation or
retardation) Fatigue/loss of energy Recurrent thoughts of death or suicide All
patients with depression should be questioned (rule out bipolar disorder) Always
ask if pt is suicidal or homicidal May appear as Pseudo-dementia in the elderly!
???Takes 4-6wk for SSRI effects to kick in ???Typically if patient doesn�t improve,
increase the SSRI dose o Electroconvulsive therapy (ECT) can be used if: ?????????o
If bipolar: SSRI therapy will ignite a manic episodeo If pt is suicidal/homicidal:
immediate hospitalization with sitter and initiate an SSRI Bipolar Disorder ?? o o
o ?? Depression is unresponsive to any pharmacotherapy Patient cannot tolerate
pharmacotherapy (depression in pregnancy is classic) Rapid reduction of depression
is needed (pts will not eat/drink/catatonic/immediate suicide risk) Risk Factors:
Family member with bipolar disorder (strongest genetic risk among mental health
diseases) Dx of cyclothymic disorder (1/3 of patients with this disease will
develop bipolar disorder) Onset typically before age 30 (most often around age 18)
Manic Episode Includes 3 (with elevated mood) or 4 (with only irritable mood) of
these criteria: Distractibility Inflated self-esteem/grandiosity Goal-directed
activity (work, social, sexual) or psychomotor agitation Decreased need for sleep
Flight of ideas/racing thoughts More talkative or pressured speech
(uninterruptable) Excessive engagement in pleasurable activities with high risk of
negative outcomes (sexual indescretion, shopping spree, etc.) 50% of manic patients
also have psychotic symptoms Often the pts require hospitalization to protect
themselves Hypomanic Episode Meets criteria for mania but isn't full-blown (Lasts
at least 4 days; No impairment in social/occupational functioning; No
hospitalization required; No psychosis) o DSM-5 ?????????????????????o o ?? o * ??
�Bipolar I: at least one episode of true mania with bouts of
depression/euthymia/hypomania * ?? �Bipolar II: at least one episode of hypomania
with bouts of depression/euthymia * ?? �Subtypes: o o o o o o o o o * ?? �Tx:o o o
Anxious distress - tense, restless, diffiuclty concentration, fear of bad events,
�loss of control� Mixed features - depressive symptoms persist during
manic/hypomanic episodes Rapid Cycling - 4 or more mood episodes (depression,
hypomania, mania) within 1 year Melancholic features - classic criteria of
depression predominate in depressive episodes Atypical features - hypersomnia,
hyperphagia, reactive mood, leaden paralysis, hypersensitivty to rejection in
depressive episodes Catatonia - catalepsy (immobility), purposeless motor activity,
mutism, bizarre postures, echolalaia (responsive to ECT) Psychotic features -
delusions or hallucinations are present Peripartum onset - occurs during or up to 4
weeks after pregnancy Seasonal pattern - occuring during a certain season Lithium -
mood stabilizer shown to reduce suicide risk, but has low therapeutic window
Carbamazepine/Valproic Acid - anticonvulsants that act as mood stabilizers ECT an
option in patients refractory to Tx, immediate danger, pregnant women o Important
to ask about suicide: 25-50% attempt at suicide with 10-15% success Bereavement
Normal sadness/grief after the loss of a loved one Patients will often be sad, but
consolable and often a bit embarrassed with their emotional outbursts Pts want to
feel better while their grieving Often many symptoms decreased around 6 months No
signs of psychoses, disorganization, or active suicidality Note! While bereavement
may seem like MDD, the pt won't meet the criteria. That if patent meets all the
criteria for MDD, even following the loss of a loved one, the diagnosis is MDD
?? ?? o o o ?? Case 26 � Post-Partum Care [Chapter 11: Postpartum Care � Topics 13,
14, 29]Puerperium � the 6-8wk process of the mother�s body returning to it�s normal
state following birth * ?? �Involution of the uterus � initial decrease in size is
from expulsion of the fetus; subsequently autolysis of intracellular myometrial
protein (decreased cell size, NOT cell number), complete by week 6 * ?? �Lochia �
basically fluid/clots that are sloughing off the uterus. Often heaviest in the
first 2-3 days post partum. Lochia rubra (blood clots/decidua), Lochia serosa
(lighter with less blood), Lochia alba (whitish, may persist for several weeks; may
be confused for pathologic discharge) * ?? �Cervix/Vagina � the cervix reforms by 1
week, with its os retaining a �fish-mouth� shape, rather than a nulliparous round
shape. The vaginal tissues return to normal and sow a hypoestrogenic state,
especially with breastfeeding as ovarian function will be suppressed. Pelvic floor
muscles will regain tone and Kegel exercises are encouraged to strengthen pelvic
floor muscles. * ?? �Return of Ovarian function � typically ovulation occurs in 45
days for non-lactating and 189 days in lactating women due to prolactin suppression
of estrogen. Function should resume within a few weeks following cessation of
breastfeeding. * ?? �Abdominal Wall � stretching resolves over weeks and aided by
exercise. Striae gravidarum become more-silvery and lighten and diastasis recti
(separation of rectus muscle and fascia) resolves. * ?? �Cardiovascular system �
blood loss from birth is balanced with shifting of extracellular fluid into
intravascular space and elevated pulse rate. There may be CV decompensation in
mom�s with heart diseases that should be monitored. * ?? �Hematopoietic system �
leukocytosis occurs during labour/puerperium which may actually mask leukocytosis
occurring from post-partum infection. * ?? �Renal System � GFR remains elevated but
returns to normal in a few weeks. Some urinary retention due to urethral edema is
to be expected but urinary incontinence >90 days should be evaluated. Management of
the Immediate Post-Partum Period * ?? �Hospital Stay � typically 48hrs (vaginal) to
96hrs (cesarean) after the day of birth. Mom may be able to be discharged earlier
with specific signs of health, but baby may not be should there still be need for
routine neonatal care to be administered. Focus should be on prepping mom for care
of baby. * ?? �Maternal-Infant Bonding � mom should be with baby as much as
possible; skin-to-skin and breastfeeding are encouraged. Should monitor for signs
for depression/poor bonding * ?? �Postpartum Complications � some moms will have
post-partum hemorrhage (1%). Some moms will have increased bleeding on days 8-14
post-partum corresponding to separation/release of the placental eschar. This is
self-limited, but delayed post-partum hemorrhage may occur, which typically
responds to medical therapy. * ?? �Analgesia � it�s common to prescribe analgesia,
especially after C-section; clinical call as to what to use * ?? �Ambulation �
encouraged after day 1 to decreased DVT * ?? �Breast Care o Breast engorgement �
occurs typically in women who do NOT breastfeed 1-2 day post-partum. Gradual,
bilateral pain without fever/symptoms. Pts should be encouraged to wear a well
fitting bra/use ice packs or analgesia to relieve pain. They should also avoid
nipple stimulation and expression of milk as it will make the process of
physiologic return to normal longer. o Galactocele � plugged duct causing gradual,
unilateral, localized pain/swelling, without fever or symptoms of sickness. Should
resolve with total breast drainage of milk. o Mastitis � infection causing sudden,
unilateral, localized intense pain with fever/symptoms of sickness. Typically
S.aureus or other local bacterium in baby�s mouth. Pt should continue breastfeeding
and receive proper antibiotics o Breast Abscess � same as mastitis but with
fluctant mass. Same management as mastitis except with additional incision and
drainage of abcess. * ?? �Immunizations � mom should receive rubella/Tdap/RhoGAM if
indicated. Baby should receive HepB surface antigen vaccine and proper screening
tests. * ?? �Bowel/Bladder Function � constipation for 1-2 days is common (esp.
since patients havn�t eaten much during labour), hemorrhoids may be exacerbated
from pregnancy, and urinary output should be monitored for 24hrs although it is
common to have some urinary retention. Normal treatment of these conditions can
occur while mom is in the hospital or in outpatient basis. * ?? �Care of Perineum �
typically there�s some pain that�s relieved with oral analgesia/warm sitz bath.
Unresponsive pain may be a hematoma, which should be evaluated. Dehiscence or
infection may also have occurred
if a woman received stitches after birth. * ?? �Contraception � 15% of non-nursing
women are fertile at 6 weeks post-partum. o Combined OCPs � don�t use post-partum;
don�t want to screw with mom�s estrogen levels o Progestin only � OK to use 3-6wks,
even if breastfeedingo Sterilization � often done surgically at the time of a C-
section OR after vaginal birth. Questioning and consent should be sought during
pregnancy as to mom�s preferences. * ?? �Sexual Activity � started when patient is
comfortable. Minimal risk of hemorrhage/infection at 2 weeks * ?? �Patient
Education � reinforce value of healthcare for her/infant. Schedule a post-partum
visit. * ?? �Weight Loss � typically loss of 2lbs per month will not affect
breastfeeding. Often moms who breastfeed will lose weight at a faster rate than
not. * ?? �Lactation/Breastfeeding � breastmilk provides the best nutrition for a
neonate and exclusive breastfeeding is recommended for 6 months, then as long as
mutually desired. o Contraindications � HIV+ mom (vertical transmission),
active/untreated TB (close contact isn�t OK, but mom can pump breast milk), mom
receiving radioactive substances (check breastmilk until cleared), mom use of
illegal drugs, infant has galactosemia. ???Typically, <1% of any medication can
appear in the breastmilk. Some drugs that contraindicate breastfeeding = lithium
carbonate, tetracyclines, bromocriptine, methotrexate, or other listed above. o
Prolactin Release � initial drop in estrogen after birth allows for release of
prolactin for breast milk production. Suckling of the infant stimulates oxytocin
for breastmilk ejection (smooth muscle contraction in lactiferous duct) via nipple
stimulation. It also stimulates uterine contraction (helps with physiologic return
of uterine size). o Colostrum � produced 5 days post-partum; high nutrient/IgA
content makes it awesome. It�s steadily replaced by milk after day 5 o Lactational
Amenorrhea � note that prolactin will inhibit release of FSH/LH, ultimately
depressing estrogen/menstrual cycling. While it helps with contraception, it is not
reliable enough alone and medical contraception should be used. o Nipple Care �
fissuring/drying of nipple is common. Use moisturizer or a nipple shield.
Anxiety/Depression in the Post-Partum period � not entirely understood, but thought
to be influenced by hormone changes. Women with personal/family history of
depression/anxiety or depression during pregnancy are good predictive things to
note. * ?? �Post-partum Blues � 70-80% of women, typically 2-4 days; mild insomnia,
tearfulness, irritability, or sadness. Typically, self-resolving with no Tx.
Increase risk for Post-partum Depression. * ?? �Post-partum Depression � 10% of
women, typically 2wk-12mo duration; irritability, labile mood, insomnia, anxiety
that often worsen in the evening. Tx: antidepressants/therapy. * ?? �Post-partum
Psychosis � 0.1% of women, variable duration; confusion attention deficit,
distractibility, clouded sensorium. Tx: Antipsychotic/antidepressant drugs.
[Chapter 11: Postpartum Care � Topics 13, 14, 29 QUESTIONS] * ?? �Don�t forget!
Uterine atony is the most common cause of PPH and occurs in one in every twenty
deliveries. * ?? �Post-partum hemorrhage can result in Sheehan Syndrome (anterior
pituitary necrosis), which may lead to loss of gonadotropin, thyroid-stimulating
hormone (TSH) and adrenocorticotropic hormone (ACTH) production, as they are all
produced by the anterior pituitary. Frequently goes unnoticed for many years after
the inciting delivery. Treatment includes estrogen and progesterone replacement and
supplementation with thyroid and adrenal hormones. * ?? �Factors related to
increased rates of infection with a vaginal birth include prolonged labor,
prolonged rupture of membranes, multiple vaginal examinations, internal fetal
monitoring, removal of the placenta manually and low socioeconomic status * ?? �The
most common cause of postpartum fever is endometritis. Rate of endometritis is most
closely related to the mode of delivery (vaginal = 2%, C-section = 10-15%). Uterine
fundal tenderness is a common additional symptom. * ?? �Postpartum endometritis are
usually polymicrobial resulting in a mix of aerobes and anaerobes in the genital
tract; most common causes amonst the polymicrobial isolates are S.aureus and
Streptococcus * ?? �Don�t forget! Post-partum Blues (lasts <2wk) and Post-partum
depression (2wk � 6mo) * ?? �A sense of incapability of loving her family and
ambivalence toward her infant are classic signs of true post-partum depression.
Baby blues are usually depressive symptoms, but not toward the baby. * ?? �The most
significant risk factor for developing postpartum depression is prior history of
depression. Others include marital conflict, lack of perceived social support from
family and friends, having contemplated terminating the current pregnancy,
stressful life events in the previous twelve months, and a sick leave in the past
12mo related to hyperemesis, uterine irritability or psychiatric disorder. * ??
�Apparently the safest method to suppress lactation is breast binding, ice packs
and analgesics. No hormonal interventions are recommended in puerperium mothers due
to increased risk of adverse cardiovascular events. * ?? �Breastfeeding is
associated with a decreased incidence of ovarian cancer and breast cancer.
Breastfeeding has NOT been shown to decrease the risk for developing coronary
artery disease, cervical dysplasia and cervical cancer or colon cancer in the
mother. * ?? �Side lying position is a good one for breastfeeding, it is important
for mother and baby to be belly-to- belly in order for the infant to be in a good
position to latch on appropriately, taking a large part of the areola into its
mouth. If poor latching occurs, baby may not feed as well as it could and mom could
end up with baby sucking around the areola, causing drying/cracking of skin. * ??
�Prolactin is responsible for the synthesis of milk; present in large quantities
during gestation, its action is inhibited by estrogen and progesterone during
pregnancy (inhibits alpha-lactalbumin production by the rough endoplasmic
reticulum). After delivery, large amounts of prolactin continue to be secreted, and
milk is produced after estrogen and progesterone decrease (alpha-lactalbumin
stimulates milk lactose production). May take about two days to occur (colostrum
often occurs in these two days) * ?? �Bugs causing Mastitis are usually sensitive
to penicillin or a cephalosporin; community-acquired organisms, and even
staphylococcal infections are typically susceptible. * ?? �Some classic
breastfeeding promotive policies: baby on the breast within a half hour of delivery
and rooming-in for the baby to ensure frequent breastfeeding on demand (i.e.
unlimited access). * ?? �Candidiasis of the nipple may occur in breastfeeding if
baby has Candida infection in the mouth o Presentation: intense nipple pain,
burning/worsening with breastfeeding; sometimes with shiny, pink nipples and
peeling at the peripheryo Dx: inspection & swab/wet mount of both mom�s nipple and
baby�s mouth o Tx: ???Mom � topical fungal ointment & topical triple antibiotic
ointment ???Baby � oral nystatin followed by oral fluconazole * ?? �Signs that a
baby is getting sufficient milk: 3-4 stools in 24 hours, six wet diapers in 24
hours, weight gain and sounds of swallowing. Little spit-ups after feeding is NOT a
sign of adequate eating * ?? �Breast Engorgement is a common occurrence after
birth. To decrease discomfort: frequent nursing, taking a warm shower or warm
compresses to enhance milk flow, massaging the breast and hand expressing some milk
to soften the breast, wearing a good support bra and using an analgesic 20 minutes
before breastfeeding. * ?? �Oxytocin is responsible for milk ejection. Its
stimulated best by suckling of the infant * ?? �Note that cortisol and insulin act
in concert with other hormones to stimulate the growth and development of the milk-
secreting apparatus. [Chapter 12: Post-Partum Hemorrhage � Topic 27]
Recognition/Early Detection � defined as >500mL blood loss per vaginal delivery, or
>1000mL blood loss of cesarean birth. However, these are average blood losses for
these events, and estimation of blood loss is extremely subjective. This emphasizes
the need for recognition of signs/symptoms of blood loss in the pt. Note that loss
can be overt hemorrhage or more insidious bleeding. * ?? �10% loss � no worries,
this is typical and tolerated by most women * ?? �20% loss � first signs of
depletion: tachycardia, tachypnea, delayed capillary refill, orthostatic blood
pressure changes, and narrowed pulse pressure (elevated diastolic pressures from
vasoconstriction). * ?? �30% loss � continued tachycardia/tachypnea, overt
hypotension * ?? �40% loss � oliguria, shock, coma, and possibly death * ??
�Typically bleeding should be stopped as best as possible, with a search for
etiology General Management * ?? �Best to identify pts at risk early on and prepare
for hemorrhage management before labour. Prolonged, augmented, and rapid labours,
Hx of post-partum hemorrhage, episiotomy, pre-eclampsia, overdistention of the
uterus, operative delivery, and chorioamnionitis all increase risk * ?? �Treatment
should be directed at a suspected cause (most commonly uterine atony) and the use
of transfusable blood products should be understood.o Packed RBCs � 1 unit
increases Hct 3% and Hb by 1g/dLo Platelets � 1 unit increases platelet count by
5000-10000/mm3 o Fresh Frozen Plasma � 1 unit increases fibrinogen by 10mg/dL o
Cryoprecipitate � 1 unit increases fibrinogen by 10mg/dL Causes/Management??
Uterine Atony � normally, the uterine muscle contracts after birth, clamping down
on the spiral arteries to stop bleeding. When this doesn�t occur, uterine
atony is diagnosed. o Presentation: uterine bleeding with �boggy� uterus on
palpation.o Dx: clinicalo Tx: listed in order of consideration * ???�3rd stage
prophylaxis � decreases PPH rates up by 70%. Oxytocin infusion before placental
passage, gentle cord traction, uterine massage, & immediate breastfeeding * ???
�Uterotonic Agents � Methylergonovine maleate (powerful smooth muscle activator,
given IM as IV will cause hypertension from arterial contraction, avoided in HTN
pts); 15- methyl prostaglandin F2a (IM or intrauterine); Dinoprostone
(suppository); Misoprostol (suppository) can all be used. Note: if uterus is firm,
these will do nothing (as they only help firm the uterus) and other etiologies of
bleeding should be sought. * ???�Surgical Compression � typically used in failure
of other interventions. B-lynch (surgical compression of the uterus), arterial
ligation of uterine arteries, and selective arterial embolization are first
considered and often successful. Hysterectomy is a last resort. * ?? �Laceration of
Lower Genital tract � lacerations are common, lacerations causing significant
bleeding are not. Typically, this will be bleeding in the setting of a contracted
uterus. These often are identified via visual inspection and treated with simple
surgical closure. * ?? �Retained Placenta � typically uterine contractions aid in
separating the zona basialis and the zona spongiosa to allow the placenta to
separate for expulsion. If retained, bleeding will continue. o After placental
expulsion, the placenta should be examined for missing cotyledons, as they may
break off and be retained within the uterus o A sheared surface or abruptly ending
blood vessels may indicate an accessory (succenturiate) placental lobe which is
prone to breaking off for retention in the uterus. o Manual sweep of the uterus
should be done to attempt to identify and remove retained tissue, although
ultrasound can be helpful if diagnosis is uncertain. o Suction curettage may be
used if manual sweep is not successfulo Placenta accreta/increta/percreta may be
the underlying cause of retained placenta, as the placenta will rip apart rather
than detach from the deeper uterine tissue. These cases often involve profuse
bleeding and typically require hysterectomy to save mom�s life. * ?? �Hematoma �
development of a bleed within tissue, typically from normal birth trauma o
Presentation: exquisite pain at the site of bleed without shock; often with a
demonstrable mass o Dx: clinicalo Tx: o ???�If <5cm diameter/not enlarging �
expectant management with close monitoring o ???�>5cm or enlarging � should be
opened and drained with ligature of active bleeding site with close monitoring of
hemodynamic status * ?? �Coagulation Disorders � any coagulopathy can make normal
bleeding worse. However, it should be noted that bleeding can, in turn, generate a
coagulopathy due to loss of blood! * ?? �Amniotic Fluid Embolism � entry of
amniotic fluid into the bloodstream; rare and sudden o Presentation: occurs as a
sequence of events after fluid entry [respiratory distress??cyanosis ??
cardiovascular collapse??hemorrhage??coma/death] o Dx: based on clinical
presentation o Tx: cardiovascular/hematologic supportive measures?? Uterine
Inversion � literal inversion of the fundus into the uterine corpus and sometimes
out into the vagina, impeding contraction of the uterine muscle. Typically occurs
with too heavy of traction on the placenta during 3rd stage of labour. o Dx:
profuse bleeding, sometimes with round tissue mass protrusion from introituso Tx:
physical placement of fist into the uterus to revert + uterine massage/uterotonic
agent administration; should reversion be difficult or impossible, utero-relaxant
agents + reversion + uterotonic agents is used; surgical hysterectomy is a last
resort.?? Uterine Rupture � tearing apart of the uterine tissue, classically
occuring in pts with previous C-section attempting a vaginal delivery.o Dx: uterine
bleeding, with loss of fetal station, and possible palpation of small parts of
fetuso Tx: depends on severity/hemodynamic status of pt. Less serious situations
may be treated with surgical revision of the opening, but hysterectomy is a
distinct possibility. Chapter 12: Post-Partum Hemorrhage � Topic 27 QUESTIONS] * ??
�Methylergonovine is an ergot alkaloid (potent smooth muscle constrictor). It is
also a vasoconstrictive agent and should be withheld from women with hypertension
and/or preeclampsia. * ?? �Prostaglandin F2-alpha (Hemabate) is a potent smooth
muscle constrictor, which also has a bronchio- constrictive effect. It should be
used with caution in any patient with a reported history of asthma. It is
absolutely contraindicated in patients with poorly controlled or severe asthma.
* ?? �Uterine inversion is an uncommon etiology of postpartum hemorrhage; major
causes are: o Excessive (iatrogenic) traction on the umbilical cord during the
third stage of delivery.o Over-distended uterus (grand multiparity, multiple
gestation, polyhydramnios and macrosomia are all risk factors) * ?? �Presence of a
low-lying anterior placenta in a patient with a history of multiple Cesarean
births, the diagnosis of the placenta accreta must be entertained. This is a
concern as delivery of the placenta may result in laceration and severe hemorrhage;
typically, only resolvable with hysterectomy. * ?? �The following are associated
with retained placenta: prior Cesarean delivery (attachment to scar), uterine
leiomyomas (attachment to smooth muscle), prior uterine curettage (attachment to
scar) and succenturiate (accessory) lobe of placenta (weak connection to main
placenta) * ?? �In a patient with post-partum hemorrhage who is NOT responding to
uterotonic agents, the least invasive treatment is placement of the Bakri balloon
(device placed into the uterus with a balloon that is filled with up to 500 cc of
sterile fluid) This places pressure on the inside of the uterus. B-lynch
compression stitch, Uterine artery ligation, and hysterectomy all require a
laparotomy and should be reserved for recalcitrant cases. Uterine artery
embolization requires placement of embolization catheters as well as interventional
radiology. * ?? �Should the shit really hit the fan and pt requires exploratory
laparotomy for assessment/resolution of bleeding: [1st line - B-lynch compression
stitch, 2nd line �Uterine artery ligation, 3rd � hysterectomy] Case 27- Congestive
Heart Failure Epidemiology: * ?? �1-2% of cases are in people ages 50-59; 6-10% are
in patients 65+ * ?? �Men: 5-year mortality is 60% with mean survival age of 3.2yr
* ?? �Women: 5-year mortality is 40% with mean survival age of 5.4yr Presentation *
?? �Right Heart Failure: fluid retention, peripheral edema, JVD, hepatojugular
reflex, hepatic ascites, splenomegaly, porto-systemic congestion, nausea/vomiting,
distention/bloating, constipation, abdominal pain, decreased appetite * ?? �Left
Heart Failure: pulmonary congestion (dyspnea on exertion, orthopnea, wheezing
tachypnea, cough), bilateral rales, S3 gallop, Cheyne-Stokes respiration, pleural
effusion, pulmonary edema * ?? �Common to Both: tachycardia, cardiomegaly,
cyanosis, oliguria, nocturia, peripheral edema Dx: 2 major criteria �OR� 1 major +
1 minor criteria * ?? �Major criteria: paroxysmal nocturnal dyspnea, JVD, rales,
CVP >15cm H20, circulation time >25sec, hepatojugular reflex, weight loss of 4.5kg
within 5 days of treatment * ?? �Minor Criteria: bilateral ankle edema, nocturnal
cough, dyspnea on exertion, hepatomegaly, pleural effusions, decreased vital
capacity by 1/3, tachycardia Workup and Labs: don�t forget, CHF is a sign of some
other pathologic process going on! * ?? �CBC??elevated WBC (infection or anemia
(lack of O2 capacity) which both increase stain on heart * ?? �Serum
electrolytes ???dilutional hyponatremia and other electrolyte abnormalities are
common * ?? �Renal function tests??fluid retention causing CHF signs could actually
be from renal failure * ?? �Liver function tests ???vascular congestion can cause
damage to the liver * ?? �Cardiac enzymes??acute MI may precipitate onset of CHF
* ?? �BNP??sign of fluid overload; >500 pg/mL consistent with CHF * ?? �EKG??may
show signs of ventricular hypertrophy or other less specific signs * ?? �CXR??
cephalization of pulmonary vasculature; perihilar infiltrates (�butterfly
pattern�), pleural effusions (more commonly on right hemithorax), and cardiomegaly
may be identified * ?? �Echocardiography??gold standard for diagnosis due to
ability to identify enlargement and failure of the heart functionally Acute CHF
Management * ?? �Oxygen (decrease heart work): 100% non-rebreather??CPAP/BiPAP??
intubation/ventilation o Continuously monitor O2 status; aiming for >90% saturation
on room air for discharge * ?? �Furosemide (pee out retained fluid): use if
pulmonary edema found on exam * ?? �IV Nitroglycerine (reduce heart O2 demand &
decrease BP): pools blood in the veins, should be used with caution as it may cause
precipitous hypotension * ?? �IV morphine sulfate (reduce heart O2 demand &
decrease BP): reduces anxiety, thus heart rate, and acts as a venodilator aiding
drop in BP * ?? �Discharge is considered with resolution of symptoms with
treatment, meeting O2 demands on room air, and exclusion of acute coronary syndrome
Chronic CHF Management * ?? �Emphasize diet, weight loss, sodium/fluid restriction
* ?? �ACE/ARB: reduce pre-load/afterload/cardiac output through reducing RAAS
influence; downside is they cannot be used in pregnancy, hypotension, hyperkalemia,
bilateral renal artery stenosis, and must be monitored in pts with renal
dysfunction * ?? �B-blockers: low dose with titration up reduce progression into
chronic heart failure; although in the acute setting they may worsen CHF * ??
�Diuretics (loop or thiazide): used to decrease fluid retention; regular weighing
to measure �water weight� allows for adjustment to a proper dose * ??
�Spironolactone: an aldosterone antagonist found to reduce mortality in CHF.
Monitor for hyperkalemia * ?? �Amlodipine: used in diastolic heart failure as it
slows the heart, allowing for more filling time; note that this is the ONLY Ca2+
channel blocker you can use. Others are shown to increase mortality. [Tips from
UWorld] Case 28 � Family Planning & Contraceptives [Chapter 26: Contraception �
Topic 33] Don�t ever forget! * ?? �Progesterone halts ovulation by inhibiting LH
* ?? �Estrogen inhibits follicle maturation by inhibiting FSH Hormonal
Contraception * ?? �OCPs (estrogen + progesterone) � suppresses ovulation (HPA
axis), regulates cycle, thickens cervical mucus, discourages implantation
(unfavorable uterus) o Contraindications: smoker >35yr, thromboembolism/vascular
occlusive disease/CVA, impaired liver function, or congenital hyperlipidemia o
Relative contraindications: migraines, severe HTN, DMII, gallbladder Dx, morbid
obesity o Function may be reduced by antibiotics, barbiturate, and antifungal
medications * ?? ��Mini-pill� (progesterone only) � thickens cervical mucus; can be
used immediately post-partum and during breastfeeding * ?? �Depo-provera
(medroxyprogesterone) � injection every 3 months; often pts cease to have a period;
worst side effects are weight gain, facial hair growth, and irregular bleeding
(only in first few months of use); fertility takes time to return after stopping
(depends on how long you were on it) * ?? �Transdermal Patch (Ortho Evra) � same
effect as OCPs, but change each week (3 on 1 off) * ?? �Intravaginal Ring
(NuvaRing) � same effect as OCPs, but leave in for 3 weeks (3 on 1 off) * ??
�Etonogestrel implant (Implanon) � progresterone only implant effective for 3
years. Similar effects to Depo-provera, but often less intense due to lower
necessary dose Barrier Methods: seeks to block the passage of sperm and egg meeting
* ?? �Condom � only latex condoms are effective in STD prevention. Wrap your dingus
boys. * ?? �Female condom � why? * ?? �Sponge � why? Can cause toxic shock
syndrome...again I ask why? * ?? �Diaphragm � needs spermicide and be left in place
6hr after sex...who would invent this? * ?? �Cervical cap � diaphragm that can be
inserted for 48hr...so you can be uncomfortable for 48hr * ?? �Spermicides alone �
dumb. Only use spermicide with a condom if you want to go this route. Intrauterine
Devices (IUDs) * ?? �ParaGard (Copper IUD) � kills sperm on contact for 10yr; can
cause increased bleeding; oddly, it�s the best form of emergency contraception if
used within timeframe * ?? �Mirena (progesterone) � local release of progesterone
for 5yr. Gives you the benefits of progesterone without the side-effects. Actually
one of the best and most popular contraceptive devices. Natural Family Planning ??
Good for someone trying to sneak a baby into their relationship. [Chapter 27:
Sterilization � Topic 32, 33, 41]Sterilization is the most common form of
contraception in the USA (esp. in people >30yrs or couples who have been married
>10yrs); it�s important to remind patients that it is permanent and although
technically reversible, typically there�s low success. ?? Men: the vasectomy is the
contraceptive procedure of choice with the benefits of faster sterilization and
easier reversal (although relatively poor outcomes) o Post-Op complications (5-10%)
� bleeding, hematoma, acute/chronic pain, infection o Some concern about post-op
depression, formation of anti-sperm antibodies, and increasing rates of prostate
cancer, however these are not substantial risks o Pregnancy occurs 1% post-op often
resulting from intercourse too soon after procedureo Multiple ejaculations are
needed to clear the collecting ducts of sperm entirely; and couples should use
another method of contraception until semen analysis confirms azoospermia
(typically occurs at 10 weeks post-op)?? Women: several methods, but all involve
alteration of the fallopian tubes. Reversal is technically possible but has low
success rateo Laproscopic: a good option as it�s minimally invasive and often
outpatient surgery. All options of technique serve to occlude the Fallopian Tubes *
???�Electrocautery � may be either unipolar (one electrified end) or bipolar (two
electrified ends clamping); unipolar has higher risk of injury but has higher
success rate * ???�Hulka clip � minimal tissue damage; easiest to reverse; highest
failure rate (1%) * ???�Falope ring � medium reversibility and failure; higher
rates of post-op pain and bleeds * ???�Filshie clip � lower failure than Hulka clip
with similar reversibility o Mini-laparotomy � most common approach in the world;
small infraumbilical incision is made, the tube is sutured into a �knuckle� and a
3-4mm portion is removed. These open portions are then sutured shut and may be
cauterized to ensure closure o Hysteroscopy � approaches sterilization through the
cervix; with placement of a small metal device into the fallopian tube causing
irritation and growth of tissue for occlusion. Pts take effective birth control
until occlusion is proven by hysterosalpingography ?? For some unknown reason,
women ho undergo tubal ligation have lower rates of ovarian cancer Complications
* ?? �Risks of surgery (infection, bleeding, pain, etc.) are always present; but
there is also increased risk of ectopic pregnancy with these form of procedures * e
�Tubal ligation via electrocautery has the highest rate (even more so than
mechanical occlusion) Reversal of Tubal Ligation * ?? �It can happen but really
doesn�t have great results * ?? �If a patient has a tubal reversal, they are
presumed to have an ectopic pregnancy until intrauterine pregnancy is firmly
established (typically by ultrasound) * ?? �Apparently 26% of pts regret having
tubal ligation, although only 1% ask for reversal. [Chapter 26: Contraception &
Chapter 27: Sterilization � Topic 32, 33 QUESTIONS] * ?? �While many women may
initially have irregular bleeding when starting Depo-Provera, this often resolves
within 2-3 months of use; 50% of women will actually stop bleeding altogether. * ??
�Apparently when a patient is requesting emergency contraception, you should also
immediately initiate OCPs as well o Remember that emergency contraception is not
considered an abortifacient and has not been shown to be teratogenic if pregnancy
is present o Plan B or other emergency contraceptives should be initiated within
72hrs of sex (best outcomes) but can be administered no later than 120hrs after sex
* ?? �Contraindications to estrogen (OCPs) include a history of thromboembolic
disease, women who are lactating, women over age 35 who smoke, or have severe
nausea with combined OCPs o These women are better suited for progestin-only or
mechanical methods * ?? �Oral contraceptives will decrease a woman�s risk of
developing ovarian and endometrial cancer due to low-dose estrogen exposure. o
Slightly higher risk of developing cervical intraepithelial neoplasiao Risk of PID,
endometriosis, benign breast changes and ectopic pregnancy are reduced * ?? �In pts
wih high BMI or previous gynecologic surgeries desiring permanent sterilization,
hysterscopic sterilization (Essure) is a great option due to increased surgical
risk o
Ptmusttakeeffectivecontraceptionfor3mofollowingsurgery,untilahysterosalpingogramcan
confirm that the tubes are occluded * ?? �Regret rate after tubal ligation
increases with decreasing age (40% of women under 25yr had regret); women who are
not married at the time of their tubal ligation, when tubal ligation was performed
less than a year after delivery, and with conflict between the woman and her
partner have higher rates * ?? �Vasectomy and tubal ligation are both 99.8%
effective; in a married patient with multiple medical problems that present high
risks for surgery, the husband getting a vasectomy may be the best option * ??
�Don�t forget! A person with Wilson�s Disease (hepatolenticular degeneration) is
not a candidate for a copper-IUD (as they can too much copper from it as a present-
source!) * ?? �The patch (Ortho Evra�), while comparable efficiency to the pill in
comparative clinical trials, has significantly higher failure rate when used in
women who weigh more than 198 pounds, likely due to significantly increased
subcutaneous fat, inhibiting hormonal diffusion. Case 29 � Adolescent Health
Guidelines for Adolescent Preventative Services (GAPS) � these are guidelines
specifically tailored to preventing major problems within the adolescent
population. Below are things that should be screened in teens: * ?? �Medical:
Hypertension, Obesity/eating disorders, hyperlipidemia (if at risk), TB (if at
risk) * ?? �Social/Emotional: Abuse (physical, emotional, sexual), learning
disabilities/school problems, substance abuse, depression, emotional problems,
suicide risk assessment * ?? �Sexual: risky sexual behavior/contraception, STIs
(esp. Chlamydia/Gonorrhea/HIV), cervical cancer * ?? �General Advisory Topics:
healthy eating/maintaining a healthy weight, regular exercise, use of
seatbelts/helmets, optimal sleep/establishing a sleep pattern, avoiding
tobacco/drugs/alcohol, limiting risky online behavior (posting nude pictures,
giving out personal info), dealing with bullying Immunizations often given to
Adolescents/Teens * ?? �Hep A, Hep B, MMR, Varicella � Often these are given in
childhood; if they have NOT been given previously, they should be given during the
adolescent years * ?? �Tdap booster (every 5 years) * ?? �HPV � given between ages
9-26 in BOTH boys and girls * ?? �Meningococcal vaccine � esp. if going to college
or enlisting in the military * ?? �Annual Flu shot � an oldie
but goodie * ?? �Pneumococcal vaccine � only if risk risk for infection (lung or
immune system problems) Sports Physicals ?? Teen present to the doctor for a sports
physical ALL THE TIME, thus it�s important to know what you�re supposed to be doing
in a sports physical. Below are some general guidelines: o Ensure compliance with
vaccine recommendations/GAPs guidelineso Check for joint health/orthopedic
abnormalitieso Ensure that any chronic disease is well controlled for sporting o
Check the heart for HOCM and heart murmurs ?? HOCM and heart murmurs o One of the
most common causes of sudden cardiac death in an athleteo
Allpts/parentsshouldbeasked:exertionalchestpain,syncope,Hxheartmurmurs,hxof HOCM,
cardiac abnormalities, or premature cardiac deaths o Signs of Marfan�s syndrome
should be assessed: arachnodactyly, arm span greater than height, pectus excavatum,
tall-thin body habitus, high arched palate, eye lens subluxations ?? Some tips from
UWorld on HOCM2678: Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal
dominant mutation typically of myosin binding protein C or cardiac beta-myosin
heavy chain gene resulting in abnormal myocardium ?? The murmur is decreased with
increased blood in the left atriumo Sustained handgrip (increased afterload),
squatting from standing (increased afterload/preload) or passive leg raise
(increased preload)o These all increase distention of the ventricle, minimizing
outflow obstruction * ?? �The murmur is increased with decreased blood in left
artriumo Valsalva, abrupt standing (decreased preload), and nitroglycerin o All
increased obstruction, thus the intensity of the mumur * ?? �Murmur is best heard
on the left, lower sternal border/apex 4673: Hypertrophic Obstructive
Cardiomyopathy (HOCM) should be suspected in a young person experiencing syncope,
chest pain, and has a creshendo-decreshendo murmur on the left sternal border.
While aortic stenosis CAN cause this murmur, it is unlikely if the patient does not
have a familial syndrome/risk factors that leads to aortic stenosis. Aortic
stenosis would be more common in older people. 2711: A CLASSIC reason for a young
athlete to get syncope/abnormal heart sounds is HOCM. Oddly, this can become more
severe as the outflow of blood along the narrowed ventricle can pull the mitral
valve leaflets into the ventricle creating outflow obstruction. This outflow
obstruction is largely blamed for clinical manifestations AND the harsh systolic
murmur that worsens with standing up suddenly. Case 30 � HypertensionHypertension
is bad. It increases the risk for heart attacks, stroke, renal failure, and many
other conditions with risk positively correlated to the elevation of blood
pressure. 30% of folks don�t even know they have it, earning it the name the
�silent killer�. Levels of hypertension are as follows: * ?? �Normal BP � <120/80 *
?? �Pre-hypertension � 120-139/80-89 * ?? �Hypertension � 140-159/90-99 * ??
�Severe Hypertension � >160/100 Diagnosis ?? Two resting blood pressures, taken
with a proper cuff size at least 4hr apartWorkup � once someone is diagnosed, the
underlying cause and damage done by HTN should be assessed * ?? �Hx � full Hx
making sure to ask about HTN risk factors in Family Hx * ?? �Physical � Vital signs
+ BP in both arms, BMI, funduscopic exam (retinopathy), oropharynx (OSA), thyroid
exam (hyperthyroid), full body auscultation (bruits/coarctation), AAA,
cardiopulmonary exam * ?? �Labs � serum K, Ca, Creatinine, blood glucose,
hematocrit, urinanalysis, and EKG Treatment * ?? �Non-Pharmacologic � always your
first option and should be part of all treatment plans. Increase physical activity,
lose weight, reduce EtOH/smoking, and DASH diet (limit sodium!) * ?? �Pharmacologic
� often employed when pt on non-pharmacologic Tx isn�t meeting goals o 1st line �
Thiazide Diuretic (well tolerated/strong effect)o Additional Therapy � ACE
inhibitor, ARB, Other diuretics, Ca2+-channel blocker, B-blocker, and aldosterone
antagonists are all options to be used in different pts ???Use if pt >20/10mmHg
above goal or with Severe HTN Some Classic Underlying Causes of HTN are outlined
below & others are covered elsewhere: Aortic Coarctation, Reno-vascular/renal
disease, Cushing�s Disease, Hyperthyroidism (elsewhere), Hyperparathyroidism
(elsewhere), Hyperaldosteronism, Pheochromocytoma, Obstructive Sleep Apnea 8819:
Aortic coarctation (late presentation): remember that this is a congenital aortic
stricture which can cause significant cardiac signs/symptoms: * ?? �Associated
findings: bicuspid aortic valve, Turner�s disease, ventricular septal defect (VSD)
* ?? �Dx: classically presents with asymptomatic HTN and epistaxis in a young
person o May also have claudication, headache, heart failure, aortic dissectiono
Brachial-femoral delay, upper extremity hypertension with lower extremity
hypotension, continuous cardiac murmur (from collateral flow)o CXR can show: LV
hypertrophy, notching of 3-8 ribs, �3-sign� of aortic indentation o Confirm with
echocardiography * ?? �Tx: balloon angioplasty +/- stenting to open stricture point
* ?? �Diabetes Mellitus (covered elsewhere) 4682: Renal artery stenosis has two
classic findings: * ?? �Systolic-diastolic periumbilical bruit: apparently if you
hear this, think renal-artery stenosis. Don�t get it confused with AAA...which will
produce a systolic bruit and have a pulsating abdominal mass! * ?? �Refractory HTN:
the patient in the vignette has a BP 190/120 on 4 different BP lowering
drugs...that ain�t right son. If you see this, consider secondary causes...of
which, renal artery stenosis is the most common. 3894: Renal Artery
Stenosis/Renovascular Hypertension * ?? �Presentation: resistant HTN (3 drug
regimen cannot control), malignant HTN (end organ damage), new severe HTN
(>180/120) after age 55, recurrent flash pulmonary edemao Asymmetric kidney size,
abdominal bruits, unexplained rise in creatinine after starting an ACE/ARB,
unexplained atrophic kidney * ?? �Dx: clinical presentation with concurrent
findings ?? Tx: o Initial: ACE/ARB administration + additional agents if needed. If
RAS is unilateral, the unaffected kidney is no longer subject to the RAAS
activation being set forth by the stenotic one, and will compensate for proper
renal function. If bilateral, kidney function can worsen o Refractory:
revascularization or renal artery stenting. Reserved for those who do not tolerate
anti-hypertensives, have flash pulmonary edema, or heart failure due to HTN.
2592/4721/4419: Cushing�s Syndrome * ?? �Presentation: central obesity, buffalo
hump, moon facies, skin atrophy with purple striae, proximal muscle weakness,
hypertension (mineralocorticoids), glucose intolerance, skin hyperpigmentation,
eccymoses, women may have hirsutism/menstrual irregularities o Labs: hyperglycemia,
hypokalemia * ?? �Etiology: exogenous corticosteroid administration (most common),
ACTH-producing tumor (Cushing�s disease), ectopic ACTH-production (small-cell lung
cancer), or primary adrenal disease * ?? �Dx: o Establish hypercortisolism with
salivary cortisol assay, 24-hr free urine cortisol, and low-dose dexamethasone
suppression test (2/3 must be positive) o If hypercorticolism present??ACTH level
measurement (see if process is ACTH dependent or independent) o If ACTH is
elevated??high-dose dexamethasone suppression test to determine if source of ACTH
is pituitary (will be suppressed) or ectopic (won�t be suppressed, likely lung
cancer) ?? Tx: aimed at underlying cause 3231/2725/3230/3832/8897:
Hyperaldosteronism Primary Hyperaldosteronism (Conn�s syndrome) * ?? �Typically,
from an adrenal adenoma or bilateral adrenal hyperplasia * ?? �Presentation:
hypertension (increased Na+), hypokalemia, high aldosterone, low renin, adrenal
changes on CT scan, and metabolic alkalosis (hypoK increases bicarb reabsorption/H+
secretion) * ?? �Dx: CT findings + aldosterone:renin ratio >20 or adrenal
suppression after oral saline administration o
Adrenalvenoussamplingcandistinguishbilateralfromunilateraldysfunction o Best first
test is the aldosterone:renin ratio ?? Tx: o Unilateral: surgical excisiono
Bilateral or surgery not an option: aldosterone antagonists (K-sparing diuretics)
spironolactone or eplerenone (note that spirono has anti-androgen effects, but
eplerenone will have less of these. Spirono is still the preferred first-line
treatment)?? Note that these patients may be on a non-K-sparing diuretic simply
because they seem to have hypertension. But K-wasting due to diuretic use will not
approach the degree that hyperaldosteronism will achieve. Often the two combined
will cause the hypokalemia Secondary Hyperaldosteronism * ?? �Typically, from reno-
vascular HTN, malignant HTN, renin-secreting tumor, or diuretic use (basically the
kidney�s normal response to poor perfusion) * ?? �Presentation: hypertension
(increase Na+), hypokalemia, high aldosterone, high renin Pseudo-hyperaldosteronism
* ?? �What looks like aldo, smells like aldo, but isn�t aldo? Basically things that
increase other �corticoids� that aren�t mineralocorticoids...but can act as
mineralocorticoids. CAH, deoxycortisone-secreting tumor, Cushing�s syndrome, or
exogenous mineralocorticoid use * ?? �Presentation: hypertension (increase Na+),
hypokalemia, low aldosterone, low renin 3976: Pheochromocytoma * ?? �Neuroendocrine
tumor of chromaffin cells producing catacholamines (typically 5-HT) o Association
with MEN2a/MEN2b * ?? �Presentation: episodic hypertension, palpitations, sweating,
pallor classically with increase intraabdominal pressure (urination, palpation,
positional change) or anesthesia/surgery o Beta blockers alone will cause
hypertensive crisis (5-HT activates a-receptors)o Must give a-blockers before
surgical removal (phenoxybenzamine) * ?? �Dx:
clinical presentation demonstration of mass on imaging * ?? �Tx: pre-treatment of
phenoxybenzamine and surgical removal 3033/4448: Obstructive Sleep Apnea ??
Presentation: daytime sleepiness, morning headaches, poor sleep with multiple
awakenings o Labs: erythrocytosis with increased EPO (reaction to hypoxemia)o Risk
factors: Obesity, tonsillar hypertrophy, excessive oropharyngeal tissue, or short
mandible o Sequlae:cor-pulmonale,right-
heartfailure,pulmonary/systemicHTN,depression,daytime accidents due to sleepiness,
impotence * ?? �Dx: nocturnal polysomnigraphy??>15 apneic or hypopnea events in a
night * ?? �Tx: directed at underlying cause Case 31 � Infantile Abdominal
Pain/VomitingIntussusception � �telescoping� of bowel with inflammation and
eventual obstruction causing symptoms ?? Presentation: infant with intermittent
vomiting/abdominal pain that resolves completely and spontaneously; episodes of
pain last approximately 20 minutes. o Typically with vomit of food??bilious
vomiting (distal intestinal obstruction)o Classically a palpable sausage shaped
mass (telescoped bowel) can be palpated on the right side of the gut (occurs most
often at the ileocecal junction)o May show �currant jelly� or mildly bloody stools
from bleeding within the gut o If not resolved, bowel necrosis will set in causing
permanent damage to gut * ?? �Dx: plain film X-ray (rule out perforation) or
contrast enema (Dx and therapeutic) * ?? �Tx: enema to relieve intusseceptum +/-
surgical resolution Hypertrophic Pyloric Stenosis � hypertrophy of the pylorus
causing obstruction in upper GI tract; most common cause of infantile GI
obstruction ?? Presentation: non-bilous projectile vomiting immediately following
meals; baby will always seem hungry despite vomiting (�hungry baby!�) o Vomiting
only food/mother�s milk directly after or during feeding sessions o Olive shaped
mass can be palpated and visible peristalsis can be seen in upper abdomen * ?? �Dx:
ultrasound imaging of thicken pylorus or upper GI contrast showing the �double-
bubble sign� * ?? �Tx: IV fluid repletion and immediate surgical resolution (near
100% success rate) Gut Malrotation with Volvulus � gut rotates around itself
cutting off blood supply due to improper mesenteric development causing poorly
secured intestines within the abdomen * ?? �Presentation: bilious vomiting with
abdominal pain that will start and NOT resolve spontaneously o Often presentation
<1mo of ageo If advanced, hypovolemia, hypotension, GI bleeding, peritonitis, and
sepsis/death can occur * ?? �Dx: upper GI series imaging showing volvulus,
�misplaced duodenum�, or duodenal obstruction * ?? �Tx: stabilization if necessary
with immediate surgical resolution Foreign Body Bowel Obstruction * ??
�Presentation: abdominal pain/vomiting, sometimes with Hx of ingestion * ?? �Dx:
plain radiographs or Hx indicative of forgeign body presence * ?? �Tx: stool checks
by parents to ensure passage (90% will pass spontaneously) o Button-shaped
batteries � require immediate surgical intervention as they will be able to conduct
electricity within the body causing perforation o Sharp objects/multiple magnets �
have a good chance to perforate the bowel wall and require surgery. If passed into
dueodenum, these may be watched with daily x-rays until passage. If object doesn�t
move in 3 days, surgery is required. Poisoning * ?? �Presentation: depends on thing
ingested; often OTC drugs are of biggest concern but insecticides/nicotine/personal
care items/fumes/etc are all possible * i �Dx: based on history of ingestion or
symptoms of ingestion (cholinergic or anti-cholintergic syndrome) * ?? �Tx:
immediate poison control consult Case 32 � Dementia Evaluation and Dx * ?? �Careful
Hx and review of medications for broad search for underlying cause * ?? �CBC, B12,
CMP, Thyroid hormone testing, and depression screening * ?? �Clock Draw � quick and
easy screen for dementia * ?? �Folstein MMSE � comprehensive mental status
assessment often used for further etsting Alzheimer�s DiseaseThe most common
dementia; present in 4% of pts >65 years old * ?? �Histology: neurofibrally tangles
and senile plaques in cortex/hippocampus * ?? �Lack of ACh production by the
nucleus basalis of Meynert is thought to drive disease symptoms * ?? �Risk factors:
o Old age, female sex, history of head trauma, Down�s syndromeo ApoE4 (chrom. 19),
Amyloid Precursor Protein (chrom. 21), Presenilin 1 (chrom. 14), Presenilin 2
(chrom. 1), a2-microglobulin mutation (chrom. 12) * ?? �Manifestation: o
Early:language/reasoning/behaviornormalwithminor�slipups�o Late: significant
impairment of language/reasoning/cognitive function, loss of independence o Very
Late: impairment of motor function, personality changes, hallucinations, delusionso
�Sundowning� is a phenomenon where symptoms become worse at night.o Impaired sense
of smell is a consistent finding in this and other dementias * ?? �Diagnosiso
Clinical signs/symptoms and progressive worseningo Elevated tau protein or low AB-
42 levels in CSFo MRI showing shrinkage of amygdala, hippocampus, and thalamuso
PET/SPECT showing bilateral tempo-parietal hypometabolismo Truly can only be
diagnosed with pathologic brain samples showing plaques/NFTs * ?? �Therapy:o Goal
is to delay progression and maximize function; disease course lasts approximately
12 years o Donepezil: cholinesterase inhibitor | Diarrhea, abdominal cramps,
hepatic toxicityo Rivastigmine:cholinesteraseinhibitor|
Diarrhea,abdominalcramps,hepatictoxicityo Memantine: NMDA-receptor antagonist |
dizziness, headache, confusiono Galantamine: cholinesterase inhibitor | Diarrhea,
abdominal cramps, weight loss Disease course lasts 9-12 years before death Vascular
(Multi-infarct) DementiaDementia resulting from cerebrovascular disease;
classically progressing in a step-wise fashion (person at a level of decreased
function, then sudden steps down to another level); ; * ?? �Causeso Macrovascular:
disease from infarction of major brain vesselso Microvascular: disease from
subcortical ischemia (lacunar strokes/deep white matter damage) * ?? �Risk factors:
HTN, diabetes, advanced age, embolic sources, atherosclerosis * ?? �Diagnosis:
Typically complex attention and executive function are affected Pt will often have
some major sign of vascular disease (bruits, etc.) o Dementia + two or more of
additional symptoms:o Focal neurologic signs | abrupt, step-wise, or stroke-related
onset | brain imaging showing multiple strokes, lacunes, or extensive white matter
damage ?? Treatment: prevent further vascular disease and treat risk factors
Dementia with Lewy Bodies Core features: * ?? �Fluctuations in cognition with
pronounced changes in attention/altertness * ?? �Visual Hallucinations are a
hallmark and often quite vivid * ?? �Parkinsonism; often mild and unilateral with
rigidity, but not full-blown movement disorder Suggestive features: * ?? �REM-sleep
behavior disorder: often parasomnias or acting out dreams (can be dangerous!) * ??
�Severe neuroleptic sensitivity: akathisia/TD/worse parkinsonism with normal dosing
* ?? �Low DA-transporter uptake in basal ganglia (SPECT or PET): often a classic
sign * ?? �Low metabolism in occipital lobe (SPECT or PET): another classic sign to
be aware of Dx: 2 core features or 1 core + 1 suggestive; definitive diagnosis on
autopsy * ?? �Imaging (CT/MRI) are useful for ruling out other possible causes of
disease phenotype * ?? �Neuropsychologic testing helps in differentiating AD from
DLB * ?? �EEG may be used, but isn�t the most useful thing * ?? �Autopsy will show
a-synuclein intranuclear Lewy Bodies Tx: no way to slow disease progression but
some can restore function * ?? �Anti-cholinesterase drugs (rivastigmine, donepezil,
galanthamine) ???cognitive/behavior problems * ?? �ECT is safe if depression occurs
* ?? �DO NOT GIVE NEUROLEPTIC DRUGS Often difficult to distinguish from Alzheimer�s
Disease; we must be able to differentiate the two Frontotempotal Lobe Dementia ??
Manifestations: o Impaired executive function (poor social function, decision
making, trouble with organization or sequencing, etc.) o Hallmark Personality
changes, often with disinhibition o Atrophy of the frontal/temporal lobes ??
Associated with abnormal tau protein TDP-43 Parkinson DiseaseDefined: progressive
disease causing bradykinesia, rigidity, and dementia * ?? �Substantia nigra shows
loss of pigmentation and/or eosinophilic Lewy Bodies * ?? �Familial variants show
mutation in the parkin gene (autosomal recessive) Signs/Symptoms: insidious onset;
average age of 60 for symptoms * ?? �Cardinal Features: onset is often asymmetric,
then generalizeso Resting (pill-rolling) tremor, Cogwheel rigidity (often seen when
checking �tone�), Hypokinesia (best correlate to severity of DA loss), with
Postural instability * ?? �Stooped/shuffling gait and difficulty arising from a
chair are classic signs * ?? �Loss of smell is nearly universal in PD patients * ??
�Pain, sialorrhea, dysarthria, cognitive deficits (esp. executive function) can
occur Dx: Ruling out other diseases is a huge part of diagnosis: * ?? �Multiple
systems atrophy � parkinsonism with less pronounced tremor/symmetric onset (�hot-
crossed bun sign� on MRI * ?? �Dementia with Lewy Bodies � parkinsonism with
dementia/hallucinations/fluctuations/myoclonus * ?? �Corticobasal ganglionic
degeneration � asymmetric parkinsonism with alien limb/dystonia/apraxia * ??
�Progressive supranuclear palsy � Pseudoparkinsonism with inability to look down,
upright posture, and early/frequent falls (because they cannot check the ground)
* ?? �Shy-Drager Syndrome � parkinsonism with extreme dysautonomia (orthostatic
hypotension is classic) * ?? �Nigrostriatal degeneration? Tx: * ?? �Levodopa-
carbidopa (carbidopa
is a COMT inhibitor to keep L-dopa levels high) � may cause dyskinesia * ?? �DA
agonists (pramipexole, ropinirole, bromocriptine) � may decrease incidence of
dyskinesia if used 1st * ?? �MAO-B inhibitor (selegiline, rasagiline) � augments L-
dopa and primarily helps disease symptoms * ?? �Amantadine (NMDA antagonist; useful
for eliminating L-dopa induced dyskinesia) * ?? �Deep Brain Stimulation of the
subthalamic nucleus Note: Anti-psychotics and anti-emetics
(prochlorperazine/metoclopramide) can induce Parkinsonism Huntington Disease
Defined: severe genetic disease causing loss of motor control/psychiatric decline *
?? �Autosomal dominant CAG repeat elongation in the huntingtin gene (4p16.3) * ??
�<25 CAG (no dx); 26-39 (sometimes dx); >40 (always dx); 60+ (earlier onset dx)
* ?? �Average age of onset 40yrs * ?? �Anticipation may occur especially if
paternally transmitted (family should all be screened) Signs/Symptoms: slow onset
of symptoms is typical * ?? �Chorea: jerky, dance-like movements affecting the
entire body; initially trouble with coordination/movement but ultimately
swallowing/choking * ?? �Dementia: personality change, disinhibition, depression,
anxiety, suicide * ?? �Westphal variant (childhood): more like Parkinsonism;
bradykinesia and rigidity; atrophy of the caudate nucleus and putamen is
characteristicDx: clinical suspicion with confirmed genetic testing; rule out drug
effects Tx: * ?? �No treatment to stop/slow disease progression * ?? �Chorea: o
Haloperidol: typical antipsychotic (D2 antagonist); stops aberrant activation of
basal ganglia. May be discontinued if TD occurs or later in disease where
bradykinesia is a bigger problem o Tetrabenazine: unknown mech; helps improve
symptoms * ?? �Depression/Anxiety: SSRIs * ?? �Swallowing/Aspiration: PEG tube
placement * ?? �Genetic counseling for family PseudodementiaDepression that mimics
dementia; typically, these pts will have dementia-like features but will often show
a lack of impairment with prodding. Classically, a patient who brings themselves
into your clinic complaining of dementia symptoms is depressed. Dementia pts are
unaware of their deficits. ?? o o o o o ?? Pseudodementia o Acute onset
'Sundowning' is uncommon Pts often answer "I don't know" to questions (may answer
properly when pressed) Pt aware of problem Antidepressants improve cognitive
functioning Dementia, by contrast: Insideous onset o o o o Vit. B12 (cobalamin)
deficiencyRemember that B12 has a complicated pathway of absorption into the body:
?? R-binder, stomach acid, intrinsic factor all play a role in transport/absorption
in the distal ileum A classic disorder resulting from several possible etiologies:
* ?? �Pernicious Anemia: antibodies against the parietal cells of the stomach (no
intrinsic factor produced) * ?? �Vegan diet: B12 is found primarily in animal
proteins; diet may restrict intake * ?? �Many others that will depend on the
clinical picture in the case Signs/Symptoms * ?? �Stocking-Glove peripheral
neuropathy (often an early sign) and Paresthesias * ?? �Beefy, smooth, sore, red
tongue (loss of papillae around edges) * ?? �Megaloblastic (pernicious) anemia and
hypersegmented PMNs * ?? �Premature hair whitening or yellow-waxy hair * ??
�Flabby/bulky frame, mild icterus, or blotchy skin pigmentation * ?? �Subacute
combined Degeneration: Demyelination of Dorsal Columns (loss of position, fine
touch, vibratory sensations)/corticospinal tract (major motor dysfunction is
usually the worse manifestation of disease * ?? �Progressive dementia and memory
loss are not uncommon to see, especially in long-term Dx: clinical suspicion,
taking B12 levels/consequences of B12 levels, MRI studies * ?? �Serum B12 <150
pmol/L * ?? �Total serum homocysteine >13umol/L or methylmalonic acid >0.4umol/L
* ?? �Folate deficiency may cause the anemia, but will NOT cause the neurologic
manifestations * ?? �MRI shows degeneration in the brain white matter of dorsal
columns/lateral pyramidal tracts Tx: replete Vit B12 (IM injection to bypass gut
absorbtion) with subsequent injections for storage Syphilis (Inc. Tabes Dorsalis
and Neurosyphilis) Signs/Symptoms: * ?? �Possible manifestations/history of
syphilis infection (may even be treated previously!)o Primary = characteristic
raised, painless lesion at site of infectiono Secondary = mucutaneous lesionso
Tertiary = endarteritis of small vessels, inflammatory neuron damage, gummas, tabes
dorsalis * ?? �Lancinating pain: a stabbing/shooting pain that�s classic of
neurosyphilis * ?? �Sensory ataxia: worse in the dark, often with a broad-based
gait and normal strength * ?? �Argyl-Robertson pupil: won�t constrict to light, but
will accommodate * ?? �Cerebellar dysfunction: Romberg sign can be (+) and can
contribute to gait * ?? �Dementia or other psychiatric manifestations Dx: clinical
signs/symptoms and history confirmed with testing * ?? �RPR/VDRL: often positive,
have questionable sensitivity for neurosyphilis; negative result prompts LP * ??
�LP: elevated protein, lymphocytes, VDRL(+), elevated IgG * ?? �FTA-ABS/TPHA/MHA-
TP: all specific tests for T. Pallidum, thus if these are negative then you know it
cannot be neurosyphilis; often these are done with high clinical suspicion but
negative prior testing Tx: * ?? �High-dose IV aqueous penicillin G (2-4million
unites, every 4 hours for 2 weeks) * ?? �Doxycycline + ceftriaxone is an acceptable
alternative if penicillin allergy 'Sundowning' is common (^confusion at night)
Confabulation is response to questions they cannot answer Pt is unaware of problem
Antidepressants do NOT improve cognitive function ?? Eradication is confirmed with
CSF testing returning normal; often neurologic losses are nor recovered fully, but
will not progress Note that HIV(+) pts have a much higher risk for contracting
syphilis and may result in an earlier presentation Normal Pressure Hydrocephalus
Idiopathic, non-obstructive hydrocephalus that typically affects the elderly. * ??
�Occurs episodically causing ventricular expansion and distortion of corona radiate
* ?? �Presentation: urinary incontinence, ataxia, cognitive dysfunction with
�magnetic gait� (feet stick to floor) with the classic �Wet, Wobbly, Wacky�
presentation * ?? �Often CT head with show abnormally large cerebral ventricles
HIV-associated DementiaProgressive cognitive function deterioration ether caused
primarily by the disease or by other infectious diseases due to immune-deficiency *
?? �Note that HIV is the most common infectious agent to cause cognitive impairment
* ?? �Worse prognosis with low CD4+, high viral titers, low body weight
Signs/symptoms: * ?? �Classic early sign is stumbling/tripping with poor
handwriting * ?? �Memory problems, poor concentration/attention are common
complaints * ?? �MRI shows diffuse atrophy of the the brain Dx: clinical suspicion,
positive HIV testing; rule out other causes ?? CT with an LP MUST be done, as HIV
can predispose to meningitis infections that could cause these signs/symptomsTx:
with HAART should prevent this from happening due to preventing HIV progression
Creutzfeldt-Jakob DiseaseRare, invariably fatal, rapidly progressive dementia ??
Thought to be caused by prion proteins, resulting in abnormal folding/degeneration
Signs/Symptoms: * ?? �Earlier signs: Rapid (within months) deterioration of memory,
personality changes, loss of coordination, poor judgement, and visual disturbances
* ?? �Later signs: changes/loss of vision, myoclonus, exaggerated startle reflex,
weakness, and coma Dx: * ?? �Rapid progression of clinical dementia symptoms * ??
�CT: normal; typically used to investigate stroke/tumor as this disease is so rare
* ?? �MRI: �pulvinar sign� seen in v-CJD on T2-FLAIR * ?? �LP: 14-3-3 protein found
in the CSF * ?? �EEG: periodic sharp wave complexes * ?? �Biopsy/Autopsy: only true
way to diagnose; may show spongiform changes and characteristic proteins Tx: no
treatment is effective; best to ease the pts symptoms and have strict protocols to
limit transmission (covering/protection, sterilizing all instruments to 269-273F)
Delerium ?? ?? ?? ?? Acute organ failure of the brain, characterized by below;
should resolve with underlying illness resolution Inattention/decreased level of
awareness/disorientation Acute development of cognitive deficits Symptoms fluctuate
throughout the day, worse at night Recent memory/language deficits R ?? Case 33 �
ObesityDiagnosis � most easily diagnosed via BMI (>30.0 is obese) with waist
circumference and truncal deposition of fat (�apple shaped figure�) increasing risk
for complications based on obesity * ?? �Labs: fasting glucose, fasting lipids,
TSH, liver enzymes * ?? �Search the body for acanthosis nigricans (a sign of
glucose intolerance) * ?? �Note that BMI is inaccurate in pts with heart failure
(H20 retention), pregnancy, body builders/pro athletes, and elderly patients
Pathogenesis � it really boils down to taking in more calories than expended.
Sadly, this is easy to do in our modern society. Obviously there are going to be
patients with glandular problems and on medications which make gaining weight
extremely easy. Don�t chalk up obesity to laziness. Often it�s more complex than
that. Treatment � recommended to start at [BMI 25 w visceral obesity] or increased
waist circumference (40cm in men and 35cm in women) * ?? �Diet/Exercise � creating
a 500-1000 cal/d produces a weight loss of 1-2lbs/wk (theoretically). Most diets
focus on creating a calorie deficit with exercise for 30min minimum 5-7day/wk.
Also, exercise without diet change is NOT effective. YOU CAN�T WORK YOUR WAY OUT OF
A BAD DIET. * ?? �Pharmacotherapy � used with BMI>30 or BMI>27 with comorbid
conditions (DMII, etc.)o Orlistat is the only drug approved by
the FDA for weight loss. It blocks pancreatic lipase and effectively stops you
from absorbing fat. You often get horrible steatorrhea (smelly greasy diarrhea;
thus nobody uses this awful drug) and Vitamin AEDK deficiencies * ?? �Bariatric
Surgery � used with BMI >40 with failure of diet/exercise or BMI >35 with co-morbid
cond. o Often pt must prove they will adhere to a special diet for weight loss
before the surgeon will perform the procedure. Many do not pass at this step sadly.
4164: Metabolic Syndrome [HIGH YIELD] * ?? �Syndrome characterized by the following
parameters:o Abdominal obesity (men >40inch waist, women >35 inch waist) o
Elevatedfastingglucose(>100-110mg/dL)o Mild hypertension (>130/80)o Elevated
triglycerides (>150 mg/dL)o Low HDL cholesterol (Men <40, women <50) * ?? �Insulin
resistance is central to the pathogenesis AND chronically high insulin levels has
huge effects on the body as a whole, which is thought to be the major cause of
these symptoms. Case 34 � HeadachesTension HeadacheYour classic headache.
Recurrent; bilateral/holocranial; tension sensation �like a vice�; ranges from 30
min � several days; lack of nausea/exacerbation by physical activity. * ?? �Dx:
clinical, although must be careful not to just lump any headache into this * ??
�Tx: NSAIDs/relaxation techniques; withdrawal from caffeine, barbiturates, and
NSAIDs may cause tension headaches so watch out for that! Migraine Headache
Overview: a super shitty headache. These are fairly common AND debilitating so
they�re important to know. ?? May be triggered by various things; classics are red
wine, cheese, chocolate, menses, and excess or deficiency of sleep (many, MANY
other things) Hallucinations/illusions (visual is most common) Disruption to
circadian rhythm Signs/symptoms: * ?? �Prodrome: often non-specific, but consistent
symptoms occurring hours-days before a migraine * ?? �Aura: typically precedes the
headache from 5min-1hr but not during. Visual auras (Scotomas, zig-zags, flashing
lights, or visual distortion) are most common. Numbness, tinginling, aphasias, and
hemiparesis may also occur * ?? �Headache: unilateral pain behind the eye/around
the ear (4-8hr in length) usually with pulsating/throbbing quality.
Photo/phonophobia are classic signs; pt typically wants to lay in a dark, quiet
room and sleep it offDx: typically, Hx alone can clue you in. Blood studies, ESR,
LP, and imaging are used mainly in ruling out other, more serious diseases that can
result in a headacheTx:Abortive therapy (stopping the migraine once it stops) * ??
�Triptans (all end with �-triptan�): 5HT-1D serotonin receptor agonists and most
effective therapy o Common side effects: N/V, numbness, tinglingo
Contraindications: concurrent ergotamine use, Hx of coronary artery disease/HTN
* ?? �Ergotamines: natural derivatives typically used if someone fails to respond
to triptans * ?? �Dihydroergotamine: similar to ergotamine but formulated for IM
and intranasal use * ?? �Midrin (acetaminophen, dichloralphenazone, isometheptene
mucate) for analgesia, muscle relaxation, and vasoconstriction (respectively); not
the most common drug, but a good alterantive Prophylactic therapy (stopping any
onset) � used with >3 migraines per month * ?? �Topiramate (anticonvulsant) is the
mainstay of therapy; concern of sedation/numbness/tinginling * ?? �Divalproex
(anticonvulsant) an alternative but may have worse side effect profile * ?? �Beta-
blockers (propranolol) � a classic treatment but not the best tolerated in patients
with normal blood pressures (concern of syncope) Cluster Headaches ?? Symptoms: o
Pain is ALWAYS unilateral, frontal, retro-orbital (�side locked�); may recur up to
8 times a day o Called �cluster� because these pop up over a course of weeks then
go away for months-years o Pain is constant, severe, non-pulsating pain (bad enough
to cause suicide) - sometimes described as �a hot poker in my eye�o Makes patients
restless and pace around the room or even banging head against the wall! o May have
unilateral conjunctivitis, rhinorrhea, Horner�s syndrome ?? Treatment:o Acute:
subcutaneous sumatriptan with 100% nasal oxygen at 6L/mino Prophylaxis: verapamil
(Ca2+ channel blocker), lithium, valproic acid, prednisone Chronic Headache
Basically any kind of headache that is occurring chronically/persistently (pt
affected >15 days per month) * ?? �Migraine/tension headaches are commonly chronic
* ?? �Occipital neuralgia: headache from inflammation of the greater occipital
nerve (runs off cervical plexus from C2 to innervate much of the posterior
neck/head). Often bilateral and tender to palpation. May be severe and patient
perceives pain behind the eyes. * b �Analgesia rebound (from long term NSAID use)
is a classic reason to get a persistent headache. It�s important to note pts
prescribed and OTC drug history when evaluating persistent headache and to get pt
off all analgesia if this is the case Non-medical treatment * ?? �Physical therapy
with head/neck rehabilitation * ?? �Massage therapy has also been helpful in
relieving tension Medical treatment * ?? �Removal of all OTC analgesics (concern of
analgesia rebound) * ?? �Addition of anti-headache therapies (triptans, ergots,
topitamate, b-blockers, etc.) all can aid in resolving these headaches * ??
�Typically, anti-convulsants have the greatest success rate for daily chronic
headaches Epidural HematomaDefined: bleed between the dura and the skull, typically
from a traumatic injury ?? Commonly the middle meningeal artery (temple area) is
damaged causing the bleed Signs/symptoms: * ?? �Classic is trauma (knocked out),
with lucid period, then rapid deterioration/confusion * ?? �Headache, N/V,
pupillary abnormalities, lower GCS, or increased ICP can all presentDx: trauma with
evidence of �lens-shaped� bleed with smooth margins/does not cross suture lines on
CT * ?? �Check CBC/PT, PTT/Fibrin products to better understand bleeding tendencies
* ?? �Air in the epidural hematoma suggests rupture of mastoid air cellsTx:
stabilize (ABCs), supportive therapy, and reduction of ICP to stop herniation * ??
�CT is always the first step of management * ?? �Elevation of the
head/Trendelenburg position to increased venous drainage of the head * ??
�Consultation of neurosurgery for evacuation/repair Subarachnoid HemorrhageDefined:
hemorrhage within the brain resulting in abrupt onset of neurologic symptoms * ??
�Sentinel Bleed: intermittent smaller hemorrhages/headaches preceding full blown
hemorrhage often occuring with physical/emotional strain, defication, sex, or head
trauma * ?? �Most common etiology is a ruptured saccular (berry) aneurysm (also has
worst prognosis) so risk factors for developing aneurysm are risk factors for this
hemorrhage (PKD, marfans, HTN, diabetes, mycotic aneurysms, oral contraception,
etc.) * ?? �Aterio-venous malformation, cocaine/amphetamine use, or trauma may also
cause them * ?? �Typically occur in anterior communicating artery or carotid artery
bifurcation * ?? �Up to 60% of pts die in the first month following the hemorrhage
Signs/symptoms: sudden onset of �worst headache of my life� with focal deficits or
altered consciousness Dx: * ?? �CT: bleeding within brain parenchyma indicates
acute hemorrhage * ?? �LP: blood and xanthochromia indicates active bleeding into
the CSF * ?? �Transcranial Doppler/CTa/conventional angiography: may show the
aneurysm in question Tx: * ?? �If neurosurgery is required: Angiography must be
done to localize the aneurysm/bleed * ?? �Endovascular coiling � superior to
clipping and can be used at any time * ?? �Clipping � needs to be used within 48hrs
or after 2 weeks post-hemorrhage (timeframe in-between has a high risk of
vasospasm, thus we�re trying to avoid that) * ?? �Triple H (hypertensive
hypervolemic hemodilution) therapy with nimodipine � give aggressive fluids to keep
perfusion up; the calcium channel blocker is to reduce vasospasm Intraparynchmal
(incracranial) hemorrhage Bleeding within the brain tissue parenchyma o
Presentation: severe headache, N/V, comao Trauma - the most frequent cause; a blow
to the head causes blood vessel rupture o Hypertension - a very common cause (some
stats say it�s the most common) ???Charcot-Bouchard aneurysm - small vessel
aneurysm in the brain from HTN * ?? �Usually occur in lenticulostriate vessels (not
seen on angiogram) * ?? �Typically causes hemorrhage in the basal ganglia/thalamus
???Treating the HTN will reduce hemorrhage risk by 50%o Arteriovenous malformation
- these misshapen vessels have a tendency to rupture/bleed ???Treat with
obliteration with coiling or surgical removal Epidural hematomaRupture of middle
meningeal artery (maxillary artery branch) often secondary to a skull
trauma/fracture (temple area)??high pressure hematoma o Presentation: * ???
�Traumatic injury with possible temporary loss of consciousness * ???�Lucid period
(up to 48 hours) with headaches, nausea, hemiparesis * ???�Rapid expansion may
cause transtenorial herniation (LOC, respiratory depression, death) or CNIII palsy
(down and out gaze) from compression o Labs: * ???�Head CT showing lens-shaped bi-
concave hyperdensity not crossing suture lines o Treatment ???Surgical: immediate
evacuation/pressure relief of bleed ???Medical: treat the raised ICP (mannitol,
hyperventilation, steroids, ventricular shunt) Giant-cell Temporal Arteritis
Granulomatous arteritis affecting medium-large arteries classically in people >age
50 in the extracranial carotid branches (ophthalmic, temporal, etc.) * ??
�Symptoms: jaw claudation with chewing, amaurosis fugax, fever, weight loss,
fatigue, �hard� prominent temporal artery * ?? �Feared complication is anterior
ischemic optic neuropathy causing irreversible blindness * ?? �Dx: elevated ESR,
elevated
C-Reactive Protein, segmental biopsy of temporal artery showing granulomatous
vasculitis (normal biopsy does NOT exclude this disease) * ?? �Tx: immediate high
dose prednisone (corticosteroid) to preserve vision Suspected Meningitis
Sign/Symptoms: classic triad of headache, fever, and neck stiffness * ??
�Macropapular rash??suspect Neisseria gonorrhea * ?? �Kernig�s sign/Brudzinki sign
are classics indicating meningitis Tx: 1. Initiate empiric antibiotic/antiviral
Tx??IV ceftriaxone + IV vancomycin + IV acyclovir and if pt is a child +
dexamethasone (steroids avoid the possible deafness/other losses seen in children)
2. Schedule STAT CT (check for masses/abnormalities) and lumbar puncture with
opening pressure a. Note that papilledema means there�s increased ICP, meaning
there is a higher suspicion of brain mass, thus a CT MUST be performed due to risk
of LP causing herniation 3. If etiology not confirmed, look for things like
fungi/TB as causative agent 4. Alter treatment based on confirmed etiology with
supportive care Disease Cell Protein Glucose Other Findings Bacterial Meningitis
PMNs (neutrophils) High Low Culture/Gram stain may be positive Viral meningitis
/Encephalitis Lymphocytes High Normal Viral PCR may be positive Pseudotumor Cerebri
(idiopathic intracranial hypertension)Classically found in young, obese women of
child-bearing age; sometimes with menstrual irregularity * ?? �CT with contrast:
Slit-like ventricles, enlarged optic nerve sheath, empty sella * ?? �High volume LP
(pt laying on side) shows increased opening pressure with normal CSF * ??
�Papilledema noted on funduscopic exam (vision greying out/obscuration are common
signs) * ?? �Other focal neurologic signs may be present o Headache: diffuse, worse
in morning, worse with Valsalva maneuver o N/V, 6th neve palsy, tinnitus, diplopia,
and others are all possible Tx: * ?? �Emergent: high volume lumbar puncture to
acutely lower ICP * ?? �Long-term: acetazolamide (carbonic anhydrase inhibitor;
will result in increased respirations, lowering ICP) or nerve sheath fenestration
surgery or shunt placement (aid in CSF drainage) Medication related headacheDon�t
forget to review medications and how the patient is using them when they complain
of headaches! Classically a medication overuse or �rebound� headache can occur with
NSAIDs, Acetaminophen, Aspirin, Caffeine use, and many other medications! Case 35 �
High CholesterolHigh cholesterol is NOT a disease in itself, but is a major
modifiable risk factor for CHD * ?? �A high cholesterol should be interpreted
within the context of overall coronary heart disease risk * ?? �Those with higher
overall risk will have more aggressive cholesterol goals * ?? �Typical cholesterol
levels: o LDL cholesterol (the bad one) optimal level is <100 mg/dL o HDL
cholesterol (the good one) optimal level is >40 mg/dL o Total cholesterol desirable
levels are <200 mg/dL * ?? �Adults older than 20yr should have lipids checked every
5 years by a fasting lipid panel Determining an LDL cholesterol goal * ?? �Based on
listed risk factors below: o Cigarettesmoking o Hypertension (either >140/90 or
currently on any medication for hypertension) o Low HDL (<40 mg/dL)o Age >45 for
men, >55 for womeno Family Hx of CHD * ?? �Note that a high HDL (>60 mg/dL) is a
�negative risk� which neutralizes any one of the risk factors Risk Categories and
LDL goals * ?? �CHD or equivalent present: <100 LDL; medications used if LDL >130 *
?? �2+ risk factors: <130 LDL; medications used if >160 * ?? �0-1 risk factors:
<160 LDL; medications used is >190 * ?? �CHD and multiple risk factors: <70 LDL;
medications always used here Management * ?? �Best to initiate therapeutic
lifestyle goals (smoking cessation, lower dietary cholesterol/saturated fat,
increased dietary plant fiber, etc.) before needing medications * ??
�Pharmacotherapy is used when a patient cannot meet their goals with TLCs alone o
�Statins� (HMG-CoA reductase inhibitors) � vvvLDL, ^HDL, vTRI ???
hepatotoxicity/myopathy (esp. with fibrates/niacin) o �Choles� (Bile Acid Resins) �
vvLDL, HDL, TRI ???diarrhea/Vit AEDK deficiency o Niacin (Vit. B3) - vvLDL, ^^HDL,
TRI???Flushed face (aspirin blocks it), hyperglycemia/hyperuricemia o �Fibrates�
(Fibric Acids) � vLDL, ^HDL, vvvTRI???gallstones, myopathy (esp. with
fibrates/niacin) o Ezetimibe (Cholesterol absorption blocker) � vvvLDL, ^^HDL, vTRI
2698/3823/4336: Guidelines for Lipid-Lowering therapy (typically a statin) * ??
�Symptomatic atherosclerotic disease??high or low intensity based on age (> or <
than 75yr) * ?? �LDL >190mg/dL??high intensity statin therapy * ?? �Age 40-75 with
diabetes ???high or low depending on 10-year ASCDV risk * ?? �Estimated 10-year
ASCVD risk >7.5%??moderate to high intensity statin therapy [Note that the
difference between statin intensity is the dose] 3822: (refer to 2698) A patient
with Type II Diabetes Mellitus over the age of 40 should always be on a statin and
initiate positive lifestyle changes according to lipid lowering guidelines. Refer
to 2698 for the complete guidelines. 4227: Statins inhibit HMG-CoA reductase thus
decreasing intrinsic cholesterol synthesis??forcing increased cholesterol uptake
from blood to meet demands on the liver. Side effects include: * ?? �Myalgias �
common, may have increased creatine kinase; thought to be due to decreased CoQ10
synthesis which is necessary for muscle energy production * ?? �Liver dysfunction �
rare but serious 3158: There are two major side effects of statin therapy and
they�re both have lab values: * ?? �Muscle damage: elevated CPK with myalgias which
may progress to severe rhabdomyolysis and renal failure (would acutely raise BUN
and Creatinine). Stop the statin if this happens * ?? �Liver damage: not as
pronounced usually, but can cause elevated liver transaminases (ALT/AST). Usually
these will trend back to normal with stopping the statins. Case 36 � Family
Violence Intimate Partner Violence * ?? �Obviously spousal abuse doesn�t just
happen to women, but can happen in any relationship * ?? �Regular screening for
this type of abuse is recommended at any regular checkup/gynecologic exam * ??
�Some Physical Signs of Abuse include o Contusions, fractures, black eyes, internal
bleeding; esp. if treatment seeking is delayed o New STI, anal/pharyngeal trauma,
or unintended pregnancyo Emotional distress, new depression/anxietyo Chronic
abdominal pain, new substance abuse or eating disorder * ?? �When asking about
violenceo Use direct questioning with the patient in the room without the abuser o
Offer resources/numbers to call in a non-directive way * ?? �Reporting varies by
state, but apparently Tennessee mandates suspicion of intimate partner violence to
report such suspicions to proper authorities Child Abuse * ?? �Often unthinkable to
a reasonable person, there are several things that could cause an increased risk
for abused of a child including parental depression, substance abuse, social
isolation, stress, low income, poor access to recreational services * ?? �Some
signs of child abuse: o
Aggression,anxiety,bedwetting,depression,regression,advancedsexualplayo Burns:
Stocking-glove burns, buttock/genital burns, cigarette burnso Shaken baby syndrome:
Retinal hemorrhage, lethargy, spinal/neck traumao Fractures: �bucket-handle
fractures�, �Spiral fractures�, posterior rib fractures, scapular fractures,
spinous process fractures, sternal fractures, complex/big skull fractures o Sexual:
genital injury, STI or genital warts, circumferential anal hematoma ?? You ALWAYS
report child abuse if in good faith, no matter what. Elder Abuse * ?? �Typically as
physical/sexual/psychologic abuse, neglect, or financial exploitation * ?? �Women
>75yr and those cognitively/physical impaired are at highest risk * ?? �Best to
interview elder alone to try and assess abuse Case 37 � Limping/Leg Pain in
Children Diagnostic Approach * ?? �Pain vs No Paino Pain � start exam focused on
that area, then branch out from there o No pain � examine the back, pelvis,
buttock, leg, and foot * ?? �Evaluation of the hip is MOST important as the hip is
the most likely to need emergent eval. o Restricted internal rotation of the hip �
most sensitive marker of hip pathologyo Lack of abduction � 2nd most sensitive
marker for hip pathology * ?? �After localizing pain/likely spot of pathology x-ray
imaging and labs should be soughto Infection or Rheumatologic cause suspected �
CBC, CRP and ESRo Gonorrhea testing of aspirated fluid in teens or Lyme disease in
endemic is OK to do * ?? �Limping without paino Leg length discrepancy (measure
umbilicus to medial malleolus)o Muscle atrophy/limb deformity or congenital
malformation (inspection/movement) Infants/Toddlers * ?? �Septic arthritis �
crying/irritability/fever, monoarticular with swelling/heat from joint. Often child
refuses to bear weight on affected joint (increased swelling/pressure in joint
capsule!) o Labs � elevated WBCs, reactive ESR/CRPo Micro � GBS/Staph (<4mo);
Staph/Strep (<5yr)o Dx � joint aspiration with gram stain/culture o Tx � urgent
surgical irrigation, debridement, and antibiotic Tx * ?? �Fractures � acute onset
of limp or simply refusal to walk/bear weight on injured bone o Screening for abuse
is clever, but Hx may not reveal much o Dx � plain film of suspected area of
fractureo Tx � immobilization for healing * ?? �Congenital Dysplasia � painless
limp/odd ambulation from time child learns to walk o
Allchildren�shipsshouldbeexaminedfordysplasia/stability/deformityo
Dx�plainfilmsshowingmisalignmentofthehips o Tx � if early, splinting for alignment;
if late, surgical correction Young Children * ?? �Transient Synovitis � self-
limited inflammation, classically of the hip, in children ages 3-10yr typically
following a viral infection o Labs � no fever, normal CBC, normal ESR/CRP and
normal X-rayo Dx � clinical presentationo Tx � watch with followup; should resolve
within a few days, although a septic joint may develop o Kocher Criteria for Septic
Arthritis Risk in Children ???Septic � Aspirate is purulent, WBC count >50,000/mcL
???Transient synovitis � Aspirate is yellow/clear with WBC count <10,000/mcL * ??
�Legg-Calv�-Perthes disease � avascular necrosis of the head in boys ages 4-8yr of
unknown origin o Gradual onset of hip/knee/thigh pain and limping over a few months
o X-ray � normal??collapse/flattening/widening of femoral head with inflammation o
MRI � necessary to confirm inflammation and make diagnosiso Tx � conservative
treatment with therapy to maintain range of motion Adolescents?? Slipped capital
femoral epiphysis � slipping of the growth plate causing displacement
medially/posteriorly often without acute injury. Often in overweight adolescent
boys o Limited internal rotation with obligate external rotation upon hip flexiono
X-ray � epiphysis widening??slippage of the femoral heado Tx � surgical pinning of
the femoral head to stop slippage ???1/3 will develop avascular necrosis of hip ???
1/3 will develop SCFE in the contralateral hip * ?? �Sprain/strains/overuse
injuries � the most common cause of limb pain in this population * ?? �Gonococcal
arthritis � get a sexual history and aspirate the joint if necessary Any Age * ??
�Pain at night � suspicious for malignancy * ?? ��Growing pains� � a dx of
exclusion that occurs only at night (NOT DURING DAY) bilaterally in the absence of
any other pathology Case 38 � Post-Operative Fever Drug Fever (Any Time) * ??
�Classically associated with rash or Lupus-like symptoms; may involve any organ
* ?? �Drugs Associated: o Antibiotics (1/3 of cases): minocycline, cephalosporins,
floroquinolones, sulfa drugs, penicillins o May happen with ANY drug; typically
more drugs = more chance to occur * ?? �Often resolves within 72-96hr after
stopping the offending drug Surgical Trauma (within 24hr) * ?? �Cutting stimulates
cytokine release, thus bigger surgeries have a higher risk for this type of fever *
?? �Often mild, but NSAIDs or steroids can help increase patient comfort Malignant
Hyperthermia (within 24hr) * M �Rare autosomal dominant disorder causing severe
reaction to anesthesia (halothane and succinylcholine are classics associated with
this reaction) * ?? �Fever (104oC), tachycardia, metabolic acidosis,
rhabdomyolysis/muscle rigidity * ?? �Treated with � stopping anesthesia, physical
cooling, IV dantrolene, O2 supplementation, antipyretics Bowel Leakage of Flora
(within 36hr) * ?? �Can invade the peritoneum resulting in a soft tissue infection
* ?? �Major signs/symptoms will be from specific bug causing infection Toxic Shock
Syndrome (within 36hr) * ?? �Bacterial infection (S.aureus most common) with Toxic-
Shock Toxin-1 (TSST-1), a super-antigen that results in massive T-cell
activation/cytokine release, resulting in loss of intravascular fluids to the
extravascular spaces and shock! * ?? �Presentation: rapid development of high
fever, Hypotension (<90 systolic), diffuse red/edematous rash (looks like sunburn),
skin desquamation of palms/soles, multisystem failureo Classically (50%) associated
with a tampon left in post-menstruation, typically arising 2-3 days after the last
menstrual period o Non-menstrual infections can also cause it (post-surgery,
sinutitis, etc) * ?? �Dx: clinical syndrome with history * ?? �Tx: supportive
therapy for shock, removal of foreign materials causing infection, anti-staph
(penicillin + vancomycin) are all part of treatment Pneumonia (within Day 5) * ??
�Often atelectasis (alveolar collapse) can occur after surgery leading to pulmonary
complication, especially in those with lung conditions (COPD, asthma, smoking, old
age, etc.) * ?? �Anesthesia and narcotic use can also decrease a patient�s
breathing, thus increasing pulm. Risk * ?? �Patients on ventilators are a HUGE risk
for VAP (considered a hospital complications) * ?? �Aspiration may occur in
patients with GERD or difficulty swallowing (gram negative bugs) UTI (within Day 5)
* ?? �Increased risk with difficulty voiding; if patient is catheterized, it needs
to be discontinued * ?? �Often IV antibiotics are used, esp. in patients with
complicated UTI DVT/PE (Day 5) * ?? �DVT: Often asymptomatic but classically with
leg tenderness, pain, warmth, and asymmetry * ?? �PE: often with pleuritic chest
pain and rapid-onset SOB * ?? �Prevented with compression stockings/anti-
coagulation Surgical Site Infection (Day 5 � 7) * ?? �Local erythema, discharge,
pain, purulent discharge at the site of incision * ?? �Prophylactic Abx (1hr before
operation; discontinued within 24hr) can decrease the risk * ?? �Sterile technique
and careful operating procedure in the OR is the other way to reduce risk Abscess
(Day 10 � 15) * ?? �Pretty much the same as an SSI, but with fluctuant mass that
needs drainage * ?? �Rare, but fever may be the presenting sign IV or Catheter
Infection (3 Days or More present) * ?? �Basically these are great sites for bugs
to crawl in and set up infection * ?? �IV/catheter sites should be assessed EVERY
DAY for signs of infection and removed ASAP when not necessary anymore. The chance
for infection is proportional to the time the line is left placed. * ?? �If
infection is suspected, line is discontinued IMMEDIATELY and the tip is cultured
for diagnosis Specific Risks of Specific Surgeries * ?? �Laproscopic surgery �
lowest risk of infection due to minimal invasion * ?? �Cardiothoracic surgery � all
patients will develop pleural effusion due to incision (5% get pneumonia) * ??
�Abdominal surgery � deep abdominal abscess & pancreatitis * ?? �OBGYN surgery �
post-op endometritis, pelvic abscess, pelvic thrombophebitis * ?? �Orthopedic
surgery � highest rate of surgical site infection * ?? �Urologic surgery �
prostatic/perinephric abscess * ?? �Neurosurgery � increased DVT due to
immobilization/less aggressive anticoagulation (protect brain) 3950: Cholesterol
Crystal Embolization typically occurs after cardiac catheterization or recent
vascular procedure in the setting of cardiovascular risk factors. * ?? �Features:
livedo reticularis, ulcers/gangrene, blue toe syndrome, renal injury, stroke,
Hollenhorst plaques (in the eye), GI ischemia/pancreatitis * ?? �Dx:o Labs:
elevated creatinine (renal damage), eosinophilia/eosinophiluria, hypocomplementemia
o Skin/renal biopsy: biconcave, needle-shaped cholesterol clefts in occluded
vessels and perivascular inflammation with eosinophils 2310: After and MI
successfully treated with cardiac catheterization, there�s a good chance,
especially with risk factors, that cholesterol plaques could rupture and send
cholesterol emboli showering throughout the body causing ischemia. This can be
manifested through livedo reticularis, blue toe syndrome, renal failure, gangrene,
ulcers, Hollenhorst plaques (yellow, shiny plaques in the retina), stroke, or GI
bleeding. * ?? �Tx: statin therapy with support for any other problems * ?? �May
happen immediately or delays (up to 30 days after) Case 39 � Wheezing in Children
(NOT asthma) Case 40 � Irritable Bowel Syndrome (IBS)Typically affects women 2-3x
more than men often occurring in teens/20s Has an odd relationship with psychiatric
illness, where IBS is often worsened by psych illness?? Treating psych illness can
often improve IBS symptoms but will not resolve them completely 4595: Irritable
Bowel Syndrome (IBS) * ?? �Common functional GI tract disorder with no identifiable
cause. A diagnosis of exclusion * ?? �Presentation: chronic, crampy abdominal pain
with alternating episodes of constipation and diarrhea. Passage of stool relieves
the pain. o Classically occurs in young womeno Alarm signs (rectal bleed, severe
pain, weight loss, or abnormal labs) should be investigated further as they point
toward something else, NOT IBD * ?? �Dx: Rome III criteria o Recurrent abdominal
pains for >3 days per month o Two of the following: ???Symptoms improve with bowel
movement???Changes in frequency of pooping???Changes in forms of poop
(diarrhea/constipation) * ?? �Tx: Diet-adjustment & treat symptoms (diarrhea =
anti-diarrheals; constipation = fiber or laxatives) Case 41 � Substance Abuse �
likely the worst written chapter in this book; my notes are from psych rotation
Alcohol Intoxication ?? ?? o ??????o Drunk ??????o ???o o ?????????o Scan: ???o
???????? Works as a CNS depressant via: Activating GABA/DA/serotonin & Inhibiting
glutamate ?? Depends on Blood Alcohol Level (BAL) Buzzed 20-50: decreased fine
motor control 50-100: impaired judgement/coordination 100-150: ataxia and poor
balance 150-250: lethargy, slumped position, anterograde amnesia, nausea/vomiting
Alcohol Poisoning Treatment 300 or more: respiratory depression, coma, death
Monitor: airway, breathing, circulation, glucose, electrolytes, acid-base status
Give: Thiamine (B1)/Folate to prevent Wernicke's encephalopathy (FIRST THING TO DO)
Naloxone as opioids are commonly co-ingested with alcohol with alcoholics D5
dextrose with electrolytes CT to rule out brain damage/bleed Support: Mechanical
ventillation if pt is respiratory depressed GI evacuation only if significant
amount of EtOH was ingested within last 30-60 minutes Alcohol Withdrawal Onset
between 6-24hr of last drink lasting 2-7 days (depends on severity of alcoholism) o
o o ?? o o o ?? Tx:o o o ??????o ?????????o o ?? o ?????????o Marijuana ?? o o o ??
o o ??????o Tx:??????Mild: irritability, tremor, insomnia Moderate: Sweating, HTN,
tahycarida, fever, disorientation Severe: Seizures, Delerium Tremens,
Alcoholic Hallucinosis Time since last drink: 6-24 hr: Present with alcohol
withdrawal symptom 12-48 hr: withdrawal may cause tonic-clonic seizures
(hypomagnesemia may precipitate this) 48-96 hr: delerium tremens may occur Mild
agitation: Benzos with slow taper (keep patient calm/lightly sedated) Severe
agitation: Benzos with possible antipsychotics and physical restraints Support:
"Banana bag" - thiamine/folate/multivitamin Monitoring: Correction of any
fluid/electrolye abnormalities Use CIWA scale to monitor withdrawal symptoms Check
for any trauma/brain damage Check for hepatic failure Tx for Alcohol Abuse First
line for drug aid: Naltrexone (Revia, IM-Vivitrol) - opioid antagonist; decreases
craving/"high" of alcohol consumption Acamprosate (Campral) - glutamate modulator;
used post-detox to prevent relapse; OK in liver disease, NOT OK in renal disease
Second line for drug aid: Disulfiram (Antabuse) - blocks aldehyde dehydrogenase
causing flushing/nausea/vomiting with alcohol consumption. Contraindicated in heart
disease, pregnancy, psychotic episodes LFTs must be monitored Only use in highly
motivated patients Topiramate (Topamax) - potentiates GABA/inhibits glutamate
receptors; reduces alcohol cravings ?? Intoxication Euphoria, perceptual
disturbances, conjunctival injection (red eyes), increased appetite ("munchies"),
dry mouth Hallucinations may occur Anxiety/paranoia may occur in the naive user
Overdose/Chronic Use You can't seem to overdose on cannabis Chronic Use Found in
50% of daily users If smoking: chronic bronchitis/asthma Any route of
administration: immune system suppression, decreased reproductive hormones, cancer
?? Withdrawal Support/psychosocial intervention Treat any other condition
precipitated by use o Irritability anxiety, restlessness, strange dreams,
depression, insomnia, decreased appetite Cocaine?? Intoxication o o o o o ?????????
?? Withdrawal o o o o 4042: Any person (especially younger) presenting with
agitation, dilated pupils, atrophic nasal mucosa, HTN, and acute myocardial
ischemia should be suspected for cocaine abuse! * ?? �a/B adrenergic stimulation =
HTN/pupil dilatation/agitation/ischemia * ?? �Cocaine also potentiates thrombus
formation o Cocaine + alcohol = cocaethylene??increased risk of coronary vasospasm
* ?? �Tx: immediate benzodiazepines/O2 + aspirin, nitrates, calcium channel
blockers * ?? �NEVER GIVE A B-BLOCKER: it will cause unopposed a-adrenergic
activity and HTN crisis! Amphetamines ?? o o o o ?? o o ?? o Opioids ?? o o o
Mimics a fight or flight response or a manic state General: euphoria, high self-
esteem, low/high blood pressure, tachy/bradycardia, dilated pupils, agitation,
chills/sweating Dangerous: Respiratory depression, seizure, arrhythmia,
hyperthemia, paranoia, hallucinations (tactile; �cocaine crawlies�) Deadly: intense
vasoconstriction causing MI/stroke/intracranial hemorrhage Tx: Mild:
reassurance/benzodiazepines Severe/psychosis: benzo/antipsychotics Post-
intoxication "crash" - malaise, fatigue, hypersomnolence, depression, anhedonia,
hunger, constricted pupils, vivid dreams, suicidality NOT life threatening
(remember how stimulant drug withdrawal is awful, but won't kill you?) Should
resolve within 3 - 14 days depending on use May need hospitalization for supportive
measures Intoxication Similar to cocaine (due to shared DA/NE increase); euphoria,
dilated pupils, tachycardia, diaphoresis, chest pain Unique feeling of
closeness/love with others, ^libido Teeth grinding Overdose Tx: Rehydration,
electrolyte correction, hyperthermia treatment if necessary Hyperthermia,
dehydration (esp. in a hot club), rhabdomyolysis, renal failure Withdrawal Ongoing
psychosis (due to long half-life) Prolonged depression Intoxication Symptomatic
support: control blood pressure (cautious with alpha-blockers), arrythmias
(cautious with anti-arrythmatics), high fever (aggressive with ice-bath, cooling
blanket, other supports) Constricted pupils, respiratory depression, constipation,
altered mental status, nausea/vomiting May progress to coma/death in OD Tx
?????????o o o ???o????o o o o o ?? o o ????????????o Inhalants ?? o o o ?? o ??
Tx:o o Hallucinogens ?? o o o PCP ?? ?? Withdrawal Ensure ABCs are intact
Ventillatory support if necessary Naloxone (opioid antagonist) for overdose (may
precipitate withdrawal!) Dysphoria, insomnia, lacrimation/rhinorrhea, sweating,
goose-bumps, dilated pupils, abdominal cramping, myalgia/arthralgia, HTN,
tachycardia, intense cravings Unpleasant, but NOT life threatening Tx While not
life-threatening, it's quite horrible, so we try to help pts get through it
Moderate symptoms: manage with common drugs Severe symptoms: Detox with Methadone
(long acting opioid agonist)/buprenorphine (partial opioid receptor agonist)
Intoxication Depersonalization, hallucinations, impaired judgement, amnesia,
ataxia, muscle rigidity, dysarthria Synesthesia (Sensory mixing: hearing a sound
produces a visual color) Agitation/aggression/assault/high pain tolerance (often
violent seemingly 'immune to pain') Overdose Nystagmus (rotary is most
characteristic, can also be vertical or horizontal) Hallucinations (visual and
tactile) Seizure, delirium, coma, death Tx: ?? Monitor vital
signs/temperature/electrolytes Minimize sensory stimulation Benzodiazepines to
treat agitation/muscle spasms/seizure Antipsychotics for severe agitation/psychoses
Withdrawal Intoxication Only lasts 15-30 minutes typically Perceptual disturbance,
paranoia, lethargy, dizziness, headache, hypoxia (if breathing in a lot), stupor,
coma, etc. (CNS depressant) Typically used by teenagers (easy substances to access)
Overdose Respiratory depression/cardiac arrythmia (fatality) Intoxication None; but
pt may have "flashbacks" due to storage of drug in adipose with gradual release
ABCs, may need hyperbaric oxygen if hypoxia is present Identify the inhalent as it
may need chelation (leaded gasoline is a good example) Perceptual changes
(illusions, hallucinations, synesthesia) Labile affect, dilated pupils,
tachycarida, HTN, hyperthermia, sweating, palpitations High typically 6-12 hours
but can last for days o ?? o o Case 42 � Heart Palpitations Workup ???
History/Physical (don�t forget psych screening, caffeine/drug use!)???12-lead EKG??
if abnormal a 24hr Holter monitor/echocardiogram/stress test may be used ???Labs:
CBC, BMP, urine drug screen, TSH/T3 Primary Rhythm Disturbances � 41%?? Paroxysmal
Supraventricular Tachycardia (PSVT) o Abrupt onset of tachycardia (60-200 bpm)
sometimes with quick movement or in response to atrial fibrillation (A-fib with
RVR!) o Must rule out arrhythmias with an EKG before calling this benign * ??
�4894: Wolff-Parkinson White syndrome occurs due to an abnormal accessory pathway
(bundle of Kent) that connects the atria/ventricles, by-passing the AV node. This
causes pre-mature ventricular excitation (delta wave of the ECG), and can result in
a re-entrant circuit resulting in supraventricular tachycardia (chest fluttering or
palpitations are usually described by the patient) and possible sudden death. * ??
�3069: In Wolff-Parkinson-White (WPW) syndrome, an abnormal accessory pathway
between the atrial and ventricles that bypasses the AV node (slow down for
coordination) is present o Atrial fibrillation is a common, and possibly deadly,
arrhythmia in WPW; the quick atrial depolarization means you�re getting consistent
quick ventricular impulses due to the accessory pathway. Thus AFib can deteriorate
in the ventricular fibrillation??sudden cardiac arrest! o Tx:???Hemodynamically
unstable??immediate electrical cardioversion???Hemodynamically stable??IV ibutilide
or procainamide for rhythm control are used ?? Brugada syndromeo Autosomal dominant
genetic disorder Na+ channelopathy o Often recognized in Asian males, average age
40 ???Usually you get ventricular tachycardia causes while asleep (Lai Tai) ???
Causes syncope or sudden cardiac deatho Malfunctioning Na+ channels cause blunted
sodium currents * ???�Shortened/failed action potentials or conduction block * ???
�This gives a greater risk for the potential to �loop back in on itself�, causing a
recurrent stream of firing called re-entrant ventricular tachycardia. This is
essentially because the impulse is small and you get a faster recovery and second
firing.o Generally an abnormal EKG is found at rest called �coved type Brugada
pattern� ???Persistent >2mm elevated ST segments in V1, V2, V3 ???Right bundle
Branch Block???Inverted T-waves present in some leads???J-point elevation
Withdrawal A "bad trip" is a high consisting of anxiety, panic, or psychoses No
real withdrawal symptoms "LSD flashbacks" may occur later in life spontaneously o A
ICD defibrillator that will automatically shock the patient�s heart is the
treatment to reset this arrhythmia ?? Long QT intervalo Remember! The QT interval
is the phase when the ventricle contracts and relaxes o Present more often in
childhood; while kids are playing/exerciseo This interval (QTc) should last 0.44
secondso Many things can cause this to happen (IHD, Low K, Ca, Mg, channelopathy,
others) o We see a pathologic increase in phase 2 ventricular contractiono Three
different major types: * ???�Congenital long QT Type 1 (LQT1) �IKS channel fail to
open (no outward K+) * ???�Congenital long QT Type 2 (LQT2) � IKR channel fail to
open (no outward K+) * ???�Congenital long QT Type 3 (LQT3) � INa channel fail to
close (too much Na+ in) o The variable repolarization time screws up coordination
causing ventricular tachycardia o Characteristically we see a torsades de points
(twisting around points) pattern on EKG due to early after-depolarizations
from multiple sites o A ICD defibrillator that will automatically shock the
patient�s heart is the treatment to reset this arrhythmia ?? Sick Sinus Syndromeo
Arrhythmias due to SA node dysfunction, typically from valvular
disease/cardiomyopathyo Typically pt has sinus bradycardia, which can lead to
arrhythmia although other variants are possible ?? Premature Ventricular
Contractions (PVCs)o Benign, but abnormal contractions where the ventricle fires
too early, leading to a �fusion beat� o Can be part of normal variation but if
several of these are occuing consistently, a more thorough cardiac workup should be
sought Mental Health Problem � 31% * ?? �Likely there are more than outlined below,
but these are common ones to cause panic palpitations * ?? �Panic Attack o
?????????o ??????????????????A sudden surge of anxiety, which may be triggered or
spontaneous intensity peaks within a few minutes resolves within 30 minutes
anxiousness may persist for hours after attack is resolved Symptoms Dizziness,
detachment from self/reality Heart palpitations/chest pain Shortness of breath
Abdominal distress/nausea Fear of going crazy/losing control Sweating, chills,
shaking o It can look a lot like a heart attack! But the EKG/proteins will be
normal * ?? �Panic Disorder o ????????????o o ?????????o ?????????* ?? �Generalized
Anxiety Disorder o ?????????o o????????? ???o ???Drugs (prescription or
recreational) � 5%Alcohol, caffeine, cocaine, tobacco, OTC decongestants, OTC
weight loss drugs, diuretics (cause electrolytic disturbance), digoxin, albuterol,
theophylline, phenthiazine Intrinsic Structural Defects in the Heart � 3% * ??
�Likely many ways for this to occur. Some Quick notes on Cardiomyopathies are below
* ?? �Hypertrophic Obstructive Cardiomyopathy (HOCM) � covered earlier * ?? �4061:
Dilated cardiomyopathy is CHF due to myocardial damage resulting in dilation of the
ventricles and diffuse hypokinesia (ventricles can�t pump as well, thus heart
failure occurs)o Dx: classically acute heart failure in a young person suggests
dilated cardiomyopathy Disorder of spontaneous, recurrent panic attacks Attacks are
often sudden ("out of the blue") Pt may also experience attacks with a trigger, but
this is not necessary for the disease Pt has debilitating worry of another attack
("fear of the fear") Pt may display 'avoidance behaviors' to avoid another attack
-> can lead to odd behavior like agoraphobia! Often appears with Major Depression
(65%), other anxiety disorders, bipolar disorder, and alcoholism Criteria
Recurrent, unexpected panic attacks without an identifiable trigger At least one
attack followed by >1 month of worry of further attacks/maladaptive changes to
behavior Not caused by a substance/medication/disease/another mental illness Tx:
Pharmacotherapy + CBT = best results First line: SSRI bridged with a benzodiazepine
if necessary Second line: TCAs Remember to start low and go slow with the SSRI; the
initial side effects may worsen anxiety in panic disorder Disorder of general
anxiety about their daily lives Pts have somatic symptoms (fatigue/muscle tension)
Often present to their primary care doc initially Anxiety is not fixated on a
specific trigger, but part of everyday life Criteria Excessive anxiety/worry about
daily events for >6 months Difficult time controlling the worry >3 of the following
symptoms: Restlessness, fatigue, impaired concentration, irritability, muscle
tension, insomnia Symptoms cause significant impairment/not cause by anything else
Tx: CBT + SSRI or SNRI Short-term benzos, buspirone, TCAs, and MAOIs are all other
viable options ???Recent viral infection is a common precipitant (3-5%) due to
direct viral and immune response damage to the myocardium (Coxsackie B, Parvovirus
B19, HHV-6, adeno, and enteroviruses) ???Thiamine deficiency (wet beri beri) is
another classic cause ???Dilated ventricles with diffuse hypokinesia on
echocardiogram confirms diagnosis o Tx: supportive for CHF and tx for precipitating
factor ?? 4238: Tachycardia-medicated cardiomyopathy: with a long-standing
tachyarrythmia of any nature (a- fib, a-flutter, rapid ventricular rhythm, etc.)
the myocardium can undergo responsive changes eventually leading to heart failure o
Symptoms: tachyarrhythmia (of any nature), CHF signs, heart palpitationso Dx:
abnormal EKG, rule out CAD, echocardiography showing diffused changes/hypokinesia o
Tx: aggressive rate/rhythm control of arrhythmia (ablations, AV node blockaid,
anti- arrythmatics)?? 2699: Restrictive cardiomyopathy: uniform/symmetric
thickening of the myocardium typically starting with prominent right heart failure,
eventually progressing to right and left heart failure.o Etiology: sarcoidosis,
amyloidosis, hemochromatosis, endomyocardial fibrosis, or idiopathic o
Hemochromatosis (iron overload) is the only REVERSIBLE cause, treated with
phlebotomy o Sarcoidosis/amyloidosis are both slowed with corticosteroids but
cannot be stopped! Non-Cardiac � 4% * ?? �Anemia � low O2 carrying capacity means
the heart ramps up efforts to deliver blood * ?? �Hyperthyroidism � high T3/T4
means increased heart rate, which could lead to palpitations * ?? �Hypoglycemia � a
classic sign for diabetics that they�re sugars are low. Kind of like anemia * ??
�Hypovolemia � like anemia. Heart compensating for inadequate blood volume * ??
�Fever � tachycardia may be the result of vasodilation/leakage of fluid into
extravascular space in response to inflammatory cytokines causing widespread
inflammation * ?? �Pheochromocytoma � release of catecholamines ramps up heart
activity * ?? �Pulmonary disease � likely other underlying signs. Heart could be
distorted from abnormal blood flow or poor oxygen saturation may lead to cardiac
compensation * ?? �Vasovagal syncope � basically you�re BP dropped neurogenically,
thus your heart is compensating Idiopathic � 16% ?? Sometimes we just don�t know. A
good negative workup can only make this diagnosis Case 43 � Bites and Stings Insect
Stings * ?? �Most commonly from Hymenoptera insects (wasp, yellow jacket, hornet,
honeybee, bumblebee, fire ant) resulting in a reaction that may range from local to
anaphylactic * ?? �Approacho Hx � focus on details of sting and ID the probable
organism causing stingo Physical � look for both local signs and systemic signs of
reactiono Remove stinger preferably by brushing (less chance of squeezing venom
out!) * ?? �Local reactionso Redness, swelling, pain, itching at site of injury due
to histamine release triggered by venom o Onset is immediate lasting a few hourso
Tx: ice and antihistamine for itching + tetanus prophylaxis if not vaccinated * ??
�Delayed Reactionso Larger area of redness/warmth (10cm) at the site of sting due
to IgE mediated reaction o Onset is between 24-48hr lasting for 3-5 dayso Note that
there is NOT an increased risk of anaphylactic reaction if a pt has a delayed rxn o
Tx: oral corticosteroids (decrease inflammation) + tetanus prophylaxis if not
vaccinated * ?? �Anaphylaxis o Mild � nausea, generalized urticaria, angioedemao
Severe � hypotenion, shock, laryngeal edema, deatho Onset typically immediately
after sting due to immediate hypersensitivity reaction o Tx: ABC management as
needed (intubation if necessary), IV access, fluids Animal Bites?? Approach * ???
�SubQ or IM epinephrine given IMMEDIATELY and 10-15 min after if symptoms not
improving. Immediately Epi-Pin use is often a good choice for patient * ???
�Antihistmaines, steroids, and broncodilators may also be needed * ???
�Hospitalization for 12-24hr to monitor response * ???�Prescription of epinephrine
pin and instruction on staying away from stings; desensitization therapy may also
be an option o ABCs, protection of current injury (splints of fractures, etc), and
control bleedingo Cleaning with soap+water, Saline irrigation of wound, and
debridement of dead tissue o Hx � in attempt to know what animal bit them/why they
were bitteno Control of infection * ???�Rabies � typically from bats, skunks,
foxes, and dogs??washing + double prophylaxis * ???�Tetanus � given to patients who
are not currently vaccinated * ???�If deep/puncture, likely primary closure should
not be done to allow for drainage * ???�5-7 days of Augmentin (Amoxacillin-
Clavulonic acid) o Micro * ???�Human bites � most common bug = Eikinella corrodens
(30%) followed by S.aureus, E.coli, Streptococcal spp. * ???�Dog bites � may
contain Pasturella spp. and should not be ignored 3002: When a person is bit by a
possible rabid animal, there are really 4 avenues for Rabies post-exoposure
prophylaxis depending on the situation: ?? High risk wild animal bite � includes
bat, fox, raccoon, coyote, skunk o If animal unavailable start PEP o If animal
available; euthanize it/test for rabies??PEP if positive * ?? �Low risk animal bite
� squirrell, chipmunk, mouse/rat, rabbit o NoPEP * ?? �Pet � if a pet (usually a
dog) DOES have rabies, they�ll show signs within 10 days o If available for
quarantine??observe 10 days??if shows signs of rabies, euthanize pet and do PEP
immediately o If not available for quarantine??start PEP?? Livestock or unknown
wild animal � call the health department PEP for rabies consists of: * ?? �Thorough
cleansing of the wound (reduce risk by 90%) * ?? �Administer rabies vaccine (if
person hasn�t gotten it before) + passive immunization (human rabies Ig) Case 44 �
Stroke/TIA Evaluation of Stroke Symptoms * ?? �Stabilize/CT without contrast??shows
hemorrhage immediately; if negative consider tPA o Try to define onset of stroke
symptoms to evaluate timeframeo MRI and CTA may also be used to assess extent of
brain damage * ?? �Evaluate patient (ABCs, Define Neurologic Deficits, underlying
conditions/medications) Transient Ischemic
Attack (TIA) * ?? �Effectively stroke symptoms that occur and resolve within 1hr
(classically 24hr) * ?? �Indicates significant transient ischemia that has resolved
(classically cocaine or drug use!) * ?? �Should be treated as a stroke and stroke
prophylaxis should be initiated * ?? �Note that severe hypoglycemia may result in
stroke-like presentation and should be treated first if found, to see if stroke-
like symptoms resolve with sugar resolution * ?? �HTN is the most important risk
factor for stroke onset Brain Ischemia � 80% of strokes are ischemic!Thrombosis:
localized occlusive processes causing blood flow obstruction * ?? �Atherosclerosis
is most common; often occurring in the large vessels in the head/neck * ?? �Primary
hematologic problems (polycythemia, thrombocytosis, hypercoagulable states) may
cause platelet clotting within the vessels * ?? �Vasoconstriction/fibromuscular
dysplasia/arterial dissection can occur * ?? �Hypertension (medial vascular
hypertrophy) commonly affects penetrating intracranial arteries Embolism: clot
forms somewhere in the body and breaks off to lodge/occlude bloodflow somewhere
else * ?? �Stroke emboli most commonly come from the heart (atrial fibrillation!)
or other major vessels * ?? �Arterial dissection can result in clot formation with
embolization * ?? �Paradoxical emboli form in veins (usually DVT) and travel
through a heart septal defect of A-V malformation in the lungs to hit the brain
* ?? �Air, fat, cholesterol, bacteria (mycotic), foreign bodies, or placental
material have a chance of entering the vessels, acting as an embolus Systemic
Hypoperfusion: not enough blood pressure means not enough perfusion! * ?? �Heart
Failure (infarction or arrhythmia) or systemic hypotension (blood loss,
hypovolemia, overwhelming infection) are the two more common causes * ?? �Watershed
regions (regions last to receive blood supply) are the periphery of perfusion zones
will be greatly/diffusely affected Stroke SyndromesThese are simply outlined on pg.
106 (BluePrints Neuro); name off the syndrome with these prompts! Anterior
Circulation Stroke Syndromes: carotid artery occlusion, MCA embolism, or hemorrhage
in basal ganglia * ?? �Left cerebral hemisphere stroke (in book) * ?? �Right
cerebral hemisphere stroke (in book) Posterior Circulation Stroke Syndromes * ??
�Lateral Medullary Stroke (Wallenberg Syndrome; intracranial VA occlusion)o
Ipsilateral: increased or reduced facial pain/temp sense, Horner�s Syndrome o
Contralateral: reduced body pain/temp sense; arm discoordinationo Bilateral:
nystagmus, ataxia; possible dysphagia/hoarseness if severe * ?? �Bilateral Pontine
Base/Medial Tegmentum Stroke (Basilar Artery)o Quadriparesis | conjugate gaze
paresis, intranuclear aphthalmoplegia, or CN VI nerve palsy o Coma may occur if
severe * ?? �Cerebellar infarction (PICA or SCA)o Gait ataxia; dysarthria;
ipsilateral dysmetria * ?? �Left PCA infarctiono Right homonymous hemianopia &
Sometimes amnesiao Alexiawithoutagraphiaifspleniumofcorpuscallosuminvolved * ??
�Right PCA infarctiono Left homonymous hemianopiao Sometimes left-sided visual
neglect Lacunar Strokes: may be anterior or posterior circulation, but will affect
penetrating arteries * ?? �Pure Motor Stroke: contralateral face/arm/leg weakness
with no sensory/behavioral losses * ?? �Pure Sensory Stroke: contralateral
face/arm/leg paresthesia without motor/visual/behavior losses * ?? �Dysarthria-
Clumsy hand syndrome: slurred speech and a clumsy hand * ?? �Ataxic hemiparesis:
weakness/ataxia of contralateral body (leg>arm) Stroke in a Young Person ??
Defined: basically it�s a stroke, but it�s odd that the person is so young, thus we
look for other etiologieso Patent Foramen Ovale: can result in a paradoxical
embolus, typically with risk factors that can predispose to clotting (heart
disease, diabetes, hyperlipidemia, etc.); best assessed with transthoracic
echocardiologyo Carotid Dissection: usually results in clot formation in the new
open space with embolization. Trauma, chiropractic manipulation, or predisposing
diseases (Marfans, Ehlers-Danlos) clue you in. Because the carotids run with the
sympathetic ganglia, may cause an acquired Horner�s syndrome o Hypercoagulable
disorder: anti-phospholipid syndrome, protein C/S deficiency, ATIII deficiency,
Factor V leiden mutation, hyperhomocystinemia, or prothrombin gene mutation o
Moyamoya disease: a classic disease of occlusion in the Circle of Willis resulting
in collateral vessel hypertrophy (moyamoya = puff of smoke); predisposes to
rupture/stroke o Arteriovenous malformation: can result in aneurysm and rupture,
thus stroke o Drugs of abuse: classically cocaine/amphetamines can cause
vasospasm??stroke ?? Tx: typically look for these more interesting etiologies and
treat accordingly Treating Acute Stroke...to give or not give tPASome major points
when considering tPA thrombolytic therapy * ?? �Timeframe: Pt is >4.5 hours away
from symptom onset -> no tPA * ?? �Hemorrhage/bleeding: hemorrhagic infarction,
tendency to bleed/anti-coagulant meds, recent surgery, thrombocytopenia, or recent
bleeding episode -> no tPA * ?? �Sugars: hypo/hyperglycemia may mimic
signs/symptoms of stroke * ?? �Blood pressure: lowering blood pressure causes less
brain perfusion, worsening an ischemic stroke! Don�t lower BP unless there�s signs
of end-organ damage from HTN After acute event, you must anti-coagulate! * ??
�Heparin, Warfarin, Aspirin, or newer Factor Xa inhibitors (Dabigatran, etc.) can
all be of use * ?? �Anti-arrythmatics can be helpful if atrial fibrillation is
present! A-fib can easily cause clots to be formed and thrown, thus stopping the
arrhythmia may aid in preventing future events * ?? �Control risk factors (HTN,
lipid abnormalities, obesity, smoking, drinking, etc.) with medication (aspirin,
anticoagulants, lipid/BP medications) and lifestyle changes (avoid fat, exercise,
smoking cessation) Case 45 � HIV & AIDS 10301: HIV screening is an assay detecting
HIVp24 antigen and HIV antibodies recommended at: * ?? �Initial screen if: Ages 15-
65, being treated for TB, or being treated for any STI * ?? �Annual screening if:
IVDU (person AND sex partners), MSM, homeless, incarceration, possible sexual
contact with a HIV+ individual * ?? �Additional screening if: new pregnancy,
occupational exposure, prior to any new sexual relationship 3583: Acute, initial
HIV infection begins as a mono-like disease and should be suspected in higher risk
pts: * ?? �Presentation: fever, lymphadenopathy, sore throat, arthralgias,
generalized rash, diarrhea/N/V * ?? �Dx: often must be made with high viral load
detection (virus isn�t being attacked by immune system yet) because the anti-HIV
abs havn�t been formed. CD4+ count often normal. * ?? �Tx: immediate HAART with
partner notification/prophylaxis 2265: Remember! Spirochete visualization on dark-
field microscopy is diagnostic for syphilis! Usually if a person has syphilis,
they�ve been engaging in some risky sexual behavior...thus they should be tested
for other STIs, especially HIV 3888: Basically, if your CD4+ count is >200 then you
can receive any vaccine (simple!) but: * ?? �All HIV pts should receive a
pneumococcal conjugate (once) and polysaccharide (every 5 yrs) vaccines * ?? �HIV
pts who are sexually active with men should get HepA vaccine (once) * ?? �If CD4+
count is <200 ???cannot receive live-attenuated vaccines o MMR, varicella zoster,
intranasal influenza, yellow fevero Should a pt be diagnosed with HIV and be
vaccinated with any of these before starting HAART, they should be vaccinated again
after HAART initiation 3252: Opportunistic infections and primary prophylaxis in
HIV/AIDS * ?? �P.jiroveci (PCP) � TMP-SMX (<200) * ?? �T.gondii (toxoplasmosis) �
TMP-SMX (<100 or positive IgG for toxo) * ?? �Mycobacterium Avium complex �
azithromycin/clarithromycin (<50) * ?? �Histoplasmosis � itraconzole (<150 or
living in endemic area) * ?? �Herpes simplex virus � acyclovir/valacyclovir
(recurrent infections, no CD4 count specified) * ?? �Note that some major HIV
related infections are NOT recommended to have primary prophylaxis o Candida �
Fluconazole: reactive treatment is extremely effective and prophylaxis is
expensive. Also concerns of resistance with prophylaxis, so we only treat
reactively o Cryptococcus � fluconazole: cost/concern for resistance are solid
reasons, but also incidence is extremely rare, thus prophylaxis is not administered
3251: If you�re exposed to HIV you immediately stop what you�re doing and initiate
PEP for HIV * ?? �Immediate prophylactic triple therapy (tenofovir, embricitabine,
and raltegrevir preferred) for 28 days * ?? �Serologic testing at immediately, 6
weeks, 3 months, 6 months * ?? �High risk exposure: blood, CSF, genital secretions,
needle-stick * ?? �Low risk exposure: urine, feces, other bodily fluids 4115: If
you see atypical pneumonia (diffuse interstitial infiltrate, tachypnea,
tachycardia, fever, non- productive cough) in an immunocompromised
(immunosuppressive drugs, chemotherapy, or AIDS) then think PCP pneumonia. If it�s
typical pneumonia??S. pneumo. Don�t overthink it hauss. 2267: Remember!
S.pneumoniae is THE most common cause of pneumonia in HIV/AIDS patients. You might
be temped to think PCP when an AIDS patient has pneumonia, but you better slow your
roll: * ?? �S.pneumoniae � unilateral, lobar infiltrate, productive cough, pleural
effusions often occur, >200 CD4 o Remember! This guy is encapsulated, thus even
people with normal immunity have a harder time clearing this infection! * ??
�P.jiroveci � bilateral, diffuse infiltrate, dry cough, pleural effusions rarely
occur, <200 CD4 3938: PCP pneumonia is one of the most common infections in AIDS
patients * ?? �Sym: dry cough, fever, exertional dyspnea
(out of proportion to CXR findings) * ?? �Signs: CXR (bilateral interstitial
infiltrates), elevated lactate dehydrogenase * ?? �Dx: bronchioalveolar lavage
demonstrating P.jiroveci * ?? �Tx: TMP-SMX (Bactrim) for 21 days + corticosteroids
(PaO2 <70) o IV pentamidine is an alternative for those that cannot take TMP-SMX
but it has a lot of side effects (damage to kidney, liver, heart, etc.) 2273/2267:
PCP pneumonia (P.jiroveci formerly carinii) * ?? �One of the most common infections
for an AIDS patient * ?? �Presentation: dry cough, dyspnea, hypoxia, CXR with
bilateral diffuse infiltrate, rarely pleural effusion * ?? �Dx: clinical suspicion
+ bronchoalveolar lavage showing P.jiroveci (little crushed ping-pong balls!) * ??
�Tx: TMP-SMX + corticosteroids (if poor O2 saturation status; PaO2 <70 or A-a
>35)??may show initial worsening of lung function due to death of bacteria and
inflammatory reactions in lung 2304: Detecting PCP you can do bronchioalveolar
lavage (high sensitivity/spec) or sputum culture (high specificity but low
sensitivity) 2269: Profuse watery diarrhea in HIV/AIDS patients is typically from a
opportunistic infection (bloody would be more high infectious things). ?? First
step in diagnosing what is causing the diarrhea is stool examination for
ova/parasites as often parasitic infections will be the cause here! 3917/3590:
Diarrhea in HIV/AIDS typically occurs with different etiologies based on CD4+ count
?? Cryptosporidium (<180) � severe watery diarrhea, wt loss, fever o Classically
from animal contact, water, or person-persono Dx: modified acid-fast stain shows
cryptosporidial oocytes (4-6mcg) o Tx: anti-retroviral therapy (resolves with CD4
receovery) * ?? �Microsporidium or isosporidium (<100) � watery diarrhea, wt loss,
cramps, no fever * ?? �Mycobacterium Avium Complex (<50) � watery diarrhea, wt
loss, high fever (>102F) * ?? �CMV (<50) � bloody/small volume diarrhea, abdominal
pain, wt loss, fever o Dx: colonoscopy with biopsy � intracytoplasmic
eosinophilic/basophilic inclusions o Tx: gancicloviro Must examine eyes to rule out
CMV retinitis 2277: Progressive multifocal leukoencephalopathy (PML) * ??
�Progressive demyelinating disease caused by [JC virus infection +
immunocompromised] * ?? �Presentation: any immunocompromised patient getting new
onset of focal neurologic symptoms should immediately be suspected to have PML * ??
�Tx: MRI showing multiple, non-enhancing white matter lesions, typically without
mass effect * ?? �Dx: no known treatment, progressively fatal 3253/11108: Kaposi
Sarcoma (HHV-8 + AIDS) * ?? �Presentation: multiple skin lesions often starting
brownish then becoming purple/red due to increased vascularization of infected
tissue; may accompany other signs of AIDSo Note that lesions may be quite
impressive if infection has been present for prolonged time (see question 11108 for
example) * ?? �Dx: clinical but biopsy and HIV/AIDS serologic evidence often used
to confirm * ?? �Tx: HAART treatment of AIDS will often cause regression with CD4+
recovery o If refractory, chemotherapy may be used to kill off the rapidly dividing
tissue 2274/8959: HIV esophagitis occurs with CD4+ count <100; occurs with painful
swallowing/substernal burning * ?? �Candida albicans � white plaques in
mouth/esophagus (oral thrush!) o Tx: 3-5 days of oral fluconazole with HAART
assessment o If patient fails this, further workup for viral causes * ?? �HSV �
herpetic vesicles with round/ovoid ulcers in esophagus, sometimes w/ HSV infection
elsewhere o Severe odynophagia (painful swallow) WITHOUT dysphagia o Dx: biopsy
with histopathology * ?? �CMV � Deep, linear ulcers in the distal esophagus o
Severe odynophagia (painful swallow WITHOUT dysphagia o Dx: biopsy with
histopathology * ?? �Aphthous ulcers � idiopathic presenting with apthous ulcers
Pill esophagitis can cause some similar symptoms but DOESN�T typically occur in
HAART regimens 3103: CMV esophagitis in AIDS pts causes substernal burning/long-
linear ulcers, and biopsy shows intranuclear/intracytoplasmic inclusions (Tx: IV
ganciclovir) 2268: Disseminated Mycobacterium Avium Complex (M. avium or M.
intracellulare): non-specific symptoms (fever, cough, abdominal pain, diarrhea,
night sweats, weight loss), splenomegaly, and elevated alkaline phosphatase. * ??
�Typically, in HIV pts with CD4+ <50; pts with this low of CD4 should be given
azithromycin prophylaxis * ?? �Dx: blood culture or lymph node/bone marrow biopsy *
?? �Tx: clarithromycin or azithromycin 2295: TB re-activation is common in AIDS
patients. The infection is kept latent in the lungs in a granuloma (macrophages
make up much of this), so when the immune system craps out...these do too,
releasing the mycobacteria. * ?? �Sign/sym: subacute mild cough, low-grade fever,
fatigue prominent in the morning (due to secretion accumulation) o CXR: superior
lobe consolidation (higher O2 levels) with cavitary lesions o Substance abuse is a
huge risk factor for TB active infection * ?? �Remember that PCP is a common AIDS
pneumonia, but cavitary lesions are uncommon 3246: TB infections (new or re-
activated) are VERY common in HIV/AIDS patients. In fact, any AIDS patient having a
PPD test show >5mm induration should be treated prophylactically immediately. ??
Tx: Isoniazid (anti-TB) + pyridoxine (B6 to fight off deficiency) for 9 months
4388: Infective endocarditis is typically due to S.aureus infection and there�s an
even higher chance with concurrent HIV/AIDS. ?? Typically, right sided (tricuspid)
endocarditis has differences than the typical mitral valve version: o Murmur less
likely (lower pressure flow across the tricuspid valve)o Less systemic signs with
more prominent lung problems (as septic emboli get in the lungs) o Chest CT can
show abscesses, infarction, pulmonary gangrene, cavities at lung periphery
3254/9885: Cryptococcal Meningoencephalitis (Cryptococcus neoformans fungus) * ??
�Classically occurs in pts with immunosuppression (AIDS is classic) * ??
�Presentation: fever, lethargy, headache, altered mental status??may progress to
coma o CSF: high opening pressure, low WBCs, low glucose, elevated protein o
Papilledema (indicating increased CNS pressure) can be an important sign * ?? �Dx:
Latex agglutination (+), cryptococcal antigen (+), India Ink (+), Sabourard Agar
growth * ?? �Tx: IV amphotericin B + flucytosine (2 weeks, induction)??oral
fluconazole (8 weeks) o Intrathecal amphotericin B if failure to respond to IV
treatment o Serial lumbar punctures to limit elevated CSF pressure 3107: Bacillary
angiomatosis (B.hensliae) * ?? �Classically due to a cat scratch * ??
�Presentation: immunosuppressed (AIDS pts most common) with bright red, firm,
friable, exophytic (extends beyond the epithelium) nodules * ?? �Tx: oral
erythromycin 2264: Treatment of toxoplamosis * ?? �Prophylaxis is TMP-SMX (Bactrim)
often for AIDS or immunosuppressed pts * ?? �Tx: empiric sulfadiazine +
pyrimethamine if the infection is actually present; diagnosis may be made if ring-
enhancing lesions are seen on brain imaging with improvement of symptoms with this
treatment regimen! 2839: Serous Otitis Media * ?? �Middle ear effusion resulting in
conductive hearing loss without infectious symptoms. Ear canal shows dull tympanic
membrane with hypomobility on pneumatic otoscopy * ?? �The most common middle ear
pathology in HIV/AIDS due to lymphadenopathy obstructing the Eustachian tube Case
46 � Jaundice2627/2935: Hyperbilirubinemia * ?? �Unconjugated more elevated:
hemolysis (overproduction), reduced uptake into liver (portosystemic shunt or drug
effect), or conjugation defect (Gilbert�s syndrome or Crigler-Najar) * ??
�Conjugated more elevated: o AST/ALT elevated: liver disease/damage
(hemochromatosis, hepatitis, cirrhosis, etc) because hepatocytes are damaged and
releasing bilirubin into bloodo Normal AST/ALT/Alk.phos: bilirubin metabolism
disorder (Dubin-Johnson or Rotor syndromes) bilirubin is built up and leaks into
bloodo Alk.phos elevated: intrahepatic cholestasis or biliary obstruction
(gallstones, malignant obstruction, intrahepatic destruction, etc.) bilirubin is
backed up and leaks into blood 2977: When assessing jaundice, positive urine
bilirubin means conjugated (direct) bilirubinemia * ?? �This makes sense, as only
conjugated bilirubin is made to be water soluble, unconjugated (indirect) bilirubin
is inherently not water soluble, thus it cannot be filtered by the kidney into the
urine. * ?? �However, a positive urine urobilinogen indicates unconjugated
(indirect) bilirubinemia, as the huge amount of unconjugated bilirubin goes through
it�s normal metabolism in the large intestine, a large amount of urobilinogen (a
normal by-product) will be made. This is NOT the case in a direct bilirubin, as a
direct bilirubinemia is caused by some obstructive process, and it would never make
it to the large intestine to become urobilinogen! 2975: When presented with a
jaundice/direct bilirubinemia, the FIRST thing to do is assess the bile duct width
with RUQ ultrasonography. A dilated biliary tree >3cm suggests extrahepatic
obstructive process. A non-dilated biliary tree (<3cm) suggests an intrahepatic
obstructive process. ?? ERCP is often performed when dilation >3cm is found as you
must figure out exactly where the obstruction is occurring to uncover etiology
2900: Acute Liver Failure?? Presentation: nonspecific symptoms (fatigue, anorexia,
nausea, etc.), RUQ pain, jaundice, pruritus, and sometimes hepatic encephalopathy
as failure worsens. Labs include:o ^PT/INR (failure to liver to make coagulation
proteins)o AST/ALT x10 normal with increased bilirubino Progression may show
AST/ALT trending down (liver death is bad that these are being released less and
less) and increasing PT/INR/bilirubin (further loss of liver
function; PT is the single most prognostic factor in Acute Liver Failure) * ??
�Dx: clinical presentation with lab values; must search for underlying cause * ?
�Tx: stabilize pt and treat underlying cause once identified 4635/2936: Chronic
Liver Disease (Cirrhosis) ?? Presentation: Jaundice, itchiness, GI bleeding,
encephalopathy, decrease in total T3/T4 (free concentration only drops in severe
cases) and gender specific signs due to poor metabolism of estrogens in liver
(increased estrogen in blood) and systemic signs o Men: hypogonadism (small/firm
testes, decreased libido, erectile dysfunction, loss of pubertal hair,
gynecomastia) o Women: amenorrhea, irregular menseso Systemic: telangiectasias,
portal HTN, ascites, hepato-splenomegaly, palmar erythema, �terry nails�,
Dupuytren�s contracture, clubbing of fingernails o May be totally asymptomatic * ??
�Dx: clinical picture; may be confirmed with liver biopsyo Endoscopy to assess for
varices as these are treatable complications of liver disease. Two other
complications (hepatic encephalopathy/acites) will be obvious from clinical exam
* ?? �Tx: stop damaging behavior/disease; some cirrhotic damage cannot be undone o
Treatment to prevent complications (B-blocker for varicies, draining of ascities,
etc.) is a major part of management alongside treatment of current complications o
Cirrhosis in patients without signs/symptoms (�compensated cirrhosis�) should be
monitored for hepatocellular carcinoma (ultrasound liver/a-fetoprotein screen every
6 months) 2911/4278: Alcoholic Hepatitis?? Presentation: signs of hepatitis
(jaundice, RUQ pain, ascites, etc.) and sometimes cirrhosis with history of alcohol
abuse and characteristic labso Labs: elevated AST:ALT (2:1, but <300), elevated
GGT/bilirubin/INR/ferritin (acute phase reactant), neutrophil leukocytosiso Note
that AST:ALT ratio is thought to be due to alcohol depletion of pyridoxyl-5-
phosphate, a cofactor needed for ALTo May have elevated MCV due to chronic
malnutrition (folate or B12 depletion) * ?? �Dx: history + clinical presentation +
labso Imaging/biopsy will show fatty liver * ?? �Tx: abstinence/supportive care
4648: Ischemic Hepatic Injury (�Shock Liver�) * ?? �Presentation: any form of shock
(septic shock is most common) with rapidly developing AST/ALT elevations (like in
the 1000-2000 range!) and normal total bilirubin/alk.phos * ?? �Dx: clinical
syndrome o Acute HepA/HepB will quickly elevate AST/ALT/Bili/Alk.phoso
Cholecystitis/Hepatobiliary obstruction will elevate Bili/Alk.phos more than
ALT/AST o Otherhepaticdiseasesmayraisetheselevels,butnotveryhigh! * ?? �Tx: treat
the underlying cause of shock and typically liver enzymes will recover as well!
Hepatitis A (HAV) * ?? �RNA picornavirus; fecal-oral (enteric) transmission * ??
�Acquired by: children, travelers to endemic areas, may be in community outbreaks o
Symptoms occur over a period of weeks (children = asymptomatic; adults = symptoms)
o Shedding of the virus in feces occurs before symptoms begin! * ?? �Causes: acute
hepatitis (often community, asymptomatic) * ?? �Testing: o Anti-HAV IgM antibody =
used to detect presence of virus/recent infection o Anti-HAV IgG antibody = used to
detect previous infection/protects from new infections * ?? �Vaccine: o Havrix:
inactived vaccine for children (2 y/o)o Twinrix: HAV + HBV vaccine for teens (18
y/o)o Human reservoir/single serotype (good chance for eradication); but it�s not
serious disease so eradication is not a huge priority?? Hand-washing is the BEST
defense against this virus! Hepatitis B (HBV)?? DNA hepadnavirus; parenteral
transmission; �Dane� particles may contribute to chronicity * ?? �Acquired through:
childbirth/unprotected sex (vaginal secretion, semen), IV drug use/needle stick
(blood); living in the same house as someone infected with HepB * ?? �Causes: acute
hepatitis, chronic hepatitis (20%), fulminant liver failure, increased HCC risk o
Higher risk of chronicity with younger age (<1yr: 90% | >5yr: 2%)o Virus course
over a year if chronic; virus shedding occurs BEFORE symptoms * ?? �Replication:o
Virus enters the nucleus with partial dsDNA, which is �fixed� into DNA in the
nucleus o Host nuclear machinery transcribes the HepB DNA into an (+)mRNA
intermediateo (+)mRNA intermediate moves into cytoplasm ???Some mRNA is transcribed
by host ribosomes into viral proteins ???Some mRNA is enveloped in these proteins
to become the new progenyo Viral reverse transcriptase converts (+)mRNA -> partial
dsDNA within the progeny virus o New HepB is released out of the cello �DNA virus
using an RNA intermediate to generate DNA� * ?? �Testing:o HBsAg = HBV surface
antigen used to detect HBV infection ???Detected during acute infection and chronic
infection o HBcAg = HBV core antigen ???Not used in detection of diseaseo HBeAg =
HBV core antigen detected during active viral replication (high transmissibility)
???Detected during acute infection or chronic-active infection o Anti-HBs =
antibody to HBsAg ???Can detect after disease resolution indicating recovered
infection or immunization ???Vaccine is ONLY surface antigen o Anti-HBc = antibody
to HBcAg ???IgM??acute infection or �window period� ???IgG??chronic infection or
recovered infection o Anti-HBe = antibody to HBeAg (low transmissibility) ???
Detected during the �window period�, chronic infection, or recovered infection * ??
�Epidemiology: sub-Saharan Africa/China (early life infections) * ??
�Immunization??patients born before 1988 probably havn�t gotten vaccinated unless
they�re in a healthcare field or from University. Anyone after that should have
gotten it as a baby or teenager Hepatitis C (HCV) ?? RNA flavivirus; does not
replicate in the nucleus; parenteral transmission o Generates one big protein and
then sues proteases to cleave it into functional unitso Proteases are a huge target
for HCV drug treatmento E2 envelope protein??hyper-mutating 30 amino-acid stretch
that is often targeted by the immune system. If it mutates then the virus will
become a �quasi species� and it�s less recognizable to our immune defenses * ?? �6
subtypes (USA commonly 1; IVDU commonly 3); each has a different drug regimen * ??
�Acquired through: IV drug abuse, unprotected sex, before 1992 blood transfusion
(now rare) * ?? �Causes: mild acute hepatitis, chronic hepatitis (80%), increased
HCC risk * ?? �Testing: o HCV-RNA test (EIA screening confirmed with PCR) indicates
infection presenceo Decreasing RNA levels = resolution of diseaseo Persistent RNA
levels = chronic disease (quasi-species causing chronic infections) ?? Alcohol use
should be discouraged completely; Tylenol is safe if less than 2g is taken ?? HEP C
IS CURABLE 2958/2232: Cryoglobulinemia secondary to Hepatitis C infection * ??
�Occurs via IgM immune complex deposition causing inflammation and damage in areas
of deposit/vascularture * ?? �Presentation: muscle/joints (arthralgias), skin
(palpable purpura, Raynaud�s), liver (elevated transaminases, ALT>AST), kidney
(moderate-to-severe glomerulonephritis), and PNS (motor-sensory axonopathy) o Labs:
decreased compliment levels, cryoglobulins, serologic evidence of HepC o Hx may
suggest Hep C exposure (IVDU is classic) * ?? �Dx: clinical presentation with
agreeing lbs * ?? �Tx: plasmapheresis (remove cryoglobulins) and
cyclophosphamide/corticosteroids (immunosupp.) 4654: Chronic Hepatitis C and
Associated Conditions * ?? �Presentation: asymptomatic or fatigue are the most
common; nonspecific symptoms (fever, anorexia, myalgia, weight loss, etc.) can also
occuro Labs: elevated or normal serum transaminaseso May progress to liver
cirrhosis (20%) or hepatocellular carcinoma * ?? �Associated diseases can clue you
into the HepC infection! o Essential mixed cryoglobulinemia (90% of cases have
HepC) � palpable purpura, arthralgias, renal complications due to IgM immune
complex deposition into medium sized vessels ???Low compliment levels are classic
for this disease o Membranoproliferative glomerulonephritis � will appear as renal
decline with characteristic biopsy histology of the glomeruli o Porphyria cutanea
tarda � fragile skin, photosensitivity, vesicular rash/erosions on dorsum of the
hands o Lichen planus � itchy, purple, raised, well demarcated plaques Hepatitis D
(HDV) * ?? �RNA delta-virus; incomplete/cannot function on it�s own * ?? �Requires
HBV infection for infectivity; uses HBV surface antigen to infect cells * ??
�Encodes delta antigen, which are capsid proteins; uses host-RNA polymerase * ??
�Causes: chronic hepatitis co-infection (less severe), super-infection
(severe/progressive), increased HCC risko Chronically infected pt with a sudden
spike in ALT??superinfection! Hepatitis E (HEV)??25 yo Afghani pregnant woman
becomes nauseated, vomiting, elevated liver enzymes, dies 7 days later. Likely HepE
(classic association); but not Hep A, as she was likely exposed in early life
because of the poor sanitation that happens in a war-torn country * ?? �RNA
calicivirus (non-enveloped ssRNA); fecal-oral (enteric) transmission (Zoonotic
illness in the USA) * ?? �Causes: acute hepatitis, fulminant hepatitis (<1%) in
pregnant women, 3rd trimester (high fatality) * ?? �Testing o Anti-HEV IgM antibody
= used to detect presence of virus/recent infectiono Anti-HEV IgG antibody = used
to detect previous infection/protects from new infections 2924/2923: Genetic
Diseases of Liver Metabolism * ?? �Dubin-Johnson syndrome � conjugated
bilirubinemia; jaundice with body stressors (illness, pregnancy, OCP use) but
otherwise no/minor symptoms (fatigue, abd. pain, weakness) and no hemolysiso More
common in Sephardic Jewso Clinically normal aside from reactionary jaundice and
black liver (epinephrine metabolites) o Labs: Bilirubin (20-25 mg/dL), normal
LFTs, normal coproporphyrin (predominantly Copro I) * ?? �Rotor syndrome � Dubin-
Johnson syndrome without the black liver * ?? �Crigler-Najar syndrome � autosomal
recessive unconjugated bilirubinemia; o Type 1: significant mental
retardation/death; Phototherapy/plasmapheresis can help conjugate the bilirubin to
buy time for curative liver transplant o Type 2: fairly benign unconjugated
bilirubinemia with jaundice; often asymptomatic, but symptoms (if occuring) can be
treated with phenobarbital or clofibrate ?? Gilbert syndrome � mild unconjugated
bilirubinemia triggered by bodily stressors; very similar to C-N syndrome II,
difference is in the enzyme defect Malignant Obstruction of the Hepatobiliary Tree
* ?? �A classic reason to get bilirubinemia, typically due to pancreatic
adenocarcinoma/cholangiocarinoma * ?? �Presentation: conjugated hyperbilirubinemia
with predominantly elevated Alk.phos, painless jaundice, and
fatigue/weakness/weight loss * ?? �Dx: Abdominal ultrasound or CT; retrograde CPG
endoscopy if imaging is negative * ?? �Tx: Resection or chemo/radiation therapy
2209: Pancreatic Cancer * ?? �Can occur in the head or the body/tail of the
pancreas causing different symptoms! * ?? �Head: painless jaundice, �double duct�
sign, Courvorsier sign (non-tender, distended gallbladder at right costal margin),
jaundice/pruritis/pale stools/dark urine * ?? �Body/Tail: abdominal pain WITHOUT
jaundice/obstruction 3585: Diagnosis of Pancreatic Adenocarcinoma * ?? �Common
symptoms: Weight loss, gnawing abdominal pain that radiates to the back, worsens
with eating, laying down, or at night * ?? �Pancreatic Head symptoms: jaundice and
steatorrhea (obstruction of hepatobiliary secretion) o Abdominal ultrasound is the
preferred technique for diagnosis * ?? �Pancreatic Body/Tail symptoms: NO JAUNDICE
o Abdominal CT is preferred technique for diagnosis 2978: Acute Cholangitis * ??
�Biliary stasis due to any number of reasons (commonly gallstone obstruction,
malignancy, bile duct stenosis) but all of them cause backup. The fear is that
disruption of the blood-bile barrier could allow for dissemination of
bacteria/toxins * ?? �Presentation: [fever, jaundice, RUQ pain], [confusion,
hypotension] (Charcot triad, Reynold�s pentad) o Labs: neutrophilia, elevated
alk.phos/GGT/AST/ALT/direct bilirubin * ?? �Dx: presentation/labs with biliary
dilatation (ultrasound FIRST, then CT if not diagnostic) * ?? �Tx: [ERCP with
sphincterotomy or percutaneous transhepatic cholangiography] +[ broad spectrum
antibiotics] 2898/2950: Primary Biliary Cholangitis * ?? �Chronic liver disease
characterized by intrahepatic biliary duct destruction by anti-mitochondial
antibodies resulting in cholestasis * ?? �Presentation: fatigue, pruritus,
jaundice, hepatomegaly, steatorrhea, portal HTN, xanthalasma, and metabolic bone
diseaseo Labs: elevated Alk.phos, hyperlipidemia, normal AST/ALTo Classically in
middle-aged women and associated with other autoimmune diseases * ?? �Dx:
ultrasound to confirm intrahepatic cholestasis ???anti-mitochondrial antibodies are
diagnostic o Liver biopsy would show ductopenia * ?? �Tx: Ursodeoxycholic acid
(delays histologic progression via increased bile transit and possible anti-
inflammatory effects o Liver transplant is the ultimate treatment 4331/3609/4347:
G6PD deficiency (glucose-6-phosphate dehydrogenase) o ?? �X-linked recessive
disorder which can result in acute anemic crises in response to certain situations.
G6PD typically used to generate glutathione to minimize oxidation damage to RBCs.
Should a oxidizing stressor come on, G6PD deficiency pts are not able to
compensate. o Classically triggered by infection, oxidant drugs (anti-malarials,
sulfa drugs, etc.), and fava bean o ?? �Presentation: acute hemolytic crisis
(fever, jaundice, abdominal pain, dark urine) due to hemoglobin denaturation and
disruption/lysis of RBCs. o Labs: normal G6PD levels are typical (as the deficient
cells were destroyed and new reticulocytes have normal G6PD levels)??re-test in 3
months after crisiso Smear: degmocytes (�bite cells�) and Heinz bodies (denatured
basophilic hemoglobin) o Urine may stain with Prussian Blue (+ is presence for
iron, thus hemolysis is occuring * ?? �Dx: clinical scenario/blood smear * ?? �Tx:
supportive care during crisis with avoidance of precipitating substances 3062/4333:
Hereditary Spherocytosis * ?? �Autosomal dominant defect in spectrin or ankyrin RBC
structural proteins resulting in RBC membrane blebbing and eventually deformation
into fragile spheres (instead of bi-concave disks) * ?? �Presentation: hemolytic
anemia, jaundice, splenomegaly classically in European-descent folks o Labs:
anemia, inc. MCHC/dec. MCV (small RBCs)o Smear: abundant spherocytes with some
shearing of RBCso Complications: aplastic anemia in Parvovirus B19 infection OR
pigmented gallstones (increased hemolysis causing increased bilirubin),
overwhelming sepsis from encapsulated organisms if spleen has been removed. * ??
�Dx: Osmotic fragility test (increased fragility), acidified glycerol lysis test
(increased lysis), or abnormal eosin-5-maleimide binding test, with negative
Coomb�s test and blood smear * ?? �Tx: splenectomy (stops RBC destruction), folate
supplementation, blood transfusions o Anti-pneumococcus, Haemophilius, and
meningococcus vaccines before splenectomy and daily oral penicillin for 3-5yrs
after surgery due to risk of sepsis post-splenectomy, which apparently lasts for
>30yrs even though our prophylaxis only goes on for about 5 years. [HGH YIELD]
4437/2248: Autoimmune Hemolytic Anemia (AIHA) ?? Warm AIHAo Hemolysis triggered by
a stressor (abx, infection, etc.) causing IgG/Anti-C3 antibody formation o
Presentation: normocytic anemia, hemolysis (jaundice, indirect bilirubinemia, inc.
serum lactate dehydrogenase, decreased serum haptoglobin), splenomegaly ???Smear:
reticulocytes, spherocytes, elliptocytes, and microspherocytes ???Concern of venous
thromboembolic diseaseo Dx: direct Coombs test demonstrating specific antibodies
bound to RBCs o Tx: high-dose corticosteroids or splenectomy (if refractory) ??
Cold AIHAo Hemolysis triggered by infection (HCV, EBV mono, or Mycoplasma) or in
lymphoproliferative disorders causing IgM/Anti-C3 antibody formationo Presentation:
Warm AIHA symptoms + livedo reticularis/acral cyanosis with cold exposure that
disappear with warming???Concern of gangrene from cold agglutinin aggregates o Dx:
direct Coombs testo Tx: avoid cold temps + rituximab +/- fludaribine Medication
induced � acetaminophen and alcohol (>3 drinks) can lead to toxic NAPQI
accumulation * ?? �Herbals like Kava, Ma Huang, etc can all cause liver damage,
thus should be investigated * ?? �Milk thistle might aid in helping resolve with
alcoholic cirrhosis, but likely does nothing Case 47 � Dyspepsia/Peptic Ulcer
Disease (PUD) Helicobacter pylori * Slender/curved gram(-) rods with polar flagella
* Associated with: � Gastritis * Peptic ulcer disease (95% duodenal, 75% gastric) *
Gastric adenocarcinoma and lymphoma * Microaerophile (requires O2, but only needs a
low level of it) * Virulence factors: * Vaculolating cytotoxin (VacA) � toxic to
cells, not well studied * Cytotoxin Associated gene A (CagA) - PAI encoding Type
III secretion system allowing for infection of VacA toxin into cells * Urease �
hydrolyses urea to make ammonia and CO2??neutralizes stomach acid for protection *
Diagnosis * Endoscopy with biopsy/culture � can be useful, although invasive. The
bacterium will sit on top of the mucosa in little clumps in the gut lumen * Stool
antigen � enzyme immunoassay used to detect antigen in the infected patient�s
stool. Fairly inexpensive and non-invasive. * Urea breath test � qualitative test
using 14C- and 13C-labelled urea can be given orally and when degraded by the
bacterial urease, labelled CO2 will equilibrate with body fluids and ultimately be
expired from the lungs into the breath. Can be used to prove absence of bacterium
and follow treatment! Somewhat expensive but non-invasive. * Serology � useful for
confirming an infection at some point by the bacterium. Titers stay high for years,
even with eradicated infection, so it�s not as useful as you may think * Tx *
Triple therapy � Amoxicillin (mitronidazole if allergic to penicillin)
+Clarithromycin + PPI * Quadruple therapy � PPI + Bismuth + Metronidazole +
Tetracycline (Pylori Being Mean? Use tetra [4]) NSAIDs � non-specific COX
inhibitors can screw up the mucus barrier in the stomach leading to ulcers
Gastroesophageal Reflux Disease (GERD)?? Reflux of acid from stomach into esophagus
due to decreased Lower Esophageal Sphincter (LES) tone o Often
heartburn/regurgitation upon lying down � may mimic cardiac chest paino Nocturnal
cough/dyspnea or adult-onset asthma � airway irritation from HCl moving up the
esophagus/into common space and down into the airwayo Enamel erosion of the teeth �
HCl getting into moutho Ulceration/stricture � total destruction of mucosa knocking
out stem cells??healing with fibrosis resulting in narrowing of lumen o Barrett�s
esophagus � discussed below ?? Risk factorso Alcohol/tobacco use, fatty diet,
obesity, caffeineo Hiatal hernia (�sliding hernia�) � herniation of gastric cardia
above the diaphragm = HCl production above the diaphragm means easier entry of HCl
into the esophagus (often more severe GERD)o Hour-glass sign � LES is pushed higher
into thoracic cavity/retains some tone; so you have Clinical Points ?? ?? 2200:
?? ?? 4335: ?? ?? Often gastroenterologist referral prudent when �alarm feature�
are present (changes in chronic disease, unresponsive symptoms, dysphagia,
vomiting, cancer concerns, anemia, etc.)Endoscopy may be useful for diagnosing GERD
(good specificity, poor sensitivity)
and often findings will clinic diagnosis (lack of findings doesn�t tell you much)
Endoscopy�s role in Evaluation of GERDBasically a person with GERD isn�t too much
of a worry as long as they�re doing OK. However there are certain situations where
further investigation is requiredLet�s say you have a patient with GERD, if: o
Male>50,symptoms>5yrs,cancerrisk(smoking,alcoholism,etc.),alarmsymptomspresent
(dysphagia, odynophagia, weight loss, anemia, GI bleeding, recurrent vomiting)??
endoscopy o They don�t have any of the above characteristics/symptoms??PPI trial 2
months ???If symptoms are well controlled??stay on that PPI???If symptoms are
refractory??consider switching PPI or increasing dose ?? If symptoms STILL
refractory??endoscopy Asthma exacerbation due to GERDPresentation: recent worsening
of asthma symptoms with normal lung exam. Often sore throat, morning hoarseness,
worsening cough when laying down (at night is common), need for inhaler following
meals, dysphagia, chest pain/heartburn, regurgitation sensation o Result of
microaspirations causing irritation and vagal hypersensitivity resulting in
proclivity to bronchospasm o Often coincides with weight gain (possibly due to a
stomach ulcer!) Tx: PPI trial esophagus??LES??cardia above the diaphragm 4346:into
the larynx) as part of their clinical picture. Note that chronic GERD patients may
have chronic cough (stomach HCl into lungs) or hoarseness (HCl 11126: Remember how
we made fun of people for misdiagnosing heart attacks for GERD? Well that shit is
real because GERD can sound a whole lot like coronary artery disease! A patient
with GERD might come complaining of chest pain with radiation!! Note the
characteristic GERD signs: * ?? �Prolonged pain >1hr, post-prandial symptoms,
heartburn/dysphagia, relief with anti-reflux drugs * ?? �Often cardiovascular
workup is necessary in these patients, but will remain unremarkable 3588: Dyspepsia
* ?? �Uncomfortable feeling of fullness or discomfort after eating; more of a
symptom than a disease * ?? �Three major routes to consider based on pt
presentation: o Typical GERD symptoms: PPI or H2 blockero NSAID/COX-2 inh. use:
stop using the NSAID/COX-2 inh. o Neither of the two above: ???Alarm symptoms
(weight loss, GI bleed, anemia, dysphagia, vomiting, early satiety): upper/lower GI
endoscopy ???No alarm symptoms: o ?? �Age >55: Scope o ?? �Age <55:o H.Pylori
testing (Breath test or stool assay) ???Treat if positive; PPI trial if negative
* ?? �If all of that fails, then have the patient undergo endoscopy Peptic Ulcer
Disease * ?? �Presentation: epigastric abdominal pain that changes (improve or
worsen) with eating, often with symptoms appearing at night spontaneously. Onset
gradual over weeks-months * ?? �Stool occult blood/anemia workup should be done to
ensure no active bleeding ulcers * ?? �Testing for H.pylori with PPI/triple or quad
therapy trial should be undertaken. Endoscopy should only be sought if these do NOT
resolve symptoms or alarm symptoms are present 3178: Perforated Peptic Ulcer
Disease * ?? �Presentation: chronic epigastric pain that suddenly worsens, with
rebound tenderness/guarding (peritonitis due to gastric contents in peritoneal
cavity), air under the diaphragm on CXR * ?? �Dx: immediate CXR, as diagnosis and
prompt treatment (<12hr) is critical to limit mortality * ?? �Tx: immediate
surgical repair 2596: MALT lymphoma (MALToma) * ?? �Gastric cancer often the result
of H.pylori infection; looks like a heaped up ulcer * ?? �Dx: endoscopy with biopsy
showing MALT-lymphoma * ?? �Tx: o Eradication of H.pylori ([omeprazole,
clarithromycin, amoxicillin] or [bismuth, omeprazole, a tetracycline, an
aminoglycoside] o Chemotherapy ([CHOP] or [CHOP + bleomycin]) can still play a role
should H.pylori eradication fail to cure the cancer 3591: Gastrinoma (Zollinger-
Ellison Syndrome) * ?? �Gastrin secreting tumor??overwhelming stimulation of
parietal cells to secrete HCl/intrinsic factor * ?? �Presentation: dyspepsia, GERD,
abdominal pain, weight loss, diarrhea, frank GI bleeding o Endoscopy: thickened
gastric folds, multiple gastric ulcers, duodenal/jejunal ulcers which are
refractory to PPI use o Often sporadic (ages 20-50) but can be associated with MEN-
1 syndrome o May result in steatosis due to acidic inactivation of pancreatic
enzymes?? Dx: if characteristic findings clinically/on upper endoscopy follow this
testing algorithm o Serum gastin level: check 1 week after stopping PPI???<110
pg/mL = not gastrinoma???110-1000 pg/mL = indeterminate, further studies are needed
???>1000 pg/mL = gastrinoma , confirm with stomach pH testing o Secretin secretion
test: a test for indeterminate levels of gastrin; secretin inhibits gastrin
producing G-cells, thus if gastrin levels drop, you don�t have a gastrinoma.
Gastinomas are stimulated by secretin, thus a rise means you have gastinoma. * ???
�Calcium infusion study: if a secretin test is negative but clinical suspicion is
still high, the calcium infusion that illicits a rise in serum gastrin points to
gastrinoma * ???�Chromogranin A: a neuroendocrine tumor marker that�s elevated in
many situations but can be elevated in gastrinoma and helpful if clinical suspicion
is high o Stomach pH testing: important confirmatory test with a diagnostic gastrin
level. Gastrin may be physiologically elevated due to achlorhydria (failure of HCl
secretion). ???pH< 4 = gastrinoma ???ph > 4 = not gastrinoma ?? Tx: surgical
resection Case 48 � Fever and Rash in a Child Case 49 � Diseases of the Breast
[Chapter 33: Disorders of The Breast � Topic 40] Anatomy * ?? �Breasts are
essentially modified sebaceous glands that have gained the ability to produce milk.
Younger women have a high amount of glandular/ductal tissue and as life progresses,
the tissue is slowly replaced by fat, a process accelerated by menopause * ?? �The
largest amounts glandular tissue is in the upper, outer quadrant of the breast;
this also explains why the majority of breast cancers first appear in this region *
?? �The breast has a rich blood supply and lymphatic system, which is great for
support, but poses problems when cancer arises. The ipsilateral lymph nodes and
internal mammary lymph nodes are the most common sites of metastases. * ?? �Breast
tissue development is primarily the result of sex hormones:o Estrogen � stimulates
growth of adipose tissue/lactiferous ducts o Progesterone � stimulates lobular
growth and alveolar budding Evaluating Breast Signs/Symptoms * ?? �Breast Cancer
Risk Factors � increasing age, Hx of breast cancer/atypical hyperplasia, BRCA1 or
BRCA2 mutation, high density breast tissue, increased estrogen exposure (early
menarche, late menopause, nulliparity, no breast feeding), long-term OCP use,
alcohol consumption, tall height, high SES, and Ashkenazi Jewish ancestry * ??
�History/Physical � history is always important. The breast exam is best done
during the follicular phase of the menstrual cycle as breast tissue will be
maximally stimulated by hormonal changes * ?? �Diagnostic Testing o Mammography �
basically an X-ray of the breast. It�s a standard screening procedure for women age
>50. Useful as it can detect lesions approx. 2yr before palpable. Also note that
lobular carcinoma is the hardest to detect. If a mass is found, scan the other
breast as well as the lymph nodes to search for other abnormalities. o
Ultrasonography � the most common modality to evaluate a breast mass in women
<40yrs (esp. adolescents / those with dense breast tissue) o MRI � may be used in
women who are high risk, but not a typical modality due to cost, no standard
imaging protocol, and inability to detect microcalcifications. o Fine-Needle
Aspiration (FNA) � if clear fluid and reduction of mass occurs, pt may be scheduled
for follow up in 4-6wk. If bloody, send to cytology and initiate a
mammogram/ultrasound. If mass re-appears upon follow-up, initiate
mammorgram/ultrasound. o Core-Needle Biopsy � often used in larger, solid breast
masses to assess cellular architecture ?? Algorithm o If it�s cystic??do an FNA???
Clear/mass disappears??no worries, follow up and reassess???Clear/mass persists??
mammogram/ultrasound???Bloody??send for cytology/perform mammogram/ultrasound ???
Nothing aspirated??perform mammorgram/ultrasound o If you�ve done a
mammogram/ultrasound???Complex cyst??FNA and consult surgery/rads???Simple cyst??
aspirate or just watch depending on symptoms ???Suspicious/intermediate/solid
mass??excisional biopsy???Normal??follow-up in 2-3mo Benign Breast Diseases??
Mastalgia � breast pain, characterized by it�s type of onset o Cyclic � begins in
luteal phase and resolves with menses. Bilateral/upper outer quadrants. The result
of proliferation of breast tissue during normal hormonal changes o Noncyclic � not
associated with menstruation and worrisome. May be idiopathic but must be worked up
for other causes. May be the result of hormone therapy (OCPs, ERT, etc.) o
Extramammary � chest wall trauma, rib fractures, shingles, you name it. Lots of
things can happen to the chest wall, so just because it�s there, doesn�t mean it�s
the breast. o Treatment can include:???Hormone suppression with danazol,
bromocriptine, GnRH agonists, Lisuride maleate (DA agonist), progestin-only
contraception, or SERMs (tamoxifen/raloxifene; only used in severe mastalgia that�s
unresponsive to conventional therapy.) ???Assessment for better fitting bra/use of
a sports bra ?? Nippleo Spontaneous, non-bloody, bilateral � fibrocystic changes or
ductal ectasiao Green, yellow, or brown-sticky bilateral � ductal ectasia or
fibrocystic changes in the breast o Milky bilateral � childbearing or endocrine
abnormalityo Purulent � infection of ducto Bloody/unilateral � intraductal
papilloma, invasive ductal carcinoma, intraductal carcinoma
???Will need workup with ultrasound, mammography, and possibly ductograpy ??
Benign Breast Mass o Signs of malignancy - >2cm, immobile, poorly defined margins,
firm, skin dimpling, skin color changes, retraction or changes to nipple, blood
discharge, or ipsilateral lymphadenopathy. o If these signs are not present, then
you�re more likely to have a benign mass o Non-proliferativelesions ???Fibrocystic
changes � dilation and scarring/inflammation that occurs normally in women that can
may be breast diffusely more dense/firm ???Adenosis � increase in number of
glands/lobular growth that can produce small masses Discharge � it�s all about the
color, consistency, and bilaterallity ???Simple Fibroadenoma � tumor of young
women; round, rubbery, mobile; do NOT have malignant potential but because they�re
made of breast tissue they can enlarge with normal cycles or pregnancy and cause
discomfort o Proliferative Lesions without Atypia � often do NOT cause a palapable
mass, but are proliferations of benign cells of either ductal or lobular epithelium
* ???�Epithelial hyperplasia � expansion of the basement membrane making for more
than 2 layers of cells along the ducts * ???�Sclerosing adenosis � increased
fibrosis/distortion and compression of the epithelium * ???�Radial scar � nidus of
tubules trapped within a hyalized stroma; mimicking invasive carcinoma as the arms
of sclerosis radiate outward. * ???�Papilloma � intraductal growths with abundant
stroma and normal lining. These are the most common cause for blood in nipple
discharge (sero-sanguinous) o Proliferative Lesions with Atypia � proliferation of
malignant epithelium lining the ducts resulting in a carcinoma in-situ. This has
malignant potential, but it not cancer yet due to an intact basement membrane by
definition. * ???�Lobualr (LCIS) � involves the lobules, often bilateral and
multicentric (multiple spots). Biggest risk for malignancy is either breast. * ???
�Ductal (DCIS) � involves the ducts, often unilateral and unicentric (in one spot).
Biggest risk for malignancy is in the breast that it�s appeared in. * ???�Both
should be evaluated with a core-needle biopsy and treated accordingly; note that
SERM usage after treatment has been shown to reduce the risk of invasive breast
cancer Breast Cancer * ?? �#2 cancer in women (behind skin cancers), with a
steadily increasing rate attributed to increase of mammographic screening, finding
small disease which would have previously gone undetected. * ?? �Risk Factors o Age
� the #1 risk factor for developing breast cancer. Older women get breast cancer
(>age 50) which is why we begin regular mammograms at age 50. o Race � White women
have higher rates (go figure!)o Genetics � if a woman is diagnosed with breast
cancer before age 40, she should have screening for genetic mutations (most notably
BRCA1/BRCA2)o Estrogen exposure � increased estrogen exposure for the classic
reasons are associated o Breast changes � women with dense breast tissue are at
higher risko Others � overweight/obesity (^estrogen) and alcohol use (unknown) are
both assocaited ?? Staging � TNM staging (Tumor characteristics, Node involvement,
and Metastases) as well as estrogen receptor testing (Her2/neu) can help predict
prognosis ?? Treatmentso Surgical * ???�Mastectomy � removal of all breast tissue
with preservation of pectoralis muscles * ???�Lumpectomy + radiation � removal of
breast tumor only. Radiation is essential and the combination of the two approaches
similar outcome rates as mastectomy * ???�Breast re-construction should always be
offered to patients after these procedures o Medical * ???�Classic chemo drugs used
as adjuvant therapy are often used with widespread disease * ???�Aromatase
inhibitors can be used to limit estrogen in post-menopausal women * ???�SERMs
(tamoxifen/raloxifene) can be used to limit estrogen exposure only in the breast.
Unfortunately, these can be agonists at other sites increasing risk of endometrial
cancer. * ???�Trastuzumab � useful if cancer is Her2-neu(+) as it targets these
cells for destruction; serious side effects of heart failure, respiratory problems,
allergic rxns can occur Screening Guidelines * ?? �Breast Self Exams are NOT
recommended any longer, as they were found to be ineffective and lead to excess
concern/testing for benign breast diseases * ?? �Breast self-awareness is now
recommended (being aware of normal breast architecture/look and voicing concern if
this changes) * ?? �Mammography value increases with increasing age, thus we begin
at age 50 for regular screening * ?? �Guidelines o Women age 20-39 � clinical
breast exam every 1-3yro Women age 40-49 � clinical breast exam every 1-3yr +/-
mammographyo Women age 50+ � clinical breast exam and mammography every yearo Women
with BRCA mutations � monthly breast self-exams starting at age 18, annual clinical
breast exams at age 18, and annual mammography +/- MRI at age 25 [Chapter 33:
Disorders of The Breast � Topic 40]?? Stimulation of the breast during the physical
examination may give rise to an elevated prolactin level and promote milky
discharge. Post partum women may continue to produce milk for up to two years after
cessation of breastfeeding o Accurate prolactin levels are best obtained in the
fasting state.o If still elevated, then a TSH level and brain MRI are indicated to
rule out a pituitary tumor. o Although pathologic factors such as hypothyroidism,
hypothalamic disorders, pituitary disorders (adenomas, empty sella syndrome), chest
lesions (breast implants, thoracotomy scars, and herpes zoster) and renal failure
can elevate prolactin levels, a non-significant benign elevation needs to be ruled
out first. * ?? �If there�s a dominant breast mass, but no obvious signs of
malignancy an FNA is a great first option. If it�s got signs of malignancy, then an
excisional biopsy may be indicated. * ?? �Fibrocystic breast changes are the most
common type of benign breast conditions and occur most often during the
reproductive years. Fibrocystic disease is often associated with cyclic mastalgia,
possibly related to a pronounced hormonal response. Caffeine intake can increase
the pain associated with fibrocystic breast changes, so recommending decreased
caffeine intake may be helpful. * ?? �The first noticeable symptom of breast cancer
is typically a lump that feels different from the rest of the breast tissue. More
breast cancer cases are discovered when the woman feels a lump. o Even though the
mass decreased in size after aspiration, the bloody discharge obtained obligates an
excisional biopsy be performed to rule out breast cancer. o If clear discharge is
obtained on aspiration and the mass resolves, reexamination in two months is
appropriate to check that the cyst has not recurred. * ?? �Most postpartum mastitis
is caused by staphylococcus aureus, so a penicillin-type drug is the first line of
treatment. Dicloxacillin is used due to the large prevalence of penicillin
resistant staphylococci. Erythromycin may be used in penicillin allergic patients.
* ?? �If you have a dominant breast mass and FNA fails to reduce it, get an
excisional biopsy. 2345: Evaluation of a Breast Mass * ?? �Step 1: Breast Mass
found/reported; do a breast exam to confirm report * ?? �Step 2: Ultrasound &
mammography for evaluation of the found mass o If <30??ultrasound +/- mammography o
If >30??mammography +/- ultrasound * ?? �Step 3: Evaluate the findings o Simple
cyst??FNA to asses fluid; if normal, come back in 2-4 months for evaluationo
Complex cyst or solid mass??core biopsy with possible excision of mass depending on
results 2607: Paget�s Disease of the Breast/Nipple * ?? �Presentation: persistent
eczematous/ulcerating rash around the nipple/areola with pain/itching without
relief from topic corticosteroid creamo 85% of these patients have underlying
adenocarcinoma * ?? �Dx: ultrasound/mammography with biopsy * ?? �Tx: excision Case
50 � Irregular Menstrual CycleNever forget, the #1 reason for an abnormal menstrual
period is pregnancy. Chapter 37: Reproductive Cycles; Ch 39: Amenorrhea/Abnormal
Uterine Bleeding � Topic 43/45 QUESTIONS * ?? �Most women resume normal menstrual
cycles after discontinuing oral contraceptive pills (OCPs), they are not usually
considered the cause of the amenorrhea. A history of irregular cycles prior to pill
use may increase the risk of amenorrhea upon discontinuation. This is sometimes
referred to as �post pill amenorrhea.� * ?? �Disorders of clotting may present with
menstrual symptoms in young women, with Von Willeberand disease being most common.
* ?? �Management of an endometrial polyp includes the following: observation,
medical management with progestin, curettage, surgical removal (polypectomy) via
hysteroscopy, and hysterectomy. o Observation is not recommended if the polyp is >
1.5 cm.o In women with infertility polypectomy is the treatment of choice. While
her inability to get pregnant may be more complicated than just her polyp, removal
of the polyp should occur prior to infertility treatments. * ?? �Abnormal uterine
bleeding is a term used to describe uterine bleeding abnormalities. This term can
encompass both structural causes (polyp, adenomyosis. Leiomyoma, or malignancy [or
hyperplasia]) as well as non-structural causes (coagulopathies, ovulatory
dysfunction, endometrial, iatrogenic or not classified). The acronym PALM-COEIN is
a means for this classification. * ?? �Hysteroscopic myomectomy preserves the
uterus, while removing the pathology causing the patient�s symptoms. A laparoscopic
approach is not indicated as the myoma is submucosal and not accessible using a
laparoscopic approach 4769: Pts who are in their first year of ovulation will
experience 90% annovulatory cycles in that year. This means that their cycles
will be irregular with breakthrough bleeds and often heavy because the lack of
ovulation means a lack of endometrial sloughing. Thus the endometrium gets built up
until the woman finally does ovulate, making for very heavy periods. ?? If periods
become more normal (1/month) and are still very heavy, bleeding disorders and
abnormalities of the uterus should then be considered, but not in the first 1-2
years of cycling. [Chapter 48: Uterine Leiomyoma and Neoplasia � Topic 53] Uterine
Leiyomyoma (�Fibroids�) ?? Presentation: vaginal bleeding with progressively
heavier menstrual flow, which is longer in duration with progressive pain that
ultimately persists beyond menstrual bleeding; iron deficiency anemia, subjective
pelvic pressure/fullness, and necrosis of the fibroid can also occur o Abnormal
uterine distortion often present in large fibroids; sometimes palpable externally
as a large, solid, midline, irregular-contoured, mobile pelvic mass. o Compression
of the ureters can cause hydrouteter/hydronephrosis * ?? �Etiology: abnormal growth
of the uterine smooth muscle for poorly defined reasons * ?? �Dx: presentation with
ultrasound/MRI confirmation of uterine distortion with masses o Surgical evaluation
may be used in pts where imaging does not confirm diagnosis but diagnosis is
strongly clinically suspected ?? Txo
MostcommonlyptsareasymptomaticanddoNOTrequiretreatmento Medical treatment:
progestin OCPs or local hormonal contraceptives with NSAIDs to minimize symptoms
until menopause; often GnRH analogous are used to reduce fibroid size (40-60%) if
surgical treatment is soughto Surgical treatment: typically used in rapidly
enlarging masses, masses unresponsive to medical treatment, and masses causing
complication (infertility, anemia, hydronephrosis) * ???�Myomectomy: removal of
only the fibroid tissue. Not a definitive treatment, but good for retention of
fertility * ???�Hysterectomy: definitive treatment for women who are done with
childbearing or in dire situations. Fibroids are the most common cause of
hysterectomy * ???�Myolysis or Uterine Artery Embolization: both seek to
shrink/destroy fibroid tissue, but rarely can take out all fibroids. May be useful
in patients who are poor candidates for surgery and only seek relief for symptoms.
Not currently recommended for women trying to continue to have children. ?? Effects
on Pregnancy: associated with infertility due to distortion of the uterine cavity
with large leiomyomas o Typically, medical treatment is strictly indicated, however
discrete pedunculated myomas may be surgically removed if easily clamped/ligated. o
Otherwise myomas should be removed at time of delivery.o Rarely, myomas can distort
the lower portion of the uterus, contributing to dystocia. If this occurs, c-
section is warranted. 8943: Uterine Leiomyoma (Fibroids) * ?? �Presentation:
progressive menorrhagia with dysmenorrhea with abnormally shaped, irregularly
enlarged uterus on exam. May cause pressure on bladder/bowels causing painful
urinartion/defecation o May prolapse through the cervical os if present
submucosally, showing a firm, whitish, smooth mass protruding through the cervical
os causing labor-like pain and cervical dilation. * ?? �Dx: pelvic ultrasound
(don�t do a biopsy or a CT/MRI!) * ?? �Tx: If asymptomatic??observation; if
perimenopausal??contraception till menopause; if definitive treatment if sought??
embolization, myomectomy, or hysterectomy are all options! 2408/2606: When
considering SERMs there�s really two: * ?? �Tamoxifen: antagonist at the breast,
but agonist everywhere else o Used as adjunctive therapy for breast cancer o Inc
risk of DVT/hot flashes/endometrial cancer and hyerplasia * ?? �Raloxifene:
antagonist at the uterus and breast, but agonist every where else o Used to treat
osteopososis when pt cannot tolerate bisphosphonate o Inc risk of DVT/hot flashes *
?? �Note that hot flashes are the most common side effect of SERMs Chapter 48:
Uterine Leiomyoma and Neoplasia � Topic 53 QUESTIONS ?? The #1 symptom in uterine
fibroids is menorrhagia (think of your lady in clinic!) due to: o Increase in the
uterine cavity size that leads to greater surface area for endometrial sloughing o
Obstructive effect on uterine vasculature that leads to endometrial venule ectasia
and proximal congestion in the myometrium/endometrium resulting in hypermenorrhea.
?? Fibroids can be detected in as high as 80% of women. Most uterine fibroids are
asymptomatic and do not require any treatment. o Fibroids may grow or become
symptomatic in pregnancy due to hemorrhagic changes associated with rapid growth,
known as red or carneous degeneration. However, this is uncommon for smaller
fibroids. o Fibroids can be located below the fetus, in the lower uterine segment,
or cervix, causing a soft tissue dystocia, necessitating delivery by Cesarean
section. o Myomectomy at the time of Cesarean section should be avoided, if
possible, secondary to the risk for increased blood loss o It is not necessary to
follow the growth of fibroids during pregnancy, except for the rare cases when the
fibroid is causing symptoms (primarily pain) or appear to be located in a position
likely to cause dystocia. * ?? �Leiomyomas are an infrequent cause of miscarriages
and subfertility either by mechanical obstruction or distortion (and interference
with implantation). o Submucosal or intracavitary myomas cause lower
pregnancy/implantation rates via: ???Focal endometrial vascular disturbance???
Endometrial inflammation???Secretion of vasoactive substances. o Submucosal
fibroids are best treated by hysteroscopic resection. * ?? �Medical management of
fibroids includes 1NSAIDs and progestin OCPs/IUDs; but if that doesn�t work 2GnRH
analogues can be used to shrink fibroids for either symptomatic tx OR easier
surgical resection. o Don�t forget! Fibroids feed off estrogen! Thus, just giving
estrogen would be a poor choice.o Often GnRH analogues are used in older women
(this lady was 49) until they reach menopause, where the fibroids will shrink due
to loss of endogenous estrogen. * ?? �This question had a woman who was worried her
big belly (BMI 37) was caused by a large fibroid. Sadly, she�s just obese and
should be counselled on diet and exercise.o Bariatric surgery may be considered
when BMI is greater than 40, or is between 35 to 39.9 accompanied by a serious
weight-related health problem, such as type 2 diabetes, high blood pressure or
severe sleep apnea. This lady had no other problems. * ?? �If patients present with
menstrual abnormalities, the endometrial cavity should be sampled to rule out
endometrial hyperplasia or cancer, even if it really sounds like fibroids. This is
most important in patients in their late reproductive years or postmenopausal
years. o If the patient�s bleeding is not heavy enough to cause iron deficiency
anemia, reassurance and observation may be all that are necessary. o Treatment with
GnRH analogues to inhibit estrogen secretion may be used as a temporizing measure.
Can be used for three to six months prior to a hysterectomy to decrease the uterine
size and increase a patient�s hematocrit; either leading to easier surgery (smaller
fibroid/less blood loss) or tide a patient over into menopause. ?? Mean uterine
size decreases 30-64% after three to six months of GnRH agonist treatment.o In a
patient who desires future fertility, this may be a good short-term option to
decrease pain/blood loss; esp. if hematocrit is decreasing.o Maximal response is
usually achieved by three months of GnRH agonist treatment. The reduction in size
correlates with the estradiol level and with body weight. ?? When treating with a
GnRH agonist: o Hot flashes are experienced by >75% of patients (3-4wk) but
shouldn�t persist for more than one to two months. o After cessation of treatment,
menses return in 4-10wk, and myoma/uterine size return to pretreatment levels in 3-
4mo. ???Fibroids will regain their normal growth after cessation of treatment; the
myth that they�ll grow faster due to hormone withdrawal is unsubstantiated.
[Chapter 49: Cancer of the Uterine Corpus � Topic 54] Endometrial Hyperplasia ??
Types:o Simple Hyperplasia (1% risk progression) � proliferation and stromal cell
proliferation together. Does NOT typically progress to endometrial carcinomao
Complex Hyperplasia (3% risk progression) � abnormal proliferation of mainly
glandular elements without accompaniment with stromal elements giving a �crowded�
appearance. o Hyperplasia with Atypia (8% if simple, 29% if complex) � either type
of hyperplasia where glandular elements show cytologic atypia and disordered
maturation (loss of polarity, nuclear enlargement, increased nuclear-to-cytoplasmic
ratio, dense chromatin, and prominent nucleoli) * ?? �Pathophysiology: overgrowth
of the endometrium due to unopposed estrogen exposure o Endogenous sources:
ovaries, fat, or granulosa cell tumor of the ovary o Exogenous sources: exogenous
estrogen of any kind (OCPs, patches, creams, etc.) * ?? �Risk Factors: all have to
do with estrogen exposure, arranged from highest to lowest risk increase: o High-
dose menopausal estrogen (10-20x), Living in N.America or N.Europe (3-18x),
Tamoxifen use (3-7x), estrogen producing tumor (5x), Obesity (2-5x), Increased
estrogen exposure from menstrual cycles (nulliparity, infertility, early menarche,
late menopause) * ?? �Presentation: abnormal uterine bleeding should prompt further
evaluation in women >35yrs or women <35yrs with risk factors * ?? �Dx: o
Endometrial evaluation: endometrial biopsy (90-98% accuracy) should be initial
evaluation. D&C and pap smear are not as accurate at diagnosiso Transvaginal
Ultrasound: if you see an endometrial thickness >4mm in post-menopause, a polypoid
mass, or fluid collection you are prompted for further
evaluation ?? Tx: o Medical: synthetic progesterones (medroxyprogesterone acetate;
decrease estrogen receptors and thin the endometrium) are used typically in pts
without atypia o OtherTx:maybetherapeuticD&Cordefinitivetreatmentwithhysterectomy
Endometrial Polyps * ?? �The result of focal, benign hyperplasic growth with
abnormal bleeding being the primary presentation * ?? �Less than 5% of polyps are
malignant; although may be removed * ?? �More often malignancy in post-menopausal
women, esp. if taking tamoxifen therapy Endometrial Cancer * ?? �Presentation:
abnormal uterine bleeding in a post-menopausal woman * ?? �Pathogenesis: o Estrogen
dependent (90%; Type I): often from estrogen exposure; good prognosiso Estrogen
independent (Type II): arise spontaneously; poorly differentiated; poor prognosis o
If invasive, cancer typically spreads through endometrial cavity, into myometrium,
then endocervix, then into the lymphatics * ?? �Risk Factors: identical to those
for endometrial hyperplasia * ?? �Dx: endometrial biopsy showing cancerous change
with pre-operative CA-125 level o Prognosis: Higher grade and deeper depth of
invasion yield a worse prognosis?? Tx: hysterectomy with complete surgical staging
and assessment of regional/retroperitoneal lymph nodes is both therapeutic and
improves survivalo If lymph nodes are positive, post-surgical
radiation/chemotherapy is critical for treatment Recurrent Endometrial Carcinoma
* ?? �If pt has not received radiation: evaluate with speculum/recto-vaginal exam
every 3-4mo for 2-3yr * ?? �If radiation therapy: less frequent surveillance is
used * ?? �If present, recurrent estrogen or progestin (+) cancer can respond well
to high-dose progestin therapy Hormone Therapy After Endometrial Carcinoma Tx ??
Post-menopausal estrogen therapy MAY be used in women who have be previously
treated for endometrial carcinoma, but good candidates must be selected based on
certain prognostic indicators and women must know of the risk they have. Uterine
Sarcoma * ?? �Presentation: progressive uterine growth in a post-menopausal woman,
post-menopausal bleeding, pelvic pain, increased vaginal dischargeo Even if they�re
on estrogen therapy, this type of growth should always be considered pathologic o
Often these tumors are extremely aggressive, thus treatment must be prompt * ??
�Dx: surgical evaluation, resection, and histologic evaluation * ?? �Tx:
hysterectomy o Radiation, chemotherapy, and and hormonal therapy do not produce
good results 2391: Abnormal Uterine Bleeding (AUB) is always concerning for
endometrial cancer, thus an endometrial biopsy is typically warranted to rule this
out. Criteria indicating an endometrial biopsy include: * ?? �Age >45 � AUB or
post-menopause bleeding ???do an endometrial biopsy! * ?? �Age <45 � AUB +
[unopposed estrogen, failed medical management of AUB, or Lynch syndrome] * ??
�Remember that a Pap smear is ONLY A SCREENING test and should never be used to
confirm suspected pathologic changes! Chapter 49: Cancer of the Uterine Corpus �
Topic 54 QUESTIONS ?? In a post-menopausal patient having abnormal uterine
bleeding, risk factors for endometrial carcinoma can help determine how likely
they�ve developed a cancer/possible severity. In order of highest conferred risk: o
Finding of complex endometrial hyperplasia on endometrial biopsy � 28% of pts have
cancer o Obesity (esp. if >50lbs over ideal body weight) � 10x normal risko
Nulliparity, early menarche, late menopause, hypertension, diabetes and exposure to
unopposed estrogens (HRT or SERMs) � all increase to different degrees * ?? �Less
than 5% of women diagnosed with endometrial cancer are asymptomatic. Approximately
80-90% of women with endometrial carcinoma present with vaginal bleeding or
discharge as their only presenting symptom. Thus, if a patient is asymptomatic and
lacks many risk factors (or all in this case) yearly regular exams are the best
course of action. * ?? �The most common symptom is abnormal postmenopausal
bleeding. This may be accompanied by abnormal vaginal discharge, lower abdominal
discomfort, and increased size of the uterus, but these are less common findings. o
Note that combination ERT does NOT increase the risk of endometrial cancer * ??
�This question has a 65y/o G2P1 with homogenous thickening of the endometrium to
5mm. Biopsy revealed rare atypical cells. D&C is the correct next step. In a woman
with persistent symptoms suggestive of endometrial cancer, AND with a negative
biopsy, further investigation with D&C to sample the entire endometrium is the best
course of action. * ?? �This question has a lady that had FIGO Grade 1 endometreoid
adenocarcinoma on endometrial biopsy. This is low-grade and the next best step is
to confirm that there�s no spread of the cancer outside the uterus, so we can
possibly have less intense treatment thus: o Routine evaluation in this setting
should include a chest x-ray as the lungs are the most common site of distant
spread. o CA-125 may be helpful in predicting those patients that may have
extrauterine spread, but is not absolutely necessary o A pelvic ultrasound is not
indicated once a pathologic diagnosis has been established, although one may have
been obtained as part of the initial evaluation of postmenopausal bleeding. o When
there is a low suspicion for advanced disease, a CT scan, MRI, PET scan, and other
invasive and costly tests are not indicated. * ?? �Recommended components of the
surgical approach to an early endometrial cancer are the extrafascial total
abdominal hysterectomy, bilateral salpingo-oophorectomy, and pelvic and para-
aortic lymphadenectomy; best done in high grade (>3) or aggressive types (clear
cell, papillary serious) o Vaginal or laproscopic approaches can also be done as
alternatives o Chemotherapy, radiation, and hormonal therapy may be utilized, but
in an adjuvant setting. * ?? �Graunlosa cell tumor (Granulosa-Theca tumor) is a
functional, estrogen secreting tumor that may cause increase bleeding, �speeding
up� of periods, and complex endometrial hyperplasia w/out atypia * ?? �Theca-lutein
cyst � typically bilateral cysts that occurs due to markedly increased B-hCG
production (most often during a molar pregnancy), causing uniformly complex, fluid
filled ovarian cysts. Often these resolved after B-hCG level return to normal. * ??
�Postmenopausal bleeding or discharge accounts for the presenting symptom in 80-90%
of women with endometrial cancer, thus if these occur, an H&P, pelvic examination,
and endometrial biopsy should occur. However, the causes for post-menopausal
bleeding are as follows: o Atrophy of the endometrium (60-80%), hormone replacement
therapy (15-25%), endometrial cancer (10-15%), polyps (2-12%), and hyperplasia (5-
10%). o Transvaginal ultrasound can be a useful tool as it can visualize polyps,
myomas, or endometrial thickening. Also, if the endometrial stripe is <5mm, there�s
a low chance for endometrial cancer to be present ?? This question had a lady with
remote hx (15yr ago) of endometrial cancer now presenting with cough, dyspnea, and
bilateral lower extremity edema. o The most appropriate next step is to refer her
to a pulmonologist (or cardiologist) for a thorough work-up. Pleural effusions and
lower extremity edema point towards a cardiopulmonary etiology and you need to rule
this out before going for cancer. o However, the finding of a solitary lung nodule
in a patient exposed to second hand smoke certainly suggests the possibility of a
primary lung cancer. ?? While Taxomifen is known to increase risk of endometrial
cancer, any woman on therapy with it should have regular yearly exams from their
gynecologist. If they�re asymptomatic, no ultrasound/biopsy studies are needed.
Case 51 � Diabetes Mellitus [Type I Diabetes] Autoimmune destruction of pancreatic
B-cells (produce insulin) ?? Juvenile onset & pathogenesis poorly understood o 95%
of pts with T1DM have HLA Haplotype DR3/DR4o Viral infections (coxsackie virs &
rubella) have been linked with developmento Girls with protracted monilial
(Candidia) vulvovaginitis may have early Type 1 DMo Autoantibodies formed � islet
cell antibodies (ICA; 85%), anti-insulin antibodies, or angi glutamic acid
dearcoxylase antibodies; often can be detected well before clinical manifestations
o Adolescents may present with DM1 during puberty growth spurt (GH and sex steroids
are antagonistic to to insulin action...resulting in setting of phenotype) ?? Prone
to diabetic ketoacidosis (DKA) o Result of nearly no uptake of sugar from the blood
into cellso Because cells can�t get sugar, they start to metabolize fat, producing
ketones at a large scale o This is the basis for a ketogenic diet (burns fat cuz no
carbs!) [Type II Diabetes] Resistance to the Effects of Insulin * ?? �Adult onset &
pathogenesis involves first the resistance to uptake causing a constant hyper-
insulin- emic state, eventually giving way to �burnout� of the pancreatic B-cells *
?? �Patients will be hyperinsulinemic for years until symptoms occur, then will be
diabetic for many more years until burnout occurs (the �insulin dependent type II
diabetic�) * ?? �Prone to Hyperosmolar Hyperglycemic State (HHS) o
Resultofpooruptakeofsugaro However, the sugar CAN (to some degree) enter the cells,
making fat burning not necessary, thus the build-up of ketones doesn�t occuro
Extreme serum osmolarity results in diuresis & dehydration causing problems
[Gestational Diabetes] 4793/12179: Gestational Diabetes Mellitus?? Presentation:
abnormal fasting glucose with onset during pregnancy o The results of B-cell
hyperplasia and physiologic peripheral insulin resistance due to hPL production by
the placenta (increase sugar availability for the fetus/placenta) ?? Dx:o At 24-
28wk: 1-Hr 50g glucose challenge??target
if <140 mg/dLo If >140 mg/dL: 100g glucose challenge; check levels each hour for 3
hrs; if 2 parts are abnormal you�ve made your diagnosis???Fasting � <95 mg/dL is
normal ???Hr 1 � 180 mg/dL is normal???Hr 2 � 155 mg/dL is normal???Hr 3 � 140
mg/dL is normal ?? Tx: 1. Dietary modifications (balanced diet with glucose
control); if not controlled then 2. Insulin (intermediate + short-acting BID; best
choice) 3.metformin or glyburide can be used as well o Weight loss is NOT
recommendedo Goals: fasting glucose <100 mg/dL and 1hr post-prandial <140 mg/dLo
Strong evidence that fasting levels <95 mg/dL provide better neonatal outcomes A
history of gestational diabetes mellitus (GDM) is the greatest risk factor for
future development of diabetes mellitus. It is thought that GDM unmasks an
underlying propensity to diabetes. While a healthy pregnancy is a diabetogenic
state, it is not thought to lead to future diabetes. About 50% of women with a
history of GDM will develop type 2 diabetes within 10 years of the affected
pregnancy. Women should be screened for DMII in the post-partum period because of
this. [Diabetes Insipidus] 3729/3899: Diabetes Insipidus * ?? �Presentation:
increased thirst, need to urinate, normal fasting glucose * ?? �Dx: o Water
deprivation test � serial measure of urine volume/osmolality until levels are
stable on approximately 2-3hrs of testing ???Diabetes Insipidus � urine will
continue to be dilute, while serum will be concentrated ???Primary Polydipsia �
urine will concentrate (>600mOsm)o Vasopressin Challenge � give vasopressin (ADH)
to see if urine concentrates ???Central DI � urine successfully becomes
concentrated (kidneys can respond) ???Nephrogenic DI � urine fails to concentrate *
?? �Tx:o Central DI � intranasal demopressin (ADH analogue)o Nephrogenic DI �
supportive care and HCTZ or other diuretics ???Discontinue offending drugs lithium,
demeclocycline, foscarnate, cidofovir amphotericin B [�Bronze Diabetes�] Hereditary
Hemochromatosis * ?? �Presentation: Skin (Hyperpigmentation, �bronze diabetes�),
MSK (arthalgias/arthropathy/chondrocalcinois), GI (elevated LFTs, with
hepatomegaly??cirrhosis, increased risk of hepatocellular carcinoma), endocrine
(diabetes, hypogonadism/hypothyroidism, diminished libido/erectile dysfunction),
cardio (restrictive cardiomyopathy/abnormal condution), and infections (Listeria,
Vibrio, and Yersinia increased susectibility) * ?? �Dx: HFE genetic mutation and
elevate iron studies * ?? �Tx: serial phlebotomy (decrease iron store) [Screening
and Diagnosis of Diabetes] 3807: Screening for Diabetes Mellitus * ?? �Available
Tests: Fasting Plasma glucose (>126), Random glucose (>200), HbA1c (>6.5), or oral
glucose tolerance test (>200) � the values indicate a diagnosis of diabetes
mellitus * ?? �All tests should be repeated to confirm diagnosis * ?? �USPSTF �
screen all patients with sustained BP >135/80 * ?? �ADA � screen all patients
>45y/o with risk factors for DM Ways to Diagnosis Diabetes Mellitus (all must be
confirmed with repeat testing) * ?? �Hemoglobin A1c level �6.5% * ?? �Fasting
plasma glucose level �126 mg/dL (no caloric intake for 8hr prior) * ?? �Random
glucose level �200 mg/dL in a patient with symptoms of diabetes * ?? �2-hour oral
glucose tolerance test value �200 mg/dL. * ?? �While a urine dipstick may be used
to screen for diabetes, it is not a diagnostic test. Some Fast Facts in Making the
Diagnosis ?? HbA1c of 6-6.5% is called �pre-diabetes� and patients should undergo
lifestyle changes to stop it. ?? Fructosamine levels can indicate glucose control
over the past 2-3wk; used in place of HbA1c in those with hemoglobinopathies or
recent intense blood loss Once the Diagnosis is Made * ?? �Fasting lipid panels
(annually) � DM has a huge association with metabolic syndrome * ?? �Serum
creatinine/urinalysis/urine microalbuminuria (annually) � diabetic nephropathy is a
big killer * ?? �Dilated eye examinations (annually) � diabetic retinopathy is a
huge blow to life quality * ?? �Regular foot exams � diabetic foot
ulcers/neuropathy are a huge killer/blow to quality of life * ?? �Thyroid Screening
(Type 1 only) � due to autoimmune nature of disease, autoimmune damage to or
activation of the thyroid gland is not uncommon [Management of Diabetes] Type I
Diabetics rely on Insulin therapy. Typically a 1.short-acting at meal time with 2.
Intermediate or long- acting once a day for baseline coverage. Type II Diabetics
should initially attempt control with lifestyle changes (it�s ALWAYS the first
intervention). However, diabetes drugs should be used to aid glucose control. The
following are considered in descending order for control: ?? Metformin (1-2% drop)
� typically first agent in DM control.o
Mec:decreasesgluconeogenesisprimarily;sensitizesperipheraltissuetoinsulinaidingin
uptake & decreases intestinal uptake of glucose secondarilyo Weight
neutral/decrease in TAGs & cholesterolo Low risk of hypoglycemiao Most commonly
causes GI upset and diarrheao Life threatening lactic acidosis with renal
insufficiency (Cr of >1.5 in men, >1.4 in women), hepatic failure or heart failure
* ?? �Sulfonylureas (glipizide; 1-2% drop) � typically added with metformin
monotherapy failure. o Mec: stimulate B-cells of pancreas to enhance insulin
secretion o Weight gain and hypoglycemia are major side effects. * ??
�Thiazoliadones (�-glitazone�; 1-1.5% drop) o Mec: improves insulin sensitivity
peripherally for enhanced uptake of glucoseo Low risk of hypoglycemia with slow
onset of action (12wk of therapy for effect) o Metabolized by the liver, thus Can
be used in renal insufficiencyo Weight gain, edema, CHF, bone fracture are all
possible. * ?? �Meglinitides (�-glinide�; 0.5% drop)o Mec: rapid onset stimulation
of insulin secretion from the pancreas o Onset within an hour; but high cost and
risk of hypoglycemia * ?? �a-Glucosidase inhibitors (Acarbose)o Mec: inhibit the
enzyme a-glucosidase, decreasing absorption of glucose from the intestines o Best
in limiting post-prandial sugar spikes, and useful in patients with sporatic eating
habits o Side effects of retention of sugar in gut causing flatulence/diarrhea * ??
�GLP-1 agonists (exenatide; 0.5-1% drop) � low hypoglycemia risk, may aid in weight
loss. Can cause acute pancreatitis and hypoglycemia when added to a sulfonylurea o
Mec: stimulates GLP-1 receptors to enhance release of insulin from pancreas o Upper
respiratory symptoms & hypersensitivity are the major side effects * ?? �DPP-4
inhibitors (�-gliptin�; 0.5% drop) � low risk of hypoglycemia, weight neural, can
be used in renal insufficiency o Mec: stops inactivation of GLP-1/GIP which are
release from the gut to stimulate the pancreas 11367: Tight glycemic control in
Diabetes Mellitus?? While glycemic control goals are between 6-7%, it doesn�t
decrease all the complications of DM: o Macrovascular complications (stroke,
atherosclerosis, etc.) don�t change with tight control o Microvascular
complications (nephropathy, retinopathy) decrease with tight controlo All-case
Mortality is not changed with tight control, but goes up with poor control
2910/3902: Tight Blood Pressure Control in Diabetes Mellitus * ?? �All diabetes
patients should be treated to keep blood pressure around 140/90 * ?? �Pts with
diabetic nephropathy should have more intese blood pressure control of 130/80 to
limit the effects of nephrotic syndrome. Typically, careful administration of an
ACE or ARB are warranted. This has been proven to decrase end-organ damage and
should be initiated at the first signs of diabetic nephropathy (microalbuminuria)
3823/4336: Guidelines for Lipid-Lowering therapy (typically a statin) * ??
�Symptomatic atherosclerotic disease??high or low intensity based on age (> or <
than 75yr) * ?? �LDL >190mg/dL??high intensity statin therapy * ?? �Age 40-75 with
diabetes ???high or low depending on 10-year ASCDV risk * ?? �Estimated 10-year
ASCVD risk >7.5%??moderate to high intensity statin therapy 3822: (refer to 2698) A
patient with Type II Diabetes Mellitus over the age of 40 should always be on a
statin and initiate positive lifestyle changes according to lipid lowering
guidelines. Refer to 2698 for the complete guidelines. 4171: Side effects of
Thiazide diuretics (HCTZ or chlorthalidone) * ?? �Glucose intolerance � worse
insulin release from pancreas AND tissue resistance to glucose uptake. Worse in pt
with diabetes or metabolic syndrome * ?? �Poor lipid metabolism with increased
LDL/triglycerides � similar to glucose intolerance. Worse in diabetes or metablic
syndrome * ?? �Hyponatremia/kalemia/magnesemia and hypercalcemia � based on
mechanism of action. Actually beneficial in staving off osteoporosis * ??
�Hyperureciemia and worsening gout � reduces renal uric acid excretion
[Complications of Diabetes] 2171/2184: Diabetic Ketoacidosis (DKA) * ?? �Often can
be the initial presentation of a young person with Type I diabetes mellitus. Often
pt will have weight loss/polydipsia and be able to compensate by simply drinking
more water. However, anything disrupting oral intake (recent illness) can throw
this off and send them into DKA * ?? �Presentation: polydipsia/polyuria, burred
vision, weight loss, altered mentation, hyperventilation, abdominal paino Labs:
hyperglycemia (250-500s), bicarb <18 (acidosis), elevated anion gap, (+)serum
ketones * ?? �Dx: presentation with specific labs * ?? �Tx: High-flow IV fluids, IV
insulin, close watch/replacement of potassium o Note the ketone level (B-
hydroxybutryate) or anion gap are the best methods by which you track response to
treatment 4247: Hyperkalemia in DKA [HIGH YIELD] * ?? �When DKA occurs, pts often
show paradoxical hyperkalemia due to 1extra-cellular shift of K in exchange for H+
ions to limit the acidosis and 2impaired
K+ entry into cells due to low insulin levels (insulin helps K+ enter into cells)
o Called �paradoxical� because the body is actually wasting K+, and overall levels
are low, however serum concerntration is high due to extracellular shift * ?? �Thus
pts in DKA should be given supplemental K+, insulin, and IV fluids because once
insulin is on board, the K+ level can tank quickly, unless it�s very high 2186:
Hyperosmolar Hyperglycemic State (HHS) ?? Presentation: old person with type II
diabetes; confusion/lethargy, fever, dehydration, gradual onset of hyperglycemia
symptoms (polyuria, polydipsia, etc.)o Labs: electrolyte abnormalities, glucose
>1000, pH around normal (7.4ish), normal bicarb, negative serum ketones, serum
osmolality >320o Pts often have paradoxical hyperkalemia driven by insulin
deficiency/hyperosmolality resulting in severe diuresis. The K+ moves out and is
peed out. * i �Dx: clinical picture with normal pH and severely high glucose
(>1000) * ?? �Tx: aggressive normal saline hydration (switch to 0.45% if sodium
replete), potassium supplementation, IV insulin NOT SUB-Q INSULIN DAMMIT and close
moitoring o Use ketone level or anion gap to track response to treatment 3800/3795:
Diabetic Neuropathy * ?? �Typically, this occurs in a stocking-glove pattern. Two
major manifestations of diabetic neuropathy: o Small fiber disease: pain/allodynia
predominate with less sensory/reflexive loss o Large fiber disease: numbness and
loss of sensation, often with loss of distal reflexes * ?? �Tx: many options
available and are listed in terms of desire: o First line: TCAs (amitriptyline,
desipramine, nortriptyline); good but may cause worsening urinary symptoms and
autonomic hypotension o Second line: Gabapentin; best used when TCA side effects
cannot be toleratedo Third line: NSAIDs (ketorolac, etc.); may worsen renal
functions, thus not as desired Neuropathy Associated with Diabetes Mellitus * ??
�Femoral neuropathy � weakness of the lower left leg, giving way of the knee, and
discomfort in the anterior thigh. Associated, but caused by conditions common to
diabetics, not the diabetes itself. * ?? �Meralgia Parasthetica � lateral femoral
cutaneous nerve neuropathy, secondary to diabetes. Numbness and paresthesia over
the anterolateral thigh with no motor dysfunction * ?? �Ileofemoral Atherosclerosis
- common complication of diabetes mellitus, may produce intermittent claudication
involving one or both calf muscles but would not produce the motor weakness noted
in this patient.? * ?? �Diabetic polyneuropathy - symmetric and distal limb sensory
and motor deficits with gradual onset 3797: Gastroparesis due to Diabetic Autonomic
Neuropathy * ?? �Presentation: decreased appetite, nausea, abdominal bloating, and
early satiety after meals in the setting of long-standing diabetes mellitus II * ??
�Dx: clinical presentation, possibly gastric emptying study showing gastroparesis *
?? �Tx: drugs (below) with small, more frequent meals o
Metoclopramide:prokinetic/antiemetic;riskoftardivedyskinesiao Erythromycin: helps
with GI kinetic activation; best used IV in acute exacerbations o Cisapride:
typically, not used for risk of cardiac arrhythmias/death 4750: Pathophys of
Diabetic Nephropathy * ?? �Caused by advanced glycation of the glomerular basement
membrane, resulting in dysfunction Ca?microalbuminuria??frank albuminuria * ??
�Histologic changes: diffuse nodular glomerulosclerosis (Kimmelstiel-Wilson
nodules) 2810: Renal Tubular Acidosis in Diabetes Mellitus * ?? �Classically Type 4
RTA (retention of K+/H+ by kidney resorption) occurs in poorly controlled DM * ??
�This results in preserved kidney function, with non-anion gap metabolic acidosis o
Labs: mild hyperkalemia, mild acidosis, diminished GFR, no anion gap [AAFP
Questions]Intensive management of hyperglycemia, with a goal of achieving
nondiabetic glucose levels, helps reduce microvascular complications such as
retinopathy, nephropathy, and neuropathy (which subsequently decreases foot
infections). o ?? �Intensive management of hyperglycemia also has a beneficial
effect on cardiovascular disease in patients with type 1 but not type 2 diabetes
mellitus. o ?? �In fact, there is data to suggest 1c that intensive glycemic
control (hemoglobin A <6.5) may be detrimental in certain populations, such as the
elderly and those with cardiovascular disease. Diabetes mellitus and cigarette
smoking are significant risk factors for intermittent claudication, as are
hypertension and dyslipidemia. Metformin and insulin are the only agents approved
for treatment of type 2 diabetes mellitus in children. The recommended time to
screen for gestational diabetes is 24�28 weeks gestation. The patient may be given
a 50-g oral glucose load followed by a glucose determination 1 hour later.Advisory
Committee on Immunization Practices of the Centers for Disease Control and?
Prevention recommended hepatitis B vaccine for all previously unvaccinated adults
between the ages of? 19 and 59 with diabetes mellitus, as soon as possible after
the diagnosis of diabetes is made. Onset of a lot of skin tags (acrochordons) are
associated with diabetes mellitus and obesity. Typically occurs in early adulthood,
and the most common locations are the neck and axillae. Testing for diabetes
mellitus should be considered in all asymptomatic adults who have a [BMI �25 kg/m2
+ one or more additional risk factors]: * ?? �Physical inactivity, a first degree
relative with diabetes, a high-risk ethnicity, hypertension, hyperlipidemia, or
polycystic ovary syndrome. In asymptomatic patients with no risk factors * ??
�Screening should begin at age 45. Treating Diabetes in Pt with renal disease ??
Glipizide is a good option as it is not eliminated renally OR has metabolites
eliminated renally ?? Metformin (avoid with Cr >1.5) is eliminated renally and
glyburide has an active metabolite that�s eliminated renally The black box warning
for thiazolidinediones (like pioglitazone) specifically addresses heart failure.
These agents are also contraindicated in patients with type 1 diabetes mellitus or
hepatic disease, and in premenopausal anovulatory women. Case 52 � Adverse Drug
ReactionsAdverse drug reactions happen all the time. There are a TON of reasons for
them. It�s important to remember: * ?? �More drugs = more problems: taking >5 meds
gives about a 33% chance of a drug rxn * ?? �Old people: changes in liver function,
kidney function, water volume distribution, and simply taking more medications puts
old people a much increased risk * ?? �Be aware: always ask, �might I have caused
this?�, when a person on polypharmacy presents. Herbal supplements and OTCs can
often play a huge role, always ask! * ?? �If unsure about problem drugs, used the
Beers Criteria list or the STOPP list to screen for drugs that are often found to
cause adverse reactions in older folks Liver * ?? �Often drugs undergo first-pass
metabolism, thus altering the liver�s ability to metabolize drugs can hugely affect
how much drug gets into the system * ?? �Liver metabolism of medications is largely
via CYP enzymes; alteration of these enzymes (alcohol, grapefruit juice,
medications, etc.) is often the culprit when investigating these problems * ??
�Albumin levels may also drop with liver function decline. Drugs that are albumin-
bound may dramatically increase serum levels if now unbound! Kidney * ?? �Many
drugs are excreted by the kidney and function may be affected by drugs! Thus it�s
important to monitor kidney function (via Creatinine) when assessing adverse drug
reactions * ?? �Pt with chronic diseases that affect the kidney (diabetes, HTN,
etc.) should be closely monitored when using renal eliminated drugs Case 53 � Low
Back PainLower back pain can range from mild and benign to severe and life
threatening. As the primary care doc, it�s your job to differentiate between the
two so interventions are prompt and appropriate. Cauda Equina Syndrome * ??
�Compression of the cauda equina as they exit the lower spine; may result in
permanent nerve damage * ?? �Presentation: low back pain often radiating down the
legs (�bilateral sciatica�); leg weakness, bladder/bowel dysfunction,
anesthesia/paresthesia in �saddle distribution�, decreased anal sphincter tone,
decreased lower extremity reflexes o Straight leg test produces pain/worsens
symptoms * ?? �Dx: clinical presentation with immediate lumbar MRI * ?? �Tx:
immediate surgical decompression of lumbar spine Infection In/Around the Spine * ??
�Osteomylitis/Pott�s Disease, paraspinous abscess, epidural abcess, or septic
discitis * ?? �Presentation: typically, low back pain with specific area of
discomfort and possibly signs of underlying infection (fever, redness, fluctant
mass, etc.) o Labs: CBC, ESRo Imaging: Osteolytic lesions in spine or abscess
formation (often plain films??CT/MRI) o Classically IV drug users could get this
disease * ?? �Dx: signs/symptoms with biopsy or strong clinical suspicion * ?? �Tx:
surgical debridement/drainage with IV antibiotcs Metastatic Cancer to the Spine
* ?? �Presentation: low back pain with insidious onset. Weight loss, worsening at
night, failure to improve after 1 month, and age >50 are all signs.o Typically,
osteoblastic lesions present in lumbar spineo MRI/radioactive bone scan should be
done to look/ID lesionso Multiple myeloma or metastatic prostate/breast/lung
cancers are most common * ?? �Dx: made with biopsy * ?? �Tx:
resection/chemotherapy/radiation therapy Herniated Disc * ?? �Squeezing out of the
spinal disc contents to compress the surrounding spinal cord * ?? �Presentation:
sharp/burning pain that radiates down the back & side of the leg. o Improves with
lying down/restingo Worsens with Valsalva, sneezing, coughing, and activity &
straight leg raiseo Specific
signs of radioculopathy (anesthesia, paresthesia, etc.) should only be confined to
one or two dermatomes corresponding with area of compression * ?? �Dx: clinical
presentation o Most occurs at the L4/L5 spinal outlet * ?? �Tx: NSAIDs (pain
control), physical therapy, or corticosteroids ???surgical resolution Spinal
Stenosis * ?? �Narrowed canals for passage of the spinal nerves causing symptoms
* ?? �Presentation: back pain, LE weakness/parasthesia, pseudoclaudication with
activity o Improves with bending over/squatting/sitting/lying down (opening up
those canals) o Most common in pts over 60yrs * ?? �Dx: clinical presentation * ??
�Tx: NSAIDs (pain control), physical therapy, or corticosteroids ???surgical
resolution Vertebral Compression Fracture * ?? �Acute damage to spine causing
compression due to altered outlets * ?? �Presentation: acute onset back pain,
classically after impact, sudden movement, lifting/bending or coughing. Pain often
moves from back to abdomen (�girdle of pain�) o Most common at T12-L2 spinal outlet
* ?? �Dx: plain X-ray of spine (shows fracture) * ?? �Tx: rest, analgesia,
treatment of underlying osteoporosis (calcitonin + bisphosphonates) Lumbar Strain �
lower back pain due to incomplete tear of the annulus fibrosis and leakage of fluid
into surrounding tissue causing inflammation, but no major damage. Often this is
the diagnosis of low back pain with a negative workup. Case 54 � Intellectual
Disability/Developmental Disorders Case 55 � Movement DisordersIdiopathic
Parkinson�s DiseaseSpontaneous neurodegenerative disorder, but has some genetic
risk factors: SNCA (a-synuclein), PARK2 (E3 ubiquitin ligase), UCHL1 (ubiquitin
carboxy-terminal esterase L1), PINK1 (PTEN-induced putative kinase 1), LRRK2
(leucine0rich repeat kinase 2) are prominent ones Pathology: brain-wide
neurodegeneration with specific concern of dopaminergic neuron loss in the vental
substantia nigra pars compacta being a main driver of disease motor manifestations
Symptoms: Four major symptoms with one less common symptom are characteristic of PD
* ?? �Pill rolling tremor: slow (3-5 Hz); evident at rest * ?? �Cogwheel rigidity:
arm passively moves in a �chunking� cogwheel fashion * ?? �Bradykinesia (slow
movement)/bradyphrenia (slow thinking) * ?? �Postural instability: failed postural
muscle reflexes needed to maintain balance * ?? �Dementia: less common (20-30%) but
recognized as a result of primary disease Tx: * ?? �Levodopa-carbidopa (carbidopa
is a COMT inhibitor to keep L-dopa levels high) � may cause dyskinesia * ?? �DA
agonists (pramipexole, ropinirole, bromocriptine) � may decrease incidence of
dyskinesia if used 1st * ?? �MAO-B inhibitor (selegiline, rasagiline) � augments L-
dopa and primarily helps disease symptoms * ?? �Amantadine (NMDA antagonist; useful
for eliminating L-dopa induced dyskinesia) * ?? �Deep Brain Stimulation of the
subthalamic nucleusNote: Anti-psychotics and anti-emetics
(prochlorperazine/metoclopramide) can induce Parkinsonism Parkinson Syndromes: some
syndromes share �Parkinsonism� as a feature but are not PD. * ?? �Progressive
supranuclear palsy: parkinsonism with characteristic ophthalmoplegia (limited
vertical gaze > limited horizontal gaze); difficulty looking down makes it hard to
walk * ?? �Cortico-basal ganglionic degeneration: parkinsonism with apraxia
(difficulty in executing motor/other actions despite normal strength/sensory
function) and alien-hand syndrome * ?? �Diffuse Lewy Body disease: parkinsonism
with early dementia, hallucinations, and extreme sensitivity to neuroleptic drugs *
?? �Vascular Parkinsonism: parkinsonism that affects mainly the lower limb
accompanied by vascular disease * ?? �Multiple systems Atrophy: parkinsonism with
early autonomic/corticospinal/cerebellar dysfunction and sometimes myoclonus or
vocal cord paresis Drug-Induced Movement DisordersOften treatment of psychotic
disorders incudes D2 DA-receptor blockage, thus it should be no surprise that these
drugs may result in movement disorders. Some big ones are below: o ?? �Akathisia �
inability to sit still (ants in the pants); Tx: anti-cholinergics, beta-blockers,
decrease neuroleptic o ?? �Neuroleptic Malignant Syndrome � muscle rigidity (^CK
levels), fever, leukocytosis, autonomic instability, and altered consciousness. Tx:
discontinue neuroleptic, antipyretics, rehydration, bromocriptine/dantrolene,
physical cooling o ?? �Tardive Dyskinesia � uncontrollable lip smacking/tongue
rolling/chewing in the context of neuroleptic use (often typical antipsychotics);
Tx: discontinue drug, DA depletion may aid in limiting symptoms but often this is
irreversible Stiff-Person Syndrome Rare autoimmune/paraneoplastic disorder of
progressive muscle rigidity with painful spasm * ?? �Tin man gait: Stiffness in
trunk/axial muscles, lumbar hyperlordosis, and restricted hip/spine mobility * ??
�Painful spasms occurring suddenly and sometimes in response to startle Dx:
clinical symptoms and continuous NMJ stimulation without evidence of other disease
* ?? �Anti-glutamic acid decarboxylase (GAD) or Anti-amphiphysin antibodies may be
found * ?? �CSF is often normal Tx: benzodiazepine and baclofen for muscle
relaxation to stop spasms ?? If autoantibodies present, immunosuppressive therapy
(steroids, plasmapheresis, IVIG) are useful TremorInvoluntary rhythmic movement of
the body. Resting (when pt at rest), postural (when pt maintains a posture for a
prolonged time), action (appears with voluntary movement), or intention (appears
when action has nearly completed) * ?? �Action/intension tremors are a feature of
cerebellar disease * ?? �Resting tremor is characteristic of Parkinsonism Essential
TremorDefined: the most common movement disorder; a simple, isolated tremor with no
serious sequelae. ?? May be a �benign familial tremor� due to autosomal dominant
gene mutation Signs/Symptoms: * ?? �Tremor: bilateral onset,
arms>head>legs>larynx>trunk, occurs with purposeful movement (�task specific
tremor�), latency is immediate onset with outstretched arms, �jerky� quality * ??
�Froment sign: some rigidity will be present in the arms; NOT COGWHEEL * ?? �Small
amounts of alcohol improve tremor * ?? �PET scan shows increased activity in the
thalamus Dx: mainly clinical with ruling out other causes of tremor Tx: * ??
�Propranolol � B-blocker, aids in decreasing the tremor; concern with
asthma/diabetes/heart problems * ?? �Primidone � anti-seizure med; used in low
doses for those who don�t respond to B-blockers * ?? �Tranquilizers/Botox may be
used to paralyze the tremor if refractory * ?? �Deep Brain stimulation in the
thalamus to limit its increased activity is a final effort ChoreaInvoluntary dance-
like movements, often with clumsiness and discoordination. Some other features
include: * ?? �Motor Impersistence: failure to sustain a motor contraction * ??
�Serpentine Tongue: cannot keep the tongue protruded, thus it writhes like a snake
* ?? �Milkmaid grip: cannot maintain grip thus the pt hand slides down like it�s
milking what their gripping Causes: There�s a huge list of causes of chorea but
some major ones include Huntington�s Disease, Post- streptococcal infection
(Syndenham chorea), SLE, thyrotoxicosis, and pregnancyTx: haloperidol (D2
antagonist) has had success BallismPoorly controlled flinging/flailing movements of
the limb (arm goes ballis-tic) * ?? �Hemiballismus: unilateral ballism; typically,
from contralateral basal-ganglia lesions or hyperglycemia * ?? �Tx: DA
depletion/blockaid is typical therapy | thalamotomy/pallidotomy may help in severe
cases DystoniaDefined: sustained muscle contraction; often contorting the pt into
uncomfortable positions * ?? �Primary Dystonia: no discernable cause is found;
diagnosed only after secondary ruled out; several different types, but the two most
common are: o DYT-1: caused by autosomal dominant glutamate deletion in torsin A
(9q34); difficult to treat; most common primary dyst. o DYT-5: dystonia responds to
dopamine agonists * ?? �Secondary Dystonia: caused by something else! Classically
medications, Wilson�s Disease, and a handful of other things will cause this
Signs/Symptoms: * ?? �Often childhood onset with worsening until a plateau in early
adulthood * ?? �Sustained muscle contractions causing twisting, abnormal posturing,
or repetitive motions Dx: * ?? �Extensive History and Physical searching for
secondary causes; classically from anti-psychotic drugs or metoclopramide (anti-
emetic) * ?? �If secondary causes ruled out, consider genetic testing to confirm
primary dystonia Tx: * ?? �Levodopa/DA agonists: stimulate basal ganglia to stop
aberrant firing of GPi and SNpr * ?? �Anti-cholinergic drugs (trihexiphendyl):
limit the aberrant ACh firing stimulated by dysregulated basal ganglia activation *
?? �Benzos/baclofen (sedative/muscle relaxant): may help relax the muscles * ??
�Deep brain stimulation of the GPi to inhibit basal ganglia activity * ?? �Benadryl
IV may help with dystonia from DA blockade as it can stimulate cholinergic activity
MyoclonusSudden �lightning-like� movements from brief, intense muscle contraction
(positive) or inhibition (negative) that can occur in 4 different contexts: * ??
�Physiologic (hiccups, hypnic jerks) � occur due to come physiologic process * ??
�Essential � no underlying etiology can be found; often improves with alcohol * ??
�Epileptic � occurs in context of epileptic seizures * ?? �Symptomatic � occurs as
a symptom of primary pathologic process Tx: clonazepam or valproic acid (both anti-
consultants) are used successfully TicsAbrupt, stereotyped, coordinated movements
or vocalizations as a result of an �inner urge� or tension that is relieved by
engaging in the tic Tourette�s syndrome is the classic tic disorder characterized
by
at least 1 motor and 1 vocal tic for >6 months causing significant
distress/impairment to the patient * ?? �Often prominent in teenage years but can
diminish into adulthood * ?? �Associated with Obsessive-Compulsive Disorder
Pediatric Autoimmune Neurologic Disorders Associated with Streptococcal-Infection
(PANDAS) * ?? �Tic/OCD exacerbation following a Group A B-hemolytic streptococcal
infection * ?? �Strep-autoantibody formation after the infection affects the basal
ganglia (unproved theory)Tx: DA-antagonists are most effective but
Clonazepam/clonidine have more favorable side-effect profiles, and are often first-
line Wilson�s DiseaseAutosomal recessive disorder due to copper-binding protein
mutation ?? Mutation??impaired copper-ceruloplasmin conjugation??copper entry to
biliary excretory pathway ?? Copper accumulates in the liver (liver damage) and
spills into the blood (deposition into tissue) Symptoms * ?? �Parkinsonism: due to
basal ganglia deposition; rigidity, tremor, dyskinesia * ?? �Cognitive Dysfunction:
due to cortical deposition; cognitive slowing, difficulty with processing * ??
�Mood/Personality changes from cortical frontal-lobe deposition * ?? �Kayser-
Fleischer ring: golden/brown/greenish discoloration in the cornea due to deposition
in Descemet�s membrane Dx: * ?? �Increased serum copper, decreased ceruloplasmin
are expected, not 100% * ?? �Increased 24-hr urine copper excretion is most
sensitive screening * ?? �Kayser-fleshcer rings in the eye are helpful clue * ??
�Liver biopsy with copper deposition is diagnostic Tx: lifelong copper chelation
with D-penicillimine or newer zinc chelators; screening for family members
Paroxysmal DyskinesiasRare disorders causing recurrent attacks of hyperkinesis with
preserved consciousness * ?? �Kinesigenic: short and abrupt; often triggered by
sudden movements * ?? �Non-kinesigenic: longer lasting; often triggered by alcohol,
fatigue, and stress * ?? �Exercise-induced dystonia (occurs with exercise) may last
for hours Tx: carbamazepine (anti-convulsants) Case 56 � Wheezing and Asthma
4617/3027: Asthma Classification and Treatment * ?? �Intermittent: daytime symptoms
<2x week | nighttime symptoms <2x month | short-acting B-agonist use <2x week with
normal baseline PFTs and no impairment of function o Tx: PRN albuterol * ?? �Mild
Persistent: symptoms >2x week but NOT daily | nighttime symptoms 3-4x month |
normal PFTs baseline with minor limitations of activititieso Tx: PRN albuterol,
inhaled corticosteroid * ?? �Moderate Persistent: daily symptoms, weekly nighttime
awakenings, moderate limitation of activites, with FEV1 60-80% predicted value o
Tx: PRN albuterol, inhaled corticosteroid, inhaled LABA * ?? �Severe Persistent:
symptoms throughout day, frequent nighttime awakenings, very limited activity, FEV1
<60% predicted valueo Tx: PRN albuterol, high-dose inhaled corticosteroid, inhaled
LABA, +/- oral prednisone 3026: B-2 agonist inhalers (albuterol) are the first line
treatment to induce bronchodilation in an acute asthma attack, however they are not
without side effects: * ?? �Low Potassium??Muscle weakness, arrhythmias, EKG
changes (B-agonism drives K+ into cells by activating the Na-K-ATPase) * ??
�Tremor, headache, and palpitations may also occur * ?? �When this complication
occurs ???check serum electrolytes to confirm K+ levels 4105/4706: Acute Asthma
Exacerbation * ?? �Presentation: dyspnea, cough, accessory respiratory muscle use,
difficulty speaking, hyperventilation/tachypnea (respiratory alkalosis, low PaCO2),
lung hyperinflation, tachycardia * ?? �Dx: clinical signs/symptoms with history of
asthma o Note that a normal PaCO2 on arterial blood gas is a sign of impending
respiratory collapse. Normally the person will hyperventilate, BUT if they�re so
fatigued from the attack that they�re starting to wear out, they can no longer
hyperventilate, PaCO2 will go back to normal and they�re getting towards the point
where they�ll stop breathing from fatigue. ?? Tx: SABA (albuterol)??+systemic
corticosteroid??+ipratropium nebulizer??+one-time infusion of magnesium sulfate
(after 1-hr without response to other therapies)??intubation/mechanical ventilation
4863: Differentiating between Major Lung Diseases with PFTs * ?? �Asthma � low
FEV1/FVC (obstructive) with resolution on bronchodilator challenge * ?? �COPD � low
FEV1/FVC (obstructive) with no resolution on bronchodilator challenge * ?? �Chest
Wall Weakness � normal to high FEV1/FVC (restrictive) with low Vital Capacity +
normal DLCO (no difficulty with air diffusion across lung tissue) * ??
�Interstitial Lung Disease � normal to high FEV1/FVC (restrictive) with low Vital
Capacity + low DLCO (trouble with getting gas across the lung tissue)o Classic is
long-tome asbestos exposure with lung calcifications??pneumoconiosis 8905:
Distinguishing Asthma from COPD ?? Clinically they can both look similar,
especially in an adult patient, but there are two major hallmarks that can set
asthma off from COPD:o Reversibility: FEV1 increase by >12% demonstrates
reversibility??asthma. COPD may be partially reversible in early stages, but never
to this degree.o DLCO: normal or increased DLCO??asthma. COPD may be normal in
early stages, but never increased.?? Note that adult onset asthma is harder to
treat (more limited response), but is usually the situation where you�re trying to
distinguish it from COPD 3050: Exercise Induced Bronchoconstriction * ??
�Bronchoconstriction/difficulty breathing often triggered by high volumes of dry,
cold air. Classically occurs in athletes with current or previous diagnosis of
asthma! * ?? �Tx: o First line: Albuterol (short acting B-agonist) inhaler 10-20
before exerciseo Second line: Anti-leukotriene inhaler 15-20 minutes before
exercise (cannot tolerate albuterol!) o Can be combined in high-performance
athletes 4335: Asthma exacerbation due to GERD ?? Presentation: recent worsening of
asthma symptoms with normal lung exam. Often sore throat, morning hoarseness,
worsening cough when laying down (at night is common), need for inhaler following
meals, dysphagia, chest pain/heartburn, regurgitation sensation o Result of
microaspirations causing irritation and vagal hypersensitivity resulting in
proclivity to bronchospasm o Often coincides with weight gain (possibly due to a
stomach ulcer!) ?? Tx: PPI trial 2842/4065: Aspirin-Exacerbated Respiratory Disease
(AERD)?? Presentation: asthmatic symptoms (cough, wheezing, chest tightness),
allergic symptoms (chest congestion, rhinorrhea, periorbital edema), and facial
flushing within 30 min � 3hr of NSAID use o Associated with Nasal polyp, asthma,
and chronic rhinosinusitis o Very similar to allergic/asthmatic flare-up, thus
symptoms may not be attributed to NSAIDo Nasal polyp development can cause bland
tasting food (caused by anosmia), recurrent nasal discharge with grey-glistening
mucoid mass in the nasal canal.o Considered a pseudo-allergic reaction that is not
IgE mediated. Instead the aspirin diverts the arachidonic acid pathway to produce
high amounts of leukotrienes = inflammation * ?? �Dx: Clinical scenario * ?? �Tx:
Surgical removal of nasal polyp, management of underlying conditions,
avoidance/desensitization of NSAIDs, and sometimes leukotriene inhibitors
(ziletuon/montelukast) 4742: Oddly enough this question painted a picture of a guy
with asthma via telling us that he had chronic rhinitis, nasal polyps, and eczema.
He likely had unstable angina and treatment may have caused him to have a dry
cough! * ?? �Aspirin = common trigger for bronchoconstriction for asthmatics * ??
�Non-selective B-blockers = limit ability to bronchodilate, thus exacerbating
asthmatics This guy was also on an ACE inhibitor...which has a classic side effect
of dry cough 4771: There are only two major mechanisms for pulsus paradoxus: * ??
�Cardiac tamponade (we�ve discussed this one!) * ?? �Severe asthma/COPD: typically,
there�s a small variation in intrathoracic pressure with inspiration (gets air to
flow in); but in asthma/COPD, air trapping raises pressure in the lungs, resulting
in a much more intense decrease in lung pressure during inspiration to allow for
inward flow (nearly 20x greater pressure drop). This results in blood pooling in
the lung vasculature (decrease preload), and inflation causes impingement on the
heart (decrease outflow). Both of these things result in less blood coming out of
the heart upon inspiration, resulting in a drop in BP with inspiration! Case 57 �
Obstructive Sleep Apnea 3033/4448: Obstructive Sleep Apnea ?? Presentation: daytime
sleepiness, morning headaches, poor sleep with multiple awakeningso Labs:
erythrocytosis with increased EPO (reaction to hypoxemia)o Risk factors: Obesity,
tonsillar hypertrophy, excessive oropharyngeal tissue, or short mandible o
Sequlae:cor-pulmonale,right-heartfailure,pulmonary/systemicHTN,depression,daytime
accidents due to sleepiness, impotence * ?? �Dx: nocturnal polysomnigraphy ???>15
apneic or hypopnea events in a night * ?? �Tx: directed at underlying cause (CPAP,
BiPAP, repositioning device, surgical therapy) 4489/4663/4413: Obesity
Hypoventilation Syndrome (Pickwickian Syndrome) * ?? �Basically these people are so
fat that it�s making chest wall expansion difficult, thus their lungs are OK but
they cannot ventilate properly??respiratory acidosiso Long-standing with metabolic
alkalosis compensation blunts the body�s response to increase respiratory drive,
leading to worsening O2 saturation * ?? �Presentation: obese patient with
difficulty breathing (SOB, orthopnea) but clear lungs and no overt signs of heart
failure but cor pulmonary/pulmonary HTN can be features o Labs: hypoxemia,
hypercapnia, polycythemia, increased bicarbonate with decreased Cl-o Obstructive
Sleep Apnea (apneic
events, difficulty sleeping, excessive daytime sleepiness) may co-exist due to
decreased nighttime respiratory drive AND poor chest wall expansion * ?? �Dx:
clinical picture * ?? �Tx: nocturnal PEEP/BIPaP (first line) + weight loss +
avoidance of sedatives. o Acetazolamide to increase respiratory drive is a last
resort 4593/4297: Cor pulmonale: process of increased lung-vascular pressure.
Untreated, causes right heart failure. * ?? �Etiology: COPD (most common),
idiopathic pulmonary HTN, interstitial lung disease, obstructive sleep apnea. Note
that LVF causing RVF is NOT cor pulmonale. * ?? �Dx: o Sym: Dyspnea, syncope, or
angina on exertiono Sign: Peripheral edema, increased JVD, hepatojugular reflex,
pulsatile liver, edema, ascities, etc. o Imaging: EKG or echo can be used but right
heart catheterization with elevated pulmonary artery systolic pressure >25mmHg is
confirmatory 2788/4677: Respiratory Acidosis from Alveolar Hypoventilation * ??
�For any reason, if a person is not ventilating enough they�re not going to be able
to blow off enough CO2 to keep blood pH at a normal level. This will result in a
respiratory acidosis. * ?? �Some causes of hypoventilation include: o
Pulmonary/thoracicdisease:COPD,sleepapnea,obesityhypoventilation,scoliosiso
Neuromuscular disease: Myasthenia gravis, Lambert-Eaton syndrome, Guillian Barre
syndrome o Drugs: illegal narcotics (heroin), sedatives, anesthesiao Primary CNS
hypoventilation: brainstem damage/stroke, herniation, post-ictal state seizure * ??
�Classically this presents with acidosis (pH <7.4), hypoxemia (PaO2 <75), and
hypercapnia (PaCO2 >45), especially within the first 48hr before the kidneys can
help compensate Case 58 � OsteoporosisOsteoporosis � low bone mass which puts pts
at risk for fractures. Defined as a Bone Mineral Density of <2.5SD below what�s
considered normal for a healthy adult ?? Osteopenia � same, but BMD is from 1.0-
2.5SD below a healthy adult Risk Factors * ?? �Classics: Low body weight, previous
fracture, a family history of osteoporosis with fracture, a history of falls,
physical inactivity, low vitamin D or calcium intake * ?? �Chronic systemic
diseases: COPD, HIV, severe liver disease, renal failure, systemic lupus
erythematosus, and rheumatoid arthritis. * ?? �Endocrine disorders: type 1 diabetes
mellitus, hyperparathyroidism, hyperthyroidism, Cushing�s syndrome, and others.
* ?? �Medications: anticonvulsants, corticosteroids, and immunosuppressants. * ??
�Nutritional risks: celiac disease, vitamin D deficiency, anorexia nervosa, gastric
bypass, and increased alcohol or caffeine intake.? * ?? �Note that obesity can be
protective (you�re constantly moving all that weight!) Prevention * ?? �Because
this typically a disease of the elderly, the normal rate of bone mineral loss can
be staved off in the hopes that a person may complete their life without symptoms
of osteoporosis * ?? �Men & Women >50yr � at risk; should have Ca2+ + Vit.D
supplementation & perform weight bearing exercise to reduce risk * ?? �Smoking
cessation & alcohol reduction are also recommended Screening ?? Women >65yr should
have a dual-energy X-ray Assessment (DEXA) of hip/lumbar spine scan to assess BMD;
if qualifying for osteoporosis based on this test, then treatment may be initiated
?? Women <65yr with risk factors of a woman >65yr based on the WHO�s FRAX 10-yr
risk calculatoro Things increasing risk are glucocorticoid use, low body weight,
previous fractures, rheumatoid arthritis, and some other risk factors?? According
to USPSTF, men of any age are not recommended to have screening o Some societies
recommend screening of men >70yr of age or men 50+ with risk factors Diagnosis * ??
�Made with DEXA scanning showing T-score -2.5 of greater * ?? �Secondary causes
should be sought (hyperthyroid, hyperparathyroid, anorexia, tobacco/alcohol abuse)
Treatment * ?? �Those who should be treated for osteoporosis o DEXA less than -2.5
at femoral neck or spineo DEXA between -2.5 and -1.0 with FRAX 10-yr risk >20% o
Aged >50 with previous Hip or Vertebral fracture * ?? �Non-pharmacologic � fall
prevention, smoking/alcohol cessation, Ca2+ 1200mg daily, VitD loading dose 50,000
IU with maintenance of 1000IU daily (goal of >30 ng/mL of 25-OH VitD on random
test) * ?? �1st line - Bisphosphnates (alendronate, risendronate, etc.) �
inhibit/kill osteoclasts to minimize bone breakdown and promote increasing bone
density. Must be taken on empty stomach with full glass of water. Large risk of
erosive esophagitis. Rare risk of osteonecrosis of the jaw after dental procedures.
* ?? �Hormone Replacement (raloxifene only) � due to risk of increasing
breast/endometrial cancer risk, these drugs are somewhat limited as a class.
Raloxifene can be used as it works as an estrogen agonist at the bone, but not the
breast or endometrium. Used in post-menopausal woman who cannot tolerate
bisphosphonates. * ?? �Calcitonin � nasal spray used as second line. Works by
promoting uptake of calcium from the blood into the bones and has a modest
analgesic effect. * ?? �Teriparatide � recombinant human parathyroid hormone
(promote Ca resorption and uptake). Will stimulate osteoblast activity, thus
contraindicated in patients with osteosarcoma, Paget�s Disease of the bone, Hx of
bone radiation, or elevated Alk.Phos levels * ?? �Denosumab � prevents osteoclast
differentiation and limits bone turnover. Works well, but risk of serious infection
is very real. Case 59 � Chronic Pain ManagementChronic pain can be frustrating for
both doctor and patient. On one hand the patient may truly have pain that they
cannot control or understand well. The doctor may have difficulty with diagnosis
and managing these patients takes a keep suspicion due to concerns for narcotic
abuse. When assessing someone with chronic pain: * ?? �Search past medical history
of clues/prior testing * ?? �Provide full Hx/Physical/Psychiatric evaluation to
search for underlying targets for treatment o Duration/type/characterization of
pain is important to establish * ?? �Provide objective assessment to establish a
baseline so further treatment may be stacked against it Non-Pharmacologic Tx * ??
�Physical therapy, psychiatric therapy, complimentary/alternative modalities of
treatment can all be part of the plan. The most important thing is patient buy
in/participation. If the patient wants to try acupuncture or whatever, it�s likely
not going to hurt them and even may help (so why not!) * ?? �It�s important to
always consider cost to the patient, as insurances may not cover many modalities of
alternative therapy. Pharmacologic Tx * ?? �NSAIDs � non-steroidals are often a
good place to start. May not help but may, who knows. Best to use a more COX-2
specific drug to minimize GI symptoms (celecoxib [Celebrex]) * ?? �Anticonvulsants
(Neurontin) � often used for neuropathic pain and a classic for folks with poorly
controlled diabetes and neuropathic pain. It�s almost like you�re depressing PNS
activity! * ?? �Muscle relaxants � often helpful with musculoskeletal pain. Not a
bad one to try. * ?? �Opioids � kill pain but at significant risk for side
effects/addiction. Best to consider long-acting drugs as the �high� is considered
less addiction forming, although short-acting may be considered for break- through
pain. o Constipation is a major side effect and should be asked about at any
followup. Typically stool softenered (Dulcolax) may be used to aid in pooping. o
Overdose/Addiction should always be on the radar in pts on long-term opioids.
Typically, patients will enter into a �contract� with the physician specifying the
exact terms of their treatment. Should they deviate, the drugs provided will be
terminated Case 60 � Lower Extremity Swelling Clinical Assessment * ?? �Most common
reason for edema in >50yr � chronic venous insufficiency * ?? �Most common reason
for edema in <50yr � idiopathic edema * ?? �Typically, assessment focuses around
finding underlying cause Making the Diagnosis * ?? �Hx � characterize
duration/pain/current medications/onset & improvement or worsening. Basically you
should always do a thorough history to see if something can explain the edema * ??
�Physical � obesity, bilateral or unilateral limb swelling, generalized, how far
does it go up (to the knee, to the sacrum, etc.), pitting or no?, varicosities,
skin changes are all good specific to note. A general heart/lung/abdominal exam
should ALWAYS be done. * ?? �Diagnostic Studies � o Unclear or heart failure
suspected � CBC, CMP, urinalysis, thyroid functions, albumin, and BNP (if CHF
suspected) are all classics in a patient >50yr to help characterize systemic
disease o Idiopathic suspected � typically a young person; water load test may be
useful. Often edema is generalized and associated with obesity/depression. o DVT �
d-dimer and examination of leg with comparison with unaffected leg are importanto
Sleep apnea � sleep studyo Liver disease � LFTs, albumin, and coagulation studies
can be usefulo Malignancy � CT chest/abdomen; often prostate, ovarian, and lymphoma
are associated with edema Tx * ?? �Idiopathic Edema � typically lifestyle
modifications (intermittent laying down, heat avoidance, low-Na diet, decreased
fluid intake, weight loss) with mild diuretics (spironolactone??thiazide +
spironolactone; loop diuretics should be avoided if possible) * ?? �Venous
Insufficiency � compression leg stockings/leg elevation; lower extremity Doppler
studies are often suggested for baseline; loop diuretics/surgical intervention may
be necessary * ?? �Lymphedema � exercise, elevation, manual lymphatic drainage, and
sometimes surgical procedure to aid in lymph drainage. Diuretics NOT helpful.
Cellulitis may be recurrent due to swelling and should be treated aggresivly. ??
Deep Vein
Thrombosis (DVT) � anticoagulation with INR goal of 2.0-3.0 should be sought.
Warfarin or equivalent NOVAC may be used. IVC filter may also be placed with
anticoagulation therapy is contraindicated to stop catastrophic clot formation. Ch.
1 The Woman??s Health Examination/Healthcare Management � Topics 1-5 * With an
abnormal Pap smear showing Abnormal Smear of Unknown Significance (ASCUS), follow-
up testing for High-risk HPV serotypes should occur.o If positive: perform
colposcopy for further examinationo Ifnegative:follow-upwithPapsmear+HPVco-
testingin3years o Ifunavailable:repeatPapsmearinoneyear * In a sexually active
patient <21y/o, pregnancy testing, testing for chlamydia/gonorrhea, and counseling
about STIs should be initiated. Pap smear should NOT be initiated before age 21
regardless of coitarche. Follow-up should be initiated for any findings. * Pap
smears are NOT necessary in [elderly pts (65+) pts with hysterectomy + 3
consecutive negative smears/2 negative co-tests], unless the hysterectomy was done
for cervical cancer or high-grade cervical dysplasia. o
Mammograms,colonoscopy,DEXAscanning,andannualbimanual+recto-pelvicexamareall
recommended in women >65y/o * From ages 30-65yrs, co-testing (pap smear + HPV)
every 5 years is the preferred method of screening. A pap smear every 3 years is an
acceptable alternative. * When a pap-smear returns a High-grade squamous
Intraepithelial Lesion (HSIL) immediate colposcopy or a loop electrosurgical
excision procedure (LEEP) are recommended o
Ifcolposcopyisinadequate:adiagnosticexcisionalprocedure(likeLEEPorotherwise)should
be undertake for removal and histologic diagnosis o LEEP is superior to
cryotherapy, which often doesn??t remove the entire lesion and doesn??t provide a
tissue specimen for histologic exam � Acute Salpingitis (Pelvic inflammatory
disease; PID)o
Presentation:fever,lowerabdominalpain,adenexaltenderness,cervicalmotiontenderness,
and vaginal discharge.o Etiology: nearly any STI or inflammatory condition could
cause this. Classically gonorrhea has worsening mucopurulent discharge following
menses * 2nd stage syphilis can classically present as non-itching vulvar rash
and ??copper penny?? macular rash of the palms/soles. If these findings are
present, you should immediately do a treponemal-specific test. Don??t forget,
treatment is with bezathine Penicillin G * Don??t forget these classic wet mount
slide findings: o Motile,flagellatedpear-shapedorganisms�Trichomonaso
Bacteriacovered??cluecells??�bacterialvaginosiso
Yeastsandhyphae�vaginalcandidiasis(??yeastinfection??)o
Multinucleatedgiantcells/inflammatorycells�sometimesHerpesinfection * Herpes
culture is the current gold-standard for diagnosis. While very specific, it is
limited with sensitivity with a 10%-20% false negative rate. Cultures are best
obtained very early in the disease course via ??unroofing?? and vigorous scraping
of blisters. Some patients may present late in the course, giving a higher chance
for false negative (virus is done shedding). Oral contraceptives DO NOT affect the
growth of the virus. PCR for Herpes virus DNA may also be useful. * Note that if a
patient with a known placenta previa is declining a C-section, you should talk to
the patient, understand what their reasoning is, and explain why the procedure is
recommended. If all else fails, it is acceptable to get a court order as a last
resort in the interest of the child??s life. * An elective C-section solely on
personal preference (this question said the pt didn??t want the pain of labor) is
OK as long as the patient is properly counseled about the risks/benefits of the
procedure. Elective C-section should be done at 39wk due to concerns for
prematurity before then. Ch.2 The OBGYN Role in Screening/Preventative Care �
Topics 3 & 7 * The birth-control methods with greatest success rate with typical
use are Depo-Provera, IUD, sterilization (male or female), and Implanon (all <1%
failure) * Typically, a DEXA scan to screen for osteoporosis is given at age 65,
unless the patient is at increased risk. Increased risk can be due to: early
menopause, glucocorticoid therapy, sedentary lifestyle, alcohol consumption,
hyperthyroidism, hyperparathyroidism, anticonvulsant therapy, vitamin D deficiency,
family history of early or severe osteoporosis, or chronic liver / renal disease *
Note that live vaccines are contraindicated in women who can feasibly become
pregnant in the next 4 weeks. Two common ones are MMR and varicella zoster vaccines
* Note that heart disease is the #1 killer of women in the USA. It??s important to
initiate early lifestyle changes to stop cardiac disease processes from occurring.
An inverse relationship between the level of physical activity and incidence of
death from coronary disease has been shown, thus initiating a regular physical
exercise routine is a great step in any patient. Yearly blood pressure readings are
also recommended! �Ch. 3 Ethics, Liability, and Patient Safety � Topic 6 *
Apparently ??patient privacy is the responsibility of physicians??. Although this
case is about a nurse leaving an open chart in the hospital, the answer puts the
onus on the physician. It also states that it??s the responsibility of ??the
physician and other healthcare providers?? to keep patient info private. Not
entirely sure what to make of this answer aside from that doctors can get
fined/sued for release of private patient information and that it should be kept
private. * A competent patient in a difficult medical situation (terminal cancer,
etc.) may elect a power of attorney while they??re still competent. If a difficult
medical decision (like whether to stay on a ventilator to prolong life) should
arise, the patient has ultimately autonomy if they are deemed competent, even if
someone else is the power of attorney. * Apparently it is ok for pharmaceutical
companies to support conferences that allow physicians to earn CME credits. Should
an investigator own stock in the company they research for, they must disclose this
possible conflict of interest and address it in presentations/papers. * Note that a
few questions address proper counselling in all patients, regardless of SES or
insurance status. Typically, the patient lacks insurance or likely won??t have a
procedure covered. The improper action is to discourage the procedure simply based
on these things. The proper thing to do is always counsel and address the issue in
a non-judgemental way so the patient is fully informed about the financial aspects
of their options. Ch. 4 Embryology and Anatomy � None here! Yay! Ch.5 Maternal-
Fetal Physiology � Topic 8 & 13 * Maternal physiologic anemia of pregnancy will
show a decreased hemoglobin BUT normal MCV (unlike folate, thalassemia, or iron
deficiency) * Physiologic SOB is common in the 3rd trimester (75%), and should
simply be assessed for other causes when seen in clinic (pulmonary embolus, anemia,
pulmonary edema, etc.) * Physiologic respiratory changes include: o
Increased:inspiratorycapacity,tidalvolume,inspiratoryreservevolume o
Decreased:functionalreservecapacity,expiratoryreservecapacity,andresidualvolume *
Common causes of acute pulmonary edema in pregnancy: tocolytic use, cardiac
disease, fluid overload and preeclampsia. Use of multiple tocolytics increases the
susceptibility of pulmonary edema, especially with the use of isotonic fluids. *
Systemic vascular resistance (SVR) is normally greater than the pulmonary vascular
resistance, but drops in pregnancy (relaxation of smooth muscle). If the pulmonary
vascular resistance exceeds the SVR, right to left shunt will develop in the
setting of a VSD, and cyanosis will develop. * In a patient presenting with molar
pregnancy a common early step in workup include a chest x-ray as the lung are a
common site of metastatic disease in gestational trophoblastic disease * Note that
right ureter compression is greater than left in pregnancy. This is because the
left ureter has some shielding from the uterus from the nearby sigmoid colon! Ch.6
Pre-conception and Antepartum Care � Topic 9 & 10 * The most accurate week for
ultrasound is between week 14.0 � 15.6 * While PAPP-A/Nuchal translucency/free B-
hCG is a fine first trimester screening test for Down??s Syndrome, the most
accurate test is the maternal cell-free DNA test. It will detect 99% of Down??s
syndrome cases, and can be used as early at 9wks. * When a pregnant patient fails
with 1-hr and 3-hr oral glucose tolerance test the first change is to
educate/initiate glucose monitoring + diabetic diet. If this fails to put person in
normal glucose ranges, then insulin or an oral hypoglycemic agent may be initiated.
Further oral glucose challenges are likely not necessary. * Shoulder dystocia,
metabolic disturbances, preeclampsia, polyhydramnios and fetal macrosomia are all
associated risks of gestational diabetes. Apparently intrauterine growth
restriction (IUGR) is a complication associated with pre-existing diabetes in
pregnancy. * According to ACOG, the recommended dose for patients not at risk for
NTDs is at least 0.6 mg/day. However, other organizations may suggest 0.4mg/day.
Regardless, women at increased risk should take 4mg/day, switching to 0.6 mg/day
after the first trimester. * Valproic acid use during pregnancy is associated with
a 1 to 2% incidence of neural tube defects, specifically lumbar meningomyelocele.
Fetal ultrasound examination at approximately 16 to 18 weeks gestation is
recommended to detect neural tube defects. * In an apparently malnourished patient,
folic acid supplementation, as well as evaluation for deficiencies in her iron,
protein and other nutrient stores should occur. In general, a patient needs
approximately 70 grams of protein a day, along with her other nutrients. Pts should
never lose weight in pregnancy, but should
adjust weight gain based on BMI. * Incorrect dating, specifically under-estimation
of gestational age, is the most common explanation for an elevated MSAFP. 90-95% of
cases of elevated MSAFP are caused by conditions other than NTDs including under-
estimation of gestational age, fetal demise, multiple gestation, ventral wall
defects and a tumor or liver disease in the patient. Next appropriate step in the
management of this patient is to obtain an ultrasound to assess the gestational
age, viability, rule out multiple gestation as well as a fetal structural
abnormality. * While Cell-free DNA screening can detect 99% of Down??s syndrome
cases, it should not be used as a rule-out for chromosomal abnormalities.
Amniocentesis or Chorionic Villus Sampling would be better choices (although the
question doesn??t explain why). The fetus in this case had a thickened NT, this
patient should be scheduled to have a detailed fetal ultrasound and echocardiogram
at 18-20 weeks to rule out anomalies. However, it is not possible to diagnose a
chromosomal abnormality with an ultrasound. Similarly, although genetic sonograms
(targeted sonogram) focus on markers associated with Down syndrome, they are not
diagnostic. * Ibuprofen is safe to take until around 32 weeks gestation, when
premature closure of the ductus arteriosis is a risk. While heparin is safe during
pregnancy, warfarin has known teratogenic effects and should not be given. If
continued anticoagulation is necessary, low molecular weight heparin is the drug of
choice. Ch.7 Genetics and Genetic Disorders in OBGYN � Topic 9 and Topic 32 * Don??
t forget! If you??re given one of those ??what??s the chances genetically??
questions note the: inheritance pattern of disease, status of mom AND dad, general
population, and do a Punnett squareo Rememberthatifitsauto-recessiveandyoumayormay-
notbeacarrier,BUTareknowntonot be affected you only have the options of ??
unaffected?? and ??carrier?? giving a 2/3 chance to have the gene, thus be able to
pass it down * Note that in screening for hemoglobinopathies a Hb gel
electrophoresis and CBC are recommended o
Thisquestionaskedspecificallyaboutsicklecell,buttheanswernotesthatanelectrophoresis
should be undertaken as milder forms and other hemoglobinopathies can be detected,
even if our only concern is sickle cell disease o Don??
tforget,asicklecellcarrierwouldnotbedetectedwithperipheralbloodsmear * Don??t
forget! Ashkenazi Jews are at increased risk of Fanconi anemia, Tay-Sach??s diseae,
Niemann Pick disease, Gaucher??s disease, Canavan disease, Bloom syndrome and
Cystic fibrosis (white people) * Note that all white people are at risk for Cystic
fibrosis (1/25 carrier status), but only Ashkenazi Jews lost the genetic lottery.
If a question asks what baby is at risk for, then always take into account the risk
factors from both parents! * Remember! Valproic Acid increases the risk for NTDs,
hydrocephalus, and craniofacial malformation. * Poorly controlled diabetes prior to
conception or during organogenesis increases the risk (x4-x8) for organ
malformation especially of the CNS and cardiovascular system. * Chorionic Villus
Sampling (CVS) takes some tissue from the chorionic frondosum (highest level of
mitotically active cells) for genetic testing of those cells. These cells can also
be used to detect chromosomal disorders/mutations (such as cystic fibrosis and
others) * Serum Screening Tests in order of sensitivity o Triple Screen (69%), Quad
Screen (81%), 1st trimester combined screen (PAPP-A, hCG, nuchal translucency;
85%), Integrated screen (if nuchal translucency not obtained, 85-88%), Sequential
Screen (1st trimester combined + 2nd trimester quad; 93%), and Cell-Free DNA (>99%)
* Note that the risk of fetal demise with CVS is approximately 1% and independent
of other pregnancies * Fragile X syndrome is the most common form of inherited
mental retardation. Note that Down??s syndrome is the most common genetic cause but
is not typically inherited. * Gestational age in the first-trimester ?? Ultrasound
crown-rump length is most reliable (+/- 4-5 days) * During a D&C for missed
abortion, you note fatty-appearing tissue coming form the curette. In this case,
the tissue is consistent with omentum and indicates possible bowel loop
involvement. Thus, the procedure should be stopped and laparoscopy should be
undertaken to assess for possible damage to the bowels. If bowel damage is
suspected, laparotomy should be done for closer look at the bowels. * Uterine
fibroids in the lower uterine segment are an indication for C-section, especially
for fetuses with head circumference >12cm. The fibroid can block the fetus??s
descent into the pelvis. * You have a G1P0 that??s been actively pushing and
exhausted. If she meets the criteria for operative vaginal delivery (complete
cervical dilation, head engaged, vertex position, fetal size/maternal pelvis have
been assessed as adequate, fetal head position is known, pain is under control, and
membranes are ruptures), she should undergo foreceps or vacuum-assisted delivery. *
In a maternal vacuum-assisted delivery, there is less risk for maternal laceration
however, there are other risks that should be known: o
Fetal:lacerationsatvacuumedges,cephalohematomaduetoscalpseparation,increasedrisk of
jaundice, and transient neonatal lateral rectus paralysis * Note that internal and
external version of the fetus is contraindicated in active labour. If the fetus is
presenting breech, then C-section should be occur to avoid risk of complications
with breech delivery. Foreceps may be used to assist head flexion, but vacuums are
contraindicated � Note that the highest risk complication with tubal ligation is
unplanned pregnancy (1/100 risk; 1/3 of these will be ectopic). This is much
greater than the risk for aspiration in pregnancy (1/1000) and the ?? post-tubal
ligation pain syndrome?? apparently is NOT a thing. Chapter 8: Intrapartum Care �
Topic 11 * Braxton Hicks Contractions � irregular, uncomfortable contractions in
the lower pelvis/groin without cervical dilation or effacement. Can happen at any
time in pregnancy (even at term!) * Group B strep. recto-vaginal swab/culture is
typically performed at 35-37wk and if positive, women should be treated
prophylactically during labour (GBS is fast growing; could grow back within 1
week!) o IfawomanhasGBSbacteuriainpregnancy??noneedtoswab,justgiveAbxintra-partumo
If a woman has Hx of GBS infection in prior pregnancy ?? no swab, just give Abx
intra-partum o GBS prophylaxis does not need to be given if a C-section is done
before membranes rupture * Upon presentation to the hospital in labor, first steps
are: review of the prenatal records with special focus on the antenatal
complications and dating criteria, a focused history and a targeted physical
examination to include maternal vital signs and fetal heart rate, and abdominal and
pelvic examination. o
Othertestsmaybeneeded(nitrazinetest,ultrasound,etc.)butthesewouldbeindicatedbythe
clinical scenario and are not routine * Remember! Fetal Heart tones MUST be
assessed during placement of an epidural (fear of fetal bradycardia). If a pt
cannot sit still for Doppler readings to be assessed during placement, a fetal
scalp electrode monitor is the way to go. Mom can move all she wants and you can
still get proper readings on baby to ensure epidural placement is OK. * In this
question, pt was presenting in labor with the fetus at +2. While initially, heart
rates were fine, the latest reading was that baby??s heart rate was in the 60s. In
this situation: o Measure mom??s heart rate to make sure Dopplers aren??t measuring
hero Encourage mom to push to try and finish the 2nd stage of deliveryo IF mom
cannot complete delivery of the baby??s head within 1-2 pushes, opt for operative
forceps or vacuum-assisted delivery to expedite the process of labor * In this
question, you were trying to place an intra-uterine pressure catheter (IUPC) and
300cc of frank blood/amiotic fluid came out! The next best thing to do is to
confirm baby is OK, thus withdraw the IUPC and check fetal heart tracings. o
Ifreassuring??attempttoplacetheIUPCagain o Ifnon-reassuring??
considerplacentalabruption/uterinedamageandgotoC-section * Some classic fetal heart
tracing changes: o Variabledecelerations�umbilicalcordcompressiono
Latedecelerations�placentalinsufficiencyo Fetalheadcompression�earlydecelerationso
Sustainedfetalbradycardia�umbilicalcordprolapseortachysystole o
Sustainedfetaltachycardia�Maternalfever/chorioamnionitis o
Lossoffetalvariability�opiatedrugstaken/administeredtothemom o
Sinusoidalwavepatterns�fetalacidosis,anemia,orhypoxemia * When umbilical cord
prolapse is diagnosed (typically through palpation of cord in the vaginal vault)
the two things to do are 1manipulate the fetus to minimize cord compression, and
2call for assistance for immediate C-sectiono Replacement of the cord, continuation
of labor, and surgical-assisted delivery are not indicated as fetal status can
quickly deteriorate or rupture of the cord can occur. * Performance of a median
episiotomy is the single greatest risk factor for third- or fourth-degree
lacerations and more highly associated with anal incontinence Chapter 9: Abnormal
Labour and Intrapartum Fetal Surveillance � Topics 22 & 26 * A patient failing to
dilate further during active labour (like they??ve been stuck at 5cm for 8 hours)
should warrant suspicion arrest of dilation. Interventions are as follows:o
Oxytocininfusion(increasecontractionfrequency/strength;promotedilation)o
Ifnotadequate:placeanIUPCandseeifcontractionsareadequate(>200MVU/10min) o
Ifnotadequate:ConsiderC-sectiono NotethatambulationDOESNOTaidinprogressingdelivery
* In the question, a patient is at term (40wk) and in severe back pain, desiring
induction of labour. She??s closed
and 20% effaced. The suggested course of action: o GiveMisoprostol(cytotec)for??
ripening??ofthecervix,theninductionwithoxytocin(Pitocin) can be initiated once a
more favorable cervix is achieved o Note that waiting till 42 weeks in this setting
severe back pain is not appropriate. The patient is at term and extremely
uncomfortable, thus ripening and induction are reasonable. Plus, going to the
absolute maximum of 42wk is associated with problems (macrosomia, oligohydramnios,
uteroplacenta insufficiency, etc.) * Prematurity, multiple gestation, genetic
disorders, polyhydramnios, hydrocephaly, anencephaly, placenta previa, uterine
anomalies and uterine fibroids are all associated with breech presentation. * Note
that prolonged latent phase is defined as >20 hours for nulliparas and >14 hours
for multiparas, and may be treated with rest or augmentation of labor. Artificial
rupture of membranes is not recommended in the latent phase as it places the
patient at increased risk of infection * Never forget! Gestational diabetes is the
biggest risk factor for macrosomia. Maternal obesity, diabetes mellitus, postterm
pregnancy, a prior delivery complicated by a shoulder dystocia, and a prolonged
second stage of labor are all associated. * Secondary arrest of dilation: lack of
cervical change in the active phase for over four hours. Management includes: o
Amniotomy (artificial ROM) as first stepo
Ifstillinadequate:Carefulobservationandoxytocinadmintoincreasecontractions o
Ifstillinadequateorfetusisnon-reassuring:considerC-section * Don??t forget!
Prolonged 2nd stage (active) labour alone is NOT an indication for operative
delivery or C-section. Fetal macrosomia, feto-pelvic disproportion, or
materal/fetal distress would all give indication for them, but not prolongation
alone! * Any Category III fetal heart tracing warrants immediate C-section. * Frank
breech is the most common type of breech presentation, occurring in 48-73% of cases
and the buttocks are the presenting part. * First Stage Labour (Active) arrest of
dilation should be assessed with the following: o
PlaceIUPCtocheckifcontractionsareadequate(>200MVU/10min)o Ifnotadequate??
consideroxytocinadministrationo Ifstillnotadequate??consideroperative-
assisteddeliveryorC-section * Note that misoprostol (Prostaglandin E1) and cervadil
(Prostaglandin E2) are contraindicated in VBAC. However, operative assisted
delivery is OK TO USE in VBAC. * Don??t forget! Amnioinfusion may be used for
repetitive variable decelerations; not for recurrent lates. * Initial measures to
evaluate and treat fetal hypoperfusion (occasional late decelerations): o
Changeinmaternalpositiontoleftlateralpositionwhichincreasesperfusiontotheuterus o
Maternalsupplementaloxygenationo Treatmentofmaternalhypotensiono Discontinue
oxytocin o Consider intrauterine resuscitation with tocolytics and intravenous
fluids, fetal acid-base assessment with fetal scalp capillary blood gas or pH
measurement Chapter 10: Immediate Care of the Newborn � Topic 12 * Some classic
physical findings in Down Syndrome: flattened nasal bridge, small size and small
rotated, cup-shaped ears, sandal gap toes, hypotonia, a protruding tongue, short
broad hands, Simian creases, epicanthic folds, and oblique palpebral fissures. *
All infants with meconium-stained amniotic fluid should not routinely receive
suctioning at the perineum. If meconium is present and the newborn is depressed,
the clinician should intubate the trachea and suction meconium or other aspirated
material from beneath the glottis. If baby is vigorous, then there is no need for
suction. * Small babies are more common with type 1 diabetes. Macrosomic (large)
infants are typically associated with gestational diabetes. Blood sugar level of
all newborns of diabetic mothers should be monitored closely after delivery, as
they are at increased risk for developing hypoglycemia. * Chorioaminonitis can
result in fetal tachycardia in-utero; coupled with minimal variability on
monitoring, the fetus may be septic! Upon birth, a septic baby will be with
fever/lethargic/pale. * Don??t forget! Infants born to diabetic mothers are at
increased risk for developing hypoglycemia, polycythemia, hyperbilirubinemia,
hypocalcemia and respiratory distress * In this question, a mother with known
opiate use delivers a baby with no respiratory effort and a slow heart rate
(90bpm). Next step should be to apply PEEP ventillation and prepare to intubate
baby.o
Notethatnaloxone(narcan)isrelativelycontraindicatedinthismom,asusecouldsendbaby
into withdrawals (life threatening seizure could occur!) * In a baby being born to
an HIV(+) mom, protocol dictates: AZT immediately after delivery. HIV testing
begins at 24 hours. Discourage breastfeeding (possible cracking of nipples and
bleeding) but encouragement of pumping of breastmilk. * When applying PEEP
ventilation in a newborn: Place child in the ??sniffing position?? (tilting the
neonate?? s head back and lifting the chin), secure the mask to the infant??s face,
squeeze the bag to observe an initial chest rise. A recommended rate of oxygen flow
is 10 L/minute. Chapter 11: Postpartum Care � Topics 13, 14, 29 * Don??t forget!
Uterine atony is the most common cause of PPH and occurs in one in every twenty
deliveries. * Post-partum hemorrhage can result in Sheehan Syndrome (anterior
pituitary necrosis), which may lead to loss of gonadotropin, thyroid-stimulating
hormone (TSH) and adrenocorticotropic hormone (ACTH) production, as they are all
produced by the anterior pituitary. Frequently goes unnoticed for many years after
the inciting delivery. Treatment includes estrogen and progesterone replacement and
supplementation with thyroid and adrenal hormones. * Factors related to increased
rates of infection with a vaginal birth include prolonged labor, prolonged rupture
of membranes, multiple vaginal examinations, internal fetal monitoring, removal of
the placenta manually and low socioeconomic status * The most common cause of
postpartum fever is endometritis. Rate of endometritis is most closely related to
the mode of delivery (vaginal = 2%, C-section = 10-15%). Uterine fundal tenderness
is a common additional symptom. * Postpartum endometritis are usually polymicrobial
resulting in a mix of aerobes and anaerobes in the genital tract; most common
causes amonst the polymicrobial isolates are S.aureus and Streptococcus * Don??t
forget! Post-partum Blues (lasts <2wk) and Post-partum depression (2wk � 6mo) * A
sense of incapability of loving her family and ambivalence toward her infant are
classic signs of true post-partum depression. Baby blues are usually depressive
symptoms, but not toward the baby. * The most significant risk factor for
developing postpartum depression is prior history of depression. Others include
marital conflict, lack of perceived social support from family and friends, having
contemplated terminating the current pregnancy, stressful life events in the
previous twelve months, and a sick leave in the past 12mo related to hyperemesis,
uterine irritability or psychiatric disorder. * Apparently the safest method to
suppress lactation is breast binding, ice packs and analgesics. No hormonal
interventions are recommended in puerperium mothers due to increased risk of
adverse cardiovascular events. * Breastfeeding is associated with a decreased
incidence of ovarian cancer and breast cancer. Breastfeeding has NOT been shown to
decrease the risk for developing coronary artery disease, cervical dysplasia and
cervical cancer or colon cancer in the mother. * Side lying position is a good one
for breastfeeding, it is important for mother and baby to be belly-to- belly in
order for the infant to be in a good position to latch on appropriately, taking a
large part of the areola into its mouth. If poor latching occurs, baby may not feed
as well as it could and mom could end up with baby sucking around the areola,
causing drying/cracking of skin. * Prolactin is responsible for the synthesis of
milk; present in large quantities during gestation, its action is inhibited by
estrogen and progesterone during pregnancy (inhibits alpha-lactalbumin production
by the rough endoplasmic reticulum). After delivery, large amounts of prolactin
continue to be secreted, and milk is produced after estrogen and progesterone
decrease (alpha-lactalbumin stimulates milk lactose production). May take about two
days to occur (colostrum often occurs in these two days) * Bugs causing Mastitis
are usually sensitive to penicillin or a cephalosporin; community-acquired
organisms, and even staphylococcal infections are typically susceptible. * Some
classic breastfeeding promotive policies: baby on the breast within a half hour of
delivery and rooming-in for the baby to ensure frequent breastfeeding on demand
(i.e. unlimited access). * Candidiasis of the nipple may occur in breastfeeding if
baby has Candida infection in the mouth o
Presentation:intensenipplepain,burning/worseningwithbreastfeeding;sometimeswith
shiny, pink nipples and peeling at the peripheryo
Dx:inspection&swab/wetmountofbothmom??snippleandbaby??smouth o Tx: * ?? �Mom �
topical fungal ointment & topical triple antibiotic ointment * ?? �Baby � oral
nystatin followed by oral fluconazole * Signs that a baby is getting sufficient
milk: 3-4 stools in 24 hours, six wet diapers in 24 hours, weight gain and sounds
of swallowing. Little spit-ups after feeding is NOT a sign of adequate eating *
Breast Engorgement is a common occurrence after birth. To decrease discomfort:
frequent nursing, taking a warm shower or warm compresses to enhance milk flow,
massaging the breast and hand expressing some milk to soften the breast, wearing a
good support bra and using an analgesic 20 minutes before breastfeeding. * Oxytocin
is responsible for milk ejection.
Its stimulated best by suckling of the infant * Note that cortisol and insulin act
in concert with other hormones to stimulate the growth and development of the milk-
secreting apparatus. Chapter 12: Post-Partum Hemorrhage � Topic 27 *
Methylergonovine is an ergot alkaloid (potent smooth muscle constrictor). It is
also a vasoconstrictive agent and should be withheld from women with hypertension
and/or preeclampsia. * Prostaglandin F2-alpha (Hemabate/Carboprost) is a potent
smooth muscle constrictor, which also has a bronchio-constrictive effect. It should
be used with caution in any patient with a reported history of asthma. It is
absolutely contraindicated in patients with poorly controlled or severe asthma. *
Uterine inversion is an uncommon etiology of postpartum hemorrhage; major causes
are: o
Excessive(iatrogenic)tractionontheumbilicalcordduringthethirdstageofdelivery.o
Over-distendeduterus(grandmultiparity,multiplegestation,polyhydramniosandmacrosomia
are all risk factors) * Presence of a low-lying anterior placenta in a patient with
a history of multiple Cesarean births, the diagnosis of the placenta accreta must
be entertained. This is a concern as delivery of the placenta may result in
laceration and severe hemorrhage; typically, only resolvable with hysterectomy. *
The following are associated with retained placenta: prior Cesarean delivery
(attachment to scar), uterine leiomyomas (attachment to smooth muscle), prior
uterine curettage (attachment to scar) and succenturiate (accessory) lobe of
placenta (weak connection to main placenta) * In a patient with post-partum
hemorrhage who is NOT responding to uterotonic agents, the least invasive treatment
is placement of the Bakri balloon (device placed into the uterus with a balloon
that is filled with up to 500 cc of sterile fluid) This places pressure on the
inside of the uterus. B-lynch compression stitch, Uterine artery ligation, and
hysterectomy all require a laparotomy and should be reserved for recalcitrant
cases. Uterine artery embolization requires placement of embolization catheters as
well as interventional radiology. * Should the shit really hit the fan and pt
requires exploratory laparotomy for assessment/resolution of bleeding: [1st line -
B-lynch compression stitch, 2nd line �Uterine artery ligation, 3rd � hysterectomy]
Chapter 13: Multifetal Gestation � Topic 20 * Two major signs of a twin gestation
are 1AFP elevation roughly x2 of what a single pregnancy should be, and 2fundal
height exceeding what would be expected (like 22cm for a 16wk gestation) *
Ultrasound markers suggestive of dizygotic (non-identical) twins: 1dividing
membrane thickness greater than 2 mm, 2twin peak ??lambda?? sign (triangular
appearance of the chorion between the twins, suggesting Di-Di preg.), 3different
fetal genders and two separate placentas (anterior and posterior) * Don??t forget!
Twin infant death rate is five times higher, risk of cerebral palsy in twin infants
is five to six times higher than that of singletons, and there??s higher incidence
of IUGR (intrauterine growth restriction) in twins/multis. 58% of twins deliver
prematurely, with an average gestational age at delivery of 35 weeks. 12% of twins
deliver very prematurely. * Incidence of congenital anomalies is increased in
twins, particularly monozygotic twins. Note: Twins typically weigh less than
singletons of the same gestational age, but their weights usually remain within the
normal range. Macrosomia is, therefore, uncommon. Rh isoimmunization is not
increased in twin gestations. * While prematurity is much more common in multiple
gestations, there is no good way of preventing it. Adequate weight gain in the
first 20 to 24 weeks of pregnancy may help to reduce the risk of having preterm and
low-birth weight babies; good early weight gains aids in development of the
placenta, possibly improving its ability to pass along nutrients to the babies.
Note that bed rest, prophylactic cerclage, tocolytic drugs, and home uterine
monitoring have all been tried and not been successful for decreasing prematurity
rate. * Superfecundation is the fertilization of two different ova at two separate
acts of intercourse in the same cycle. * Don??t forget! Monochorionic gestations
are at heightened risk for Twin-twin transfusion syndrome BUT when forced to choose
between mono-di or mono-mono, mono-di is more common overall. * Twin-Twin
transfusion syndromeo Poorprognosis;70-100%perinatalmortalityofeithertwino
Survivinginfantshaveincreasedriskofcerebralpalsyandhydropsfetaliso
Donortwin�plethora,hypervolemia,macrosomia,cardiomegaly,tricuspidregurg o Recipient
twin � anemia, hypovolemia, restricted growth * In multiple gestation, prematurity
has the most significant consequences as it is associated with an increased risk of
respiratory distress syndrome (RDS), intracranial hemorrhage, cerebral palsy,
blindness, and low birth weight. Intrauterine growth restriction, intrauterine
death of one or more fetuses, miscarriage and congenital anomalies are all more
common. � Note that when referring to twins ??Twin A?? is the first twin out and ??
Twin B?? is the second twin out. Should a pregnancy feature Twin A in a breech or
sideways lie, C-section is always the way to go, even if Twin B is vertex!
Apparently, there??s some advocacy for external cephalic version of Twin A, but
this has been shown to have similar outcomes to breech delivery and is not
recommended. Chapter 14: IUGR and Macrosomia � Topic 31 * In this question, the
patient had significant medical diseases (severe HTN, class F diabetes) that are
affecting her vasculature and, ultimately, limiting the substrate availability to
the fetus with resultant uteroplacental insufficiency. The vascular disease is
evidenced by retinopathy and proteinuria. o
Geneticfactors,congenitalanomalies,tobaccosmoking,andperinatalinfectioncanallcause
IUGR. BUT uteroplacental insufficiency is a heavier hitter given the scenario. *
When a pregnancy is complicated by fetal growth restriction, various fetal
physiologic parameters require assessment o
Oligohydramniosduetoreducedfetalbloodvolume,renalbloodflowandurinaryoutput. Chronic
hypoxia is responsible for diverting blood flow from the kidney to organs that are
more critical during fetal life. 90% of patients with oligohydramnios delivered
growth restricted infants. These infants experienced a high rate of fetal
compromise. o Systolic/diastolic (S/D) ratio of the umbilical artery is determined
by Doppler ultrasound. An increase in the S/D ratio reflects increased vascular
resistance. A normal S/D ratio indicates fetal well-being. As vascular resistance
increases, the S/D ratio increases. With severe resistance, there is absence and
ultimately reversal of end-diastolic flow. These findings are associated with an
increased rate of perinatal morbidity and mortality, and a higher likelihood of a
long- term poor neurologic outcome. o Optionsforantenataltestinginclude:non-
stresstest,contractionstresstest,andbiophysical profile to detect possible fetal
asphyxia and assess fetal wellbeing. While fetal kick counts may be of value,
additional fetal testing such as twice weekly NST with AFI and weekly umbilical
artery Doppler studies is indicated in monitoring fetuses with IUGR. � To
accurately confirm gestational age at term, one of the following should be met:o
Fetalhearttonesdocumentedfor20wkbyanon-electronicfetoscopeor30wkbyDopplero It has
been 36 weeks since a positive serum or urine HCG pregnancy test was performed by a
reliable laboratoryo Ultrasoundmeasurementofthecrown-
rumplength,obtainedatsixtotwelveweeks,supports a gestational age of at least 39
weeks (most accurate, within 5-7 days)o Ultrasound obtained at 13-20 weeks confirms
the gestational age of at least 39 weeks, determined by clinical history and
physical examination. * Asymmetric growth restriction: fetuses have normal
length/low weight with a head-sparing effect (head/brain is spared of the reduced
blood flow). Thus, the fetal abdomen measures below normal and the head remains
very close to normal. Usually detected during the third trimester and reflects
uteroplacental insufficiency. * Symmetric growth restriction: all fetal
measurements are below normal; indicates an intrinsic growth failure or an ??early
event?? secondary to one or more organ system anomalies, fetal aneuploidy, or
chronic intrauterine infection. Infectious diseases are known to cause IUGR
(rubella, CMV, syphilis, varicella, and toxoplasmosis). There are no bacteria known
to cause IUGR. Symmetrical growth restriction is usually detected in the mid-
trimester of pregnancy. * Don??t forget! Oligohydramnios (low fluid) is associated
with IUGR (bloodflow away from kidneys) and polyhydramnios is NOT associated with
IUGR. * Note that epidemiologic studies indicate that fetal growth restriction is a
significant risk factor for the subsequent development of cardiovascular disease,
chronic hypertension, chronic obstructive lung disease and diabetes. Osteoporosis
is NOT associated with IUGR. * Induced delivery is indicated in a fetus with IUGR
at 36 weeks gestation with oligohydramnios and abnormal umbilical artery Doppler
studies. There??s an increased incidence of fetal intolerance of labor, BUT
induction of labor is generally preferred over elective Cesarean delivery. o
Delivery at term is indicated in fetuses with IUGR with reassuring fetal testing
including a normal amniotic fluid volume. * Macrosomic newborns of diabetic mothers
experience excessive rates of neonatal morbidity, including birth trauma (shoulder
dystocia/brachial plexus injury), higher rates of severe hypoglycemia, neonatal
jaundice, neonatal acidosis (occurs with poor glycemic control, inc. risk fetal
demise). While poorly controlled pre-existing diabetes is associated with an
increased risk
of congenital anomalies, gestational diabetes is not associated with increased
risk of congenital anomalies. Chapter 15: Preterm Labor � Topic 24 * In most cases,
preterm labor is idiopathic (i.e. no cause can be identified). Dehydration, uterine
distortion (uterine fibroids or structural malformations) can be associated with
preterm labor. Preterm labor may also be from iatrogenic causes (like early
induction) * In preterm labor, ampicillin is indicated for this patient as her
Group B Strep status is unknown and should be continued until a culture result is
negative or her labor stops. A tocolytic (such as nifidipine) and a steroid (such
as betamethasone) are also indicated. * In this question, pt has fever, a tender
fundus, and elevated white blood cell count, (concerning for an intra-amniotic
infection). Delivery is warranted. In the case of reassuring heart tones, there are
no contraindications for labor induction and a Cesarean section is not indicated at
this time. Tocolytics should not be used in intra-amniotic infection. Conservative
management with observation would delay diagnosis and would not be appropriate. *
Contraindications for certain Tocolytic therapies: o Nifidipine�HTN o
Tertbutaline/Ritodrine�diabeteso MagnesiumSulfate�myastheniagravis,signsofoverdoseo
Indomethacin�usebeyond32wk(hastenedclosureofDuctusArteriosus) * Betamethasone from
24 to 34 weeks gestation has been shown to increase pulmonary maturity and reduce
the incidence/severity of RDS (respiratory distress syndrome) in the newborn. Also
associated with decreased intracerebral hemorrhage and necrotizing enterocolitis in
the newborn. It has not been associated with increased infection or enhanced
growth. * Fibronectin is an extracellular matrix protein that is thought to act as
an adhesive between the fetal membranes and underlying decidua normally found in
cervical secretions in the first half of pregnancy. Its presence in the cervical
mucus between 22 and 34 weeks is thought to indicate a disruption or injury to the
maternal-fetal interface. o
FetalfibronectinisFDAapprovedforuseinwomenwithsymptomsofpretermlaborfrom24to 35
weeks and during routine screening of asymptomatic patients from 22 to 30 weeks
gestation. (good rule-out test) o
Negativepredictivevalueof99.2%insymptomaticwomen�99outofevery100patients with a
single negative test result will not deliver in the next 14 days. o
Inasymptomaticwomen,anegativefetalfibronectintesthasanegativepredictivevalueof
96.7% for delivery before 35 weeks. o
Positivepredictivevalueinsymptomaticwomenis16.7%�17outof100womenwitha positive test
will deliver within 14 days. Chapter 16: Third Trimester Bleeding � Topic 23 * In
this question, a patient with polyhydramnios was ripened/induced but experienced a
precipitous labor going from 3cm/75% to 10cm/100% shortly after ROM. She was noted
to have heavy bleeding after ROM. Polyhydramnios with rapid decompression of the
intrauterine cavity is a major risk factor for placental abruption (it??s like the
placenta gets pulled off the wall!) * Don??t forget! Hx of C-sections can
predispose to placenta accreta, especially with a low/anterior placental insertion.
The scar tissue from surgery interrupts proper placentation and it grows into the
myometrium. * Don??t forget!o
FreshFrozenPlasma�containsallclottingfactors,butnoRBCs/Platelets/vWFo
Cryoprecipitate�containsFactorsVIII/XIII,vWF,andfibrinogen,notRBCs/Platelets *
Placental Abruption o Presentation: abdominal pain, bleeding, uterine hypertonus
and fetal distress.o
Riskfactors:smoking,cocaineuse,chronichypertension,trauma,prolongedprematurerupture
of membranes, and history of prior abruption.o
Tx:emergentCesareandeliverywithappropriateresuscitation � A double set-up exam is a
special situation where a mom is suspected to have placenta previa but there is
insufficient evidence to confirm the diagnosis: o Check for previous records that
may show placentation (previous ultrasounds); if placental location is confirmed,
then a vaginal delivery is OK o
Ifplacentalrecordsareunsure;attempttoelucidateplacentalplacementwithultrasound;if
still unsure manage pregnancy until 37wk o
Ifplacentalrecords/examinationsunsureat37wks,proceedwithdoubleset-up o Doubleset-
upexam * ?? �Mom is taken to OR with OB and surgical teams present and blood
products available with mom ready to receive with IV * ?? �1. Sterile speculum
exam: if placenta is seen in the Os, dx confirmed. If no, go to step 2. * ?? �2.
Careful palpation of uterine fornicies: if spongey, dx confirmed. If fetal head is
palpated, dx ruled out. If neither, go to step 3 * ?? �3. Cautious digital exam: if
spongey tissue, dx confirmed. If fetal parts or membranes without spongey tissue,
dx ruled out. If not sure, do C-section o If any of these steps confirm dx of
placenta previa, perform C-section. If placenta previa gets ruled out, proceed with
vaginal delivery. * During pregnancy the cervix is extremely vascular and may even
be described as ??friable??. Because of this, dilation may cause a small amount of
bleeding may occur. This bloody show is not of clinical significance and often
occurs with normal labor and often described as ??bloody discharge?? rather than
frank bleeding * Frustratingly, this question had a sexually active pregnant
teenager in the 2nd trimester with vaginal bleeding. Speculum exam revealed a
friable cervix. While this could be for many reasons, cervicitis is a classic
reason for this age/2nd trimester presentation. If it was in the first trimester,
it would be called a threated abortion (but these ONLY occur in 1st trimester by
definition) and if it occred later in the 3rd trimester (esp. with labor) it would
be the bloody show as a result of dilation/loss of the mucus plug. * In this
question, a 45y/o pt with hx of smoking presents with vaginal bleeding during
pregnancy. Exam showed a hard lesion on the cervix which easily bleeds. o
Dx:Cervicalcancer�it??srock-hardlesionthateasilybleeds;biopsy/txshouldbesoughto
Cervicalpolyp�typicallysofter,butmaycausealesionandbleedingo
Nabothiancyst�acervicallesionoftenappearingasa??bump??.Willrarelybleedasit??sfilled
with mucus and poorly vascularized. Chapter 17: Premature Rupture of Membranes
(PROM) � Topic 25 * Remember! When suspecting PROM, it??s important to confirm the
diagnosis with testing. Two early tests to go are the nitrazine test or a ferning
test. These importantly must test the fluid leaking into the vaginal vault, NOT
cervical mucus. Testing cervical mucus may lead to false positive test results. o
Digital vaginal exams should be minimized, as they introduce bacteria increasing
infection risk, especially in the setting of PROM. * Use of steroids in PPROM is to
help advance fetal lung function to increase change of survival. Tocolysis (while
use is controversial) is typically used simply to complete a course of
corticosteroids, NOT to delay labour until 35 weeks (except in select situations
where you??re close to 35wks). Tocolytics should not be used more than 48hrs in
PROM/PPROM due to risk of infection through the ruptured membranes. o Note that
even with intact membranes with preterm labor, tocolytics are only used for 48hrs *
Don??t forget! Variable decelerations are from cord compression, which is often
from oligohydramnios. In PPROM/PROM, there is active leakage of fluid, which can
result in oligohydramnios and variable declerations. * Remember! Antibiotics are
used to extend the latency period in PPROM. Ampicillin and erythromycin is the ACOG
recommended abx, shown to prolong the latency period by 5-7 days, as well as reduce
the incidence of maternal amnionitis and neonatal sepsis. * Uterine tenderness in
the setting of PPROM will prompt consideration of delivery as it??s a sign of
maternal genital tract infection. AFI or oligohydramnios does not warrant immediate
delivery unless fetal heart tones start to look non-reassuring. If possible, fetal
lung maturity should be achieved to limit morbidity/mortality, but this is not a
requirement if immediate delivery is indicated. * With PROM <25wk, Pulmonary
hypoplasia is often seen due to the lack of amniotic fluid interferes with the
normal intrauterine breathing process. The result is failure of normal development
and growth of the respiratory tree. * In some cases of PPROM, amniocentesis may be
performed to detect intra-amniotic infection. Amniotic leukocytes may be present,
but has the lowest predictive value. Interleukin-6 would be increased, and low
amniotic fluid glucose is a classic indication of intra-amniotic infection * In a
patient with Hx of PPROM 17 alpha-hydroxyprogesterone has been shown to reduce the
risk of premature labor; it??s administered weekly (starting between 16-20 weeks)
until 36 weeks gestation. * In a patient at >35wk with PPROM who is NOT in labor,
augmentation of labor for induction is indicated. While expectant management may
seem OK, delaying labor in the setting of ruptured membranes increases the risk of
chorioamnionitis. o Steroidsarecontraindicatedafter32wks o Tocolytics are
contraindicated at 36wks Chapter 18: Post-term Pregnancy � Topic 30� Postterm
pregnancies should be followed with antepartum fetal surveillance because perinatal
morbidity and mortality increases beginning at 41 weeks of gestation. Many
practitioners use twice- weekly testing with some evaluation of amniotic fluid
volume beginning at 41 weeks of gestation. A modified BPP should be adequate: o
Non-stress test: fetal heart tones are monitored; a normal test shows two
spontaneous accelerations of 15bpm/15sec in the course of 20 minutes o
Amnioticfluidvolumeassessmenttypicallywithultrasound(AFI>5) * Apparently postterm
pregnancies are associated with placental sulfatase deficiency, fetal adrenal
hypoplasia, anencephaly, inaccurate or unknown dates and extrauterine
pregnancyo Placentalsulfatasedeficiency(??X-linkedIchythyosis??):anX-
linkedgeneticdeletionofthe Steroid Sulfatase (STS) enzyme. Manifests as
dry/scaly/grey-brown skin patches, often subsiding in summer * While post-term
babies are more often macrosomic, there is no evidence to support induction of
labor as a preventive measure for macrosomia in these cases. Typically, post-term
pregnancies are induced at 42 weeks. * Management for the patient with an
unfavorable cervix at 42 wk is controversial. o Induction of labor in a patient
with a reactive tracing and an unfavorable cervix will minimize any risk of
antepartum fetal demise; but increases risk of Cesarean section compared to a
patient who goes into spontaneous labor. o It is reasonable to follow a patient who
is 41 weeks with antepartum fetal testing, such as twice weekly NSTs with amniotic
fluid assessment. * If you ever have a woman whose dating is based on LMP, always
get a dating ultrasound first. It??s critical to management to have an accurate
ultrasound dating. * Amnioinfusion is reasonable approach in the treatment of
repetitive variable decelerations, regardless of amniotic fluid meconium status. o
Meconiumstainingofamionticfluidismorecommoninpost-termpregnanciesbecauseof 1more
mature vagal system in fetus and 2higher chance of fetal hypoxia. Amnioinfusion is
NOT indicated for meconium stained fluid and doesn??t impact chance of meconium
aspiration syn. * Note that ??favorable cervix?? means that it??s begun to
dilate/efface. If a post-term pt has a favorable cervix, augmentation/induction of
labor is indicated o
Withaccuratedatingshowing42wkorfavorablecervix,prenatalfollowingwithtwice-weekly
testing is NOT recommended * Note that 3rd trimester ultrasound is uncertain with
+/- 3wks. In a patient with 3rd trimester ultrasound, the dating is sufficiently
uncertain that prenatal biweekly testing is not unreasonable. It??s best to simply
follow the pt with twice-weekly testing and wait for spontaneous labor or induce
with non-reassuring testing (non-reactive NST or oligohydramnios) * Fetal
Dysmaturityo Presentation: fetus born appearing withered, meconium stained, long-
nailed, fragile and have an associated small placenta * ?? �Increased incidence
after 43wk gestation (10%) due to placental insufficiency * ?? �Typically occurs
due to unsure dating resulting in a very post-term delivery * If wanting to induce
post-term labor use of prostaglandins for cervical ripening is necessary if pt has
an unfavorable cervix. Artificial ROM and oxytocin may be done after cervix has
begun to dilate. Chapter 19: Ectopic Pregnancy and Abortion � Topics 15, 16, 34� In
a patient suspected of ectopic pregnancy, stability of the patient will drive
further management. o
Ifptisstable:confirmectopicpregnancyviaultrasound(ifpossible).Ifb-hCGisbelowthe
discriminatory zone, then it is reasonable to get a 48hr b-hCG and confirm with
ultrasound once discriminatory zone has been reached. ?? Once confirmed (fetal pole
seen outside the uterus), methotrexate or surgical resolution of ectopic pregnancy
may be used o
Ifptunstable:immediatehospitalizationwithexploratorysurgeryfordxandtreatment. �
Risk factors for Ectopic Pregnancy: o x10 for prior history of ectopic pregnancy.o
x3foragebetween35and44yearsoldo
Increaseforpriorabdominalsurgery,historyofsexuallytransmittedinfections,sterilizati
on failures, endometriosis and congenital uterine malformations * Note that
spotting/cramping is common in the 1st trimester. Reassuring signs are x2 b-hCG
rise in 48hrs and progesterone >25ng/mL * In an abnormal intrauterine pregnancy (b-
hCH/progesterone indicated) expectant management is typically the way to go to
avoid surgical risks as long as patient is stable. o Misoprostol, manual vacuum
aspiration, or dilation and curettage may all be used to pregnancy termination in
this situation, but all carry their own riskso Laparoscopy and methotrexate are not
indicated as this is a confirmed intrauterine pregnancy. � While corpus luteum cyst
and ectopic pregnancy may present similarly on ultrasound, there are some key
features to distinguish the two: o o o o Visualization of fetal pole outside the
uterus on ultrasoundo Patient B-hCG above discriminatory zone (typically >2000) BUT
no intrauterine pregnancy seen o Inappropriately rising B-hCG levels that do not
fall after D&C � To initiate methotrexate therapy for ectopic pregnancy, pt must:o
Hemodynamic stability with non-ruptured ectopic pregnancyo
Sizeofectopicmass<4cmwithoutafetalheartrateor<3.5cmwithfetalheartrateo
Normalliverenzymes,renalfunction,whitecellcountandtheabilityofthepatienttofollowup
rapidly (reliable transportation, etc.) if her condition changes. * There are
several complications that can occur after an optative (suction) abortion: o
Uterine perforation: lower abdominal pain, nausea, scant bleeding, and fevero
Retainedproductsofconception:similartoperforationbutoftenprofusevaginalbleeding o
Uterinelaceration:moderatebleedingwithoutnausea/fever * First trimester spontaneous
abortion is typically caused by genetic abnormalities involving the conceptus (50
to 60 percent of embryos) * Autosomal trisomy is the most common abnormal karyotype
encountered in spontaneous abortuses, accounting for approximately 40-50% of cases.
Triploidy accounts for approximately 15%, tetraploidy 5% of cases, and Monosomy X
(45X, 0) identified in 15-25% of losses. * insulin-dependent diabetes (either Type
I or severe Type II), increase the rates of spontaneous abortion and major
congenital malformations. The risk appears related to the degree of metabolic
control in the first trimester. * Environmental factors, such as smoking, alcohol
and radiation are causes of spontaneous abortion Positiveb-
hCGpregnancytest�suggestsectopicpregnancy??Ring of fire?? sign on Doppler
ultrasound � suggests ectopic pregnancy
Freefluidinperitoneum(hemoperitoneum)�mayoccurineither � Diagnosis of ectopic (vs
intrauterine) pregnancy include: * In a hemodynamically unstable pt in the first
trimester presenting with bleeding/vital sign changes, immediate surgical treatment
consisting of dilation and suction curettage is necessary. This patient is actively
bleeding and is anemic, and needs to have the products of conception removed to
control bleeding and save her life. * Patients experiencing early pregnancy loss
can safely consider several different treatments, including expectant management,
provided the patient is hemodynamically stable and reliable for follow-up.
Expectant management portends no increase in risk of either hemorrhage or infection
compared with surgical or medical evacuation. Regardless of method chosen, the
patient??s blood type should be checked and rhogam administered as indicated. * In
a patient with incompetent cervix (dilation without labor in the 2nd trimester,
causing pregnancy loss) a cervical cerclage is placed at 14 weeks. Pregnancy loss
in the late second trimester is not usually related to genetic abnormality of the
conceptus and most clinicians delay placement of a cerclage until after the first
trimester, given the high background prevalence of first trimester pregnancy
wastage. * It is important to rule out systemic disease in a patient with recurrent
abortion (three successive first trimester losses) via: o Testing for lupus
anticoagulant, diabetes mellitus and thyroid diseaseo Maternal and paternal
karyotypeso Uterine imaging to exclude a septum or other anomaly is routinely done
using hysteroscopy or hysterography and not CT or MRI scanning * A single, prior
first trimester surgical abortion does NOT increase the risk of subsequent first
trimester pregnancy loss. Indeed, first trimester surgical abortion confers no
subsequent obstetric disadvantage, particularly when compared with an appropriate
control population. * Septic Abortiono
Presentation:abdominalpain,bleeding,fever,anddilationofthecervixwith(+)pregnancytes
t o Treatment:uterineevacuationwithbroad-spectrumantibioticcoverage. * Recurrent
pregnancy loss: >2 consecutive or >3 spontaneous losses before 20 weeks gestation o
Etiologies:anatomiccauses,hyper/hypothyroidism,lutealphasedeficiency,parental
chromosomal anomalies, immune factors such as lupus anticoagulant and idiopathic
factors.o Anti-phospholipid antibodies workup includes anticardiolipin and beta-2
glycoprotein antibody status, PTT, and Russell viper venom time.o Note that Factor
V Leiden mutation is NOT associated with recurrent pregnancy loss * Pts with Anti-
phospholipid syndrome wishing to get pregnant should be placed on aspirin + heparin
* Abortion options o Medicalabortion�Mifepristone(anti-progestin)
+misoprostol(prostaglandin)toinduce contractions * ?? �May be preferred due to no
surgery needed (96% effective) * ?? �Associated with higher blood loss than
surgical abortion. * ?? �Does NOT affect future fertility o
Surgicalabortion�surgicalremovalofconceptus;canbeprimaryorbackupinthecaseof failed
medical abortion o Anyabortioncanbepsychologicallyscarring * Manual vacuum
aspiration is more than 99% effective in early pregnancy (less than eight weeks)
but is contraindicated after 8wk gestation * Pts presenting with retained products
of conception are managed best by performing a dilation and curettage to stop
bleeding Chapter 20, 21, 22, 24 � Topic 17 * While macrosomia is a classic
complication of diabetes in pregnancy, fetal growth restriction is more of a
concern in a patient with long-standing diabetes, especially with known vaculopathy
(retinopathy, poor renal function, limb necrosis). Often Type 1 diabetics have this
complication due to the long-standing nature of Type 1 Diabetes * ACE inhibitors
(Lisinopril) and ARBs (??-sartan??) beyond the first trimester of pregnancy has
been associated with oligohydramnios, fetal growth retardation
and neonatal renal failure, hypotension, pulmonary hypoplasia, joint contractures
and death * If a mom has HIV/AIDS, she should always be offered anti-retroviral
therapy regardless of viral load. Baseline transmission rate of HIV to newborns can
be reduced from about 25% to 2% with all three of the following: o
1.HAART(highlyactiveantiretroviraltherapy)protocolantepartumo 2. Continuing through
delivery with intravenous zidovudine in laboro 3.Zidovudinetreatmentfortheneonate.o
Note that Cesarean section prior to labor can reduce this rate to 2% (although the
benefit is less clear in women with viral loads). * Don??t forget about sepsis! If
you see a patient with fever, signs of intravascular depletion (low BP,
tachycardia, tachypnea), leukocytosis with a suspected infection think septic shock
(not hemorrhagic shock!) o
AcutePyelonephritisisthemostcommoncauseofgestationalsepticshock o Chorioamnionitis
could cause septic shock, but is less common. * Asthma generally worsens in 40% of
pregnant patients. One of the indications for moving to the next line of treatment
includes the need to use beta agonists more than twice a week.o Inhaled
corticosteroids or cromolyn sodium/Theophylline (refractory patients)o Subcutaneous
terbutaline and systemic corticosteroids would be used in acute cases. * Acute
treatment of thyroid storm may include thioamides (i.e. PTU), propranolol, sodium
iodide and dexamethasone. Oxygen, digitalis, antipyretics and fluid replacement may
also be indicated. Maternal mortality with thyroid storm exceeds 25%. * Pregnant
women with syphilis and with a history of penicillin allergy can be skin tested to
confirm the risk of immunoglobulin E (IgE)-mediated anaphylaxis. If skin tests are
reactive, penicillin desensitization is recommended and is followed by
intramuscular benzathine penicillin G treatment. This is to ensure no vertical
transmission (50-80%) o
Erythromycin(11%failure)anddoxycycline(teratogenic)areacceptablealternativesfornon-
pregnant women, but not pregnancy * Patients of average risk for gestational
diabetes, screening is performed at 24-28 weeks while those at high risk (severe
obesity and strong family history) screening should be done as soon as feasible. *
Apparently in patient with bacterial vaginosis, there is no need to treat the
partner, even if there is suspicion of infidelity. * Patients with pulmonary
hypertension are among the highest risk for mortality during pregnancy, a 25-50%
risk for death and should be encouraged to not become pregnant. Similar mortality
rates are seen in aortic coarctation with valve involvement and Marfan syndrome
with aortic involvement. * Many people have mitral valve prolapse and are
asymptomatic. However, pregnancy/anxiety/other conditions may make it symptomatic.
If symptomatic, b-blocking drugs are given to decrease sympathetic tone, relieve
chest pain and palpitations, and reduce the risk of life-threatening arrhythmias. *
Mild Microcytic anemia in the setting of normal ferritin (18-115) may be indicative
of a-thalassemia trait. It poses no threat to the pregnancy, but may be useful for
diagnosis in the child. * Don??t forget! The two most common causes of anemia
during pregnancy and the puerperium are iron deficiency and acute blood loss *
Apparently if a pregnant woman with Lupus (SLE) is having problems due to SLE then
it??s appropriate to simply treat as you would a non-pregnant woman * Don??t give
radiotherapy/chemotherapy for women with breast cancer during pregnancy.
Therapeutic levels are radiation are easily teratogenic and surgical treatment
would be prudent during pregnancy. * While SSRIs are typically considered safe in
pregnancy, One SSRI, paroxetine (Paxil) has been changed to a category D drug
because of the increased risk of fetal cardiac malformations and persistent
pulmonary hypertension o
BupropionisOKinpregnancy;apparentlystudiesgiveevidencetothisclaim * Pruritus
gravidarum, a common pregnancy-related skin condition that is a mild variant of
intrahepatic cholestasis of pregnancy is awful. There is retention of bile salt,
and as serum levels increase they are deposited in the dermis causing causes
pruritus. Skin lesions are secondary to scratching and excoriation. o
Antihistamines and topical emollients may provide some relief and should be used
initially. o Ursodeoxycholic acid relieves pruritus and lowers serum enzyme levels.
o Another agent reported to relieve the itching is the opioid antagonist naltrexon.
Chapter 23: Hematologic and Immunologic Complications During Pregnancy � Topic 18,
19 * The classic signs of magnesium toxicity include muscle weakness, loss of deep
tendon reflexes, nausea, and respiratory depression. If magnesium is given in high
doses, cardiac arrest is possible (This question had 2g/hr). o Tx: Discontinuing
the magnesium sulfate, administration calcium gluconate to restore her respiratory
function. * Dx of Pre-eclampsia: persistent elevation of BP (>140/90 with two
measurements separated by 4hrs & >3g protein in a 24-hr urine sample * Don??t
forget! Definitive treatment of Pre-eclampsia/eclampsia is delivery. MgSO4 should
be infused with regular Mg checks until 24hrs post-partum. * Magnesium sulfate is
the treatment of choice for eclampsia if delivery is not possible. Valium,
hydantoin, tiagabine, and barbiturates can also be used to treat seizures, but are
not first-line therapy for eclampsia. They can be added as second agents, or used
if magnesium is contraindicated * Note! Previous history of spontaneous abortion
does not increase risk of pre-eclampsia * Therapeutic MgSO4 is 4-7 mEq/L. Remember
to look for physical signs of magnesium toxicity when administering MgSO4. Some
quick ones to remember are:o Loss of deep tendon reflexes occurs at a level of 7-10
mEq/L. o Respiratory decline/arrest occurs at a level of 11-15 mEq/L o
Cardiacarrestmayoccuratalevelof15mEq/L. * When expectantly managing pre-
eclampsia/eclampsia there are several things that can warrant immediate delivery: o
Thrombocytopenia(<100,000),failuretocontrolBPwithmaxdoseof2antihypertensives,non-
reassuring fetal heart tracings, LFTs x2 of normal, eclamptic seizure, and oliguria
o Proteinuriaatanylevelisnotawarrantfordelivery * Antihypertensive use is indicated
for blood pressures persistently greater than 160/105 o First-
lineagentsincludehydralazine(adirectvasodilator;5mgIV??5-10mgdosesIVat20- minute
intervals; maximum dose = 40 mg); or labetalol (combined alpha & beta-adrenergic
antagonist; 10-20 mg IV ?? 20 mg, then 40 mg, then 80 mg IV every 10 minutes;
maximum dose = 220 mg). o
Goalisnotanormalbloodpressure,buttoreducethediastolicbloodpressureintoasafe range
of 90-100 mmHg to prevent maternal stroke or abruption, without compromising
uterine perfusion. * Don??t forget! Rh-isoimmunization typically occurs in the
previous pregnancy. While procedures during a pregnancy may cause leakage of fetal
blood into mom, she will likely not make significant titers until after delivery.
Often problems manifest in the 2nd pregnancy where mom has already been sensitized.
* While RhoGAM eliminates much of the chance of isoimmunization, there??s only a 2%
chance antepartum, 7% chance with full term SVD, and 7% with each subsequent
pregnancy. Thus a G1P1 with an uneventful pregnancy will have only about a 9%
chance of isoimmunization o This chance depends on the degree of feto-maternal
hemorrhage occuring in pregnancy; which about 45% of pregnancies experience *
Remember! Middle cerebral artery peak systolic velocity in the management of
fetuses at risk for anemia because of red cell alloimmunization has emerged as the
best test for the noninvasive diagnosis of fetal anemia. (faster flow = more
hemolysis) * Fetal hydrops is easily diagnosed on ultrasound due to decreased
hepatic protein production from the liver needing to make more RBC proteins. o
Dx:collectionoffluidintwoormorebodycavities,suchasascites,pericardialeffusion,pleur
al effusion, or scalp edema o
Placentomegaly,polyhydramnios,andhepatsplenomegaly(extramedullaryhematopoiesis)can
all occur as well � 300mcg of RhoGAM can neutralize 30cc of fetal blood (or 15cc of
fetal RBCs). Typically, 300mcg of RhoGAM is given at 28wk gestation, after a
Direct-Coombs test proves there is not already Anti-D antibodies made, to prevent
sensitization to Rh-factor. RhoGAM is also administered: o
Within72hrsofbirthinaRh(-)momwith(+)pregnancyo
Followingspontaneousabortion,antepartumhemorrhage,amniocentesis,orchorionicvillus
sampling in a Rh(-) mom with (+) pregnancyo Note if mom AND dad are Rh(-), the baby
is definitively Rh(-) and RhoGAM is not needed * Don??t forget! Lewis antibodies
are IgM antibodies and do not cross the placenta, therefore are not associated with
isoimmunization or hemolytic disease of the fetus (Lewis Lives!) o Also, Rh(+) moms
will be Rh-Antibody negative by definition. * In a severely erythroblastotic fetus,
the amniotic fluid is stained yellow. The yellow pigment is bilirubin, which can be
quantified most accurately by spectrophotometric measurements of the optical
density between 420 and 460nm, the wavelength absorbed by bilirubin. * If labs
indicate severe hemolytic disease of the newborn (Zone 3 of the Liley curve, fetal
death within 7- 10 days) the fetus should be immediately be delivered if at term.
However, if the baby is preterm, the following should be done to prolong the
pregnancy) o Intrauterineintravascularfetaltransfusiono If this is not possible;
Intraperitoneal transfusion with maternal plasmapheresis should be done (slower
correction of anemia)� Don??t forget! Although we routinely give RhoGAM for Rh-
factor (D-antigen) other blood antigens are not protected against (Duffy, Kell,
etc.) thus, can still occur from normal blood transfer during labour Chapter 25:
Neurologic/Psychiatric Disorder During
Pregnancy � Topic 17, 29� Many antipsychotic and neural-active drugs are
contraindicated in pregnancy. These recommendations are based on a drug rating
system below:o CategoryAdrugs,thereareadequate,well-
controlledstudiesinpregnantwomenthathavenot shown an increased risk of fetal
abnormalities to the fetus in any trimester of pregnancy.o
CategoryB,animalstudieshaverevealednoevidenceofharmtothefetus;however,thereare no
adequate and well-controlled studies in pregnant women or animal studies that have
shown an adverse effect, but adequate and well-controlled studies in pregnant women
have failed to demonstrate a risk to the fetus in any trimester. o Category C drugs
have animal studies that show an adverse effect and there are no adequate and well-
controlled studies in humans, but potential benefits may warrant use of the drug in
pregnant women despite potential risks. o CategoryDdrugshaveadequatewell-
controlledorobservationalstudiesinpregnantwomen and are known risks to the fetus. o
Category X drugs should not be used in pregnancy, because adequate well-controlled
or observational studies in animals or pregnant women have demonstrated positive
evidence of fetal abnormalities or risks. * In using SSRIs, the most common side
effect is insomnia/sleep disturbance. Other common side effects include sexual
dysfunction, decreased libido and delayed/absent orgasm * Recommendations state
that SSRI medications can be safely used during lactation. Several studies show
that SSRIs are secreted in breast milk, however no detectable levels of the drug
were found in the infants?? serum. * Third trimester maternal use of SSRIs can be
associated with abnormal muscle movements (extrapyramidal signs or EPS) and
withdrawal symptoms (agitation, abnormally increased or decreased muscle tone,
tremor, sleepiness, severe difficulty breathing, and difficulty in feeding) o
Symptoms often subside within hours or days and do not require specific treatment;
other newborns may require longer hospital stays o SSRI use during pregnancy is not
associated with newborn seizures, intracranial hemorrhage or temperature
instability. Chapter 26: Contraception & Chapter 27: Sterilization � Topic 32, 33 *
While many women may initially have irregular bleeding when starting Depo-Provera,
this often resolves within 2-3 months of use; 50% of women will actually stop
bleeding altogether. * Apparently when a patient is requesting emergency
contraception, you should also immediately initiate OCPs as well o Remember that
emergency contraception is not considered an abortifacient and has not been shown
to be teratogenic if pregnancy is present o Plan B or other emergency
contraceptives should be initiated within 72hrs of sex (best outcomes) but can be
administered no later than 120hrs after sex * Contraindications to estrogen (OCPs)
include a history of thromboembolic disease, women who are lactating, women over
age 35 who smoke, or have severe nausea with combined OCPs o
Thesewomenarebettersuitedforprogestin-onlyormechanicalmethods * Oral contraceptives
will decrease a woman??s risk of developing ovarian and endometrial cancer due to
low-dose estrogen exposure.o
Slightlyhigherriskofdevelopingcervicalintraepithelialneoplasiao
RiskofPID,endometriosis,benignbreastchangesandectopicpregnancyarereduced * In pts
wih high BMI or previous gynecologic surgeries desiring permanent sterilization,
hysterscopic sterilization (Essure) is a great option due to increased surgical
risk o Pt must take effective contraception for 3mo following surgery, until a
hysterosalpingogram can confirm that the tubes are occluded * Regret rate after
tubal ligation increases with decreasing age (40% of women under 25yr had regret);
women who are not married at the time of their tubal ligation, when tubal ligation
was performed less than a year after delivery, and with conflict between the woman
and her partner have higher rates * Vasectomy and tubal ligation are both 99.8%
effective; in a married patient with multiple medical problems that present high
risks for surgery, the husband getting a vasectomy may be the best option * Don??t
forget! A person with Wilson??s Disease (hepatolenticular degeneration) is not a
candidate for a copper-IUD (as they can too much copper from it as a present-
source!) * The patch (Ortho Evra�), while comparable efficiency to the pill in
comparative clinical trials, has significantly higher failure rate when used in
women who weigh more than 198 pounds, likely due to significantly increased
subcutaneous fat, inhibiting hormonal diffusion. Chapter 28: Vulvovaginitis � Topic
35 * Tx for BV is either Metronidazole 500 mg orally BID for seven days, or vaginal
Metronidazole 0.75% gel QHS for five days. * Phimosis is resorption of the clitoris
* Trich. treatment is metronidazole 2 grams orally in a single dose or
metronidazole 500mg orally twice daily for seven days with empiric treatment of
sexual partner * Treatment for uncomplicated vulvo-vaginal Candidiasis consists of
short-course topical Azole formulations (1-3 days), which results in relief of
symptoms and negative cultures in 80%-90% of patients who complete therapy. *
Vestibulodynia (formally vulvar vestibulitis) syndrome consists of a constellation
of symptoms and findings limited to the vulvar vestibuleo
Presentation:abruptonsetsevere,??sharp/burning/raw??
painonvestibulartouchorattempted vaginal entry, tenderness to pressure, erythema
* ?? �Symptoms can occur with tampon insertion, tight clothing, or sex * ??
�Typically, a primary inciting event cannot be identified o Dx:clinicalpresentation
o Tx: * ?? �Medical: Tricyclic antidepressants to block sympathetic afferent pain
loops, pelvic floor rehabilitation, biofeedback, and topical anesthetics. * ??
�Surgical: vestibulectomy is reserved for patients who do not respond to standard
therapies and are unable to tolerate intercourse. * Treatment of
Gonorrhea/Chlamydia mucopurulent cervicitis is ceftriaxone + azithromycin * If you
get an elderly (>55 y/o) woman with a vulvar lesion causing her pain, the next step
is to perform a biopsy to evaluate for vulvar cancer. * Detrusor instability o
Presentation:urinaryfrequency/incontinencewithnegativeUTI/STDworkupandnormalpost-
void residual volume * ?? �Inability for the detrusor muscle to relax to allow for
bladder filling * ?? �Parasympathetic system stimulation via muscarinic ACh
receptors allows for normal bladder emptying o Dx: clinical presentation o Tx:
anti-cholinergic drug administration (e.g. oxybutynin); note that TCAs are
anticholinergics but are really dirty drugs and not really the best first line Tx
Ch. 29 STDs/Ch. 30 Pelvic Support Defects, Incontinence, UTIs � Topic 36, 37 *
Don??t forget! Herpes (HSV) can begin with a prodrome of viral/flu-like illness
followed by onset of vaginal itching/burning before the onset of vesicular rash.
While HIV can also have a flu-like illness associated with initial infection,
there??s rarely vulvar-vaginal itching and burning. * Hep B transmission is through
sexual contact in 38% of infections; if exposed, PEP should be administered as soon
as possible but no later than 7 days if blood exposure and 14 days if sexual o
SourceHepB(+)�giveimmediateHBIG+HepBvaccineserieso
SourceHepB(-)orunknown�onlygiveHepBvaccineserieso
IfinoculatedisHepBimmune�nofurthertreatmentneeded * In treating STDs/PID
adolescents have no better outcomes from inpatient vs outpatient therapy, but
hospitalization ensures compliance and aggressive treatment may prevent UG tract
scarring. The recommended regimen for inpatient IV treatment for
gonorrhea/chlamydia is either [cefotetan or cefoxitin + doxycycline or clindamycin
+ gentamicin.] * The rate of tubal infertility has been reported as 12% after one
episode of PID, 25% after 2 episodes and 50% after three episodes. Recurrent STDs
or PID can result in significant long-term sequelae, such as chronic pelvic pain,
hydrosalpinx, tubal scarring and ectopic pregnancy. * When assessing urinary
incontinence, a normal post-void residual (PVR) is 50-60 cc. An elevated PVR,
usually >300 cc, is found in overflow incontinence. * Apparently, women with a
family history of POP have up to a 2.5 fold increase in prolapse and it??s a huge
risk factor for development. o
Althoughhysterectomyisassociatedwithanincreasedriskofapicalprolapse,studiesshow
mixed results on in the development of prolapse. The risk of future prolapse may be
highest when hysterectomy is performed in women with existing prolapse, while the
risk in women with normal pelvic support is less clear. * In comparing surgical
procedures for stress incontinence due to urethral hypermobility or intrinsic
sphincter deficiency (ISD): o Retropubicurethropexysuchastension-
freevaginaltapeandotherslingprocedureshavethe best five-year success rates for
patients with stress incontinence due to hypermobility. o Urethral bulking
procedures are best for ISD with little to no mobility of the urethra. These are
minimally invasive and have 80% success rate. o
Needlesuspensionsandanteriorrepairshavelowerfive-yearsuccessratesforGSI. o
Colpocleisis is one option to treat uterine prolapse, and is not indicated for
urinary incontinence. * A ??drain-pipe urethra?? is simply another name for
intrinsic sphincter deficiency (ISD). The resemblance is that a drain pipe is very
wide at the top, then narrows, just as the widened proximal portion of the urethra
looks with ISD. * Oxybutynin apparently is the classic anti-cholinergic drug to
give for urge urinary incontinence * Often when a pelvic organ prolapse occurs, the
prolapsing organ is affixed to abdominal fascia: o
Centralandlateralcystocelesarerepairedbyfixingdefectsinthepubocervicalfasciaor
reattaching it to the sidewall, if separated from the linea alba. o
Defectsintherectovaginalfasciaarerepairedinrectoceles.o
Enteroceles are repaired by either vaginal or abdominal enterocele repairs.o
Vaginalvaultprolapseistreatedeitherbysupportingthevaginalcufftotheuterosacralor
sacrospinous ligaments, or by sacrocolpopexy� Don??t forget! If the patient has
pelvic organ prolapse but isn??t symptomatic...intervention is NOT necessary at
this point. � In a patient with high surgical mortality risk (this lady was 90y/o
with heart disease and diabetes) colpocleisis is a good option; it??s a procedure
where the vagina is surgically obliterated and can be performed quickly without the
need for general anesthesia. o Sacrospinousfixation(cufftosacrospinous-
coccygeuscomplex)orsacrocolpopexy(cuffto sacral promontory using interposed mesh)
require regional or general anesthesia and is not the best option for this patient
with high surgical morbidity. Chapter 31: Endometriosis � Topic 38 * Don??t forget!
An endometrioma (??chocolate cyst??) endometriosis that??s present within a cyst
(often on the ovary) seen as a complex mass on imaging. * Surgery is the gold
standard in the diagnosis of endometriosis, but often is not the initial treatment
as suspected endometriosis is often managed medically. The role of surgery is often
to manage the symptoms and can be conservative (laparoscopic ablation or excision
of implants, excision of endometriomas) or definitive (total hysterectomy/BSO). o
Inayoungpatientwhofailsmedicaltherapy,conservativesurgeryisthenextoptionto preserve
fertility * Typically, medical management of endometriosis involves combined OCPs
and NSAIDs to interrupt the HPA axis and control pain. o
GnRHagonistsalsoexertnegativefeedback,butcanbeusedshorttermonlyandhavemore side
effects o
Danazolisasyntheticandrogenusedtotreatendometriosis,butduetoitsandrogenicside
effects (weight gain, increased body hair and acne, and adverse affect on blood
lipid levels) o Laparoscopy is indicated in the patient who fails medical treatment
and/or is planning pregnancy in the near future * There is no imaging study or
blood test that can confirm the diagnosis of endometriosis; only laparoscopy and
visualization can achieve this. * Don??t forget! Oral contraceptives are
contraindicated in this patient, as she is older than 35 and smokes. * A Doppler
ultrasound to check the blood flow to the ovaries is controversial, as normal flow
does not rule out ovarian torsion. If a paitnet most likely has ovarian torsion,
they need to be surgically explored, immediately. Further imaging studies will not
help beyond the information obtained on a normal ultrasound. * A patient with a
known history of endometriosis, who is unable to conceive and has an otherwise
negative workup for infertility, benefits from ovarian stimulation with clomiphene
citrate, with or without intrauterine insemination. In-vitro fertilization and
adoption can be offered if other treatments fail. Chapter 32: Dysmenorrhea and
Chronic Pelvic Pain � Topic 39 & 46� This question had a 17y/o patient with
heavy/painful menses since onset at age 14, qualifying as chronic pelvic pain.
Pelvic exam and abdominal ultrasound were normal and she had no coagulopathy. o
Nextstep??diagnosticlaparoscopyo
MostofthesepatientswillhavefibroidsORendometriosis,bothofwhichcanbe
diagnosed/treated laproscopically. While this patient is young, rates of
endometriosis are the same as if she were older; thus we must find a diagnosis to
stop her pain. � Interstitial cystitis (IC) is a chronic inflammatory condition of
the bladder o
Presentation:recurrenturinaryurgencyandfrequency,intheabsenceofobjectiveevidenceof
another disease, Pelvic pain (70% of women), and dyspareunia. o
Thespecificetiologyisunknown� Irritable bowel syndrome (IBS) is a common functional
bowel disorder of uncertain etiology. o
Presentation:chronic,relapsingpatternofabdominalandpelvicpain,andboweldysfunction
with constipation or diarrhea. ?? IBS is one of the most common disorders
associated with chronic pelvic pain and occurs more commonly in women with chronic
pelvic pain o
DiagnosisisbasedontheRomeIIICriteriaforIBS,whichhasatleast12weeks(neednotbe
consecutive) in the last 12 months of abdominal discomfort/pain with two of three
features: * ?? �1) relief with defecation * ?? �2) onset associated with a change
in frequency of stool * ?? �3) onset associated with a change in stool form or
appearance. � Gonadotropin-releasing hormone (GnRH) agonists are analogues of
naturally occurring gonadotropin- releasing hormones that down-regulate
hypothalamic-pituitary gland production and the release of luteinizing hormone and
follicle-stimulating hormone leading to dramatic reductions in estradiol level. o
NumerousclinicaltrialsshowGnRHagonistsaremoreeffectivethanplaceboandaseffectiveas
Danazol in relieving endometriosis-associated pelvic pain. o Danazol,a17-alpha-
ethinyltestosteronederivative,suppressesthemid-cyclesurgesofLHand FSH. * Studies
have found that 40-50% of women with chronic pelvic pain have a history of abuse.
Whether abuse (physical or sexual) specifically causes chronic pelvic pain is not
clear, nor is a mechanism established but the link between abuse and chronic pelvic
pain may be psychologic or neurologic * It is estimated that chronic pelvic pain is
the principal preoperative indication for 10-12% of hysterectomies. This patient,
although with minimal disease noted, has recurrent pain from endometriosis. Since
the patient had a tubal ligation and does not desire any more children, the best
option is removal of ovaries with or without a hysterectomy. * Ovarian remnant
syndrome occurs following surgical removal of the ovaries, with subsequent
development of cyclical pain due to ovarian tissue that was left behind
inadvertently. * Pelvic congestion syndrome is a cause of chronic pelvic pain
occurring in the setting of pelvic varicosities. These veins are thin walled and
unsupported, with relatively weak attachments between the supporting connective
tissue. The cause of pelvic vein congestion is unknown. o Presentation: pain of
variable intensity and duration; worse premenstrually, during pregnancy, and with
standing, fatigue and coitus. Pelvic ??fullness?? or ??heaviness,?? which may
extend to the vulvar area and legs. Vaginal discharge, backache and urinary
frequency. Menstrual cycle defects and dysmenorrhea are common � Nerve entrapment
syndrome is a commonly misdiagnosed neuropathy that can complicate pelvic surgical
procedures performed through a low transverse incision when a low transverse
incision is extended beyond the lateral border of the rectus abdominus muscle, into
the internal oblique muscle. o Iliohypogastric nerve (T-12, L-1) - exit the spinal
column at the 12th vertebral body and pass laterally through the psoas muscle
before piercing the transversus abdominus muscle to the anterior abdominal wall,
then courses medially between the internal and external oblique muscles, becoming
cutaneous 1 cm superior to the superficial inguinal ring. ?? Provides cutaneous
sensation to the groin and the skin overlying the pubiso Ilioinguinalnerve(T-12,L-
1)-exitthespinalcolumnatthe12thvertebralbodyandpass laterally through the psoas
muscle before piercing the transversus abdominus muscle to the anterior abdominal
wall, then follows along with the ilihypogastric nerve a bit lower. ?? Provides
cutaneous sensation to the groin, symphysis, labium and upper inner thigh. o
Obturator nerve damage during lymph node dissection would result in the inability
of the patient to adduct the thigh. * Note! The progestin in oral contraceptives
causes endometrial atrophy. Since prostaglandins are produced in the endometrium,
there would be less produced. Dysmenorrhea should be improved. * This patient has
classic symptoms of leiomyomata, including menorrhagia BUT an endometrial biopsy
should be performed on all women over age 40 with irregular bleeding to rule out
endometrial carcinoma. Chapter 33: Disorders of The Breast � Topic 40 � Stimulation
of the breast during the physical examination may give rise to an elevated
prolactin level and promote milky discharge. Post partum women may continue to
produce milk for up to two years after cessation of breastfeeding o
Accurateprolactinlevelsarebestobtainedinthefastingstate.o
Ifstillelevated,thenaTSHlevelandbrainMRIareindicatedtoruleoutapituitarytumor. o
Althoughpathologicfactorssuchashypothyroidism,hypothalamicdisorders,pituitary
disorders (adenomas, empty sella syndrome), chest lesions (breast implants,
thoracotomy scars, and herpes zoster) and renal failure can elevate prolactin
levels, a non-significant benign elevation needs to be ruled out first. * If
there??s a dominant breast mass, but no obvious signs of malignancy an FNA is a
great first option. If it??s got signs of malignancy, then an excisional biopsy may
be indicated. * Fibrocystic breast changes are the most common type of benign
breast conditions and occur most often during the reproductive years. Fibrocystic
disease is often associated with cyclic mastalgia, possibly related to a pronounced
hormonal response. Caffeine intake can increase the pain associated with
fibrocystic breast changes, so recommending decreased caffeine intake may be
helpful. * The first noticeable symptom of breast cancer is typically a lump that
feels different from the rest of the breast tissue. More breast cancer cases are
discovered when the woman feels a lump. o Even though the mass decreased in size
after aspiration, the bloody discharge obtained obligates an excisional biopsy be
performed to rule out breast cancer. o
Ifcleardischargeisobtainedonaspirationandthemassresolves,reexaminationintwo months
is appropriate to check that the cyst has not recurred. * Most postpartum mastitis
is caused by staphylococcus aureus, so a penicillin-type drug is the first line of
treatment. Dicloxacillin is used due to the large prevalence
of penicillin resistant staphylococci. Erythromycin may be used in penicillin
allergic patients. * If you have a dominant breast mass and FNA fails to reduce it,
get an excisional biopsy. Chapter 34: Gynecologic Procedures � Topic 41� Management
of LSIL found on Pap smear is initial colposcopic examination (unless the woman is
pregnant, postmenopausal or an adolescent). These are typically done a few weeks
after the finding, as it takes time for analysis of the Pap. o
AnotherPapsmearrepeatedpriortosixtoeightweeksfollowingthelastone,reparative changes
may still be happening to the cervix, limiting it??s use. o
Papsmearismerelyascreeningtestandupto20%ofpatientswithLSILonPapsmearhave high-grade
squamous intraepithelial lesion (HSIL) on colposcopically-directed biopsy. o
Incontrast,upto50%ofpatientswithLSILonPapsmearhaveanegativecolposcopy.o
LSILmaybefollowedwithserialPapsmears;however,atissuediagnosisoracolposcopy without
evidence of HSIL changes must be done initially. o An excisional procedure (knife
biopsy or LEEP) is not warranted without a tissue diagnosis of dysplasia. * If a
patient has high grade CIN (II, or III), endovervical curettage should be
undertaken to see if disease is confined to the cervix. If it??s only in the
cervix, a LEEP/cold-knife conization procedure to remove diseased tissue is now
indicated. o Spontaneous regression of dysplasia may occur with a high-grade
lesion, but the rate of regression is much lower than with LSIL. On the other hand,
the progression rate of HSIL to invasive cancer is much higher (up to 12%) * In a
stable patient complaining of menorrhagia and abnormal uterine bleeding, the first
step is always an endometrial biopsy. It could be anything from fibroids to
endometrial cancer and you must rule things out before further evaluation. * Risk
factors following a LEEP-procedure include infection, bleeding, cervical stenosis,
persistent disease, and possibly risk for preterm delivery (cervical insufficiency)
* In a woman who had LSIL on PAP smear with biopsy showing CIN-I: She requires
follow up Pap smear in one year. Excisional or ablative procedures are not
indicated for LSIL, and cervical tissue should be watched as it may progress or
(more likely) spontaneously resolve. * A vulvar lesion unresponsive to treatment
needs a biopsy. In addition to testing for invasive cancer, the biopsy can also
ensure that your diagnosis and treatment are correct. * In a patient who had a
properly placed IUD that cannot be removed, hysteroscopy is the next step o This is
easily performed either in the office or in the operating room, and the IUD could
then be removed under direct visualizationo If the IUD had been seen outside the
uterus, laparoscopy could be offered for removal � Even in a patient with a likely
benign, new palpable breast mass, needle aspiration of the mass or lymph node
allows for pathologic diagnosis of the mass needs to be performed. o
Resultscorrelatewellwithexcisionalbiopsyresults.o
Observationorwaitingforthepatienttodecreasecaffeineintakewouldnotberecommended for
a patient with a new finding of a palpable breast mass, especially in a patient
with a family history of breast cancer. * In a patient with severe, symptomatic
endometriosis who does not desire fertility and wants definitive treatment,
hyperstectomy with bilateral salpingo-oopherectomy is the correct choice. Likely
much of the endometreiosis can be removed during procedure and the removal of
primary estrogen production will decrease the endometriosis. * In a stable patient,
pelvic ultrasound would be the best way to begin a workup for an incidental finding
of an adnexal mass; one can distinguish an adnexal mass from other structures, as
well as note the characteristics of the mass (simple vs. complex, solid vs. cystic,
thin or thick walled, size, and ancillary structures involved) allowing for a
management plan may be constructed. Chapter 35: Human Sexuality � Topic 56 *
Estrogen cream is a typical treatment for a post-menopausal woman who is
experiencing symptoms of vaginal atrophy. While water-based lubricant is indicated,
petroleum jelly can irritate vaginal mucosae and should be avoided! * Apparently if
a woman is enjoying masturbation, it??s still possible that she??ll have
dyspareunia AND dyspareunia is the most common thing to cause sexual dysfunction in
post-menopausal women. Chapter 36: Sexual Assault/Domestic Violence � Topic 57/58 *
If a woman reports rape and is acting odd, even with a story that makes it seem
like she cooperated, she is likely in shock following the event. Don??t assume that
because of the odd story that it didn??t happen or happened with consent. * ALL
reported cases of child abuse must be reported to the police for investigation.
Even if the mom states she doesn??t want anything to be done...the child is in
danger and this trumps her wishes. * Yeast infections (vaginal discharge, itching,
erythematous vulva) are common after antibiotic therapy, even in very young girls.
Scratching can appear like abuse is taking place. To examine a child, even with a
nasal speculum, is traumatic. If a foreign body is suspected, an exam under
anesthesia may be necessary, if ultrasound is not successful or indicated. *
Children will often place things in body orifices, the vagina included. If a child
comes in that??s asymptomatic but with some report of ??vaginal discharge??, a
foreign body placed in the vagina may be suspected. Toilet paper is the most common
foreign body found. * Sexual trauma and vaginal lacerations can occur during
consensual sexual behavior and do not necessarily indicate sexual abuse. However,
aggressive sexual activity can result in serious injuries, especially if mechanical
or foreign objects are not safely used. * In a case of date rape, the best course
of action is to ensure that the patient does not get pregnant. The patient should
also have screening for sexually transmitted diseases, with consideration to being
offered antibiotic prophylaxis. Although the risk of infection is unknown among
victims of sexual assault, it may be higher compared to consensual sexual
encounters. * Antibiotic prophylaxis for STDs should be offered to all adult rape
victims. Although patients are often reticent to do so, they should be gently
encouraged to contact/work with the police. This has been associated with improved
emotional outcomes for victims * The best place to have domestic violence
literature is where there is the most privacy such as an office restroom. In the
other areas cited, an abuser may see the information and prevent his/her spouse or
partner from obtaining it. * Some classic signs of Elder Abuse are spiral
fractures, bruising/lacerations explained by those around them, and malnutrition.
Older patients with dementia or mental illness may be at higher risk. In cases of
elder abuse, social services must be notified for case management/placement. *
Victims of domestic violence frequently present with vague physical and emotional
complaints that are consistent with PMS. Victims will rarely volunteer information
on first physician encounters, but subsequent visits give opportunities to offer
resources for assistance. It is the patient??s choice as to whether she would like
to involve the police. Social work consultation, family counseling and relocation
are all reasonable options that fall under the resources that may be discussed with
the patient, but must be arranged at the patient??s request and with her consent. *
Domestic violence does not always have to manifest in physical abuse. Disagreements
and arguments, even heated discussions, are part of a normal relationship. However,
physical violence or other abusive behaviors are not. o
Signsofbeinginvolvedinanabusiverelationshipmaycomeinseveralformsandscreeningall
women at routine ob-gyn visits, during family visits and during preconception
visits are recommended. o
Forthepregnantwoman,screeningshouldoccuratthefirstprenatalvisit,atleastonceper
trimester, and at the postpartum checkup. Chapter 38: Puberty � Topic 42 * The true
first change in puberty is growth acceleration (this is NOT the growth spurt), but
it universally goes unnoticed. The recognized sequence of events is breast budding
(around age 10), then adrenarche (hair growth), a growth spurt and then menarche. o
Inaminorityofcases,pubarche(pubichairgrowth)canoccurbeforethelarche(breast/areolar
development). * For menses to begin, body weight of 85 - 106lbs with adequate sleep
and optic exposure to sunlight. o
Psychosocialcausesofdelayedpubertyincludeeatingdisorders,excessiveexerciseandstress
or depression.o WeekendsportswouldlikelyNOTcauseexcessiveexercise * Turner syndrome
is the absence of one of the X chromosomes. These females have:o Failure to
establish secondary sexual characteristics (streak ovaries)o
Shortstatureandcharacteristicfeatures:pterygiumcolli,shieldchestandcubitusvalgus.o
Partial deletions of the long arm of the X chromosome also cause premature ovarian
failure * Average age of puberty in females with Down syndrome is the same as
normal females. * In Noonan Syndrome pts typically have normal puberty and
fertility and normal karyotype, although it?? s sometimes called the ??male version
of Turners??. They may have short stature, webbed neck, heart defects, and abnormal
faces. * Kallmann syndrome is characterized by olfactory tract hypoplasia and the
arcuate nucleus does not secrete GnRH. Therefore, these females have no sense of
smell and do not develop secondary sexual characteristics. Treatment is pulsatile
GnRH replacement therapy. * In true precocious puberty, the HPA-axis is prematurely
activated and the patient must have a thorough neurologic, adrenal, and gynecologic
workup before diagnosis can be made. o Tx is with GnRH agonist administration to
suppress HPA-axis until
appropriate puberty age * Normal age for menarche is between nine and 17. While
this patient hasn??t started menses yet, she has secondary sexual characteristics
and normal anatomy, she should be offered reassurance that she is normal and her
menses will probably start soon. * Renal anomalies occur in 25-35% of females with
Mullerian agenesis. The uterus and cervix are absent, but the ovaries function
normally and, therefore, secondary sexual characteristics are present. You would
expect the karyotype in this patient to be 46,XX and testosterone levels in the
female range. * Imperforate hymen where the genital plate canalization is
incomplete. Amenorrhea, cyclic abdominal pain (menstrual blood will collect in the
vagina and uterus) and bluish mass protruding from the labia. Treatment involves
surgical correction Chapter 37: Reproductive Cycles; Chapter 39:
Amenorrhea/Abnormal Uterine Bleeding � Topic 43/45 * Most women resume normal
menstrual cycles after discontinuing oral contraceptive pills (OCPs), they are not
usually considered the cause of the amenorrhea. A history of irregular cycles prior
to pill use may increase the risk of amenorrhea upon discontinuation. This is
sometimes referred to as ??post pill amenorrhea.?? * Disorders of clotting may
present with menstrual symptoms in young women, with Von Willeberand disease being
most common. * Management of an endometrial polyp includes the following:
observation, medical management with progestin, curettage, surgical removal
(polypectomy) via hysteroscopy, and hysterectomy. o Observation is not recommended
if the polyp is > 1.5 cm.o In women with infertility polypectomy is the treatment
of choice. While her inability to get pregnant may be more complicated than just
her polyp, removal of the polyp should occur prior to infertility treatments. *
Abnormal uterine bleeding is a term used to describe uterine bleeding
abnormalities. This term can encompass both structural causes (polyp, adenomyosis.
Leiomyoma, or malignancy [or hyperplasia]) as well as non-structural causes
(coagulopathies, ovulatory dysfunction, endometrial, iatrogenic or not classified).
The acronym PALM-COEIN is a means for this classification. * Hysteroscopic
myomectomy preserves the uterus, while removing the pathology causing the patient??
s symptoms. A laparoscopic approach is not indicated as the myoma is submucosal and
not accessible using a laparoscopic approach Chapter 40: Hirsutism and Virilization
� Topic 44 � Masculinizing Tumors of Women o Sertoil-
LeydigCellTumor�testosteroneproducingtumor,unilateral,sized7-10cm;presents with
acne, hirsutism, amenorrhea, and virilization over 6mo or less time. Dx is with
inspection and measurement of low FSH/LH/androstenedione and high testosterone. Tx
is surgical resection with inspection of contralateral ovary. o
Gynandroblastoma�raretumorwithbothtestosteroneandestrogenproducingfeatures.Odd
clinical presentation with masculinization as well as endometrial
hyperplasia/irregular uterine bleeding. o
LipidCellTumor�smallovariantumorwithsheetsofround,clearstaining,palecellswith
characteristic overproduction of 17-ketosteroids. Will produce masculinization. o
HilarCellTumor�overgrowthofmaturehilarcells,typicallyseeninolderwomen.Small,
unilateral benign ovarian tumor. Hilar cells are homologues of Leydig cells,
producing testosterone and masculinization in these older women. Pathognomonic
Reinke albuminoid crystals are the hallmark of this tumor. * For some reason Asian
people are less likely to have a predisposition to idiopathic hirsutism. Asians
with polycystic ovarian syndrome are less likely to present with overt hirsutism
than other ethnic groups. * Don??t forget! Isolated elevated DHEAS support the
diagnosis of an adrenal tumor as the etiology of female masculinization. * Don??t
forget! In polycystic ovarian syndrome, a patient would have increased
androstenedione and testosterone. A normal serum testosterone levels make it a less
likely diagnosis. Also, while these patients should be tested for insulin
resistance, it isn??t helpful for diagnosis of PCOS. * Don??t forget! Idiopathic
hirsutism is a diagnosis of exclusion, often being made after thorough workup for
hormonal/genetic problems that may cause it. Pts are thought to have a heightened
level of 5a- reductase, thus making the normal testosterone levels they have more
potent at the hair follicle from increased DHT production. * If Cushing's syndrome
is suspected, either a dexamethasone suppression test or a 24-hour urinary
measurement for cortisol can be performed. * Acanthosis nigricans is associated
with elevated androgen levels and hyperinsulinemia. * Postpartum telogen effluvium
(hair loss) affects 40-50% of women postpartum. o High estrogen levels in pregnancy
increase the synchrony of hair growth. Therefore, hair grows in the same phase and
is shed at the same time. o Occasionally, this can result in significant postpartum
hair loss at 1 to 5 months postpartum with 3 months after delivery being most
common time. * Hyperthecosis is a more severe form of polycystic ovarian syndrome
(PCOS)o Associatedwithvirilization(highandrostenedione/testosteronelevels) o
Moredifficulttotreatwithoralcontraceptivetherapy.o More challenging to achieve
successful ovulation induction. * Spironolactone, an aldosterone antagonist
diuretic, can also be used in addition to the oral contraceptives for hirsutism. o
Lupron and Depo-Provera are also reasonable as second-line treatments of hirsutism,
if your patient is not already on oral contraceptives o
Danazolisprimarilyusedforthetreatmentofendometriosisandmayactuallyworsen hirsutism
and acne. Chapter 41: Menopause � Topic 47 * The principal symptom of endometrial
cancer is abnormal vaginal bleeding. Although the patient??s worsening menopausal
symptoms make HRT an important consideration, the specific organic cause(s) of
abnormal bleeding must be ruled out prior to initiating therapy. o Apparently
HTN/Diabetes are NOT contraindications for hormone replacement therapy. * DonDot
forget! Premature ovarian failure occurs before age 35. * Calcium absorption
decreases with age due to a decrease in biologically active vit D. o A positive
calcium balance is necessary to prevent osteoporosis.o Calcium supplementation
reduces bone loss/fractures in individuals with low dietary intakes.o
Inordertoremaininzerocalciumbalance,postmenopausalwomenrequireatotalof1200mg of
elemental calcium per day. � In this question, the patient has many of the major
risk factors for osteoporosis (history of fracture as an adult, low body weight,
current smoker) o Patients who already have had an osteoporotic fracture may be
treated on this alone.o
Priortobeginningtreatmentwithbisphosphonates,abonemineraldensity(BMD)shouldbe
documented and repeated at two-year intervals to monitor treatment.o Dual-energyX-
rayabsorptiometry(DEXA)scanisthetestofchoiceformeasuringBMD.o A nuclear medicine
bone scan is useful to rule out pathologic fracture from metastatic disease. o
General recommendations for the prevention of osteoporosis include eating a
balanced diet that includes adequate intake of calcium and vitamin D, regular
physical activity, avoidance of heavy alcohol consumption, and smoking cessation.�
ACOG recommendations considers hormone replacement therapy (HRT) the most effective
treatment for severe menopausal symptoms that include hot flashes, night sweats and
vaginal dryness.o Counselling about the risks and benefits before initiating
treatment is essential.o ACOGrecommends??
thesmallesteffectivedosefortheshortestpossibletimeandannual reviews of the decision
to take hormones.??o
HRTshouldnotbeusedtopreventcardiovasculardiseaseduetotheslightincreaseinriskof
breast cancer, myocardial infarction, cerebrovascular accident, and thromoboembolic
events. o Awomanwithanintactuterusshouldnotuseestrogen-
onlytherapybecauseoftheincreased risk of endometrial cancer. � Expectant management
is reasonable in this patient, as she notes minimal menopausal symptoms. o Her
vaginal dryness is not interfering with her ability to enjoy intercourse, and she
has only occasional hot flashes; if she is not experiencing significant symptoms,
HRT should not be initiated at this time.o
AnFSHlevelisnotindicatedasbydefinitionsheismenopausal(amenorrheafor>than12mo) *
Treatment of hot flash symptoms with estrogen is most effective, and the current
recommendation is for the lowest dose for the shortest duration of time; especially
in a patient without a uterus. o Hot flashes will resolve completely in 90% of
patients receiving this therapy.o
Raloxifene,aselectiveestrogenreceptormodulator,mayactuallycausehotflashestoworsen
in a patient who has not stopped having these symptoms completely.o
SSRIantidepressants,someanti-seizuremedicationsandalternativetreatments,suchassoy
products and herbs, have not been shown to be as effective as estrogen. * Recent
data have confirmed the overall positive effects of hormone therapy on serum lipid
profiles. o Reduction in LDL cholesterol (increases LDL catabolism, as well as
lipoprotein receptor numbers and activity) o Increase in HDL cholesterol (inhibit
hepatic lipase activity, which prevents conversion of HDL2 to HDL3, thus increasing
HDL levels) � Osteopenia:o World Health Organization (WHO) definition = BMD -1.0 to
-2.5.o ACOGCommitteeOpinionrecommendsthatphysiciansinterpretTscoresbetween?1.0and?
2.5 in combination with the patient??s risk factors for fractureo Postmenopausal
women in their 50s with T scores in the osteopenia range and without risk factors
may well benefit from counseling on calcium and vitamin D intake and risk factor
reduction to delay initiation of pharmacologic intervention. ?? Thus, after seeing
an osteopenia range BMD score ?? risk for fracture is to be assessed o
Riskfactorsforfractureincludepriorfracture,familyhistoryofosteoporosis,race,dementi
a,
history of falls, poor nutrition, smoking, low body mass index, estrogen
deficiency, alcoholism, and insufficient physical activity.� Estrogen production by
the ovaries does not continue beyond menopause. However, estrogen levels in
postmenopausal women can be significant due to the extraglandular conversion of
androstenedione and testosterone to estrogen. This conversion occurs in peripheral
fat cells and, thus, body weight has been directly correlated with circulating
levels of estrone and estradiol. Since menopausal ovaries are known to continue
production of androgens, surgical removal of postmenopausal ovaries may result in
the resurgence of menopausal symptoms from the abrupt drop in circulating
androgens. Chapter 42: Infertility � Topic 48� Reassurance and observation is most
appropriate as the patient has only been trying to conceive for three months.o
Afteronemonth,20%ofcoupleswillconceive;afterthreemonths,50%;aftersixmonths,75%; and
after 12 months, 90% will conceive.o Primary infertility is defined as the
inability to conceive for one year without contraception. � This patient is having
difficulty conceiving after trying for one year. Based on her history, the most
likely underlying factor is tubal disease, as she has a history of being
hospitalized for a pelvic infection, most likely pelvic inflammatory disease. o
Cancauseadhesionsandblockageofthetubes,whichisbestassessedwitha hysterosalpingogram
to evaluate the uterine cavity and tubes. o After a single episode of salpingitis,
15% of patients experience infertility.� In a patient suspected of PCOS,
Testosterone levels as a single test will be helpful to confirm the diagnosis,
especially in the presence of hirsutism.o
Onceadiagnosisisestablished,progesteronelevelsarehelpfulduringmedicaltreatmentto
check if the woman is ovulating. o
AnincreasedLH/FSHratioisobservedtobeelevatedinPCOSpatientsbuteachtest separately
will not aid in the diagnosis. o 1st line Tx for ovulatory dysfunction due to PCOS:
Weight loss, metformin, and ovulation induction agents (clomiphene citrate) * This
patient has hyperprolactinemia due to imipramine and should be weaned off
imipramine (minimize withdrawal symptoms) and placed on a more appropriate
medication for her depression. Once she is off imipramine and the cause of her
elevated prolactin levels is confirmed, her normal menses should resume. * If you
get a patient struggling to get pregnant and hormonal workup shows both
hyperprolactinemia and hypothyroidism (High TSH, low T4), the best first step is to
assess they thyroid gland. Often there is a problem with thyroid cause
hypothyroidism, BUT the increased TRH (causing inc. TSH) can sometimes lead to a
hyperstimulation of the pituitary (with physiologic enlargement) resulting in
hypothyroid induced hyperprolactinemia. o The infertility and hyperprolactinemia
should resolve with proper treatment of the underlying cause of the hypothyroidism.
* Exercise-induced hypothalamic amenorrhea, characterized by normal FSH and low
estrogen levels. o The best treatment is to encourage the patient to gain weight by
decreasing exercise and increasing caloric intake.o
Ifhermensesfailtoresume,shemaybetreatedwithexogenousgonadotropins(LHandFSH)to help
her conceive * A clomiphene challenge test, which consists of giving clomiphene
citrate days five to nine of the menstrual cycle and checking FSH levels on day
three and day 10, will help determine ovarian reserve. This would be an appropriate
first step in older women without other problems having trouble with conception. *
A semen analysis or sperm penetration assay is not necessary as a first step if a
patient was able to conceive from her husband previously without problems. * Women
are most fertile during the middle of their cycle when they are ovulating. o
Assuming normal cycles every 28 days, a woman is most likely to ovulate on day 14.
Since sperm can live for up to three days, intercourse up to three days before
ovulation can still result in pregnancy.o Since this patient has cycles that vary
in length, she can best tell when she is ovulating by using an ovulation predictor
kit (measures LH surge, which rises 24hr BEFORE ovulation)o The basal body
temperature charts tell when a patient ovulated retrospectively (temperature rise
occurs 24hr AFTER ovulation), so it cannot be used to time intercourse to conceive,
as the egg is only viable for about 24 hours. This is best used for charting when
ovulation normally occurs in women to make a good guess for next period. Chapter
43: PMDD � Topic 49� PMDD is a psychiatric diagnosis, describing a severe form of
premenstrual syndrome in which the diagnostic criteria include five out of 11
clearly defined symptomso 1Functional impairment and prospective charting of
symptoms present during the 2last week of the luteal phase that 3begin to resolve
with the beginning of the follicular phase. o All three areas of symptoms need to
be represented for the diagnosis of PMDD. * Vitamin deficiency of A, E and B6 have
been associated with an increase in PMS. Replacement of these vitamins might
improve PMS symptoms and avoid further medical therapy. * A calendar of symptoms
can clarify if there is a cyclic or constant nature of the symptoms. Often women
will mistakenly attribute their symptoms to their menstrual cycle. Different self-
reporting scales have been written to assist patients track their symptoms. * This
woman has premenstrual syndrome (PMS) with symptoms that warrant treatment.
Patients with PMS and premenstrual dysphoric disorder (PMDD) experience adverse
physical, psychological and behavioral symptoms during the luteal phase of the
menstrual cycle. Mild symptoms of PMS often improve by suppressing the
hypothalamic-pituitary-ovarian axis with oral contraceptive pills. * Even with mild
symptoms, hypothyroidism can mimic typical symptoms of PMS, but symptoms occur more
constantly throughout the cycle. Diagnosis involves complete work-up to rule out
medical illnesses, including hypothyroidism. * When suspecting the diagnosis of
PMDD, obtaining further history with a menstrual calendar determines the cyclic
nature of the PMS or PMDD symptoms and helps guide appropriate therapy. While
dietary changes may help, it is first important to establish the diagnosis. *
Selective serotonin reuptake inhibitors increase the amount of active serotonin in
the brain and have been found to be effective in alleviating PMS and PMDD symptoms.
Patients can take the medication either every day or for 10 days during the luteal
phase. * Exercise increases circulating endorphins in the brain which are ??feel
good?? hormones and act similar to serotonin. Therefore, in addition to being a
benefit to cardiovascular health, regular exercise can significantly decrease
symptoms of PMS. * Risk factors for PMS include a family history of premenstrual
syndrome (PMS) and Vitamin B6, calcium, or magnesium deficiency. PMS becomes
increasingly common as women age through their thirties, and symptoms sometimes get
worse over time. Previous anxiety, depression or other mental health problems are
significant risk factors for developing premenstrual dysphoric disorder (PMDD).
Chapter 44: Cell Biology/Principles of Cancer Therapy � No questions yay! Chapter
45: Gestational Trophoblastic Neoplasia � Topic 50 * Risk of molar pregnancy
increases with the following: o Asian race (1/800 vs Caucasian women that are
1/2000) o Age<20yror>40yro Consuminglessbeta-caroteneandfolateo
Having>2miscarriages o Having an aneuploidy pregnancy is NOT a risk factor for
molar pregnancy * Recurrent risk for molar pregnancies ranges from 1 to 2%, which
is a 20-fold increase from background risk. The risk of recurrence after two molar
pregnancies is 10%. * After evacuation of molar pregnancy patients must be followed
regularly with serial Beta-hCG levels to insure spontaneous regression. o Pregnancy
should be avoided during this follow-up period, and for the following six months. o
Effective contraception (OCP or other hormonal contraception) is strongly
recommended to prevent confusion in interpreting a rising Beta-hCG as a post-molar
recurrence/progression versus a new, spontaneous pregnancy. * In this question, a
patient presented with findings consistent with a complete molar pregnancy;
however, a vaginal nodule was also found on exam. This nodule is suspicious for
metastatic disease and staging should be done due to high vascularity of GTD. o
CTchest/abdomen/pelvisisappropriateforstagingmetastaticGTNo
ABrainMRImayalsobedonetoensurenometastaticspreado
PETscanning(noteffective)andbiopsy(mayspreaddisease)arenotindicated * Post-molar
GTD may be due to persistent (retained or invasive) disease in the uterus or
metastatic disease (often to the lungs), most often from a complete molar
pregnancy, even with complete uterine evacuation o Persistent disease can easily be
cured with chemotherapy, if it develops, and is therefore not routinely given
prophylactically, except in high-risk situations (e.g. non-compliant patient who
will be lost to follow-up). * Diagnosis of choriocarcinoma (GTN) is made once the
presence of Beta-hCG is confirmed. So if you??re concerned about GTN, you must
confirm with a B-hCG. Chapter 46: Vulvar and Vaginal Disease/Neoplasia � Topic 51 *
ALWAYS biopsy first; never go straight to vulvectomy * Given the findings of
obvious, moderately differentiated carcinoma, definitive treatment can be
recommended with radical vulvectomy and groin node dissection. Only microinvasive
squamous cell carcinoma of the vulva can be treated by wide local excision, but it
is a diagnosis that is only made after pathology evaluation of a small (<2 cm),
well-differentiated lesion, with invasion <1.0 mm. * Squamous cell carcinoma
accounts for approximately 90% of vulvar cancers. Typically presents
with a lump with long-standing history of pruritus (chronic itch-scratch cycle) o
Paget??s disease of the vulva is associated with white plaque-like lesions and
poorly demarcated erythema, not a discrete mass. o Verrucous carcinoma has
cauliflower-like lesions.o Melanoma typically presents as a pigmented lesion.o
Hidradenitisisachronic,unrelentingskininfectioncausingdeep,painfulscars/fouldischar
ge. * Melanoma represents 5% of vulvar cancer, which is not insignificant given the
lack of sun exposure and the relatively small surface area. Typically, lesions are
flat and pigmented with abnormal shape. Biopsy must be performed to confirm
diagnosis. * Any finding of a new Bartholin gland cyst in a post-menopausal woman
should be further investigated. For any woman over the age of 40 with a mass in
this area, a biopsy should be obtained. Primary vulvar adenocarcinomas most likely
arise from the Bartholin gland * VIN III should be treated with local superficial
excision. Even with complete removal of all gross disease, recurrence is still
possible; close surveillance is needed. It is inappropriate to do radical surgery
in this setting as cancer has not been diagnosed * This question had a lady on
immunosuppressive therapy of Lupus with a history of HPV related condyloma
accuminata. After being on immunosuppression, she had vaginal itching with
widespread whitish, flat papules. While this could be a resurgence of HPV, this
could also represent HPV related neoplasia and a biopsy should be taken. * Don??t
forget the classic description of Paget??s Disease of the Vulva: ??fiery red
background with mottled whitish hyperkeratotic areas?? Chapter 47: Cervical
Neoplasia and Carcinoma � Topic 52 * The majority of risk factors for cervical
cancer are related to HPV exposure: early-onset sexual activity, multiple sexual
partners, a sexual partner with multiple partners, history of HPV or other sexually
transmitted diseases, immunosuppression, smoking, low socioeconomic status and a
lack of regular Pap tests * Apparently if you have a girl who has a Pap smear (+)
for ASCUS; then you can immediately test her for HPV. If HPV is negative, then you
can safely resume normal Pap smears at every 3 years. * Apparently if you have a
visible cervical lesion that suspicious of cancer, you can go straight to biopsy
and bypass colposcopy with acetic acid wash. You already have the lesion in your
sights. * A white plaque found on the cervix is called leukoplakia and should be
biopsied directly or under colposcopic guidance as soon as possible, regardless of
Pap test outcome. Pap tests have a false- negative rate as high as 20-30%. * When
examining the cervix under acetic acid washed colposcopy: o Punctuations and
mosaicism represent new blood vessels on end and on their sides, respectively.
Atypical vessels usually represent a greater degree of angiogenesis and, thus,
usually a more concerning lesion.o Ectropion is an area of columnar epithelium that
has not yet undergone squamous metaplasia. It appears as a reddish ring of tissue
surrounding the external os.o Acetowhite epithelium can represent dysplasia but, in
most cases, is less concerning than the above vascular changes. * Don??t forget! If
an entire lesion cannot be visualized, this colposcopy is unsatisfactory and severe
dysplasia and even invasive cancer cannot be ruled out. While endocervical
curettage may be nice to do, but it has a relatively low sensitivity (i.e. a high
amount of false negatives). The endocervical canal must be histologically examined.
A cervical conization should be performed to obtain a pathologic specimen *
Cervical cancer is caused by HPV; just never forget that. * Although the risk of
HPV correlates with the lifetime number of sexual partners, the risk is still
relatively high even in those with one partner (up to 20%). At least 75 to 80% of
sexually active women will get a genital HPV infection by age 50. Cervical cancer
is not genetically inherited. * The use of talc does not increase risk of cervical
cancer. * Cervical dysplasia is graded based on extent of involvement of the
epithelial layer but does not extend below the basement membrane. o Carcinoma in
situ (CIS) represents abnormal cells involving the entire epithelium to the
basement membrane.o In cancer, the cells invade beyond the basement membrane. o
Inmicroinvasivecancer,theyinvadelessthan3mm. Chapter 48: Uterine Leiomyoma and
Neoplasia � Topic 53� The #1 symptom in uterine fibroids is menorrhagia (think of
your lady in clinic!) due to: o Increase in the uterine cavity size that leads to
greater surface area for endometrial sloughing o
Obstructiveeffectonuterinevasculaturethatleadstoendometrialvenuleectasiaandproximal
congestion in the myometrium/endometrium resulting in hypermenorrhea. � Fibroids
can be detected in as high as 80% of women. Most uterine fibroids are asymptomatic
and do not require any treatment. o Fibroids may grow or become symptomatic in
pregnancy due to hemorrhagic changes associated with rapid growth, known as red or
carneous degeneration. However, this is uncommon for smaller fibroids. o Fibroids
can be located below the fetus, in the lower uterine segment, or cervix, causing a
soft tissue dystocia, necessitating delivery by Cesarean section. o
MyomectomyatthetimeofCesareansectionshouldbeavoided,ifpossible,secondarytothe risk
for increased blood loss o
Itisnotnecessarytofollowthegrowthoffibroidsduringpregnancy,exceptfortherarecases
when the fibroid is causing symptoms (primarily pain) or appear to be located in a
position likely to cause dystocia. * Leiomyomas are an infrequent cause of
miscarriages and subfertility either by mechanical obstruction or distortion (and
interference with implantation). o Submucosal or intracavitary myomas cause lower
pregnancy/implantation rates via: * ?? �Focal endometrial vascular disturbance * ??
�Endometrial inflammation * ?? �Secretion of vasoactive substances. o Submucosal
fibroids are best treated by hysteroscopic resection. * Medical management of
fibroids includes 1NSAIDs and progestin OCPs/IUDs; but if that doesn??t work 2GnRH
analogues can be used to shrink fibroids for either symptomatic tx OR easier
surgical resection. o Don??tforget!Fibroidsfeedoffestrogen!
Thus,justgivingestrogenwouldbeapoorchoice.o Often GnRH analogues are used in older
women (this lady was 49) until they reach menopause, where the fibroids will shrink
due to loss of endogenous estrogen. * This question had a woman who was worried her
big belly (BMI 37) was caused by a large fibroid. Sadly, she??s just obese and
should be counselled on diet and exercise.o
BariatricsurgerymaybeconsideredwhenBMIisgreaterthan40,orisbetween35to39.9
accompanied by a serious weight-related health problem, such as type 2 diabetes,
high blood pressure or severe sleep apnea. This lady had no other problems. * If
patients present with menstrual abnormalities, the endometrial cavity should be
sampled to rule out endometrial hyperplasia or cancer, even if it really sounds
like fibroids. This is most important in patients in their late reproductive years
or postmenopausal years. o If the patient??s bleeding is not heavy enough to cause
iron deficiency anemia, reassurance and observation may be all that are necessary.
o TreatmentwithGnRHanaloguestoinhibitestrogensecretionmaybeusedasatemporizing
measure. Can be used for three to six months prior to a hysterectomy to decrease
the uterine size and increase a patient??s hematocrit; either leading to easier
surgery (smaller fibroid/less blood loss) or tide a patient over into menopause. �
Mean uterine size decreases 30-64% after three to six months of GnRH agonist
treatment.o Inapatientwhodesiresfuturefertility,thismaybeagoodshort-
termoptiontodecrease pain/blood loss; esp. if hematocrit is decreasing.o
MaximalresponseisusuallyachievedbythreemonthsofGnRHagonisttreatment.The reduction
in size correlates with the estradiol level and with body weight. � When treating
with a GnRH agonist: o Hot flashes are experienced by >75% of patients (3-4wk) but
shouldn??t persist for more than one to two months. o
Aftercessationoftreatment,mensesreturnin4-10wk,andmyoma/uterinesizereturnto
pretreatment levels in 3-4mo. ?? Fibroids will regain their normal growth after
cessation of treatment; the myth that they??ll grow faster due to hormone
withdrawal is unsubstantiated. Chapter 49: Cancer of the Uterine Corpus � Topic 54
* In a post-menopausal patient having abnormal uterine bleeding, risk factors for
endometrial carcinoma can help determine how likely they??ve developed a
cancer/possible severity. In order of highest conferred risk: o
Findingofcomplexendometrialhyperplasiaonendometrialbiopsy�28%ofptshavecancer o
Obesity(esp.if>50lbsoveridealbodyweight)�10xnormalrisko
Nulliparity,earlymenarche,latemenopause,hypertension,diabetesandexposureto
unopposed estrogens (HRT or SERMs) � all increase to different degrees * Less than
5% of women diagnosed with endometrial cancer are asymptomatic. Approximately 80-
90% of women with endometrial carcinoma present with vaginal bleeding or discharge
as their only presenting symptom. Thus, if a patient is asymptomatic and lacks many
risk factors (or all in this case) yearly regular exams are the best course of
action. * The most common symptom is abnormal postmenopausal bleeding. This may be
accompanied by abnormal vaginal discharge, lower abdominal discomfort, and
increased size of the uterus, but these are less common findings. o
NotethatcombinationERTdoesNOTincreasetheriskofendometrialcancer * This question has
a 65y/o G2P1 with homogenous thickening of the endometrium to 5mm. Biopsy revealed
rare atypical cells. D&C is the correct next step. In a woman with persistent
symptoms suggestive of endometrial cancer, AND with a negative biopsy, further
investigation with D&C to sample the entire endometrium is the best course of
action. * This question has a lady that had FIGO Grade 1 endometreoid
adenocarcinoma on endometrial biopsy. This is low-grade and the next best step is
to confirm that there??s no spread of the cancer outside the uterus, so we can
possibly have less intense treatment thus: o Routine evaluation in this setting
should include a chest x-ray as the lungs are the most common site of distant
spread. o CA-125 may be helpful in predicting those patients that may have
extrauterine spread, but is not absolutely necessary o
Apelvicultrasoundisnotindicatedonceapathologicdiagnosishasbeenestablished,although
one may have been obtained as part of the initial evaluation of postmenopausal
bleeding. o When there is a low suspicion for advanced disease, a CT scan, MRI, PET
scan, and other invasive and costly tests are not indicated. * Recommended
components of the surgical approach to an early endometrial cancer are the
extrafascial total abdominal hysterectomy, bilateral salpingo-oophorectomy, and
pelvic and para- aortic lymphadenectomy; best done in high grade (>3) or aggressive
types (clear cell, papillary serious) o Vaginal or laproscopic approaches can also
be done as alternatives o
Chemotherapy,radiation,andhormonaltherapymaybeutilized,butinanadjuvantsetting. *
Graunlosa cell tumor (Granulosa-Theca tumor) is a functional, estrogen secreting
tumor that may cause increase bleeding, ??speeding up?? of periods, and complex
endometrial hyperplasia w/out atypia * Theca-lutein cyst � typically bilateral
cysts that occurs due to markedly increased B-hCG production (most often during a
molar pregnancy), causing uniformly complex, fluid filled ovarian cysts. Often
these resolved after B-hCG level return to normal. * Postmenopausal bleeding or
discharge accounts for the presenting symptom in 80-90% of women with endometrial
cancer, thus if these occur, an H&P, pelvic examination, and endometrial biopsy
should occur. However, the causes for post-menopausal bleeding are as follows: o
Atrophy of the endometrium (60-80%), hormone replacement therapy (15-25%),
endometrial cancer (10-15%), polyps (2-12%), and hyperplasia (5-10%). o
Transvaginalultrasoundcanbeausefultoolasitcanvisualizepolyps,myomas,orendometrial
thickening. Also, if the endometrial stripe is <5mm, there??s a low chance for
endometrial cancer to be present � This question had a lady with remote hx (15yr
ago) of endometrial cancer now presenting with cough, dyspnea, and bilateral lower
extremity edema. o
Themostappropriatenextstepistoreferhertoapulmonologist(orcardiologist)fora thorough
work-up. Pleural effusions and lower extremity edema point towards a
cardiopulmonary etiology and you need to rule this out before going for cancer. o
However, the finding of a solitary lung nodule in a patient exposed to second hand
smoke certainly suggests the possibility of a primary lung cancer. � While
Taxomifen is known to increase risk of endometrial cancer, any woman on therapy
with it should have regular yearly exams from their gynecologist. If they??re
asymptomatic, no ultrasound/biopsy studies are needed. Chapter 50: Ovarian and
Adnexal Disease � Topic 55� While specific factors in carcinogenesis of ovarian
cancer are not well established, risk factors include family history (greatest risk
factor), estrogen exposure (nulliparity, early menarche/late menopause), white
race, increasing age and residence in North America and Northern Europe. o
SmokingdoesNOTincreasetheriskforovariancancero
UseofcombinedOCPsdecreasesriskofovariancancer(likelyduetodecreasedovulation) with
5-years use decreasing ovarian cancer rates by 50%o BRCA1 and BRCA2 mutations are
typically seen in cases of hereditary ovarian cancers and account for 5-10% of
breast cancers and 10-15% of ovarian cancers among white women in the United States
o RoutinescreeningforovariancancerhasNOTbeenestablishedyet. � Functional ovarian
cysts are a result of normal ovulationo
Presentasanasymptomaticadnexalmassorbecomesymptomaticoftenwithapalpablemass and
abdominal discomforto
Ultrasound:unilocularsimplecystwithoutblood,softtissueelementsorexcrescences. o
Otherclassicadnexalcysticmasseshavedifferentfindings: * ?? �Endometrioma is an
isolated collection of endometriosis involving an ovary and often is not a simple
cyst on ultrasound. * ?? �Serous cystadenomas are generally larger than functional
cysts and patients may present with increasing abdominal girth. * ?? �Mucinous
cystadenomas tend to be multilocular and quite large. * ?? �Dermoid cysts usually
have solid components or appear echogenic on ultrasound, as they may contain teeth,
cartilage, bone, fat and hair. � The most useful radiologic tool for evaluating the
entire peritoneal cavity and the retroperitoneum is computerized tomography. This
question had an elderly patient with ascites and a large pelvic mass of unknown
etiology; she needs to be assessed for neoplasia and find the extent of disease
involvement. o This woman would likely benefit from an abdominal/pelvic CT to look
for signs of neoplastic growth; if suspicion of lung involvement on physical exam,
chest CT may also be prudento PET scan, to date, has not been shown to play a role
in the initial evaluation of women with a suspected ovarian malignancy. However,
PET scan may play a role in evaluating women with a known diagnosis of ovarian
cancer who have a suspected recurrence� The three main histologic sub-types of
ovarian cancer include germ cell tumors (5%), sex-cord stromal tumors (1-2%), and
epithelial tumors (90%) o
Epithelialovariantumorsarethemostcommonandcanaffectwomenofallages,buttypically the
malignant types occur in women in their 70s. o Granulosacelltumor(sex-
cordstromaltumor)arefunctionaltumorsthatsecretehighlevelsof estrogen, which can
ultimately stimulate the endometrium to undergo hyperplastic changes and even lead
to endometrial cancer. * ?? �Approximately 25-50% of women with GCT will have
endometrial hyperplasia on biopsy, and 5-10% will have endometrial cancer. * ??
�Granulosa cell tumors represent 70% of sex-cord stromal tumors and typically
affect women in their 50??s (most common type is the adult GCT � 95%; the juvenile
type affects females before puberty) o
Germcelltumorstypicallyaffectwomenofyoungeragegroups(ages10-30),comprise20-25% of
ovarian neoplasms overall (benign and malignant), being 70% of tumors in this age
group. * Don??t forget! If a young, sexually active female comes in with acute
abdomen, always get a B-hCG first as ectopic pregnancy is a life threatening
condition. * Tumor stage is directly correlated with the five-year survival of
patients with epithelial ovarian cancer o
Volumeofresidualdiseasefollowingcytoreductivesurgeryisalsodirectlycorrelatedwith
survival; optimally debulking (generally <2 cm or <1 cm maximal residual tumor
diameter) gives significant improvement in median survivalo Histologic grade of
tumor is important; poorly differentiated tumors or clear-cell carcinomas typically
have a worse survival than those with well to moderately differentiated tumorso
Tumorsize,bilateralityandasciteswithoutcytologicallypositivecells,areNOTconsideredt
o be of prognostic importance. � All patients with advanced ovarian cancer, post-
operative chemotherapy with a combination of a taxane and platinum adjunct is
considered standard of care in the United States. o
Surgicalcytoreduction,followedbychemotherapy(4-6cycles),haveabetteroverallsurvival
rate than those who undergo surgery alone with overall response rate at 60-80% o
Theoverallfive-yearsurvivalforwomenwithstageIIIandIVdiseaseisapproximately30%. o
Secondlooklaparotomyisnolongerconsideredstandardofcare.� The most common tumor
found in women of all ages is the dermoid tumor (dermoid cyst or teratoma).o
Medianageofoccurrenceis30years;80%occurduringthereproductiveyears.o Dermoids may
contain differentiated tissue from all three embryonic germ layers. (teeth, hair,
sweat and sebaceous glands, cartilage, bone, and fat) UWorld Miscellaneous OBGYN
4122: Osteoporosis Risk Factors * Modifiable � hormones (low estrogen),
malnutrition, low Ca2+/Vit.D consumption, chronic use of glucocorticoids or
anticonvulsants, immobility, cigarette smoking, and excess alcohol consumption *
Non-Modifiable � female gender, advanced age, small body size, late menarche/early
menopause, White or Asian race, or family history of osteoporosis * Note that
obesity is actually protective for osteoporosis. While it strains the joints, the
extra weight acts like weight bearing exercise, and the extra estrogen decreases
effects of menopause. 10505: Inheritance of Hemophilia A * Hemophilia A is an X-
linked recessive disease of Factor VIII deficiency * A daughter born to a father
with the disease will always be a carrier (always get a screwed up X) * A woman
carrier of hemophilia A has a 25% chance to have a child with the disease phenotype
(.5 to pass on the affected X, .5 to have a boy; .5 x.5 = .25 or 25% 2806:
Hyperemesis Gravidarum * Presentation: severe vomiting during 1st/early 2nd
trimesters associated with weight loss, volume depletion, ketonuria, and metabolic
alkalosis.o Thought to be caused by B-hCG and associated with multiple
gestations/molar pregnancies * Dx: clinical presentation * Tx: 4193/4518:
Alloimmunization * When an Rh(-) mom is pregnant with a Rh(+) baby, there??s a
chance for alloimmunization; typically this happens after her first pregnancy and
can be checked via anti-D titers. * This can be prevented with RhoGAM
administration first at 28wk, and then within 72hr of delivery; this will destroy
any fetal RBCs getting into mom??s blood so her immune system won??t pick them up.
o Standarddoseis300mcgat28wko Some moms may be more after delivery, placental
abruption, or a procedure
* If there??s concern for fetal-maternal hemorrhage a Kleihauer-Betke Test can be
performedo Mom??
scirculatingbloodistakenandaffixedtoaslideandexposedtoanacidicsolutiono
TheadultHbAwilllysetheRBCwiththissolutionbutthefetalHbFwillnotcausethistohappen o
The remaining fetal RBCs are counted and the %fetal RBCs are used to calculate
dosage * If this test is not done, mom may have the risk of developing anti-D
immunoglobulins despite RhoGAM treatment, as it was an inadequate dose to
neutralize all fetal RBCs in her circulation * If mom is already sensitized to Rh-D
antigens from a previous pregnancy; RhoGAM is not useful. 4162: ABO
alloimmunization * While mom will have antibodies against A or B antibodies
depending on her blood type, these typically only cause mild disease, resulting in
jaundice at worst in most pregnancieso ABO antibodies have a less robust IgG
response, thus less can cross the placentao A and B blood antigens are found in
food and gut bacteria, thus even in the first pregnancy, baby can get damaged by
the antibodies * Rarely, these can cause hemolytic disease of the newborn, but this
is rare (although more common in people of African descent) 2543: Indications for
RhoGAM administration in a Rh-antigen negative mom: at 28-32 weeks; within 72 hr of
abortion or episode of vaginal bleeding; ectopic pregnancy; hydatidaform molar
pregnancy; CVS or amniocentesis, abdominal trauma, 2nd or 3rd trimester bleeding,
if external cephalic version is done. 3748: This question had a post-term woman
with a fetus showing macrosomia/oligohydramnios and under fetal distress. She was
totally informed about the indications for C-section but she refused. She was
counseled about how she could die and her baby could die and she still wanted a
vaginal delivery. If this occurs you can consult the hospital ethics committee, but
moms have ultimate reign over their unborn child as long as they??re deemed to have
capacity and properly informed of risk. Therefore, you let mom make a dumb decision
and prep for emergent C-section or a horrific perineal tear. 4225/12034: Post-
Partum Urinary Retention * Presentation: inability to void after labor (anesthesia,
perineal swelling, bladder over-distention, etc.) * Risk Factors: nulliparity,
prolonged labor, perineal injury, epidural anesthesia, instrumental delivery * Dx:
pt unable to void 6hr following delivery or 6hr following catheter removal after C-
section; typically post-void volume >150mL is a good marker for atonic bladder *
Tx: catheterization, ambulation, and pain control until bladder function returns �
8899: Pre-Menstrual Disorder (PMS) and Pre-Menstrual Dysphoric Disorder (PMDD) *
Both are on a similar spectrum of symptoms with menstruation o
PMS:physicalsymptomswithlesspronouncedbutpossiblypresentpsychiatricsymptoms o
PMDD:physicalsymptomswithpronouncedpsychsymptoms(anxiety,depression,etc.) *
Presentation: symptoms occurring during luteal phase (2nd half) of cycle o
Physical:bloating,fatigue,headache,hotflashes,breasttenderness o
Psych:anxiety,irritability,depression,moodswings,decreasedlibido * Dx: symptoms
occurring 1-2wk before bleeding as evidenced by a menstrual symptom diary with
resolution during the follicular phase AND significant social/work impact * Tx:
SSRIs daily or only in luteal phase (treat psych problems) or combined OCPs
(minimize periods) 3233: This question has a patient who has been diagnosed with
HIV and does not want her husband to know. You should encourage her to tell her
husband as well as tell her that HIV must be reported to the health department
(which will contact the patient??s contacts) 4192: Lithium Exposure to the Fetus *
1st trimester: Ebstein??s Anomaly (Atrializatin of the ventricle) * 2nd/3rd
trimester: goiter or transient neonatal neuromuscular dysfunction 4194: In
evaluation of an infertile couple, a semen analysis should be done as an initial
screening to rule out male factor as the cause for infertility. It accounts for
about 20-30% of infertile couples. 4715: Rheumatic Heart Disease (often Mitral
Stenosis) can go asymptomatic for years before being uncovered during pregnancy.
The increase in circulating volume/heart rate raises left atrial pressure. Because
mitral stenosis is already present, this additional increased pressure from
pregnancy can pathologically increase and dilate the left atrium resulting in
atrial fibrillation with RVR (if heart rate >100bpm) 2552: Pseudocyesis�
Presentation: belief and some physical signs (breast enlargement, abdominal
enlargement, weight gain, amenorrhea, morning sickness, sensation of fetal
movement) of pregnancy, but pregnancy is not present. Considered a form of
conversion disorder that the belief causes hormonal changes o A confusing aspect is
that patient may self report a positive pregnancy test, but the office pregnancy B-
hCG will be negative o Ultrasound will show no present conceptus with normal
endometrial stripe * Dx: presentation with negative pregnancy findings * Tx:
psychiatric evaluation and therapy 3914: In some patients combined OCPs can raise
blood pressure and approx. 5% of patients can develop overt HTN due to OCP use. In
a patient with persistent HTN and a negative workup for more common causes, a trial
of another type of birth control is warranted. This may resolve the HTN. 2372:
Posterior Shoulder Dislocation may occur in patients having violent seizures (like
in Eclampsia). * Presentation: shoulder held in adduction/internal rotation with
visible flattening of the shoulder and prominence of the coracoid processo
Radiographic evidence of dislocation may also be sought * Dx: clinical presentation
* Tx: closed reduction of dislocation 2400: In treating pregnant moms for
hypertension in pregnancy always remember ??Hypertensive Moms Love Nefidipine?? ??
Hydralazine, Methyldopa, Labetalol, and Nefidipine are all 1st line agents 4734:
Congenital Rubella Syndrome * Presentation: eyes (cataracts/glaucoma), ears
(sensoneurial hearing loss), heart malformation (patent ductus arteriosis; ??
continuous machine-like murmumr??)o
Mommayhavemildfever,cough,conjunctivitis,ormacropapularrasho
Virustransmittedthroughplacentao Rare in USA from vaccination, but moms from other
countries at higher risk * Dx: clinical presentation * Tx: vaccination before
pregnancy; the vaccine (MMR) is live-attenuated, thus contraindicated in pregnancy.
Testing for mom??s rubella IgG titers in 1st trimester can tell you if she??s
immune or not; 2nd/3rd trimesters are not useful as infection may cause increased
IgG titers. Sadly, the baby is in poor condition and will need lots of advanced
care o IfmomisfoundtobeexposedtoRubellainpregnancy,shemaybeofferedpregnancy
termination; if she decides to keep it, then rubella IgG is administered as soon as
possible. 2925: Intrahepatic Cholestasis of Pregnancy * Presentation: intense
itching, prominent at palms/soles/at night; skin excoriations/jaundice may occur o
Labs:increasetotalbileacid,cholestaticpatternofLFTs(inc.directbiliandalk.phos.) *
Dx: clinical presentation + labs + rule out HELLP/AFLPTx: ursodeoxycholic acid and
fetal testing for lung maturity by amniocentesis at 36wk. If lung maturity is
documented, delivery can be initiated 2925: Acute Fatty Liver of Pregnancy �
Presentation: 3rd trimester malaise, abdominal pain, N/V; eventally leading to
acute liver failure (ascites, jaundice, hypoglycemia, encephalopathy, coagulopathy,
AKI) o Labs:severelyelevatedLFTs � Dx: � Tx: 2925: Pruritic Urticarial Papules and
Plaques of Pregnancy (PUPPP) * Presentation: 3rd trimester skin condition with
itchy abdominal rash of red papules with striae, spares the umbilicus and sometimes
spreads to extremities; rarely involves palms/soles/face. o
Labs:noabnormallabsshouldbenoted * Dx: clinical presentation * Tx: 2405: Amniotic
Fluid Embolism * Presentation: sudden hypoxemia respiration failure, cardiogenic
shock, DIC, and coma/seizures following delivery (commonly in complicated
pregnancies)o Results from amniotic fluid entering maternal veins during birth *
Risk Factors: advanced maternal age, >5 gestations, C-section or instrument
delivery, placenta previa, or abruption, pre-eclampsia * Dx: clinical presentation
* Tx: respiratory/hemodynamic support (intubate/ventilation/pressors); may need
blood transfusion 2399: UTI in Pregnancy � Asymptomatic Bacteriuriao
Presentation:nosymptoms,but>100,000cfufoundonurinanalysis(screenat12-16wk)o
Tx:Nitrofurantoin(5-7day);Amoxacillin-ClavuronicAcid(3-
7days);Fosfomycin(singledose) ?? AVOID ?? all fluoroquinolones and TMP-SMX * Acute
Cystitis o Presentation:dysuria,frequency,urgency,(+)urineculture/urinalysis o
Tx:sameasasymptomaticbacteriuria * Pyelonephritis o Presentation: flank pain,
fever, CVA tenderness +/- cystitis symptomso
Tx:HospitalizeandIVantibiotics;avoidaminoglycosidesifpossible;afterpatientafrebrile
for 24hr, switch to a 10-14 day course of oral antibiotics UWorld
Pregnancy/Childbirth OBGYN 2523/2524/11969: Placenta Previa � Presentation:
painless 3rd trimester uterine bleeding, possibly with hemodynamic changes in mom o
Result of placenta implantation partially covering of overlying the cervical oso
Bloodismaternal;thuschangestobabyhemodynamicsshouldnotbeaffectedo
RiskFactors:priorplacentaprevia,C-section/uterinesurgery,multipartiy,advancedage,
smoking * Dx: clinical picture + ultrasound evidence of placentation * Tx: C-
section delivery at 36-37wk o Digitalexamsandintercoursearetotallycontraindicatedo
If found in 1st trimester, uterine growth may resolve previa spontaneously 3111: If
a patient is receiving BPPs for assessment, a score of 10/10 means they??re OK and
they should be having regular weekly BPPs until delivery. This ensures the baby is
OK in the womb. If score should fall, delivery should be considered
2549/4745/4775/4776:
Intrauterine Fetal Demise� Presentation: demise of a pregnancy after 20wk
gestation prior to delivery; moms often feel a lack of fetal movement before
presentingo Often the cause is not known (50%) and could be fetal/placenta/maternal
in origin o MomshouldbewatchedfordevelopmentofDICifexpectantlymanagingconceptus o
Investigationforcausesforfuturecounsellingshouldinclude: * ?? �Fetal � autopsy,
placental/membrane/cord examination & histology, karyotype * ?? �Mom � Kleihauer-
Betke testing, Antiphophlipid antibodies, and coagulation studies o
Morelikelythannot,momcouldnothavedoneanythingtopreventitandshouldbe reassured. She
should also be informed that examination may yield more info as to cause. * Dx:
ultrasound showing lack of fetal heart movement * Tx: expectant vaginal delivery
(20wk or greater) or dilation/evacuation (20-23wk); typically delivery can be
delayed till spontaneous or induced if patient wants it (no change in outcomes)
2542: Types of Abortions * Missed: no cardiac activity visible on ultrasound <20wk;
no bleeding, Os is closed, no passage of tissue * Threatened: cardiac activity
present, bleeding <20wk, cervical Os closed, no passage of tissue * Inevitable:
bleeding <20wk, dilating cervical Os, tissue present or palpable but not yet passed
* Incomplete (partial): bleeding <20wk, dilated Os, some tissue passage but some
still present * Complete: episode of vaginal bleeding/tissue passage, but now
resolved with closed Os * Septic abortion: retained POC w/ purulent discharge,
fever, signs of shock (suction curettage, blood/endometrial cultures, broad-
spectrum Abx; hysterectomy indicated if no response to Tx) 4797/12015:
Chorioamnionitis (intra-amniotic infection) * Presentation: fever, abdominal pain,
fetal/maternal tachycardia, fever, smelly leakage of fluid; early labor or PPROM
may occur due to thiso Polymicrobial infection of the placental tissue, assceding
from the vagina. More common in prolonged rupture of membranes (>18hr) * Dx:
Maternal fever + (uterine tenderness, maternal/fetal tachycardia, leukocytosis,
malodourous amniotic fluid, or purulent discharge) * Tx: immediate delivery
induction (oxytocin) + broad spectrum antibiotics for mom + antipyretics +
corticosteroids if preterm 4530: Screening for STDs is important early in pregnancy
and should be done to all moms in the 1st trimester. HIV, HepB, C.trachomatis,
N.gonorrhea and syphilis are all common ones to screen for. � Note that GBS
swabbing is only done at 35-37wk or if patient goes into labor. This is because
it??s a fast- growing bug and early negative swabs can become positive later in
pregnancy. 12117/3118: Abnormal Fetal Lie * If a fetus is not vertex/cephalic early
on in pregnancy, it??s not a big deal as most fetuses will spontaneously move the
cephalic lie during gestation. Fetal lie should simply be monitored. * External
Cephalic version � used when fetus is NOT is vertex position in 3rd trimester. This
has about a 50/50 shot at working, but if it does, vaginal delivery can be
attempted. If not, C-section is indicated o May be performed at 37wk gestation as
long as fetal well-being is good * Internal Cephalic version � used in twin
gestations where 2nd fetus is not presenting vertex. Can help orient fetus to
proper position for a 2nd vaginal delivery, but not 100% guaranteed to work.
2535/2530/2528/2407: Placental Abruption * Presentation: sudden-onset painful
vaginal bleeding, abdominal/back pain, frequent low-intensity contractions,
tender/distended uteruso Risk factors: blunt trauma, cocaine/tobacco use,
HTN/preeclampsia/eclampsia/prior abruption o Fetal heart monitoring changes
(tachycardia, declarations, loss of variability) indicate hypoxia o
MommayexperienceDIC(tissuefactorduetodecidualbleeding)orhypovolemicshock. * Dx:
clinical presentation; ultrasound may show retro-placental hemorrhage * Tx:
immediate delivery o If mom is hemodynamically unstable, give aggressive IV
crystalloids and turning mom on her left side to increase venous return from IVC to
maximize hemodynamic status o Vasopressors or blood transfusions may need to be
used if mom does not respond. 4777: Note that white coat hypertension may cause
abnormal readings in the office, but will not produce diastolic pressures >105mmHg.
If these pressures are present, the patient is considered to have true HTN and must
be managed accordingly. 8945/2411/4759: Ectopic Pregnancy * Presentation: abdominal
pain, amenorrhea, vaginal bleeding; if ruptured, acute hemorrhagic shock, adnexal
tenderness possibly with palpable masso
RiskFactors:previousectopic,HxPID,Hxpelvicsurgery/tuballigation * Dx: (+)B-hCG
without Trans-vaginal ultrasound visualization of fetus in the uterus; possible
visualization of pregnancy elsewhere (tubes, pelvis, etc.) o IfTVUSisnon-
diagnosticrepeatB-hCGintwodays,whichmayshowthathormonesarenot rising fast enough.
Once B-hCG is >1500, it should put you into a range that the fetus will be detected
on ultrasound; so you can repeat the TVUS * Tx: Stable = Methotrexate; unstable =
surgical resection 4050: Increased lumbar lordosis and relaxation of ligaments
supporting sacroiliac joints/pelvic girdle are thought to be the main contributors
to low back pain in 3rd trimester pregnancy. While some strain may be present, it??
s likely more just the adjustments to keep center of gravity. 11966: Note that
vaginal delivery is contraindicated in women who have had a classical (vertical) C-
section or an abdominal myomectomy where the uterine cavity was entered. * Low
transverse (horizontal) C-section ?? TOL is OK and encouraged * Myomectomy where
uterine cavity was not pierced ?? TOL is OK and encouraged 12037/12038: Variable
decelerations are most often caused by umbilical cord compression. If happening
intermittently, no treatment is needed as baby tolerates these well. But if
occuring with >50% of contractions (recurrent) then treatment is needed. � Tx:
maternal repositioning (Left-lateral decubitus; reduce cord compression) should be
tried first; if this is unsuccessful amino-infusion (increase amniotic fluid
padding) is reasonable. If baby??s status worsens, induction of labor of emergency
C-section may be necessary. 3106: Vaccines During Pregnancy * Routine � Tdap,
Inactivated Flu * Used in Special Situations � Hep A (high risk), Hep B (high
risk), Pneumovax (2nd/3rd trimester high risk), H.flu (if asplenic), Meinigococcus
(if age 19-21/live in college dorm and not vaccinated before age 16) Rh-D (RhoGAM;
in Rh- moms) � Contraindicated � HPV, MMR, varicella, smallpox, live attenuated Flu
o While the waiting period used to be longer, receiving a live-vaccine 28 days
before pregnancy is considered safe. Also the rubella vaccine (MMR), while a live
vaccine, has been studied and showed that even close to pregnancy, it does not
cause known ill effects on conceptiono Thus, if patients have had these vaccines in
proper waiting periods, they can be reassured 9984/12017: If a woman comes in
complaining of lack of fetal movement a NST is non-reactive, she should likely be
offered a BPP to ensure fetal health. The results will guide further management. �
While a NST can be helpful, a lack of accelerations may simply be the result of a
fetal sleep cycle. Tracing should still be variable, but fetal sleep cycles can
last up to 40min and is the most common cause of lack of accelerations with
reported fetal movements. 4198/8868: Classic Palsies of Shoulder Dystocia * Erb-
Duchenne Palsy (C5-C6 damage) � ??waiter??s tip?? extended elbow, flexed wrist,
pronated forearm; decreased Moro/biceps reflex on affected side * Klumpke Palsy
(C8-T1 damage) - ??claw hand?? extended wrist, flexed interphalangeal joints, and
absent grasp reflex. Moro/biceps reflexes intact; may also feature Horner??s
syndrome (ptosis, myosis, anhydrosis on affected side) due to damage T1 nerve root.
* Many times these are just strain on the nerves and will resolve in approx. 3
months with gentle massage to the affected area to prevent contractures 4794:
Management of Shoulder Dystocia (BE CALM) * Breath and do not push. Lower the head
of the bed. * Elevate knees to McRoberts Position (sharp hip flexion in supine
position) to open bony pelvis * Call for help (nurse, anesteiology, pediatricians,
other phyisicians) * Apply suprapubic pressure (oblique setting of fetal shoulders
to decrease diameter) * Consider episosotomy if soft tissue appears to be under
extreme strain, however this is not favored as bony pelvis is what??s causing the
dystocia. * Attempt to manipulate baby out of pelvis; if all else fails invoke the
Zavanelli maneuver and return baby into uterus for emergent C-section 2415: Hyper-
Androgenism During Pregnancy * Presentation: hirsutism, acne, and a benign ovarian
mass occurring during pregnancy * Etiology: o Luteoma�yellow-
brownmass;solidonultrasound(50%bilateral);regressafterdelivery;high risk of fetal
virilization o ThecaLuteumcyst�bilateralcysticmassesassociatedwithhighB-
hCGlevels;lowriskforfetal virilization; regress spontaneously after delivery. o
KrukenergTumor�bilateralmassesonultrasound;evidenceofmetastaticprimaryGIcancer. *
Dx: clinical presentation/ultrasound visualization of tumor; monitoring to ensure
mass effect doesn??t affect pregnancy viability * Tx: expectant management as
delivery should cause regression; If not regressing, surgical resection may be
indicated 4793/12179: Gestational Diabetes Mellitus � Presentation: abnormal
fasting glucose with onset during pregnancy o TheresultsofB-
cellhyperplasiaandphysiologicperipheralinsulinresistanceduetohPL production by the
placenta (increase sugar availability for the fetus/placenta) � Dx:o At24-28wk:1-
Hr50gglucosechallenge??targetif<140mg/dLo If >140 mg/dL: 100g glucose challenge;
check levels each hour for 3 hrs; if 2 parts are abnormal
you??ve made your diagnosis * ?? �Fasting � <95 mg/dL is normal * ?? �Hr 1 � 180
mg/dL is normal * ?? �Hr 2 � 155 mg/dL is normal * ?? �Hr 3 � 140 mg/dL is normal �
Tx: 1. Dietary modifications (balanced diet with glucose control); if not
controlled then 2. Insulin or other diabetes management drugs are indicated. o
Weight loss is NOT recommended 4780: Management of Pre-Eclampsia� Anti-
hypertensives are indicated when mom has BP >160/110 (severe HTN) o IV Labetalol
(contraindicated with maternal bradycardia, thus if this is present don??t use); IV
hydralazine or PO nefidipine are possible alternatives (may cause reflex
tachycardia, thus not contraindicated like Labetalol) ?? Note that Methyldopa is
NOT used to treat materal acute HTNo
Magnesiumsulfateshouldbeusedtopreventeclampticseizure(withregular??Magchecks??)
3279/3280: Fetal Growth Restriction * Asymmetric � typically due to poor bloodflow
to fetus, causing re-distribution of fetal flow; baby shunts blood to head (only 1
wk too small) away from abdomen (6wk too small). HTN, diabetes, preeclampsia,
antiphospholipid syndrome, Lupus damage to vasculature, and substance abuse
(tobacco, cocaine, or alcohol) can all cause this * Symmetric � the entire baby is
small, usually due to problems with the fetus, not bloodflow. Genetic disorders,
congenital heart malformations, or TORCHES infection can cause this (CMV infection
the most common cause of symmetric IUGR) o Note that caffeine is NOT associated
with growth restriction 4148: In pregnancy, mom??s kidneys are working overtime and
renal blood flow and GFR both increase, likely due to increased cardiac output and
increase blood volume. The renal basement membrane is also more permeable. This
results in increased filtration (gradually but upto 50% increase by 2nd/3rd
trimesters): * Decreased serum creatinine and decreased BUN * Increased urine
protein 4915/12098: Don??t forget! The biggest risk factor for pre-term delivery is
prior preterm delivery! Although there are LOTS of other risk factors (multiple
gestation, short cervix, tobacco use, cervical surgery, etc.) a classic principle
of OBGYN is the biggest risk factor is the event happening before! * If concerned
for risk of cervical insufficiency ?? cervical measurement via Trans-vaginal
ultrasound in 2nd trimester should be taken to assess cervical length objectively;
a digital exam is very subjective and only give a vague idea of risk * A short
cervix is defined as <2cm (no hx preterm birth) or <2.5cm (hx of preterm birth) *
Tx: o Progesteroneadministration(maintainuterinequiescence)duringgestationo
Cervicalcerclageplacementtokeepcervixclosed;usedifcervixisobjectivelyshort o
SerialTVUStoassesschangestocervixuntil24wk 4809: Post-Partum Uterine Atony *
Presentation: enlarged, soft, boggy, poorly-contracted uterus after birth; most
common cause of post- partum hemorrhage in any womano Risk factors: prolonged
labor, chorioamnionitis, uterine over-distension, retained placenta * Dx: clinical
presentation/physical exam * Tx: bimanual uterine massage, IV fluids, and
uterotonic agents (IV oxytocin, methylergonovine, carboprost, or misoprostol) with
physical removal of retained POC if present. o If patient is unstable, go to the OR
for exploratory laparotomy 10441: If there??s any question that wants you to do
screening for the baby and ??cell free DNA testing?? is an answer choice...just
choose that one. Although it isn??t diagnostic (you??ll need a CVS or amniocentesis
for that) you can get great screening results to guide further testing. 2569: 2nd
trimester Quadruple Screening Classic Findings: * Trisomy 21: MS-AFP low; B-hCG
low; Estriol low; normal inhibin A * Trisomy 18: MS-AFP low; B-hCG high; estriol
low; inhibin A high * NTDs or abdominal wall defect: MS-AFP high; all other normal
o ThemostlikelycauseofanelevatedMS-AFPisfetalabdominalwalldefect(gastroschesisor
omphalocele); but NTDs and multiple gestations can do it as well o AFP is like the
albumin of the fetus, thus if the gut is open to the amniotic fluid, AFP riseso
NotethatelevatedAFPwarrantscarefulultrasoundevaluationforstructuralabnormalities
2568: In a patient with abnormal triple/quad screening results; the next best step
for assessment is an ultrasound. While you may be temped to go straight to
CVS/amniocentesis, the ultrasound can be used to check for anatomic abnormalities
associated with congenital defects as well as guide you for the best place to do
the amniocentesis. CVS/amnio will get done, they??ll simply need an ultrasound
first. 11998: Uterine Leiomyomata (Fibroids) * Presentation: progressive
menorrhagia/dysmenorrhea with pain eventually occuring in-between periods. May
press on surrounding structures causing urinary symptoms/difficult defecating
with ?? pelvic pressure??. o The result of overgrowth of uterine smooth muscle
(often a circular mass)o Classically an irregular shaped uterine contour due to
changes in uterus.o Histologyshows??
white,whorledappearance??;maybeseenongrossspecimen * Dx: clinical picture with
normal endometrial biopsy (rule out cancer) and laparoscopic visualization * Tx:
estrogen receptor blockers (usually used in perimenopausal women), myomectomy
(preserve fertility) or hysterectomy. 3171: In the 3rd trimester, patients may
start coming in with ??labor pains?? but they can be totally wrong! * False Labor:
mild, "uncomfortable" contractions that are longer than 5min apart and not constant
without cervical change; ??Braxton-Hicks Contractions?? * Latent Labor: the first
part of labor where regular contractions occur and cervix begins to dilate * Active
Labor: intense, painful contractions <3-5min apart with rapid cervical change. You
will never mistake these if you??re the mom. 2404: Routine Prenatal Visit Labs *
First visit: Rh-D type/antibody screen; Hb/Hct/MCV, diseases (HIV, VRDL/RPR, HBsAg,
Chlamydia PCR), Rubella/varicella immunity, urine culture, urine protein * 24-28wk:
Hb/Hct, Antibody screen with RhoGAM admin (If RhD-), and 50g 1-hour glucose
challenge * 35-37wk: GBS swab and culture 12087: If a patient has an incidental
finding of endometriosis and is asymptomatic, then observation with surveillance
for future symptoms is the best course of action. No need to treat what isn??t
causing problems. 2563: Oddly, you may have patients who have SLE presenting with
acute renal decline (like proteinuria!); pregnancy can muddle the picture making is
confusing if it??s Lupus or Pre-E causing the problem. Symptoms favoring lupus are:
� Rapid aggravation of proteinuria, other signs of SLE, and RBC casts/RBCs in
urine; often these patients will have a history of SLE and it rarely occurs the
first time during pregnancy. 4757: While some patients with PROM can be candidates
for immediate delivery, if they are GBS(+) they should be give IV penicillin (Abx)
to prevent transmission! This can be confusing as antibiotics are given in PROM to
increase latency. As a general rule, give Abx to women in PPROM/PROM unless they
are known to be GBS(-) and past 34wk. 2561: THE FIRST STEP IN MANAGING MAGNESIUM
TOXICITY (like if you??re giving MgSO4 to a pre-ecamptic mom) is to ADMINISTER
CALCIUM-GLUCONATE BOLUS, THEN STOP THE MAGNESIUM. * Because MgSO4 is eliminated
from the kidneys, renal insuffiency is a common cause for toxicity * Signs of
toxicity o Mild:hyporeflexia,nausea,headache,flushing o
Moderate:areflexia,hypocalcemia,somnolence o
Severe:cardiacarrest,respiratoryparalysis 3116: Disorder of Active Labor *
Protracted Labor � cervical changes are moving slower than expect with/without
adequate contractions. Tx: oxytocin * Arrest of Labor � no cervical change with
>4hr with adequate contractions (>200 MVU/10min) or no cervical change with >6hr
with inadequate contractions. Tx: C-section 11963: * Presentation: attachment of
the placenta to the uterine myometrium or deeper (not to the endometrium). If
unknown, the placenta will improperly separate from the uterus, tearing and causing
extreme hemorrhage * Dx: antenatal with ultrasound findings of abnormal placental
interface and intraplacental villous lakes * Tx: planned C-section with
hysterectomy 3109: In regards to exercise in pregnancy, 20-30min of moderate, non-
contact exercise is recommended for most days (or all) of the week) if
normal/health pregnancy. * Contraindications to Exercise: amniotic fluid leakage,
cervical insufficiency, multiple gestations, placental abruption or placental
previa, premature labor, Pre-eclampsia/eclampsia * Unsafe activities: contact
sports, high-risk sports of falling, scuba diving, and hot yoga 4220: Evaluation of
Amenorrhea should first start with a pregnancy test; then if negative, you should
investigate endocrine causes with prolactin, TSH, and FSH levels to check for other
common pathologies. Placenta Accreta 2299: The most common site of metastases in
GTN is the lung. Thus, this disease can present with difficulty breathing/lung
nodules/hemoptysis, classically after recent delivery. The best thing you can do in
this situation is to check a B-hCG level; if (+) then you should investigate
Gestational Trophoblastic Disease more closely. But if not, then you have some
other lung pathology occurring! 4146: Hypotension is a common side-effect of
epidural anesthesia (10% of pts). It??s the result of sympathetic neuron blockage
in the spine causing vasodilation and pooling of blood in the legs. This poor
venous return can ultimately lead to fetal acidosis, thus prevention includes
aggressive IV fluids prior to epidural, placement of mom on her left side, and
vasopressor administration if necessary. 2423: In women with Graves?? Disease, the
TSH-receptor antibody can move transplacentally causing neonatal hyperthyroidism.
Levothyroxine and T3/T4 do not cross the placenta, instead baby makes their own
thyroid hormones
with their thyroid gland. * Affected babies are often irritable, warm,
tachycardic, poorly gain weight, and low birth weight * Often will resolve within 3
months of birth * Some babies are give b-blockers and methimazole to help temper
symptoms and stop any effects it could have on neonatal nervous system development
3337: Normal change in the early-post partum period are uterine contraction with
lochia rubra (red-brown discharge, but no active bleeding), transient
rigors/chills, peripheral edema, and breast engorgement. � These signs are NORMAL
and should be taken care of with normal post-partum care.3676: The classic triad of
congenital toxoplasmosis is chorioretinitis, hydrocephalus, and intracranial
calcifications UWorld Female Reproductive System12012: Absolute contraindications
to combined OCPs include: migraine with aura (inc. stroke risk), age >35 smoker
(>15 cigs/day), severe HTN (160/100), Hx of DVT, PE, or stroke, breast cancer,
cirrhosis/liver cancer, major surgery requiring prolonged immunization, and <3wk
post-partum * This question specifically had a woman needing breast cancer
treatment and had to go on effective contraception. Due to her BRCA2(+) breast
cancer, the added hormones would be a terrible choice. A copper IUD may be a metter
method as it avoids hormones all-together * In pt <3wk post-partum, often
progesterone-only pills or Depo-provera are used for contraception 4787: Copious,
white vaginal discharge is not necessarily pathologic; in fact, it may be totally
normal for some women, as normal vaginal discharge is mixed with sloughing off
cells, making it white. � If a woman has lots of discharge, but no symptoms and no
signs on wet-mount, then there??s really no concern for infection and you should
just let her be; don??t get it confused with Candida 2391: Abnormal Uterine
Bleeding (AUB) is always concerning for endometrial cancer, thus an endometrial
biopsy is typically warranted to rule this out. Criteria indicating an endometrial
biopsy include: * Age >45 � AUB or post-menopause bleeding ?? do an endometrial
biopsy! * Age <45 � AUB + [unopposed estrogen, failed medical management of AUB, or
Lynch syndrome] * Remember that a Pap smear is ONLY A SCREENING test and should
never be used to confirm suspected pathologic changes! 2362: Fat Necrosis of the
Breast can be quite scary, as it presents with palpable, irregular, fixed mass in
the breast. The first step would be biopsy or imaging, which would show
calcifications prompting excision. Upon histologic exam, the tissue should show fat
globules and foamy macrophages, indicating fat necrosis. � Classically these
patients have a history of breast trauma (seatbelt injury) or breast surgery which
caused the fatty tissue damage. 4769: Pts who are in their first year of ovulation
will experience 90% annovulatory cycles in that year. This means that their cycles
will be irregular with breakthrough bleeds and often heavy because the lack of
ovulation means a lack of endometrial sloughing. Thus the endometrium gets built up
until the woman finally does ovulate, making for very heavy periods. � If periods
become more normal (1/month) and are still very heavy, bleeding disorders and
abnormalities of the uterus should then be considered, but not in the first 1-2
years of cycling. 12026: Never forget! Age is the #1 risk factor for breast cancer.
There are lots of modifiable and non- modifiable risk factors but AGE IS THE
BIGGEST ONE. If you have to choose a risk factor for cancer, go with age. 4810:
Lichen Sclerosus� Presentation: intense itching, dyspareunia, dysuria, and painful
defecation with white ??cigarette paper?? change to the vulvar/anal skin (??figure
8??). Itching/scratching leads to obliteration of the external genital folds/labial
retraction. o Autoimmune pathology causes the itching/scratching; can co-exist with
other autoimmune dxo
Sparesthevagina/cervix,thustheseshouldbenormalonexam,butmayinvolveotherexternal
structures * Dx: punch biopsy to confirm diagnosis and rule out SCC of vulva o Note
that LS is a premalignant lesion and increases risk for SCC * Tx: topical
corticosteroids to decrease inflammation 11972: * Presentation: unilateral bloody
nipple discharge without associated ??breast lump?? o If a lump was associated, it
would more likely be an intraductal carcinoma * Dx: mammography showing single
dilated breast duct/biopsy for confirmation * Tx: Excision to halt bleeding,
although it??s a benign condition 2612: When someone is diagnosed the breast
cancer, one of the biggest indicators of prognosis is what available effective
treatments there are. FISH gene amplification or IHC staining of biopsied tissue
can tell if the tissue is HER2/neu(+). If it is then GOOD NEWS, you can use
Traztuzumab (Herceptin), which will effectively treat the current cancer! 12020:
Don??t forget! When trying to parse out adenomyosis vs uterine fibroids, the
clinical presentation can be very similar (progressive dysmenorrhea with
menorrhagia); however a key is in the uterine structure: * Fibroids will have an
irregularly shaped uterus with firm and normal portions on palpation * Adenomyosis
will have a boggy/soft uterus that??s uniformly enlarged 3339: Note that
levonogestrel-containing IUD (Mirena) works locally by thickening cervical mucus
and impairing implantation of the egg. The nice side effects are that you can stop
having periods all-together. There are minimal systemic side effects AND it will
not make weight loss challenging. � Thus, this patient that wants contraception,
lighter periods, and wants to lose weight is a great candidate for Mirena. Intra-
ductal Papilloma 3509: Don??t forget that the urine protein-to-creatinine ratio or
24-hr urine protein tests are the gold standards for assessing pre-
eclampsia/eclampsia! Either of these tests combined with 2 separate hypertensive
readings in pregnancy are diagnostic! 12178: Don??t forget! Cervical conization
surgery can cause both cervical insufficiency in pregnancy AND cervical stenosis
due to possible scarring that can occur after the surgery. It really screws with
cervix! 8943/8948: Uterine Leiomyoma (Fibroids) * Presentation: progressive
menorrhagia with dysmenorrhea with abnormally shaped, irregularly enlarged uterus
on exam. May cause pressure on bladder/bowels causing painful urinartion/defecation
o May prolapse through the cervical os if present submucosally, showing a firm,
whitish, smooth mass protruding through the cervical os causing labor-like pain and
cervical dilation. * Dx: pelvic ultrasound (don??t do a biopsy or a CT/MRI!) * Tx:
If asymptomatic ?? observation; if perimenopausal ?? contraception till menopause;
if definitive treatment if sought ?? embolization, myomectomy, or hysterectomy are
all options! 2408/2606: When considering SERMs there??s really two: * Tamoxifen:
antagonist at the breast, but agonist everywhere else o Used as adjunctive therapy
for breast cancer o IncriskofDVT/hotflashes/endometrialcancerandhyerplasia *
Raloxifene: antagonist at the uterus and breast, but agonist every where else o
Usedtotreatosteopososiswhenptcannottoleratebisphosphonate o Inc risk of DVT/hot
flashes * Note that hot flashes are the most common side effect of SERMs 12021:
Don??t forget! While OCP use can decrease the number of ovulatory cycles, thus
decrease ovarian cancer risk, it DOES NOT decrease breast cancer risk. Apparently a
great intervention to decrease breast cancer risk is alcohol cessation. 3340: Don??
t forget, breastfeeding keeps a high prolactin level resulting in suppressed GnRH
secretion resulting in low FSH/LH causing ovulation suppression/amenorrhea. This is
actually rather effective contraception in women who are breastfeeding for about 6
months. � Note, in Sheehan syndrome, FSH/LH will be absent; but if a women is
breastfeeding properly, she cannot have Sheehan syndrome (main symptoms include
inability to produce breast milk!) 2346: Inflammatory Breast Carcinoma is a rare,
aggressive cancer causing rapid onset of cutenaneous thickening an ??peau??d??
orange?? appearance of discoloration/dimpling/swelling of the breast due to lymph
node blockage. Often itching/nipple changes as well as palpable lymphadenopathy are
present as well. * Dx: Mammography/ultrasound with tissue biopsy to confirm
diagnosis are necessary * Tx: likely involves mastectomy and systemic
chemotherapeutic treatments 4756: In an aging woman who have previously conceived,
but not having trouble decreased ovarian reserve (loss of eggs!) is a likely
culprit. Ovaries lose a lot of eggs over a lifetime and some women may have true
difficulty conceiving at age >35yr 2611: In a woman presenting with benign cystic
breast mass that disappears with aspiration, an appointment should be scheduled for
follow-up in two months. Cyst fluid can often re-accumulate over 2-4 months and it
should be re-examined in this time frame. 12052: Sadly, the best way to
visualize/diagnose a suspected malignant adnexal mass is exploratory laparoscopy.
Typically, if an older woman (>50) has an adnexal mass, you??d need to do
laparoscopy to rule out cancer. Pelvic ultrasound can show you some things, BUT
you??ll likely need to operate anyway. � NEVER biopsy a potentially malignant
adnexal mass; it??ll run the risk of seeding the peritoneum. 2608: An
echocardiogram is recommended for anyone initiating Trastuzumab therapy, as
combination chemo + Trastuzumab can lead to cardiac toxicity and a baseline cardiac
function should be established. 8903/12050/12051: Epithelial Ovarian Carcinoma *
Presentation: classically occurring in an older woman (>50); this the most common
subtype of ovarian carcinoma, resulting from abrnormal proliferation of epithelial
cellso Acute:SOB,constipationorintestinalobstruction,bloating,pain,orearlysatiety o
Subacute:pelvic/abdominalpain,bloating,earlysatietyo
Maybeanasymptomaticadnexalmass * Dx: clinical presentation often with pelvic
ultrasound and CA-125 if post-menopausal patient; if CA- 125 is elevated or mass is
suspicious on ultrasound, then further imaging/laparoscopy will be necessary o
Labs:elevatedCA-125(50%) o
Ultrasound:solidmass,cystwiththickseptations,ascitesoftheabdominalcavity * Tx:
exploratory laparotomy ultimately with resection/staging 4496: Aromatase Deficiency
� Presentation: failure of aromatase production of estrogens results in
virilization of females o Adult: primary amenorrhea, lack of sexual development,
clitoromegaly, high testosterone/androstenedione, low estradiol/estrone, high
FSH/LH, cystic ovaries o
Neonate:ambiguousgenitalia,withnormalinternalgenitals/ovaries,XXkaryotype o
Momduringpregnancy:virilizationsymptoms(terminalhairgrowth,acne,etc.) * Dx:
clinical syndrome * Tx: ??? 2345: Evaluation of a Breast Mass * Step 1: Breast Mass
found/reported; do a breast exam to confirm report * Step 2: Ultrasound &
mammography for evaluation of the found mass o If<30??ultrasound+/-mammography o
If>30??mammography+/-ultrasound * Step 3: Evaluate the findings o Simplecyst??
FNAtoassesfluid;ifnormal,comebackin2-4monthsforevaluationo Complex cyst or solid
mass ?? core biopsy with possible excision of mass depending on results 2607:
Paget??s Disease of the Breast/Nipple * Presentation: persistent
eczematous/ulcerating rash around the nipple/areola with pain/itching without
relief from topic corticosteroid creamo 85% of these patients have underlying
adenocarcinoma * Dx: ultrasound/mammography with biopsy * Tx: excision 4758:
Management of HSIL **Look up management of ASCUS/LSIL/HSIL guidelines tomorrow
Chapter 1: Nausea, Vomiting, and Left Groin Mass � Hernia Differential Diagnoses
for a Groin Mass (MINT) *?M (malformation) � Hernia, Undescended testicle,
Varicocele, hydrocele o Hernias protrudes with straining and can reduce with
pressure *?I (infection/inflammation) � mononucleosis, abscess, sarcoidosis,
lymphogranuloma verneum o Typically, ??shotty?? reactive inguinal lymph nodes with
mass with be this differential*?N (neoplastic) � lymphoma, lipoma, metastatic
lymphadenopathy (anal/cutaneous/genital) o Testicular cancer will NOT produce
inguinal lymphadenopathy as it often metastasizes to retroperitoneal lymph nodes *?
T (traumatic) � hematoma, femoral artery aneurysm, pseudoaneurysm o Femoral
aneurysm will have a pulse on palpation of the mass Pathophysiology * *?�There are
three components to a hernia � abdominal wall defect, hernia sac, and contents of
the sac * *?�The ??neck?? of the hernia sac is the portion that is actually
protruding through the defect. o Wide neck � more common for abdominal contents to
come through, but easier to reduce o Narrow neck � less common for protrusion, but
harder to reduce/higher chance of incarceration/strangulation of the herniated
abdominal contents*?Strangulated hernia � hernia where protruding bowel contents
have compromised blood supply o More common in old folks, hernias of short duration
(new defect often narrow), femoral hernias (narrow/rigid canal), and with narrow
neckso Signs � fever, tachycardia, elevated WBCs, erythema of skin, and pain o This
is a surgical emergency and requires emergent bowel resection Types of Hernias*?
Direct Inguinal Hernia � protrusion thru Hesselbach??s triangle (inguinal ligament,
inferior epigastric artery/vein, medial border of rectus abdominus) through an
abdominal wall defect medial to the inferior epigastric artery. They pass through
the wall and enter into the inguinal canal to exit via the external (superficial)
inguinal ring o Typically, due to an acquired weakness in the transversalis fascia
in the anterior abdominal wall (straining, injury, etc.). Hesselbach??s triangle is
only composed of a thin layer of transversalis fascia, making it the prime place
for defect/herniation o Abdominal Peritoneum lines the hernia sac o Least likely to
incarcerate (flabby walls to protrude through) and more common in men*?Indirect
Inguinal Hernia � protrusion thru internal (deep) inguinal ring lateral to the
inferior epigastric artery and eventually trough the external (superficial)
inguinal ringo Typically, due to congenital defect of the processus vaginalis
allowing for hernia to slip into the inguinal canal and possibly into the
scrotum/labia following the path of the spermatic cord/round ligament
(respectively)o Processus vaginalis lines the hernia saco Most common hernia in all
people (men, women, and children!) *?Umbilical Hernia � protrusion through the
umbilicuso Typically occur in children. Associated with congenital hypothyroidism
(cretinism)o In children, often are asymptomatic and resolve spontaneously without
interventiono In adults, associated with high intra-abdomnial pressure (ascites,
pregnancy, weight gain, etc.) *?Femoral Hernia � protrusion thru the femoral canal
into the empty space (NAVEL) medial to the femoral vein and below the inguinal
ligament o Typically occur in women with multiple pregnancies, as the femoral veins
dilate with pregnancy causing dilation of the entire canal o Abdominal Peritoneum
lines the hernia saco Most common to become incarcerate/strangulate due to thick
fibrous lining of the canal! * *?�Ventral (incisional) Hernia � herniation at the
side of previous surgical incision; may appear weeks to months to years after
actual procedure that caused the defect * *?�Richter??s Hernia � hernia where only
a portion of the bowel wall has protruded into the hernia sac * *?�Spigelian Hernia
� herniation through two layers of the abdominal wall (not all of them). Is NOT
palpable, thus must be diagnosed with imaging and clinical suspicion * *?�Sliding
Hernia � when a retroperitoneal organ herniates with the sac, making up the
posterior wall of the herniated contents through the wall defect. Often posterior
wall of hernia feels ??thickened?? Workup *?Hernias are clinically diagnosed with
H&P o A reducible abdominal mass is practically diagnostico A non reducible mass
that bulges with straining (Valsava) is also another very clear signo In an infant,
the diagnosis can be made by observing a bulging mass with crying or lifting the
infant??s arms to they struggle (revealing the mass) *?Imaging can be used when H&P
does not yield diagnosis o Often it??s hard to appreciate the mass in obese
patients or in a Spigelian hernia o Ultrasound + Valsalva � cheap and can often
diagnose an inguinal hernia easily o Cross-sectional CT/MRI � can be used for any
hernia diagnosis. Management * *?�Often operative management is sought when hernia
is symptomatic or risk of damage to organs * *?�Direct Hernia � simple reduction of
the sac with repair of the weakened wall of the inguinal canal with tension free
mesh placement or a tensioned-tissue based repair * *?�Indirect Hernia �
operatively open up the sac, assess herniated contents (often bowel) for viability,
resect non-viable contents, reduce viable contents, and perform high ligation of
inguinal canal (at internal ring) to close the patent processus vaginalis o If
muscles in area are weak, tension free mesh may be placed for reinforcement of abd.
wall o If present in a child/adolescent, there is a 5-10% chance of bilateral
indirect hernia, thus the contralateral side should be assessed and corrected as
needed * *?�If hernia is acutely incarcerated an attempt for non-operative
reduction should be made, however if this is not possible, prompt operative
reduction with repair of hernia should be sought * *?�Umbilical hernias in infants
often close by age 2; repair should occur if it does not resolve by age 4, a >2cm
defect is present or progressive enlargement after 1yr occurs Complications *?Nerve
Injury � transection, stretching, compression by adhesions/suture are not uncommono
Genital Branch of genitofemoral nerve � cremaster reflex loss & anterior scrotum or
labia majora loss of sensationo Ilioinguinal Nerve � base of penis, mons pubis, and
inner thigh loss of sensationo Iliohypogastric Nerve � suprapubic loss of sensation
o Lateral femoral cutaneous nerve (meralgia paresthetica) � lateral thigh loss of
sensation extending down to the knee (often with laproscopic repair) * *?�Damage to
testicular artery/vas deferens � indirect hernias must be separated from these
structures, thus making them prone to damage during separation. Note that
testicular artery damage will rarely cause ischemia to the testicle due to other
avenues of perfusion * *?�Disruption of venous drainage of testicle � often in
indirect hernias with a large hernia sac, the distal portion of the sac will be
adherent to the scrotum. The dissection needed to remove it can damage the
testicular veins, leading to failure of drainage and ischemia/death (swollen
painful testicle after surgery). Often this portion is left adherent while the rest
of the sac is dissected for this reason. Chapter 2: Abdominal Pain, Nausea, and
Vomiting � Small Bowel Obstruction (SBO) Presentation *?Acute onset colicky
abdominal pain, nausea, vomiting, & constipation with high-pitched bowel sounds o
If due to strangulated hernia: fever, tachycardia, leukocytosis, and localized
abdominal tenderness can all be present * *?�Often with dehydration (dry mucous
membranes, pre-renal azotemia [high BUN:Cr]) * *?�Recurrent emesis may result in
hypochloremic-hypokalemic metabolic acidosis * *?�Differentiating different types
of Bowel Obstruction o Complete SBO � acute onset of symptomso Partial SBO � slower
onset of symptoms with passage of stool/gas 6-12hr after onseto LBO � if proximally
involved, presentation may be similar; however, symptoms are typically
chronic/progressive and may involve constipation, bowel distention/suprapubic
cramping, and rarely feculent vomitingo Post-operative
Ileus � typically the small bowel (24hr), stomach (48hr), and large bowel (3-5
days) all take their own amount of time to ??re-start?? after surgery/anesthesia.
While this may present with similar symptoms to SBO, pain is often constant and
dull with mainly hypoactive bowel sounds from the beginning of complaint. ??If
patient initially was fine post-op, then complaints occurred, SBO is considered ??
CT is often used to distinguish SBO from POI in equivocal cases Pathophysiology *
*?�Hernia is the most common cause of SBO worldwide due to closed loop obstruction
* *?�Prior abdominal surgery is the most common cause of SBO in industrialized
countries due to adhesions o Appendectomy is the most common surgery to cause this
complication; followed by colon resection and gynecologic procedures * *?�Crohn??s
disease (stricture/fistulas), gallstone ileus (direct obstruction/pneumobilia),
intussusception (target sign/palpable mass), volvulus (omega sign), and neoplasms
(Hx) may all cause SBO * *?�When the bowel is obstructed, fluid/gas accumulate
causing dilation, prompting the bowel to increase motility in an attempt to relieve
the blockage o Bowel dilation = nausea, abdominal pain with contractions (colicky),
and emesiso Initially bowel sounds increase from increased peristaltic activity
(high pitched/tinkling)o Progressive dilation causes inability to contact leading
to eventual decrease/absence of sounds *?Major problem is fluid loss due to emesis
and third spacing (blockage/bacterial overgrowth-->dilation -->starling forces
moving solute into bowel wall-->movement of blood serum into bowel wall) Work-Up *
*?�Labs � CBC, CMP, and serum lactate to assess dehydration (hemoconcentraction,
pre-renal azotemia, hypoCl/K acidosis) and bowel ischemia severity (leukocytosis,
elevated serum lactate) * *?�Imaging � abdominal series followed by
abdominal/pelvic CT with oral & IV contrast o What are each of these tests looking
for???Upright chest radiograph � free air under diaphragm-->bowel perforation ??
Upright abdominal radiograph � air-fluid levels-->obstruction ??Supine abdominal
radiograph � assess level/area of distention ??CT w/contrast � assess level/area of
distentiono Small bowel shows lines going the full length of the tube (plica
circularis) while large bowel will only have lines going partially through
(haustra)o Pneumatosis (CT) is presence of gas in the intestinal wall, often
indicating ischemia/necrosis o Portal venous gas (CT) is a late presentation of
pneumatosis where the air passed into the portal venous circulation because it had
been there for some time Management*?First Step � aggressive isotonic IV fluid
replacement, nasogastric tube placement (suction of bowel gas), and placement of IV
catheter to monitor urine outputo Partial obstruction � conservative management for
up to 2-3 weekso Complete obstruction � conservative management with close watch on
clinical status for 24hr *?Lack of improvement or clinical deterioration should
prompt surgical resolution, likely with a bowel resection for non-viable small
bowel o Non-viable bowel appears blue/pale, has no peristalsis, & lacks mesenteric
arterial pulsation o Ultrasound doppler is useful to assess bowel blood-flow when
assessing questionable bowels o IV fluorescein dye with Wood??s Lamp can be used,
as bowel that lights up is getting bloodo If you still can??t make up your mind,
but the section in question is small it??s acceptable to simple remove the small
section and call it a dayo If you can??t make up your mind, but the section is
large, it??s acceptable to terminate the operation, further resuscitate the
patient, and have a second look surgery. *?Shouldo 10-14 days post-op = OK re-
operation be necessary: o After 10-14 days post-op = not OK due to highly
vascularized adhesion formation.??Instead initiate conservative treatment for 4-6wk
to allow for less vasularization to be present on re-opteration??Emergent re-
operation may be necessary if peritonitis ro bowel compromise are seen Chapter 3:
New Palpable Mass in Breast � Breast CancerA new breast mass can be MANY things and
the differential can be big. Make sure to review the following on Pages 25-26 in
regards to benign and malignant differentials: * *?�Benign: fibrocystic change,
fibroandenoma, indaductal papilloma, fat necrosis, abscess, galactocele * *?
�Malignant: DCIS, LCIS, IDC, ILC, mucinous carcinoma, inflammatory carcinoma,
phyllodes tumor Key physical features of benign vs malignant breast nodules *?
Benign: well circumscribed, rubbery, mobile mass with no gross abnormalities of the
breast *?Malignant: o Overall breast: asymmetry, overlying skin changes, nipple
discharge/crustingo Mass itself: single dominant lesion that feels hard, immobile,
and has irregular borders o Lymph nodes: painlessly enlarged, firm, immobile,
and/or matted Different Types of Nipple Discharge * *?�Physiologic: clear,
bilateral, multiductal often from hormonal changes in the body (post-lactation,
regular cycling/puberty nipple stimulation) * *?�Milky: can be physiologic (post-
birth) or from prolactinoma, hypothyroidism (TRH can act like PRH), or medications
(DA inhibitor anti-psychotics come to mind) * *?�Bloody: most commonly from
intraductal papilloma, up to 15% can be from invasive breast cancer. * *?�Purulent:
may be the result of infection! Risk Factors for Breast Cancer largely have to do
with two things: * *?�Estrogen exposure: menarchal age <12, menopause >55,
nulliparity, obesity, hormone replacement therapy, age of first birth >30 * *?�DNA
damage/defect: mother/sister with breast cancer, previous breast cancer, radiation
exposure, known BRCA1/BRCA2 mutation, age >70yr Pathology/Patholophys o *?�While
fibrocystic changes are often benign, ductal hyperplasia, sclerosing adenosis, and
atypical hyperplasia all carry a risk of cancer if seen histologically o *?�Peau
d??Orange: red-orange discoloration of the breast skin, swelling, dimpling and
nipple retraction due to compromised lymphatic outflow due to malignant invasion.
Often caused by inflammatory carcinoma of the breast o *?�Nipple retraction:
malignant invasion of the Cooper??s ligaments causing thickening and pulling back,
resulting in retraction of the skin of the nipple, signifying breast cancer Workup
* *?�Triple Test: a clinical tool for physical exam of new breast mass consisting
of exam, imaging, and tissue sampling giving 1 (benign), 2 (suspicious), or 3
(malignant) ratings to each test. * *?�Imaging: o Under 30yr: young breasts are
denser with fibrous tissue, making mammography less useful. Ultrasound is first
line for imaging these women, mainly to differentiate cystic vs solid masses o Over
30yr: mammography is most useful here *?Biopsy: o Simple cystic masses may be left
or drained if symptomatic; clear fluid with the mass reducing is a normal finding;
bloody fluid or a non-reducing mass require further cytology and biopsy o Solid or
suspicious masses are assessed via core needle biopsy * *?�Tumor Antigen testing:
testing for estrogen (Er), Progesterone (Pr), and HER-2neu receptors are done to
determine options for treatment and prognosis in a malignant breast mass. If none
of these receptors are present the tumor is deemed ??triple-negative?? and often a
poor prognosis * *?�Metastatic Workup: LFTs (liver), alkaline phosphatase/serum
calcium (bone), CXR (lung) are used as a basic workup in low-stage cancers without
symptoms o CT, and other symptom driven testing may be undergone based on clinical
situation o Stage 3 cancer requires an additional CT C/A/P + bone scintigraphy *?
Staging: can be reviewed on page 29 Management * *?�Lumpectomy + SLNB + chest wall
radiation � basically cutting out the cancer with clean margins, making sure there
aren??t mets, and radiation for anything residual o Contraindications: multiple
primary tumors in 2+ quadrants, diffuse malignant microcalcifications, previous
chest wall radiation, positive surgical margins with repeat excisions, and 1st
trimester of pregnancy o Nipple/Breast Skin sparing can be part of the operation,
especially in lower risk cases * *?�Simple mastectomy + SLNB (no radiation) � more
tissue gone but a more definitive treatment * *?�Simple mastectomy + ALND +/-
neoajuvant chemotherapy � used for stage 3 or greater tumors, especially with
larger tumors that need to be shrunk for better surgical outcomes * *?
�Chemotherapeutic Drugs o There can either be hormonal treatments or classic chemo
drugs listed on Pages 32 and 33 o Note that before starting Trastuzumab (Herceptin)
all patients should receive an echocardiogram and MUGA scan (assess left/right
ventricular function) to determine ejection fraction as there is significant risk
of cardiomyopathy Complications*?Nerve Damage due to Lymph Node Dissection o Long
Thoracic nerve � weak upward rotation/abduction, and winged scapulao Thoracodorsal
nerve � weak extension/adduction/internal rotation of the shoulder o Medial
pectoral nerve � weak internal rotation of humeruso Lateral pectoral nerve � weak
flexion, adduction, and internal rotation of humerus *?Lymphedema (swelling, pain,
compromised immune system) is the most morbid comorbidity of lymph node dissection.
Also lymphangiosarcoma risk is increased with lymphedema Things that can get you in
Trouble * *?�Mistaking Inflammatory Breast Carcinoma for Cellulitis � don??t do it
* *?�Ignoring a breast mass in pregnancy o First trimester � make the diagnosis;
but you can??t treato Second trimester � make the diagnosis; chemo can be giveno
Third trimester � make the diagnosis; wait till birth until treatmento Note that
hormonal therapy and therapeutic radiation are total contraindicated in pregnancy
*?Ignoring a breast mass in an elderly male � old men can definitely get breast
cancer (esp. in 60s/70s).
Sadly, it??s often diagnosed in later stages, sometimes giving a worse prognosis
Chapter 4: Abnormal Screening Mammogram � DCIS/LCIS Recommendations for Breast
Cancer Screening *?While fairly controversial, most guidelines advise:o Regular
breast awareness and/or exams starting at age 20o Mammograms at some yearly
interval starting around either age 40 or 50 * *?�It is thought that after age 50,
the radiation risk of a mammograms outweighs the risk of breast cancer * *?�While
helpful, the use of mammograms can be dependent on the patient and the skill of the
tech and interpreter of the films, lending unwanted variability Pathophysiology o
*?�Several reasons for abnormal findings on mammogram are listed on page 38 o *?
�Benign calcifications on mammogram are often larger and more dense o *?�Malignant
calcifications are more often smaller and more ??hazy?? as they are the result of
individual cell death & calcification from malignant overgrowth o *?�DCIS o
Malignant epithelial cells within the mammary ducts that have not invaded the
basement membrane of the tissue; considered a pre-malignant lesion o Often presents
as incidental micro-calcifications on mammorgramo Comedo pattern is highly
suspicious of malignancy and is the most worrisome for metastasis o Treatment
includes excision to a negative margin with SLNB in some cases as this can
technically be invasive, but only in small amounts *?LCIS o Malignant epithelial
cells within the mammary lobules, often incidentally found on biopsyo Not
considered pre-malignant, but is a major risk factor for development of breast
cancer in either breasto Treatment is excisional biopsy to search for surrounding
malignancy with tamoxifen use in some to decrease the risk of malignancy
development. Chapter 5: Chest Pain, Diaphoresis, Nausea � Heart AttackRisk factors
� increased age, male, HTN, hypercholesterolemia, diabetes, smoking, family Hx of
CAD * *?�A patient presenting with acute chest pain can be scary, but the lack of
these risk factors may mean you should search of other etiologies! * *?�Young age
(men <40, women <50), female gender, no cardiac risk factors (smoking, diabetes,
family Hx, etc.), and character of chest pain (exertional, relieved with rest,
signs of angina) that suggest non- cardiac etiology put people at LOW RISK for MI *
*?�Postmenopausal women are at increased risk for MI as estrogen helps maintain the
vascular intimal layer. The loss of this maintenance leads to stiffening of
arteries, thus heighted risk! Presentation o *?�Chest pain (radiation to neck/left
arm), diaphoresis, anxiety, tachycardia, tachypnea, nausea/vomiting o *?�Heart
failure may occur in large MIs (dyspnea, rales, JVD, new S3/S4, new murmur, shock)
o *?�Women most often have atypical (??silent??) presentations (dyspnea, epigastric
pain, N/V, no chest pain!) Pathophysiology *?Acute Coronary Syndrome � pathologic
process involving narrowing/damage to the coronary arteries resulting in varying
degrees of myocardial ischemiao Unstable Angina � non-occlusive thrombosis causing
ischemia but NOT myonecrosiso NSTEMI � occlusive thrombosis where only part of the
myocardium (sub-endocardial segment) is damaged causing myonecrosis/cardiac enzyme
elevation, but not ST-segment elevationo STEMI � occlusive thrombosis affecting the
entire myocardial wall causing myonecrosis/cardiac enzyme elevation/ST-segment
elevation. This is the classic heart attack. *?There are two major mechanisms for
MI o Primary coronary event � plaque rupture with thrombosis; often needs immediate
intervention to re-establish myocardial perfusion o Non-primary � decreased O2
supply (hypoxia, hypotension, anemia, etc.) or increased myocardial oxygen demand
(tachycardia, tachyarrythmia, sepsis, etc.); often addressing the primary problem
is needed for resolution of ischemia *?Variant (Prinzmetal) Anginao A vasospatic
angina that typically occurs in young women without cardiovascular risk factors,
onset in the middle of the night, and often exacerbated by smoking.o May be
precipitated by exercise, hyperventilation, emotion, cold exposure, cocaine abuse;
but will not be consistently exacerbated with exercise like Typical Anginao EKG can
show transient ST elevation w/ complete return to baseline after ischemic vasospasm
o May be associated with other vasospastic disorders (migraines or Raynaud??s
phenomenon)o Tx: nitrates or Ca++ channel blockers (vasodilation) Workup * *?�First
Steps: relevant H&P + 12-lead EKG + cardiac enzyme blood assay QH8 for 24hr + chest
radiograph (rule out non-MI causes of acute chest pain) +/- echocardiogram (if not
delaying treatment!) * *?�Cardiac enzyme characteristics o Troponin-I � slower rise
(3hr) and peak (6hr) and gradually decreases over 1 week; highest
sensitivity/moderate specificity o Creatinine phosphokinase Myocardial fraction
(CKMB) � quickly rises (peak 12-40hr) and quickly falls (48-72hr); low
specificity/moderate sensitivity; best used to diagnose re-infarction o Note that
in renal failure, the half-life of these enzymes will be increased *?EKG o Left-
anterior descending (LAD) � most common site of thrombosis; branch of Left coronary
artery; supplies anterior L.ventricle & anterior 2/3 of septum; V2, V3, V4 changes
o Circumflex branch � branch of left coronary artery; supplies lateral/posterior
L/ventricle and left atrium (including SA node); aVL, V5, V6 changes o Posterior
Descending Artery � branch of right coronary artery (80% of people); supplies
inferior L.ventricle and posterior 1/3 of septum; II, III, aVF changes Management*?
Initial Steps (initial stabilization for STEMI or as total management for NSTEMI):
o Aspirin (chewed) + Clopidogrel + IIb-IIIa inhibitor � inhibits platelet
aggregationo Heparin � prevents further clot formationo B-blocker � decrease heart
rate/contractility (less O2 demand); contraindicated in shock o Nitroglycerine �
vasodilatation (decrease pre-load/afterload) to decrease O2 demando ACE inhibitor
(or ARB if not tolerated) � prevents cardiac remodeling, reduces mortality o
Supplemental O2 � increase O2 saturation (if O2 sats are low)o Morphine � alleviate
pain (give if 3 doses of nitroglycerine don??t do the trick!)o Atorvastatin �
decreased cardiac events and speeds resolution of ST-elevation *?Percutaneous
Coronary Intervention (PCI) - threading a catheter into the heart and inflating a
balloon on the end to open up a stenotic artery causing MI. A stent is usually
placed to keep it upon until about 3 months when it??s removed, as the artery has
adapted o Indication??STEMI � emergent PCI, always!??NSTEMI � not needed unless pt
has recurrent angina, CHF, high-risk findings, ejection fraction <40%, hemodynamic
instability, V-tach, PCI within past 6 months, or prior CABG o Timing ??Within 90
minutes of onset of the MI; can be done up to 6hr with decreasing benefit ??If 90
minutes has passed, patient should be considered for IV tPA thrombolysis o If PCI
is unsuccessful -->?emergent CABG *?Coronary Artery Bypass Graft (CABG) � taking a
blood vessel from somewhere else to create a route around the area of blockage in
the coronary artery o Indication for emergent � rare??presentation after 12hr of
symptom onset ??cardiogenic shock upon presentation??failure of PCI to resolve
ischemia o Indication for elective � more common??>50% stenosis of L.main coronary
or >70% stenosis in any coronary artery??stenosis of the LAD + another coronary
artery or stenosis of 3 or more coronary arteries ??obstruction at a place where
you cannot stent (like a bifurcation point!) o Best conduit for CABG is the
internal mammary artery (off the subclavian) which 95% of these guys are patient
>10yrs post-CABG ??Greater saphenous vein, radial artery, and gastroepiploic
arteries may also be used ??>2 coronary grafts being placed has been shown to
increase long-term survival versus 1 o CABG is more invasive, but has better
outcomes than stenting ??Use of aspirin, B-blockers, statins, and Abx post-op have
better outcomes ??You must stop clopidogrel before CABGo Preoperative shock,
emergent surgery, >65%, and low LVEF denote higher M&M post-op *?Complication of MI
include:o Immediate - Cardiogenic shock, CHF (both often from cardiac hypomobility)
o 2-3 days � pericarditis, arrhythmia (V-fib most deadly; common cause of death the
hospital)o 3-14 days � cardiac tamponade, rupture (intraventricular septum, free
wall, or papillary muscle) o Long term � ventricular aneurysm, Dressler??s syndrome
Areas to get you in trouble*?Not evaluating for aortic dissection � note that
Stanford Type A (toward the heart) can compress the coronary vasculature and cause
a full blown MI. CXR as initial work-up can help find this. Chapter 6: Chest Pain +
Syncope � Aortic Stenosis/Disease Presentation *?Typical symptoms:o Chest pain: LV
hypertrophy may result causing increased O2 demand and anginao Exertional syncope:
pt will be doing something (jogging) and will get lightheaded/pass out without
confusion afterwardo Pulsus parvus et tardus (??delayed and diminished carotid
pulse??): because the aortic valve is obstructing bloodflow the carotid pulse will
be delayed after the S1 sound; the bicuspid valve closes but the blood won??t make
it out of the heart until latero Signs of CHF: pumping against that stenotic valve
can cause buildup of pressure and LV dysfunction result in typical CHF signs*?Heart
Murmur: mid-systolic crescendo-decreshendo murmur; heard best in upper right
sternal border o Single/soft S2 with an S4: the S2 is diminished as the aortic
valve doesn??t ??click?? shut, it??s fused together. S4 from increased pressure of
contraction to maintain perfusion (LVH) o Intensity of the murmur has NO
correlation with severity of diseaseo Timing of murmur can indicate severity with
later being worse (takes
more systolic pressure to finally pop open the valve)o Valsalva (decreases sound
with decreased preload), Handgrip (decreases sound with increased afterload), and
Leg raise (increases sound with increased preload)o HOCM may mimic aortic stenosis
but will be affected in the opposite way with Valsalva/handgrip/leg raise. *?
Special Signs o Pulsus alternans � alternating strong/weak peripheral pulses.
Occurs with LV dysfunction (possible with aortic stenosis); poor ejection fraction
in one beat leads to overfilling and better ejection in the next beat o Pulsus
bisferiens � ??double peak?? pulse during systole seen with aortic regurgitation
(can be part of aortic stenosis). The mechanism is actually not well understood. *?
IV drug use may be an important history component, as it may result in infective
endocarditits (discussed below). Valvular vegetations may result in outflow
obstruction � stenosis. Etiology * *?�Senile calcific aortic stenosis: accumulation
of calcium deposits in the aorta due to aging. Only affects people aged >70 * *?
�Bicuspid aortic valve: an inborn abnormality of the valve results in easier
calcification...occuring in those aged <70yr (usually younger than this though!).
If the patient is in their 40s...has no history or signs of Rheumatic fever...and
has aortic stenosis-->consider bicuspid aortic valve! * *?�Rheumatic heart disease:
classic infectious cause of aortic stenosis, especially in immagrants with poor
healthcare! Presents with several signs and aortic stenosis (while uncommon and
severe) can occur. Will nearly always occur alongside mitral valve damage.
Rheumatic damage to the aorta is actually less commonly than bicuspid aortic valve!
Workup o *?�Labs: CMP, Coagulation panel, and cardiac biomarkers (troponin, CK-MB,
BNP, and D-dimer) to check for signs of underlying disease processes and CHF o *?
�EKG to rule out MI or search for signs of heart failure *?Imagingo CXR: can show
signs of CHF (large heart, increased lung markings, etc.) and can rule out other
causes of chest pain (aortic dissection, etc.)o Echocardiography: thickened aortic
valve leaflets and hypokinesia of the heart Management*?Asymptomatic aortic
stenosis: medical control of HTN/cardiac risk factors; echocardiography every 3-
5yr; elective replacement of valve if undergoing heart surgery for another reasono
Note that while statins may help in decreasing complication risk, they DO NOT stop
calcification of the aortic valve. This process is not dependent on
atherosclerosis! *?AS + CHF (??symptomatic AS??): immediate aortic valve
replacement Things to Get You in Trouble * *?�Drugs to avoid: any drug that
decreases BP can result in significant hypotension in aortic stenosis (diuretics,
B-blockers, vasodilators, etc); thus decreased dosing with warning about this
complication is considered safe * *?�Elective non-cardiac surgery: remember that
anesthesia causes vasodilatation (thus hypotension), thus those with aortic
stenosis may enter into shock under GAS; it??s important to identify AS pre-
operatively to avoid such a terrible complication Tips From UWorld4668: Infective
endocarditis can present with weird, vague symptoms that may not be entirely
obvious * *?�Systemic emboli (cerebral, pulmonary or splenic infarcts) * *?�Mycotic
aneurysms or infections due to septic emboli * *?�Janeway lesions: nontender, red,
raised lesions on palms/soles from emboli in superficial emboli * *?�Roth??s spots:
hemorrhages of the retina from emboli * *?�Osler nodes: painful fingertips,
sometimes with nodules * *?�Arthritis: swollen joints, especially of the hands/feet
* *?�Proteinuria or hematuria from kidney damage 3068/3014: Infective endocarditis
is easy to spot on exams but classic bacterial associations must be memorized. o *?
�S.aureus: implanted devices (catheters, valves, defibrillators, etc.) and IVDU o
*?�Viridians Group Strep: dental/respiratory procedures, esp with previously
damaged valve o *?�Coagulase-neg staph: implanted devices (catheters, valves,
defibrillators, etc.) o *?�Enterococci: nosocomial UTIs (classic is after UG
procedures) o *?�Strep. Bovis (gallolyticus): colon carcinoma/IBD Chapter 7: Chest
+ Back Pain � Aortic DissectionRisk Factors: hypertension, connective tissue
disease (Marfan??s, Ehlers-Danlos), old age, atherosclerosis, pregnancy, cocaine
use, aortic injury, bicuspid aortic valve, or aortic coarctationPresentation * *?
�Classic Symptoms: sudden painful ??tearing?? sensation in chest, radiating toward
the back; uneven pulses either between arms (aortic arch), or arm vs leg (infra-
renal abdominal aorta) * *?�Symptoms due to surrounding tissue
compression/involvement: o Cardiac Ischemia (coronary arteries): signs of acute MI;
most often the RCAo Cerebral ischemia (brachiocephalic or carotid arteries): signs
of strokeo Spinal Cord Ischemia (Artery of Adamkiewicz): paraplegiao Kidney failure
(renal artery): oliguria, elevated BUN, elevated Cro Mesenteric Ischemia (SMA): out
of proportion abdominal pain/nausea/bloody diarrhea o Limb ischemia (subclavian or
iliac arteries): 5 Ps of ALI o Aortic regurgitation (aortic root dilatation):
widened pulse pressure/??water hammer pulse?? o Pericardial Tamponade (pericardial
sac): hypotension, JVD, muffled heart sounds, hepatojugular reflex, pulsus
paradoxus, & electrical alterans; narrowed stroke volume (<30) Pathophysiology * *?
�Intimal Layer tearing is typically in inciting event in an aortic dissection; the
small tear gives access to the medial layer, allowing for high-pressure arterial
blood to rip apart the aortic medial layer * *?�Formation of a false lumen with an
inner layer (intima + inner media) and outer layer (outer media + adventita)
propagates down the aorta, causing symptoms * *?�Marfan??s syndrome (fibrillin-1
malformation) is one of the most common connective tissue diseases; the
malformation of connective tissue can cause cystic medial necrosis of the CT laden
media later of the aorta (needed for stretching to accommodate high pressure flow)
Classification *?Stanford classifications are based on how we would clinically
treat a dissection o Stanford A � any ascending aorta/aortic arch involvement (may
also involve descending) o Stanford B � only descending aorta involvement*?DeBakey
classifications are based on more specific anatomic involvement o DeBakey I �
involves ascending/arch/descending aorta o DeBakey II � involves only ascending
aorta/archo DeBakey III � involves only descending aorta Workup * *?�Labs: blood
type/cross, cardiac biomarkers, EKG (these are to rule out other causes) * *?
�Imaging o CXR (first image): widened mediastinum (15-20% will be NORMAL)o CT chest
w/contrast: can show false lumen and better characterize location of disease o MRI:
may be used, but often less widely available in emergency settings *?If
hemodynamically unstable: take to OR immediately for intervention; but get a
transesophageal echocardiography (TEE) in the OR to confirm diagnosis. If (+) then
immediately proceed to operate Management*?First Step: IV B-blocker � allows for
decreasing BP to decrease propagation of dissection o Contraindicated in tamponade
or severe regurgitation (may result in severe hypotension resulting in cardiac
arrest or shock!) * *?�Type A dissection � urgent trip to OR for median sternotomy
+ aorta removal & grafting/aortic valve replacement/coronary artery re-implantation
(bad prognosis) * *?�Type B dissection � ICU admission with close blood pressure
monitoring; open thoracotomy with endovascular repair may be done should
complications arise (good prognosis) Chapter 8: Incidentally Discovered Adrenal
Mass on CT scan History and Physical * *?�Adrenal ??Incidentaloma?? � non-
functional adrenal tumors are very common (85% of all adrenal tumors) and about 5%
of CT scans (and 10% of autopsies) will incidentally show an adrenal mass. * *?
�Cushing??s Syndrome (ACTH) � central obesity, buffalo hump, moon facies, skin
atrophy with purple striae/ eccymoses/easy bruising, proximal muscle weakness,
hypertension (mineralocorticoids), glucose intolerance (glucocorticoids), skin
hyperpigmentation, women may have hirsutism/menstrual irregularities * *?�Conn??s
Syndrome (aldosterone) � hypertension (increased Na+), hypokalemia, high
aldosterone, low renin, adrenal changes on CT scan, and metabolic alkalosis (hypoK
increases bicarb reabsorption/H+ secretion) * *?�Pheochromocytoma (Epi/Noreepi) �
episodic hypertension, palpitations, sweating, pallor classically with increase
intraabdominal pressure (urination, palpation, positional change) or
anesthesia/surgery * *?�Adrenocortical Carcinoma � often grow unnoticed until
lethal; 60% are functional (Cushing??s syndrome >>> virilization > feminization)
but may be non-functional (abdominal mass, abdominal pain, nausea, anorexia, early
satiety); typically they??re >6cm on abdominal CT Pathophysiology *?Functional
regions of the Adrenal Cortex (GFR-->Salt, Sugar, Sex) o Glomerulosa �
mineralocorticoids o Fasiculata � glucocorticoidso Reticularis � sex hormones *?
Adrenal medulla synthesizes catecholamines (epinephrine, norepinephrine, etc.)
Imaging * *?�CT scan with fine cuts preferred; but MRI is an acceptable alternative
* *?�Benign lesion: size <4cm, homogenous appearance, well-defined borders, high
levels of intracellular lipid (based on Hounsfield unit density), rapid washout of
contrast, low vascularity * *?�Malignant Lesion: size >6cm, irregular borders,
necrosis/calcification/hemorrhage in the mass, ill- defined borders, invasion of
adjacent tissue, low intracellular lipids, high vascularity Management for a non-
functional adrenal mass o *?�Size - <4cm (watch with interval CTs), 4-6cm (either
watch or resect based on perioperative risk), >6cm (resect as it??s more likely to
be malignant) o *?�Follow-up imaging
if not resecting -->?6, 12, 24 months o *?�Follow-up labs if not resecting -->?
every year for 4 years Adrenalectomy * *?�May be done laproscopically, but open is
preferred in malignancy or in tumors >8cm * *?�Adrenal blood supply is from
inferior phrenic artery (superiorly), aorta (medially), and the renal artery
(inferiorly) * *?�Venous drainage o Left adrenal vein-->left renal vein-->IVC o
Right adrenal vein-->IVCf. 2592/4721/4419: Cushing??s Syndrome*?Presentation:
central obesity, buffalo hump, moon facies, skin atrophy with purple striae/
eccymoses/easy bruising, proximal muscle weakness, hypertension
(mineralocorticoids), glucose intolerance (glucocorticoids), skin
hyperpigmentation, women may have hirsutism/menstrual irregularities o Labs:
hyperglycemia, hypokalemia * *?�Etiology: exogenous corticosteroid administration
(most common), ACTH-producing tumor (Pituitary adenoma ??Cushing??s disease??),
ectopic ACTH-production (small-cell lung cancer), or adrenal adenoma/hyperplasia *
*?�Dx: o Establish hypercortisolism with midnight salivary cortisol assay (positive
is >5mcg), 24-hr free urine cortisol (positive is >150mcg), and low-dose
dexamethasone suppression test (positive is >5mcg in morning following
dexamethasone admin)-->2/3 must be positive for diagnosis o If hypercorticolism
present-->ACTH level measurement (positive is <5 pg/mL) to see if process is ACTH
dependent or independent o If ACTH is elevated-->high-dose dexamethasone
suppression test to determine if source of ACTH is pituitary (will be suppressed)
or ectopic (won??t be suppressed, likely lung cancer) *?Imaging: CT scan with fine
cuts; but MRI is an acceptable alternative *?Tx: aimed at underlying cause, but
likely resection of the masso Note that glucocorticoid replacement
perioperative/postoperatively is required due to tumor??s suppression of normal
adrenal function, possibly for months/years following surgery!
3231/2725/3230/3832/8897: Hyperaldosteronism Primary Hyperaldosteronism (Conn??s
syndrome) * *?�Typically, from an adrenal adenoma or bilateral adrenal hyperplasia
* *?�Presentation: hypertension (increased Na+), hypokalemia, high aldosterone, low
renin, adrenal changes on CT scan, and metabolic alkalosis (hypoK increases bicarb
reabsorption/H+ secretion) * *?�Dx: CT findings + aldosterone:renin ratio >20 or
persistently elevated after oral saline/oral salt tablet administration (would
normally be suppressed by the Na coming in) o Adrenal venous sampling can
distinguish bilateral from unilateral dysfunction o Best first test is the
aldosterone:renin ratio *?Tx:o Unilateral: surgical excisiono Bilateral or surgery
not an option: aldosterone antagonists (K-sparing diuretics) spironolactone or
eplerenone (note that spirono has anti-androgen effects, but eplerenone will have
less of these. Spirono is still the preferred first-line treatment)*?Note that
these patients may be on a non-K-sparing diuretic simply because they seem to have
hypertension. But K-wasting due to diuretic use will not approach the degree that
hyperaldosteronism will achieve. Often the two combined will cause the hypokalemia
Secondary Hyperaldosteronism * *?�Typically, from reno-vascular HTN, malignant HTN,
renin-secreting tumor, or diuretic use (basically the kidney??s normal response to
poor perfusion) * *?�Presentation: hypertension (increase Na+), hypokalemia, high
aldosterone, high renin Pseudo-hyperaldosteronism o *?�What looks like aldo, smells
like aldo, but isn??t aldo? Basically things that increase other ??corticoids??
that aren??t mineralocorticoids...but can act as mineralocorticoids. CAH,
deoxycortisone-secreting tumor, Cushing??s syndrome, or exogenous mineralocorticoid
use o *?�Presentation: hypertension (increase Na+), hypokalemia, low aldosterone,
low renin 3598/2170: Androgen Producing Adrenal Tumor * *?�Women generate
androstenedione (AS)/dehydroepiandrosterone (DHEA)/testosterone (T) in the adrenals
and the ovaries. Dehydroepiandrosteone-sulfate (DHEA-S) is only produced in the
adrenals, thus elevated DHEA-S is the most specific for an adrenal androgen
producing tumor * *?�Presentation: signs of virilization (pubertal hair, menstrual
suppression, cliteromegaly), negative pregnancy test, and no abnormalities of the
uterus/ovaries * *?�Dx: adrenal tumor on CT scan with presentation * *?�Tx:
excision Chapter 9: Fatigue, Constipation, and Depressed Mood �
Hypercalcemia/Hyperparathyroidism Differential for Hypercalcemia * *?
�Thyrotoxicosis (most common outpatient) � hypermetabolic state causing increased
bone breakdown * *?�Primary hyperparathyroidism � results in too much PTH secretion
(familial, sporatic, or in MEN 1 or 2) * *?�Malignancy (most common inpatient) o
PTH-rP secretion (80%) � effectively too much PTH secretion (lung, head&neck, renal
cancers) o Direct osteolysis (20%) � cancer spreads to the bone causing breakdown
(breast, multiple myloma, prostate cancer) * *?�Hypervitaminosis A � works on RAR
or RXR receptors to stimulate osteoclasts/inhibit osteoblasts, resulting in
increased bone turnover (vitamin A over-supplementation or Analogue acne
treatments) * *?�Immobilization � poorly understood, but thought to be a lack of
osteoblast activation due to poor bone stimulation without loss of osteoclast
activation. (post-surgery, elderly, paralyzed for any reason) * *?�Paget??s Disease
of Bone � excessive remodeling of bone causing large Ca2+ release into serum * *?
�Hypervitaminosis D � increased absorption of Ca2+ (over-supplementation) * *?
�Granulomaous Disease (Sarcoid, TB, Hodgkins disease) � epitheliod
histiocytes/granulomas can convert 25-OH VitD-->1,25-OH VitD * *?�Milk-alkali
syndrome � calcium over-supplementation (Ca-antacids or osteoporosis supplements) *
*?�Mediations o Thiazides (HCTZ or chlorthalidone) � decreased calcium excretion
based on mechanism o Lithium � poorly understood, but may affect both the kidney
and parathyroids * *?�Rhabdomyolysis � massive myocyte hemolysis causing Ca2+
release into blood * *?�Adrenal Insufficiency � poorly understood; possibly from
hemoconcentration secondary to loss of aldosterone production and diuresis Anatomy
and Embryology of the Parathyroid Glands o *?�Superior Parathyroids � 4th
pharyngeal pouch; 95% located adjacent to the tubercle of Zuckerkandl posterior to
the terminus of the recurrent laryngeal nerve; 5% along esophagus, prevertebral
fascia, near the super thyroid artery, or intrathyroidal o *?�Inferior Parathyroids
� 3rd pharyngeal pouch; less consistent with location (65% on inferior thyroid
gland, 35% on thymus, thyrothymic ligament, carotid sheath, behind the esophagus or
partially intrathyroidal) o *?�15% of people will have more than 4 parathyroid
glands! 4308/4134/4309/3102: Evaluation of Hypercalcemia * *?�Step 1: Confirm
hypercalcemia (repeat Ca2+ level/measure serum albumin to correct for it) * *?�Step
2: Determine the source (measure PTH) o High/normal PTH: PTH dependent
hypercalcemia??Primary hyperparathyroidism, familial hypocalciuric hypercalcemia,
or lithium o Low PTH: PTH independent hypercalcemia * ??�Malignancy (Ca >15) from
bone mets or PTHrP production (suppression of PTH) * ??�Vit D toxicity (too much
Ca++ retaining), granulomatous diseases (makes Vit. D), thiazide toxicity (Ca+
resorbtion), milk-akali syndrome (over ingestion of Ca++), thyrotoxicosis
(increased bone resorbtion), Vit. A toxicity (direct osteoclast simulation in high
doses), prolonged immobilization (increased osteoclastic activity without matching
osteoblastic activity) � often more mild elevations 3083: DON??T FORGET!!! THIAZIDE
DIURETIC HYPECALCEMIA IS MILD AND WON??T CAUSE SYMPTOMS. 2599: Treatment of
Hypercalcemia *?Mild (<12), Moderate (12-14) or asymptomatic � no emergent
treatment. Avoid diuretics/lithium and give hydration to ensure hemoconcentration
does not occur. Initiation of bisphosphonates helps slow osteoclastic activity and
decrease risk of pathologic. Classically due to bone lesions from metastatic
cancer. *?Severe (>14) or symptomatic (hypercalcemic crisis) � immediately give IV
saline + calcitonin (dilute it out)-->after euvolemic, loop diuretics to aid in
peeing out Ca2+-->Long-term give bisphosphonates to decrease the amount of Ca2+
being introduced to the body through bone resorption. Hyperparathyroidism is a
common cause, especially on tests; so let??s examine how it happens: *?1o �
typically parathyroid adenoma (one dominant thyroid gland with other atrophy) o
Constitutional PTH overproduction; kidney responds to it o Hyper-calcemia, hypo-
phosphatemia, high PTH*?2o � hypocalcemia or low Vit.D; classically from end-stage
renal failure; parathyroid glands are normal sizedo PTH overproduction via
physiologic response to low Ca2+; kidney responds poorly o Normal/hypo-calcemia &
hyper-phosphatemia, high PTH *?3o � long-standing renal failure resulting in
constitutional parathyroid hyperplasia with symptoms present after with renal
transplant to correct the problem o Parathyroids got so ripped during time of
secondary hyperparathyroidism, they can??t stop pumping out PTH...so the underlying
cause is fixed, but parathyroids are still crushing it o Hyper-calcemia, hypo-
phosphatemia, low PTH 2176/4304: Primary Hyperparathyroidism*?Presentation:
typically, asymptomatic, but may present with fatigue, constipation, abdominal
pain, renal stones, bone pain, or neuropsychiatric symptomso ??Stones, bones,
groans, psychiatric overtones?? -->?Hypercalciuria (renal stones), bone pain
(resorption of calcium from bone), nausea/vomiting/constipation/pain (intense
absorption) and confusion/depression/psychosis/sleep disturbance/memory
impairment/stupor/coma (often represents hypercalcemic crisis!) o Typically found
in post-menopausal womeno Labs: hypercalcemia, low phosphate elevated
PTH, elevated chlorine, elevated urinary calcium excretion ??Serum Cl:Phos ratio
of >33 is suggestive of hyperparathyroidism (PTH causes excretion of bicarb and
phosphate alongside resorption of chloride and calcium) ??DEXA scan may show
osteopenia/osteoporosiso MEN1a (menin mutation) or PRAD1 mutation is associated
with parathyroid adenoma! Note that MEN1a will likely cause all 4 parathyroids to
be mutated and possibly abnormal * *?�Physiology: PTH causes excessive Vit D
activation, leading to renal calcium resorption, GI absorption, and bone breakdown
* *?�Etiology: parathyroid adenoma (or other tumor), parathyroid hyperplasia * *?
�Dx: diagnostic labs with clinical picture o Sestamibi scan (99-m Technetium) �
radioactive scan that can show abnormal parathyroid activity. May also by take up
by thyroid gland, obscuring parathyroid localization. o Ultrasound may also be used
to localize parathyroid adenomas *?Tx: o Medical � bisphosphonates used to decrease
response to PTH in the bones with regular monitoring of electrolyte levels and DEXA
scanning o Surgical - parathyroidectomy if symptomatic (osteoporosis, renal
manifestations), age <50, extremely high serum (>1mg/dL) or urine (>400g) calcium,
BMD with T-score of -2.5 at any site. Or if patient cannot undergo surveillance
* ??�May be removal of adenoma (if present) or if 4-gland hyperplasia, removal of
3.5 glands with the last 0.5 of a gland implanted into the arm or SCM. If patient
develops high PTH again, doing surgery again is less risky in those implantation
spots * ??�Note that even if localizing scans are negative, surgery can still be
considered with high suspicion * ??�Complications � hematoma, hoarseness (recurrent
laryngeal), perioral numbness, or tingling in the fingers (hypocalcemia) * ??�If
post-op hypocalcemia: Ca2+ supplementation post-op & hospitalization to monitor
2165: Familial Hypocalciuric Hypercalcemia *?Benign, autosomal dominant mutation in
the calcium-sensing receptor (CaS-R) of the parathyroid glands. This causes
increased elevation of serum Ca2+ to activate them to stop PTH secretion. This
results in increased Ca2+ resorption in the renal tubules o Differentiated from
primary hyperparathyroidism by calcium urine excretion *?Presentation: asymptomatic
with normal renal function o Labs: hypercalcemia with low urine calcium excretion
(<100mg/24hr) *?Dx/Tx: lab abnormalities, no treatment needed in the absence of
symptoms 4307: Hyperthyroid Bone Disease * *?�Excess thyroid gland activity
sitmulate osteoclastic acivity, thus causing bone resorbtion. The resulting
hypercalcemia inhibits PTH production ultimately leading to hypercalciuria and net
calcium wasting. * *?�Brittle bones, tenendcy toward bone fracture, and decreased
bone density are all possible problems! * *?�Note that a hot nodule (functional,
likely toxic goiter) is nearly NEVER NEOPLASTIC, as it??s an area of isolated
hyperacitivty/hypertrophy. A cold nodule is an area of low activity but growth,
which is high suspicious of thyroid cancer. 3083: Milk-Alkalai syndrome o *?�Occurs
due to over-supplementation with calcium and absorbable alkalai. Essentially you
take too much result in renal vasoconstriction, decrease in GFR, Na/K/2Cl
inhibition (diuresis) o *?�Presentation: N/V, constipation, polyuria/polydipsia,
AKI, suppressed PTH in the setting of calcium supplementation (this patient was
taking supplements for osteoporosis) o Labs: hypercalcemia, hypomagnesiemia,
hypophosphatemia, metabolic alkalosis * *?�Dx: clinical presentation * *?�Tx:
discontinue supplementation with IV fluids/furosemide to flush out the kidneys
Hyperthyroidism-Jaw Tumor syndrome o *?�Odd genetic condition that predisposes
patients to parathyroid carcinoma + fibroma of the jaw o *?�May be predisposed to
other cancers 8876: Hypocalcemia *?Presentation: fatigue and weakness; may
classically occur after parathyroidectomy to treat hypercalcemiao Labs: low Ca2+o
Chvostek??s sign � facial twitch in response to tapping the facial nerve (early
tetany sign due to hypersensitivity of neurons)o Trousseau??s sign � flexion of
fingers/wrist in response to inflation of a blood pressure cuff *?Dx:o Low
magnesium? Drugs that cause hypoCa? Recent Blood transfusion?-->correct it if yes.
o If no, measure PTH level??Low/normal PTH � surgical damage to parathyroids,
autoimmune destruction of parathyroids, or some infiltrative disease (Wilson??s,
hemochromatosis, etc.)??High PTH � Vit D deficiency (check 25-Vit D levels), CKD,
sepsis, tumor lysis syndrome Chapter 10: Intermittent Episodes of Sweating,
Palpitations, and Hypertension 3976: Pheochromocytoma *?Neuroendocrine tumor of
chromaffin cells producing catacholamines (typically Epi/Noreepi) o Association
with MEN2a/MEN2b, Neurofibromatosis type 1, and von-Hippel-Lindau *?
Presentation: ??pressure (episodic OR constant hypertension), palpitations,
perspiration, pallor, pain (headache)??, classically with increase intraabdominal
pressure (urination, palpation, positional change) or anesthesia/surgery (may
present with intra-operative crisis!) o Constant HTN = catecholamines are
slowly/constantly releasedo Episodic HTN = catecholamines are released in bursts
with elevated intra-abdominal pressure o May rarely produce dopamine which does NOT
present with hypertension, but instead shows water diarrhea as the major symptom
due to gastric hyper-motility o Labs ??Elevated hematocrit (constant a-activity or
EPO production) and hyperglycemia (constant a-activity) are common lab
abnormalities *?Anatomyo Adrenal medulla > abdomen > bladder/prostate > thorax >
head/necko Commonly, abdominal pheo occur in the para-aortic Organ of Zuckerkandl
explaining an alternative name for the tumor of ??para-gangliomas??o These tumors
theoretically can occur anywhere along the sympathetic nervous system *?
Pathophysiologyo Norepinephrine/Epi will stimulate all of the following receptors
??a1 receptors � smooth muscle contractions, gluconeogenesis/glycogenolysis ??a2
receptors � smooth muscle contraction, platelet aggregation??B1 receptors �
increasing heart rate/contractility, sweat gland activation??B2 receptors � smooth
muscle relaxation o Note that norepinephrine is produced predominantly, as N-
methyltranferase (converts norepi -->epi) isn??t always very present in tissues
where the pheochromocytoma pops up o The adrenals are a common place for pheo
because norepi production is dependent on glucocorticoids...which are produced in
high concentrations in the adrenals *?Imaging: CT or MRI abdomen/pelvis with
contrasto Nuclear imaging (I131-MIBG or 18F-DOPA PET/CT) can be used for better
imaging & localization of other areas of neoplastic growth*?Dx: 24hr urine
metanephrines (>x2 normal limit) +/- imaging of mass o Biopsy is NOT advised as it
can set off a hypertensive episodeo Note that b-blockers, decongestants,
antidepressants, and antipsychotics can all cause false elevation of catecholamines
and should be discontinued 2 weeks prior to testing o Plasma chromogranin A may be
a useful adjunctive testo Metanephrines = metanephrine, normetanephrine, and
vanillylmandelic acid *?Tx: pre-treatment of phenoxybenzamine and surgical removalo
Must give a-blockers for 10-14 days before surgical removal (phenoxybenzamine)o
Beta blockers alone will cause hypertensive crisis (Epi/noreepi activate a-
receptors)o In a patient with multiple tumors (like MEN2), the pheochromocytoma is
taken care of first! *?Follow-up:o Pts should always be referred to genetic
counselling with testing after surgical resectiono Catecholamine levels should be
measured 2 weeks post-surgery to measure success; then every 3 months for the first
year, then every 1 yearo Complications include hypertension (residual disease),
hypotension (residual a-blockade, loss of catecholamines), hypoglycemia, and
arrhythmia 3587/3520/2630/3494: Multiple Endocrine Neoplasia (MEN) *?MEN1: o
Primary Hyperparathyroidism (hypercalcemia, high urine calcium, high PTH)o
Enteropancreatic tumors (most commonly gastrinoma causing Zollinger-Ellison
syndrome; VIPoma, glucagonoma, and insulinoma all possible)o Pituitary adenomas
(most commonly prolactin secreting) *?MEN2a: RET-protooncogene mutationo Medullary
Thyroid Cancer (parafollicular C-cells, produce calcitonin)o Pheochromocytoma
(elevated plasma metanephrines, episodic hypertensive crises), o Parathyroid
Hyperplasia *?MEN2b: RET-protooncogene mutationo Medullary Thyroid Cancero
Pheochromocytomao Mucosal/cutaneous neuromas, Marfanoid habitus Chapter 11: Neck
Mass that Moves with Swallowing Hyperthyroidism * *?�Signs: progressive
nervousness, difficulty concentrating, palpitations, weight loss, moist skin, fine
resting tremor, dyspnea on exertion, diarrhea, and heat intolerance * *?�Symptoms:
Rapid pulse, elevated BP (systolic > diastolic), and rarely atrial fibrillation
Hypothyroidism *?Signs: lethargy, depressed affect, sluggish mentation,
forgetfulness, weight gain, dry skin, constipation, cold intolerance; may be
confused with depression (women) or dementia (elderly) o 1o hypothyroidism will
show a high TSH but low T3/T4 (poor thyroid function)o 2o hypothyroidism will show
a low TSH -->?TRH administration is used diagnostically ??A normally functioning
pituitary will respond and TSH will rise. If it doesn??t then there??s something
wrong with the pituitary (get imaging of the pituitary) ??If the pituitary responds
then there may be something wrong with the hypothalamus (not making TRH, thus no
TSH production) * *?�Symptoms: low blood pressure, bradycardia, non-pitting edema,
hair loss, dry/cracked skin, slowly relaxing reflexes, and rarely myoedema * *?�Tx:
thyroid hormone replacement (typically 1.7 mcg/kg daily) o Children (use a lot for
growth) and pregnant women (increased TBG) may need increased
doses o Elderly (decreased TBG) may need decreased doseso TSH is regular follow-up
for adequate response 4 weeks after any changes in dose 4324/4588: Evaluation of
Hyperthyroidism*?Any suspicion of thyroid problems should begin with TSH/T4 lab
values o TSH low/T4 normal with signs of hyperthyroid -->?measure T3??Normal T3--
>subclinical hypothyroid, early pregnancy, non-thyroid problem ??High T3-->If signs
of Grave??s disease, it??s Grave??s disease. If no signs, do a Radioactive Iodine
Uptake (RAIU) scan o TSH low/T4 high with signs of hyperthyroid -->?consider
primary hyperthyroidism ??If signs of Grave??s Disease, then you??re good; if not
then RAIU scan o TSH normal - high/T4 high with signs of hyperthyroid -->?consider
secondary hyperthyroidism ??MRI of pituitary for TSH secreting tumor *?Radioactive
Iodine Uptake (RAIU) scan performed when hyperthyroid is considered, but Grave??s
disease is not likely due to symptoms o Low uptake -->?measure thyroglobulin (Tg)
levels??Low Tg-->likely exogenous use of thyroid hormone??High Tg-->thyroiditis,
extra-glandular production, or iodide exposure o High uptake diffuse -->?Grave??s
diseaseo High uptake nodular -->?Toxic adenoma, or multinodular goiter 4324:
Central Hyperthyroidism (TSH secreting adenoma) * *?�Presentation: signs of
hyperthyroidism (weight loss, tachycardia, palpitations, etc) with tumor mass
effect signs (headache, visual symptoms, impaired secretion of other pituitary
hormones) * *?�Dx: TSH high with high T4 & MRI showing mass location * *?�Tx:
surgical excision or ablation 4415/3488/4726/4132/2179: Grave??s Disease *?
Presentation: hyperthyroidism, exophthalmos, diffusely enlarged thyroid gland o Low
TSH with high T3 or T4 * *?�Dx: clinical picture with confirmed TSH receptor-
antibodies * *?�Tx: three major options o Radioiodine ablation � basically goes in
and destroys the thyroid gland cells. Apparently the point of this treatment is to
become euthyroid and complete destruction is NOT intended. However, pts very often
have the side-effect of hypothyroidism. * ??�Initial worsening of
symptoms/exophthalmos (10%) in first week or so due to release of stored thyroid
hormone from cell destruction. Often OK in young, healthy pts. * ??�Pre-treatment
with glucocorticoids often minimizes treatment symptoms * ??�Hypothyroidism (80%)
may develop, and is most likely in Grave??s Disease as the entire thyroid gland is
dysfunctional, instead of just part. o Surgery � removal of the thyroid is always
on the table ??Risk of damage to recurrent laryngeal nerve or hypoparathyroidism
due to damage or unintentional removal of parathyroids o Propylthiouracil (PTU) or
methimazole (MMA) � thioamides that block production of T3/T4 * ??�MMA a teratogen
in the 1st trimester, may cause cholestasis * ??�PTU can cause hepatic failure,
ANCA-associated vasculitis, and agranulocytosis * ??�Does not permanently cure
disease. Typically used in pts that cannot tolerate other treatments (old people
that cannot handle worsening symptoms or surgery) 2178/3487: The life-threatening
side-effect of Propylthiouracil/Methimazole is agranulocytosis (0.3%). This
classically presents with fever and sore throat within 90 days of treatment
initiation. Should this occur: 1. Stop PTU/MMA immediately and check WBC levels. 1.
WBC >1,500 � PTU isn??t causing the problem 2. WBC <1000 � PTU should be
discontinued for life 2. Get throat culture, give oral penicillin/acetaminophen,
administer broad spectrum antibiotics before even knowing the result as lack of
immune response could be fatal. Pseudomonas is especially worrysome in these
patients 3952: Thyrotoxicosis can largely affect the heart causing changes in
rhythm (atrial fibrillation, PACs/PVCs, and sinus tachy), hemodynamics (increased
CO-->systolic HTN and increased myocardial O2 demand), heart failure, and angina.
4307: Hyperthyroid Bone Disease * *?�Excess thyroid gland activity stimulate
osteoclast activity, thus causing bone resorption. The resulting hypercalcemia
inhibits PTH production ultimately leading to hypercalciuria and net calcium
wasting. * *?�Brittle bones, tendency toward bone fracture, and decreased bone
density are all possible problems! * *?�Note that a hot nodule (functional, likely
toxic goiter) is nearly NEVER NEOPLASTIC, as it??s an area of isolated
hyperacitivty/hypertrophy. A cold nodule is an area of low activity but growth,
which is high suspicious of thyroid cancer. 4286/10958/11277: Thyroid Storm *?
Presentation: high fever, cardio (tachycardia, HTN, CHF, atrial fibrillation), CNS
(agitation, delirium, coma), hyperthyroid (goiter, lid lag, tremor), GI (nausea,
vomiting, diarrhea, jaundice)o Typically caused by: thyroid/non-thyroid surgery,
acute illness, childbirth, or acute iodine load (such as in IV contrast!)o Most
common cause of death is high output cardiac failure (often post-op patients with
undiagnosed Graves?? disease) * *?�Dx: clinical presentation with precipitating
factor * *?�Tx: propranolol (decrease adrenergic effects), propylthiouracil
(decrease thyroid hormone production), glucocorticoids (suppress TRH/T3-->T4
conversion), and ID trigger to treat/remove 3483: Metabolic changes in
hypothyroidism include hyperlipidemia (decrease in LDL receptors), hyponatremia,
and asymptomatic elevations of CK (>10x normal). o *?�Note that hyperlipidemia may
persist for months despite adequate replacement therapy o *?�Statins will increase
the chance of hypothyroid myopathy, thus are used with caution 3878/4382:
Hypothyroid Myopathy *?Presentation: normal hypothyroidism signs with elevated CK
(mild) to rhabdomyolysis/polymyositis o CK elevation can be present years before
clinical signs of hypothyroidism o Typically, normal reflexes*?Dx: any pt with
unexplained elevated CK/myositis should have TSH/T4 checked as this may be the
manifestations of hypothyroidism early on.o If normal, then muscle biopsy should be
considered *?Tx: treat underlying cause 4154: Oddly enough, oral estrogen
replacement therapy will increase Thyroid Binding Globulin (TBG) levels due to
decreased breakdown of TBG in the liver. * *?�Pts with a normal thyroid function
will make more and compensate without trouble. * *?�Pts on levothyroxine for
hypothyroidism will have to increase the dose (as the TBG increase will mean less
free T4 present). The increased dose will saturate the increased TBG, and restore
euthyroidism. * *?�*transdermal estrogen does not have this effect as it bypasses
the liver 3495: Euthyroid Sick Syndrome (??Low T3 syndrome??)*?Presentation: acute,
severe illness accompanied by abnormal thyroid function tests o Labs: low T3 with
normal T4 and TSHo Result of of decreased deiodination of T4 from caloric
deprivation, glucocorticoids, and acute phase reactants * *?�Dx: typically thought
to be hypothyroidism, but often thyroid levels are unreliable in acute illness * *?
�Tx: treatment of underlying disease should resolve the abnormal tests 3496:
Thyroiditis Hashimoto??s Thyroiditis o *?�Presentation: predominantly hypothyroid
symptoms with non-tender diffuse goiter o *?�Dx: Anti-thyroid peroxidase (TPO) or
anti-thyroglobulin antibodies in high-titer o Note that nearly 10% of the normal
population is (+) for anti-TPO antibodies o The most common cause of hypothyroidism
is the USA Silent (painless) Thyroiditis * *?�Presentation: variant of Hashimoto??s
with a mild, brief hyperthyroid phase (destruction and release of T3/T4), with a
small, non-tender goiter and slowly going back to euthyroid * *?�Dx: Anti-TPO
antibodies and low radio-iodine uptake Subacute (DeQuervain??s) thyroiditis o *?
�Presentation: post-viral inflammatory disease causing prominent fever /
hyperthyroidism with painful/tender goiter o *?�Dx: presentation with elevated
ESR/CRP and low radioiodine uptake 2191: Struma Ovarii *?Rare thyroid hormone
producing ovarian teratoma. Classically in women over age 40 with pelvic mass,
ascites, and abdominal pain 4318: Toxic Adenoma * *?�Presentation: thyrotoxicosis
with single hot thyroid nodule on exam * *?�Dx: demonstration of single, hot nodule
on radioactive iodine scan o Note that toxic multinodular goiter would have a
patchy distribution on RAIU scan *?Tx: ablation or removal Evaluation of a Thyroid
Mass * *?�Always start with careful H&P and TSH/T4 levels to get your baseline for
thyroid function * *?�Imaging: bedside ultrasound (characterize mass, lymph nodes,
and guide FNA) o If signs of malignancy -->?consider cross-sectional CT or MRIo
Nuclear imaging (I123 RAIU scan) may be useful to differentiate a ??hot?? from ??
cold?? nodule, but apparently aren??t as widely used today; most useful when FNA is
non-diagnostic *?Fine needle aspiration (FNA)o Yes: Nodules >1cm, malignant
ultrasound features (microcalcification, hypoechoic, irregular margins), or with
recent history of growtho Yes: suspicious cervical lymph nodeso No: <1cm, purely
cystic, benign sonographic features *?Interpreting FNA results & Managemento
Malignant -->?total thyroidectomy with possible neck dissectiono Suspicious for
malignancy -->?totally thyroidectomy OR diagnostic thyroid lobectomy o Suspicious
for follicular neoplasm -->?diagnostic thyroid lobectomy ??Simple biopsy is NOT
recommended as you??ll likely not be able to control bleeding, you??ll likely seed
the tumor cells, and lobectomy doesn??t affect thyroid function o Undetermined
significance (AUS/FLUS) -->?Repeat FNA (often benign); if still undetermined,
proceed to diagnostic thyroid lobectomy o Benign -->?annual follow-up +
ultrasonographyo Inadequate -->?Repeat FNA (often benign); if still undetermined,
proceed to diagnostic thyroid lobectomy 3498/3499/3497: Thyroid Malignancy*?
Papillary � arises follicular cells (epithelial), unencapsulated, most common, best
prognosis o Typically
metastasizes to the lymph nodes, but prognosis is based on local invasion presence
o Increased risk from family history and childhood radiation of head/necko FNA
often reveals large cells with pale, grooved nuclei; Often has Psamomma bodieso
Management -->?lobectomy if small (<1cm); total thyroidecetomy if large, multiple
nodules, high malignancy, family history, or history of ionizing radiation??
Concentrates iodine (thus this may be used therapeutically) *?Follicular - arises
follicular cells (epithelial), encapsulated, decent prognosiso Early hematogenous
spread (lung/brain/bone) and invasion of thyroid capsuleo FNA often shows normal
looking follicular cells. Invasion through capsule/hemotgenous spread is necessary
for diagnosis of carcinoma (vs adenoma), thus surgical diagnosis must be made to
see if invasion outside the capsule occurs (FNA/frozen sections are non-diagnostic)
o May demonstrate Hurthle Cells (large eosinophilic epithelial cells; worse
prognosis!)o Management -->?total thyroidectomy ??Concentrates iodine (thus this
may be used therapeutically) unless it??s a Hurthel cell subtype (these rarely
concentrate iodine) *?Medullary � parafollicular c-cell origin, good prognosis,
produces calcitonin, 80% are sporadic o Associated with MEN2a/MEN2b; screening for
these diseases is recommendedo Typically contains amyloid & commonly spreads to
regional lymph nodeso Symptoms often include diarrhea and flushing due to high
calcitonin levels! o Management -->?total thyroidectomy??Does NOT concentrate
iodine (it??s make of C-cells!!) *?Anaplastic � epithelial origin, rare,
classically in old peopleo Poor prognosis, death within 6 months typicallyo May
involve other adjacent structures (trachea/esophagus/etc.) due to rapidly enlarging
thyroid mass o Management -->?often palliative but can include tumor shrinking
therapies for symptom management. Often early tracheostomy is done as tumor invades
airway! *?Primary Thyroid lymphoma � rare, typically in the setting of Hashimoto??s
thyroiditis o Has rapidly enlarging thyroid gland but good prognosiso Typically
occurs as B-cell non-Hodgkin lymphoma * *?�Metastases to the thyroid � primary
often the kidney, breast, lung, or skin (melanoma) * *?�Fast facts o Note that
because thyroid cancers are often indolent, it can be prudent to wait till after
pregnancy to evaluate and treat the problem in a pregnant woman o The greatest risk
factor for thyroid cancer is exposure to ionizing radiation before age 15. The
developing thyroid gland is very sensitive to mutagenesis. Most common sources are
childhood radiation exposure, lymphoma treatment, and nuclear fallout o Typically,
patient with thyroid carcinoma are euthyroid! o Worrisome sign is that the thyroid
mass does not move on swallowing. This can indicate that the mass has invaded local
tissue and is not moving alongside the thyroidcartilage/lig. of Berry o Frozen
sections are typically NOT useful in evaluating thyroid cancer! Most cancers can be
diagnosed via FNA, and with follicular (FNA won??t work), the frozen section will
only show a few slices...making evaluation of the capsule impossible. o If lymph
nodes are palpable, they should be dissected out with either lateral or central
neck dissection. Frozen section IS helpful when used on suspicious lymph nodes *?
Post-surgical managemento Radioactive iodine ablation-->useful only in tumors that
concentrate iodine, but can reduce recurrenceo Suppressive thyroxine therapy -->?
suppresses TSH, thus suppressing thyroid tissue growth *?Follow-upo Thyroglobulin
and anti-TG antibody tests every 6 monthso If medullary carcinoma -->?serum
calcitonin every 6 months o Neck ultrasound every year *?If recurrence-->labs +
ultrasound eval + RAIU scan Complications of Thyroid Surgery * *?�Recurrent
laryngeal nerve damage � branch of CNX; innervates most larynx muscles below vocal
cords, thus damage results in vocal cord paralysis. Unilateral damage = hoarseness
& aspiration risk; bilateral damage = airway compromise needing tracheostomy * *?
�External branch of superior laryngeal nerve damage � allows speaking/singing in
high pitch; often damage isn??t a big deal unless patient is a singer/voice
professional * *?�Parathyroid glands damage � hypoparathyroidism needing
calcium/calcitrol supplementation * *?�Post-op ??tense?? looking wound � likely
from hematoma and may cause airway compromise. Needs emergent bedside decompression
with return to OR for evacuation/irrigation/hemostasis Chapter 12: Progressively
Hoarse Voice � Laryngeal Cancer Differential for Hoarseness o *?�Viral laryngitis �
acute fever, hoarseness, sore throat, cough or other URI symptoms (most common) o
*?�Vocal Cord Paralysis � hoarseness with breathy voice & no other obvious signs;
typically idiopathic or iatrogenic (recurrent laryngeal nerve damage) o *?�Vocal
cord nodules/polyps/cysts � often due to damage to vocal cords
(singing/screaming/intubation) o *?�HPV of the vocal cords � unfortunate but
totally possible (typically HPV 6 or 11) o *?�Spasmodic dysphonia or Parkinson??s
Disease � often more ??vocal tremor?? but may sound hoarse o *?�Laryngeal Cancer �
often hoarseness in older person, Hx of smoking, +/- lymphadenopathy Presentation *
*?�Hoarseness, Hx of tobacco/alcohol use, hemoptysis, possibly cancer ??B signs??
(weight loss, etc.) * *?�Characterizing ??hoarseness?? o Breathy � incomplete
closure of vocal cords causing excess air to escape when phonating. Often the
result of one vocal cord being dysfunctional o Aphonia � inability to phonate due
to lack of airflow, can be from locked-in abduction, swelling (causes stiffening so
they can??t move), or irregularities of the vocal cords stopping vibration o
Strained � narrowed vocal cords like forced adduction or mass causing narrowing o
Tremulous � neurologic disorder causing abnormal vibration (Parkinsons, spasmotic
dysphonia) *?Note the most common type of laryngeal cancer is squamous cell
carcinoma (remember how it??s mucosal tissue encountering a noxious stimulus,
causing metaplasia-->neoplasia? The mucosal cells want to become squamous cells as
squames are more durable against damage) *?The most common site of malignant
laryngeal lesions is the glottis Pathophysiology * *?�Superior laryngeal nerve �
branch of CNX with sensory (supraglottis) and motor (inferior constrictors,
cricothyroid muscles) functions * *?�Recurrent laryngeal nerve � branch of CNX with
sensory (glottis and subglottis) and motor (all intrinsic laryngeal muscles save
cricothyroid) functions Work-up * *?�You should consult an ENT when hoarseness
lasts >3-4wk (viral laryngitis rarely lasts >2wk) * *?�Typically, if hoarseness in
not self-limited, then Flexible laryngoscopy is undergone o Here, the vocal cords
and other structure can be visualized in a minimally invasive way*?If Laryngeal
cancer is suspected on flexible larngyscopy -->?intraoperative direct layngoscopy
and biopsy is needed to histologically characterize the lesiono If cancer, TNM
staging is done and therapy is based on early or late stagingo CXR is routinely
done to search for lung metso CT neck is often done for late-stage cancers to
search for metastatic lymph nodes Management * *?�Early stage (TNM I or II) �
surgical resection of tumor OR radiation of tumor; both with good outcomes * *?
�Late Stage (TNM III or IV) � any two or all three of
surgery/radiation/chemotherapy are used * *?�Note that the goal of treatment is
preservation of the larynx * *?�Note that the larynx is the narrowest part of the
human airway. A mass may very easily compromise the airway and emergent airway
management with tracheostomy may be necessary at any time! Chapter 13: Lump on Neck
Increasing in Size � Head and Neck Cancer Differential for ??Lump on Neck?? � ??
KITTENS?? o *?�K � Congenital � thyroglossal duct cyst, branchial cleft cyst,
dermoid cyst, laryngocele, thymic cyst o *?�I � Infection/Inflammation � abscess,
lymphadenitits, TB, toxo, cat scratch disease, antinomycosis o *?�T � toxin �
metals/drugs (esp. cigarette smoking) o *?�T � trauma � hematoma, foreign body,
aneurysm o *?�E � endocrine � thyroid hyperplasia/tumor, ectopic thyroid gland o *?
�N � neoplastic � (any kind) o *?�S � systemic � AIDS (lymphadenopathy) or Kawasaki
disease Salivary Gland Tumors *?Most frequent site is parotid glands, but may occur
in any salivary gland *?Subtypes o Pleomorphic adenoma (mixed tumor) � most common
benign tumoro Papillary cystadenoma (Warthin??s tumor) � 2nd most common benign
tumor o Mucoepidermoid carcinoma � most common malignant tumoro Adenoid cystic
carcinoma � 2nd most common malignant tumor Head and Neck Abscesses * *?
�Peritonsilar � typically occurs in older children (fever, odynophagia, trismus);
should be aspirated through the tonsillar bed for drainage * *?�Retropharyngeal �
typically occurs in younger children (fever, odynophagia, drooling, airway
obstruction); should be treated with intubation and drainage for posterior-
pharyngeal wall * *?�Parapharyngeal � all age groups, esp with dental
infections/tonsillitis; should be drained through the lateral neckRisk Factors
(head & neck cancer) o *?�Male, Age >40, poor dental hygiene, radiation exposure,
African American race o *?�Leukoplakia and Erythroplakia are pre-malignant lesions
Quick Facts * *?�Note that Virchow??s Node (left supraclavicular node) may appear
in metastatic head & neck cancer; it always appears on the left side due to the
cisterna chyli (dilated lymph sac) being at the base of the thoracic duct * *?�The
oral cavity is the most common site of head & neck cancer followed by larynx, &
pharynx * *?�Note that a new neck mass represents metastatic spread until proven
otherwise (85% of tumors) * *?�Most common type of head and neck cancer is squamous
cell carcinoma
(90%) Pathology *?Typically the upper aerodigestive tract (pulmonary +
mouth/oropharynx/etc.) is constantly exposed to carcinogens (food, smoke, etc.);
this constant regular exposure can produce a grossly normal appearing organ with a
field of interspersed cancerous cells that have acquired mutations (field
cancerization) Symptoms * *?�Otalgia (ear pain) � due to nerve compression of CN IX
(Jacobson??s branch), CN X (Arnold??s branch), or CN V3 (supplies external auditory
ear canal) * *?�Dysphagia (difficult swallowing) � physical compression of
esophagus or interference with swallow mechanism due to nerve compression * *?
�Odynophagia (painful swallowing) � tumor-related inflammation can cause irritation
* *?�Dysphonia (difficulty speaking) � lesion on vocal cords or nerve paralysis *
*?�Trismus (difficulty opening mouth) � pterygoid muscle invasion * *?�Stridor
(high pitched breath sounds) � airway compression/invasion narrowing the airway *
*?�Hemoptysis (bloody sputum) � tumor ulceration in upper airway or lower airway
tissue destruction Workup * *?�An enlarged cervical lymph node can be observed: if
1the patient has red flag symptoms (listed above) and 2has had the enlarged node of
less than 3 weeks. When encountering these patients, schedule follow-up in 3 weeks;
if persistent, then further investigation is needed. * *?�If node is suspected to
be due to metastatic head/neck cancer o Imaging (CT of head/neck with contrast +
CXR) are used to look for primary tumor and any further signs of metastases; can
also allow for staging ??If initial imaging does not show primary tumor in the head
and neck-->CT chest (it may be lung cancer) ??Whole body PET may be useful for
finding mets, but is controversialo Labs (CBC, Coags, LFTs, CMP with renal
function, TSH) are to gain baseline info o FNA is done as soon as possible to gain
histologic diagnosis. ??If initial FNA, FNA with ultrasound should be performedo In
addition to the physical exam, flexible nasopharngoscopy is used when a suspected
metastatic lymph node is detected to help find the primary tumor site*?If the above
fail to show primary tumor site panendoscopy (triple endoscopy) is done o
Laryngoscopy, esophagoscopy, and bronchoscopy under general anesthesia to find
primary o Allows for visualization of primary and biopsy of primary tumor*?If the
above fail an open neck biopsy should be performed and the frozen section is
examined o It??s hard to control bleeding in the head/neck and open biopsy risks
the chance of tumor seeding. It??s advised to use these as a final diagnostic
technique o Note is squamous cell carcinoma is found, an immediate open neck
dissection for removal of malignant tissue to minimize seeing of tumor cells from
biopsy site Management*?Tailored to specific cancer type; you??d hand the reigns
over to oncology here. Chapter 14: Aural Fullness, Hearing Loss, and Tinnitus
Differential for Childhood Hearing Loss * *?�Acute otitis Media (AOM) � discussed
below * *?�Otitis Media with Effusion � discussed below * *?�Chronic Otitis Media �
often recurrent bouts of AOM result in TM damage/perforation/otorrhea * *?
�Cholesteatoma � formation of yellow-ish mass of keratinized, desqamated epithelium
in middle ear. Often the result of Eustachian tube dysfunction or COM * *?
�Labyrinthitis � often viral with vertigo, gait instability, N/V, hearing loss, and
nystagmus * *?�Otitis externa � discussed below * *?�Congenital hearing loss
(hereditary, acquired like TORCH infections) * *?�Cerumen impaction/foreign body,
or trauma causing damage to ear � most typically presenting with unilateral
fullness/ear pain/hearing loss Additional Differential in Adult with Hearing Loss o
*?�Exposure to loud noises over the years o *?�Drugs � aminoglycosides, aspirin,
loop diuretics, or cisplatin are all known to cause hearing loss o *?�Tumors �
vestibular schwannoma (CNVIII involvement) o *?�Meniere??s disease � hearing loss,
vertigo, ??fullness?? of the ear, tinnitus Note that sudden deafness is associated
with viral infections (often herpes viruses); mainstay of Tx is steroids and
antivirals Testing for Hearing Loss *?Conductive - sound waves of 512Hz fork cannot
vibrate the basilar membrane of the cochlea properly o Rinne: abnormal (bone > air)
o Weber: localizes to the affected ear o Causes: * ??�Ear wax/foreign object -
soundwaves can??t get to the eardrum; removal fixes problem * ??�Tympanic membrane
perforation - can??t vibrate! May be fixed surgically * ??�Otitis media w/ effusion
- fluid in middle ear dampens vibrations * ??�Otosclerosis - overgrowth of staples
bone, causing stiffening/sound transmission failure * ??�Cholesteatoma - overgrowth
of keratin debris within the middle ear space; may erode ossicles/mastoid air cells
*?Sensorineural - neural transmission interrupted either from failure of 2o sound
waves or nerves o Rinne: normal (air > bone)o Weber: localizes to the unaffected
ear o Causes: ??Cochlear/CNVIII disorders or damage??Prebyacusis - general.
Progressive loss of high frequency hearing with aging ??Viral infection - Measels,
Mumps, Rubella, CMV, HIV??Ototoxic drugs??Meniere??s disease or vestibular
schwannomas (discussed below) *?Noise-Induced - damage to the hair cells
w/stereocilia in the organ of Cortio Isolated high frequency hearing (around
4000Hz) lost first; may progress if damage continues o Eardrum perforation may
occur with sudden, extremely loud noises Acute Otitis Media (AOM)*?Presentation:
ear pain, fever, and sometimes URI symptoms with duration <3wk o Tympanic membrane:
immobile without air-fluid levels, opaque, bulging/??full??, redness *?Dx: clinical
presentation *?Tx: similar to OME 2839: Otitis Media with Effusion (OME or Serous
Otitis Media) *?Epidemiology o Most commonly occurs between ages 2-6yr & is pretty
rare in adultso Risk factors: male, African American, cigarette exposure, low birth
weight, low SES, lack of breastfeeding during infancy, supine feeding positiono The
most common middle ear pathology in HIV/AIDS due to lymphadenopathy obstructing the
Eustachian tube; also common caused by cancer obstruction of Eustachian tube in
adults *?Pathophysiology o AOM and Eustachian Tube Dysfunction are the two major
causes of OME as fluid persists within the ear canal leading to bacterial growth
and chronic inflammation o Normal function of the Eustachian tube is to allow for
pressure equalization & drainage in the middle ear to the throat. ??Children <6yr
have shorter/flimsier tubes, thus the chance for dysfunction and failure of the
tube causing OME is more common o Micro: typically, viral (URI pathogens) but may
become bacterial (superimposed)*?Presentation: Middle ear effusion resulting in
conductive hearing loss without infectious symptoms. o Tympanic membrane: immobile
with air-fluid levels, opaque, but no bulging/rednesso Language regression or
language developmental delay are also common presentations. Classic is an infant
who stops babbling or a child with poor speech skills and trouble in schoolo
Otorrhea is suggestive of TM perforation and should be evaluated seriously!o
Tympanosclerosis can result in permanent conductive hearing loss due to
inflammation o Complications (rare) � mastoiditis, meningitis, brain abscess,
subdural empyema * *?�Dx: clinical presentation, ear swab/culture, pneumatic
otoscopy * *?�Tx: often resolves spontaneously within 3 months o Autoinflation �
pinching the nose and gentle blowing out to raise pressure and drain the middle
ear. Can be used to speed spontaneous resolution o Antibiotics � only 33% of these
are bacterial; thus it??s not routinely recommended??While steroids/antibiotics
give short-term benefits, antihistamines and decongestants are not usefulo
Tympanostomy Tubes � little tubes to allow the Eustachian tube to remain patient.
Typically reserved for pts with 1hearing impairment, 2significant symptom impact on
quality of life, 3recurrent disease, or 4children at risk (Down??s syndrome, etc.)
Otitis Externa (Swimmer??s Ear)*?Presentation: ear pain/itching worse with
manipulation, sometimes with inflamed/swollen external ear canal with drainage and
discharge. Tympanic membrane typically appears normal.o Classically occurs after
warm water exposure or instrumentation in the ear canalo Micro: Staph, Strep, and
rarely Pseudomonas (swimmer??s ear; most common in diabetics) * *?�Dx: clinical
presentation * *?�Tx: irrigation, debridement, and antibiotics (IV for 4-6wk if
bones involved) 2828: Malignant (necrotizing) Otitis Externa *?Presentation:
intense, unrelenting ear pain that??s worse at night. Purulent drainage/feeling of
fullness that does not respond to topical medication. Ear canal shows granulation
tissue/edema. May progress to osteomyelitis of the skull base with cranial nerve
involvement (facial droop) or TMJ involvement (pain worsened by chewing) o
Associated with poorly controlled diabetes/immunosuppression in elderly patients o
Typically caused by Pseudomonas Aeruginosa (classic in diabetics) * *?�Dx: clinical
presentation with swab/culture and CT/MRI evidence of infection * *?�Tx: IV
ciprofloxacin (first line) o Fluoroquinolone resistant: other IV anti-pseudomonals
(Pip-tazo/cefepime/ceftazidime) o Failure to respond to Abx: surgical
debridement/biopsy to exclude cancer Chapter 15: Post-Prandial RUQ Pain � Biliary
Colic and Gallstone DiseaseRisk Factors for Developing Gallstones (Classic the the
4Fs � Fat, Female, 40, fertile) * *?�Obesity � decreases bile salts (unknown mech)
leading to formation of cholesterol supersaturation * *?�Crohn??s Disease/Terminal
ileum resection � bile salt loss in the inflamed/resected bowels leads to
cholesterol supersaturation * *?�Female Gender/Pregnancy/OCPs � estrogen increases
cholesterol secretion into the biliary system and
progesterone slows gallbladder emptying. Thus, these two together can cause
cholesterol super- saturation and stasis, resulting in cholesterol stones! * *?
�Total Parenteral Nutrition � without protein/nutrients entering the duodenum,
secretin (which could cause gallbladder contraction) is not released and
gallbladder stasis can result in it??s contents to coalesce into stones! * *?
�Partial/Full Bowel resection � results in a decreased ability to absorb/recycle
bile acids. This can occur to a point where the cholesterol:bile acid ratio
increases to the point of cholesterol super-saturation! * *?�Hemolytic anemia � the
huge amount of heme released from massive RBC destruction results in huge amount of
bilirubin to be conjugated in the liver and sent into the bile (heme-->bilirubin).
Thus bilirubin can become super saturated causing pigmented gallstones. Physiology
* *?�Remember that fatty foods trigger release of Cholecystokinin (CCK) trigger
gallbladder contraction. When this contraction occurs, gallstones are pushed into
the biliary duct, causing gallbladder obstruction/distention/compression of
capillaries/ischemia/inflammation * *?�The three main components in bile are bile
salts, cholesterol, and lecithin; water, electrolytes, proteins, pigment, and
bacteria are all present as well * *?�Types of Gallstones o Cholesterol: most
common in USA & form when cholesterol cannot be properly dissolved by bile
salts/lecithin (too much cholesterol or not enough bile salts/lecithin)o Black
stones: pigmented stones associated with hemolytic disease (high amounts of
unconjugated bilirubin isn??t dissolved well). Found within the gallbladder.o Brown
stones: larger/softer/found in ducts; bacteria/parasites cause these; common in
Asia Micro: E.coli, Bacteroides fragilis, Klebsiella, Enterobacter, Enterococcus,
and Pseudomonas spp Note that asymptomatic gallstones should not be treated 4433:
Biliary colic (Symptomatic Cholelithiasis)*?Presentation: post-prandial RUQ pain
with tenderness to palpation, shoulder/subscapular pain (referred pain),
nausea/vomiting with resolution within 4-6hr after onseto Occurs due to gallbladder
contraction in response to fat in meal. Classically a gallstone gets stuck in the
cystic duct, causing the pain. Resolution is with gallbladder relaxation.o NO
fever, leukocytosis, changes to vitals, and Murphey??s sign (-)o Classic question
of ??what??s a better term?? due to the fact that colicky pain waxes and wanes
during it??s course, when this pain is constant but resolves. *?Dx: RUQ ultrasound
showing gallstones without other signs *?Tx: symptomatic treatment or
cholecystectomy 2904: Acute Cholecystitis*?Presentation: RUQ pain after a fatty
meal, referred pain to the shoulder, Murphey??s sign (halt on inspiration with
palpation of gallbladder), fever, nausea/vomiting, leukocytosiso 90% are caused by
gallstone impaction in the cystic duct-->uncomplicated, causes mild elevations of
LFTs/bilirubino If gallstone goes into the common bile duct -->?complicated,
icterus & very high Alk.phos o Gangrene, perforation, abscess, or peritonitis may
be complications *?Dx: RUQ ultrasound showing stones, fluid surrounding the
gallbladder, gallbladder wall thickening (>4 mm), and possible dilation of the
common bile duct (CBD) o Normal CBD � 4-5mm which increases 1mm every decade after
40yro CBD of >6mm nearly always abnormally dilatedo Emphysematous Cholecystitis �
air in gallbladder wall due to necrosis from Clostridia spp. *?Tx: hospital
admission -->?NPO/IV fluids/IV Abx (gram -) -->?laparoscopic cholecystectomy within
48hr 2978: Acute Cholangitis * *?�Biliary stasis due to any number of reasons
(commonly gallstone obstruction, malignancy, bile duct stenosis) but all of them
cause backup. The fear is that disruption of the blood-bile barrier could allow for
dissemination of bacteria/toxins * *?�Presentation: [fever, jaundice, RUQ pain],
[confusion, hypotension] (Charcot triad, Reynold??s pentad) o Labs: neutrophilia,
elevated alk.phos/GGT/AST/ALT/direct bilirubin * *?�Dx: presentation/labs with
biliary dilatation (ultrasound FIRST, then CT if not diagnostic) * *?�Tx: [ERCP
with sphincterotomy or percutaneous transhepatic cholangiography] + broad spectrum
antibiotics 3732: Porcelain Gallbladder *?Characteristic pathologic deposition of
Calcium salts intra-luminally in the gallbladder; often occurs due to chronic
irritation/inflammation from gallstoneso Appears with a ??bluish?? color and ??
brittle?? consistency on gross specimen o Increased risk of gallbladder
adenocarcinoma *?Presentation: RUQ pain with firm, non-tender RUQ masso CXR/CT:
hyper-dense rim-like calcification on the gallbladder * *?�Dx: imaging studies with
characteristic findings * *?�Tx: cholecystectomy (esp. if symptomatic) 2946:
Acalculous Cholecystitis * *?�Acute inflammation of the gallbladder WITHOUT
gallstones typically in critically ill, hospitalized pts resulting in cholestasis
or ischemia-->distention, necrosis, 2o infection of gallbladder * *?�Predisposing
factors: recent surgery, severe trauma, extensive burns, sepsis/shock, prolonged
fasting/TPN, mechanical intubation o Thought to be due to biliary stasis (NPO
status) and ischemia (hypovolemia/shock) *?Presentation: unexplained fever,
leukocytosis, RUQ abdominal pain/mass, jaundice, abnormal LFTs o Gallbladder
inflammation may cause gangrene, perforation, or emphysematous cholecystitis
(infection with gas-producing bacteria causing gas in the gallbladder)*?Dx:
Abdominal ultrasound is preferred (thickening and pericholecystic fluid); CT
abdomen or cholescintigraphy (HIDA scan) are more sensitive/specific and can be
used in unclear ultrasound (lack of gallbladder visualization is positive *?Tx:
medical management (abx/anti-inflammatory)-->urgent cholecystectomy (percutaneous,
laproscopic, or open depending on how sick the patient is) 2930: Gallstone
Management * *?�Gallstones without symptoms -->?no treatment necessary, simply
monitor * *?�Gallstones with biliary colic -->?elective laparoscopic
cholecystectomy or ursodeoxycholic acid * *?�Complicated gallstones (acute
cholecystitis, choledocolithiasis, or gallstone pancreatits)-->?cholecystectomy
within 48hr Post-Op for Lap. Chole. *?Common Bile Duct injury � feared complication
of surgery. o Recognition during surgery-->If <50% of duct is damaged, stenting is
acceptable. If >50% damage then a Roux-en-Y hepaticojejunostomy must be done to
place the intestines above the area of damage. o Recognition later -->?abdominal
pain, anorexia, bloating, elevated LFTs often occur. ??Abdominal ultrasound or CT
to search for fluid collection??If yes or LFT elevation-->are they septic? * *?�If
yes then drain fluid then do a HIDA scan * *?�If no then do a HIDA scan??If bile
leak or no bile flow to duodenum-->ERCP to find major problem for fixing 2943:
Post-cholecystectomy syndrome *?Presentation: persistent
pain/dyspepsia/nausea/vomiting/pruritis following cholecystectomy o Can occur
immediately months, or even years post-operativelyo The pain ??never went
away??, ??is new after surgery??, or ??has come back!??o Caused by biliary
(retained stone/sludge/etc, inflammation, dyskinesia) or extra-biliary (PUD,
pancreatitis, coronary artery disease, etc.) * *?�Dx: imaging (endoscopic
ultrasound, endoscopic retrograde cholangiopancreaticography [ERCP], or MRI
cholangiopancreatography) to elucidate the underlying cause * *?�Tx: directed at
underlying cause Chapter 16: Right Upper Quadrant Pain, Fever, Nausea, and Vomiting
� Impacted Gallstone Presentation *?Charcot??s Triad (50%) � fever, RUQ pain,
jaundiceo Pain often acute onset; jaundice most prominent in
eyes/palms/soles/tongue base o Jaundice clinically visible when >2.5 *?Reynold??s
Pentad (5%) � fever, RUQ pain, jaundice, hypotension, and altered mental status o
Essentially the triad + SIRS *?SIRS criteriao Temp <96.8 or >100.4 o HR >90bpmo RR
>20 or PaCO2 <32mmHg or pt mechanically ventilatedo WBC >12 or <4 or >10% bandso
Remember that sepsis is SIRS criteria with suspected infection Pathophysiology * *?
�Gallstones can easily harbor bacteria and clog the biliary tree, thus they??re the
most common cause * *?�If stone persists, abscess formation, severe sepsis, and
death may all occur Work-Up * *?�Labs: CBC, CMP, LFTs (AST, ALT, GGT), alk. phos *
*?�Imaging: RUQ ultrasound-->gallstone visualization or ductal dilation of >4mm o
4mm rule occurs till age 40yr; then add 1mm for every decade past 40 o Good rule in
but not good rule out testManagement (if presenting with Triad + SIRS) � all steps
should be done in this order * *?�Aggressive IV fluid resuscitation * *?�Broad
spectrum abx within the first hour of arrival * *?�Two sets of blood cultures
(ideally before abx) * *?�ICU admission * *?�Drain infected bile o Preferred: ERCP
with spincterotomy and stentingo Alternatives: percutaneous transhepatic drainage
or operative placement of T-tube in common bile duct*?Laproscopic cholecystectomy
(prevent future attacks)-->used to be the initial step of treatment, but higher
mortality rates were seen when putting septic patients under general anesthesia.
Better to control the sepsis, then go under the knife. Chapter 17: Severe
Epigastric Pain with Nausea/Vomiting 2982/4434/2965/2929: Acute Pancreatitis *?
Pathophysiology: intra-pancreatic activation of pancreatic enzymes causes autolysis
of pancreatic tissue, and eventually peripancreatic tissue. This results in massive
inflammation and damage. o Premature Trypsin Activation -->?damage to pancreas -->?
damage to rest of bodyo Gallstones causing pancreatitis are often small and don??t
get stuck in the Ampulla of Vater. They are there transiently, causing enough
backup to damage the pancreas, but almost always pop out to be digested. ERCP is
NOT
useful in evaluation because of this.o Ethanol??s mechanism isn??t fully
understood, BUT it??s proposed that EtOH metabolites cause damage to the pancreas,
eventually resulting in enzyme activation after years of damage o Hypocalcemia �
due to fat necrosis sequestration of calcium (saponification) *?Presentation:
severe acute abdominal pain, fever, nausea/vomiting, abdominal guarding, hypoactive
bowel sounds, sometimes xanthomas o Causes (??GET SMASHED�) Gallstones (40%),
Ethanol (40%), Tumors (obstruction of pancreatic head), Scorpion stings (lol),
Mycoplasma/Mumps, Autoimmune (SLE or polyarteritis nodosa), Surgery/Trauma,
Hypertriglyceridemia (classically >1000), Embolism (ischemia), Drugs/toxins o
Imaging: sentinel loop (dilated loops of bowel near the pancreas) or colon cutoff
(bowel distention until sudden collapse in upper left splenic flexure) on plain
films o Labs: elevated WBCs, elevated amylase/lipase, elevated LFTs *?Dx: two of
the following o Acute epigastric abdominal pain radiating to the backo Increased
amylase or lipase (more spec) x3 the normal limit -->?typically the first step in
workup o Diffuse pancreatic enlargement with contrast enhancement (CT) or
hyperechoicity (ultrasound) and sometimes with fat-stranding; Ultrasound is
preferred in patients suspected with gallstones as underlying cause
(fat/40/fertile/female = gallstone) *?Prognosis (Ranson Criteria) o At Admission:
Glucose (>200), Age (>55), LDH (>350), AST (>250), WBCs (>16,000)o At 48hr: Ca
(<8.0), Hct drop (>10%), PaO2 (<60), BUN rise (>5), Base deficit (>4), Fluid
sequestration (>6L)o Each individual value is worth 1 point-->0-2 (2% mortality),
3-4 (15%), 5-6 (40%), 7-8 (100%) o Most common cause of mortality in 1st week--
>multiorgan failure resulting from SIRS/sepsis o Most common cause of mortality
after 1st week -->?pancreatic necrosis/abscess -->?often a patient develops
fever/leukocytosis 3wk into course -->?stat CT to assess *?Tx: supportive care
(pain control/fluids) as most cases are self-limited (4-7 days) o If caused by
something that can be treated (gallstone, EtOH, drug, infection, etc) then treat
that once initial episode begins to resolve o Meperidine (over morphine) may be
preferred for pain control as it doesn??t cause contraction of the Sphincter of
Oddi; however, it lowers seizure threshold 4603: Severe Acute Pancreatitis*?
Pancreatitis + evidence of organ failure due to release of pancreatic enzymes into
the vasculature. This causes increased vascular permeability in/around the
pancreas, causing shock & organ failure o Shock � systolic blood pressure <90mmHgo
Organ failure � PaO2 <60mmHg; Creatinine >2.0 after rehydration; GI bleed
>500cc/24hr *?Presentation: pancreatitis symptoms with additional oneso Organ
dysfunction due to fluid overload (dyspnea, tachypnea, abdominal distention, etc.)
o Cullen sign: periumbilical blue-ish coloration indicating retroperitoneal
hemorrhageo Grey-Turner sign: red-brown coloration around the flanks indicating
retroperitoneal bleed o Remember! The Pancreas is retroperitoneal...thus bleeding
goes into this area! *?Risk factors: >75yrs, obesity, alcoholism, pulmonary
infiltration on X-ray o Labs at 48 hrs-->CRP >150mg/dL, Rising BUN and Creatinine
*?Tx: aggressive IV fluid resuscitation to replace lost volume 3833: Drug induced
Acute Pancreatitis*?Anti-seizure (valproate), Diuretics (furosemide, HCTZ), Drugs
for IBD (sulfasalazine, 5-ASA), Immunosuppression agents (azathioprine), HIV-
medications (didanosine, pentamidine), Antibiotics (metronidazole, tetracyclines),
and possibly many others! 4362/4919: Chronic Pancreatitis * *?�Etiology: alcoholism
(most common adults), cystic fibrosis (most common kids), duct obstruction
(malignancy or stones), autoimmune * *?�Presentation: chronic epigastric pain
radiating to the back, improved with leaning forward/sitting up (intermittent
remission/relapses), malabsorption (steatorrhea, AEDK deficiency, weight loss),
diabetes o Amylase/lipase may be normal or decreased (??burnt out pancreas??)o
CT/MRCP showing pancreatic calcifications, dilate ducts, enlarged pancreas o May
result in fat-soluble vitamin (AEDK) deficiencies o Steatorrhea occurs with 90%
loss of pancreatic function*?Dx: clinical presentation with radiographic evidence
(calcifications are the best thing to see) o Fecal fat assays (Sudan Stain) may
sometimes be used*?Tx: pain management, alcohol/smoking cessation, frequent small
meals, pancreatic enzyme supplementation during meals 2897: Pancreatic Pseudocyst*?
Presentation: palpable mass in epigastrum following acute pancreatitis or in
chronic pancreatitis, often with pain radiating to the backo ??Cyst?? actually
lacks a proper epithelium and is covered by a thick, fibrous capsuleo Filled with
fluid/tissue/debris that contains high levels of pancreatic amylase/lipase, thus it
can leak into the circulation causing elevation of pancreatic enzymes o If cyst
erodes into a blood vessel, hemorrhage into pseudocyst may occur as an acute
complication, requiring immediate surgical attention * *?�Dx: presentation with
ultrasound visualization * *?�Tx: often symptomatic as cyst will resolve itself o
Drainage indicated if: persistence for >6wk, size >5cm, or secondary infection
Chapter 18: New Onset of Painless JaundiceThere??s a long differential for jaundice
but it can be conveniently divided into three types (page 192): * *?�Prehepatic �
hemolytic anemia, Gilbert??s syndrome * *?�Hepatic � ischemic/viral/toxic liver
injury, primary biliary cirrhosis, Wilson??s disease * *?�Posthepatic �
choledocholithiasis, chronic pancreatitis, mirizzi syndrome, pancreatic/ampullary
carcinoma, cholangiocarcinoma Presentation *?Fatigue, mild vague abdominal pain or
no pain, low appetite, weight loss, jaundice, itchingo Jaundice is often noticeable
at bilirubin >2.5 mg/dL, most prominent on palms, soles, under tongue, and sclera
of the eyes (less photodegeneration)o Courvoisier??s sign � palpable non-tender RUQ
mass due to enlarged gallbladder. Enlargement due to distal biliary tree
obstructiono ??Sandy?? stools � poor bilirubin entry into gut -->?less stercobilin
to color the stoolo ??Tea colored?? urine � back-up of direct (conjugated)
bilirubin which gets filtered out by kidneys o Sister Mary Joseph Nodule �
periumbilical mass, sometimes seen w/ metastatic GI malignancy o Blumer??s Shelf
� ??step off?? felt in rectal exam due to metastatic disease in Pouch of Douglas *
*?�Labs: elevated total bilirubin/direct bilirubin/LFTs/alk.phos * *?�Risk factors:
chronic pancreatitis > smoking > high-fat diet > male gender > family history
Pathophysiology *?Bilirubin is a heme breakdown product and its metabolism drives
much of the symptoms here o Heme -->?unconjugated bilirubin (albumin bound) that
goes to the livero Un-bili -->?conjugated bilirubin in the liver, then stored in
the gallbladdero Con-bili -->?excreted into the small intestine and converted into
urobilinogen ??Urobili-->absorbed and converted into urobilin (makes pee yellow)??
Urobili-->metabolized by bacteria in large intestine to stercobilin (makes poop
brown) Workup * *?�Labs: CBC, LFTs (AST, ALT, GGT), Alk. Phos, bilirubin levels *
*?�Imaging: o Painful jaundice = RUQ ultrasound (most likely gallstone)o Painless
jaundice = Triple Phase CT +/- endoscopic ultrasoundo ERCP is not routinely needed
for diagnosis, but can be helpful in unequivocal cases and if stent
placement/biopsy are needed for delination*?Tumor markers CA 19-9 and
Carcinoembryonic Antigen (CEA) may be used to monitor treatment response but are
not useful in diagnosis/prognosis Management *?Pancreaticoduodenectomy (Whipple
Procedure) � removal of the pancreatic head, duodenum, proximal jejunum, distal
stomach, and gallbladder o Complications: Gastroparesis (most common, treat with
metoclopramide), pancreatic leak (milky grey-white fluid drainage with ??sheen??;
test for pancreatic amylase), biliary leak (green leakage), hemorrhage (sanguinous
leakage), malabsorbtion, weight loss & weight loss are all possible complications
of surgery o Yellow-red drainage is normal post-surgically * *?�Typically,
resectability is determined by review of triple-phase CT +/- endoscopic ultrasound
* *?�Things that make pancreatic cancer unresectable (not a surgical candidate) o
Superior mesenteric, celiac, or hepatic artery invasion o Any sign of metastatic
disease*?If patient is unresectable, palliative procedures may be done to relieve
symptoms/suffering o Chronic abdominal pain � celiac nerve block, external beam
radiationo Gastric outlet obstruction � gastrojejunostomy, gastric tube or PEG tube
placement o Symptomatic biliary obstruction � ERCP + biliary stent is preferred *?
Patients who are borderline resectable may receive neoadjuvant chemotherapy to
shrink to tumor to an appropriate size before surgical intervention (33% of
patients will become resectable; this does NOT increase survival) 2977: When
assessing jaundice, positive urine bilirubin means conjugated (direct)
bilirubinemia * *?�This makes sense, as only conjugated bilirubin is made to be
water soluble, unconjugated (indirect) bilirubin is inherently not water soluble,
thus it cannot be filtered by the kidney into the urine. * *?�However, a positive
urine urobilinogen indicates unconjugated (indirect) bilirubinemia, as the huge
amount of unconjugated bilirubin goes through it??s normal metabolism in the large
intestine, a large amount of urobilinogen (a normal by-product) will be made. This
is NOT the case in a direct bilirubin, as a direct bilirubinemia is caused by some
obstructive process, and it would never make it to the large intestine to become
urobilinogen! Chapter 19: Bright Blood per Rectum (may want to just read again;
doesn??t translate well into notes) Differential Dx-->diverticulosis,
neoplasia, iatrogenic, colitis (infectious, ischemic, inflammatory, or radiation),
angiodysplasia, anorectal bleeding (hemorrhoids, anal fissure, rectal varicie,
rectal ulcer) *?Some of these are discussed in more detail below Management * *?
�Initial Steps � place 2 large-bore IVs; send labs (type & cross, CBC, H&H, CMP,
PT/INR); start IV fluids followed by packed RBCs as needed * *?�2nd step � place NG
tube to rule out upper GI bleed depending on aspirate o Blood/??coffee grounds?? �
upper GI bleed confirmedo Bile � upper GI bleed ruled out completelyo Clear fluid �
upper stomach bleed ruled out, but NOT duodenal bleed *?If patient Unstableo Admit
to ICU for close monitoring and expedited work-up of bleedo 1st line test �
colonoscopy (bowel prep if possible, but do not delay if urgent) o 2nd line test �
if the colonoscopy fails to visualize the bleed, consider: ????o 3rd line ????
Diagnostic arteriography � needs brisk bleeding (1mL/min); can be therapeutic/dx
Tagged RBC scintigraphy � slower bleeding (0.1mL/min); only dxtest � at this point
the bleeding may have stopped or notStopped bleed/suspect small bowel � Meckel??s
nuclear scan, capsule endoscopy, or enteroscopy Stopped bleed/no clue of source �
repeat 1st or 2nd line tests Continued bleeding � emergent laparotomy with total
colectomy (save their life)o Note that if embolization fails to stop a known bleed,
partial bowel resection is the next step *?If patient Stableo Age <40-->anoscopy
(basically a scope of the anus) ????Typically yields hemorrhoids, which will often
resolve with symptomatic treatment or minor surgery to remove them ??If no source
sound, do a sigmoid or colonoscopyo Age 40-49 without red flag signs -->?
sigmoidoscopy/colonoscopyo Age >50 or red flags-->?colonoscopyo Red flags include:
recent bowel habit changes, abdominal pain, weight loss, anemia, or family history
of colon cancer 4086: Diverticulosis*?Outpouchings of inner colonic tissue through
the outer layers of the colon due to weakened areas encountering pressure, thus
bulging out. The vasa recta are stretched out over the pouch, resulting in an
increased chance for bleeding o Associated with constipation and oddly enough, may
worsen existing constipation!o Most diverticular occur in the sigmoid colon as
stool is harder/dryer and the lumen decreases in size (thus more pressure for
damage to bowel!)o May produce massive painless bleeding, especially with bowel
movements *?Complications: diverticular hemorrhage, diverticulitis, perforation,
abscess formationo Adequate fruit/vegetable fiber in the diet and physical activity
lower risk of complications o Meat, aspirin/NSAIDs, obesity, advanced age, and
smoking increase risk of complications *?While these often pose no problem, it??s
important to take steps to limit the risk of complication in those with
diverticulitis with lifestyle changes 4389: Colorectal cancer: signs/symptoms*?An
older man (>60) with abdominal pain, microcytic anemia, (+)fecal occult blood, and
hepatomegaly with a hard liver edge -->?prompt you to think infiltrative colon
cancero Any old person with microcytic anemia (esp. men) or blood in stool-->colon
cancero Hepatomegaly with a hard liver edge-->liver cancer (most often from
metastatic colon cancer) o Mildly elevated AST/ALT/Alk.phos in this setting -->?
infiltrative/cholestatic disease (which metastatic liver cancer would be a part
of!)*?Dx: because this pt has signs of colon cancer and liver abnormalities without
significant elevations in LFTs, an abdominal CT should be sought as metastatic
malignancy is suspected. Ischemic Colitis (look in Surgery UWorld notes for better
explainations) * *?�Lack of bloodflow to the typically blood-thirsty colon causing
mucosal damage with prolonged ischemia resulting in full-thickness damage * *?
�Presentation: left sided abdominal pain, bloody diarrhea, especially those with
volume depletion (dehydration, heart failure, shock, trauma) o Classically
affects ??watershed?? areas first (splenic flexure poorly perfused by SMA/IMA)o Can
be due to any ??low flow?? state (low BP, low cardiac output, dehydration, heart
failure, extreme exercise, vascoconstrictive drugs, etc.) o 80% will resolve
spontaneously * *?�Dx: clinical presentation * *?�Tx: rehydration supportive
therapy Chapter 20: Right Lower Quadrant Abdominal Pain � Acute Appendicitis
Differential Diagnoses *?General Stuff: IBD, pancreatitis, cholecystitis,
appendicitis, gastroenteritis, perforated duodenal ulcer, pyelonephritis,
nephrolithiasis, sigmoid/cecal/Meckel??s diverticulitis * *?�Women Stuff: PID,
ovarian torsion, Mittelschmertz, ruptured ectopic * *?�Children Stuff: mesenteric
lymphadentitis, Yersinia enterocolitica (pseudoappendicitis), gastroenteritis,
intussusception Presentation o *?�Classic progression: anorexia -->?vague abdominal
periumbilical pain -->?vomiting -->?pain shift to RLQ o *?�Other symptoms:
paralytic ileus (absent bowel sounds from inflammation), Hamburger sign (pt would
not like to eat their favorite food), Rovsing??s sign (RLQ pain w/ palpation of
LLQ), Psoas Sign (RLQ pain w/ active flexion of hip or passive extension; often
Pelvic Appendix), Obturator Sign (RLQ pain w/ internal rotation of hip), McBurney??
s Point Tenderness (tenderness w/ palpation at McBurney??s point) o *?�Often
children will initially present with viral URI, then the lymphoid hyperplasia
resulting from fighting the URI can cause obstruction and appendicitis o *?�Lumbar
triangle palpation may be painful in those with retrocecal appendicitis. The cecum
will shield the appendix from many signs mentioned above, thus this can be an
important test! Pathophysiology *?Transition from vague pain-->localized RLQ pain
occurs due to diff. peritoneal layers getting affected o Visceral peritoneum �
innervated by autonomic nerves responding to stretch or distention; sensation is
poorly localized; this level is affected first as it??s more internalo Parietal
peritoneum � innervated by spinal nerve (somatic innervation of T10-T12); as
inflammation progresses, this level will be affected resulting in localized pain *?
Whereo Foregut � [mouth -->?ligament of Treitz (2nd part of duodenum)] -->?
epigastric paino Midgut � [3rd part of duodenum -->?proximal 2/3 of transverse
colon] -->?periumbilical pain o Hindgut � [1/3 distal transverse colon -->?rectum]
-->?hypogastric pain * *?�??Cutaneous hyperesthesia?? � sensitivity to touch with
peritoneal inflammation * *?�??Closed loop obstruction?? of the appendix � the
appendix is a blind loop of bowel o Obstruction -->?increased pressure -->?
distention/inflammation/ growth of appendix bacteria o Eventually pressure is so
great that venous flow is compromised-->backup of arterial flow o Bloodflow
congestion -->?ischemia/gangrene -->?weakening of the appendix wallo Weakened wall
+ increased pressure -->?rupture! *?Important causes of appendix obstructiono
Fecalith � most common in adults; hard poop rock!o Lymphoid hyperplasia � most
common in children; often after viral URIo Oral barium (bariolith) � occurs after
radiologic studies with oral barium contrast o Tumor � carcinoid tumor,
adenocarcinoma of appendix, etc.o Ingested seeds � aren??t digested well and get
stuck in appendixo Parasites � reproduce and grow in the GI tract; can get stuck in
appendix Workup * *?�Labs: CBC (leukocytosis with left shift), CRP (elevated), B-
hCG pregnancy test (if of child-bearing age), urinalysis (sterile pyuria) * *?
�Imaging: used if H&P is equivocal or to rule out gynecologic problems/pregnancy in
women o CT a/p if non-pregnant female or adult man (periumbilical fat stranding and
appendix >6mm diameter, free abdominal fluid, phlegmon) o Ultrasound if pregnant
female or child (dilated, tubular structure in RLQ with thickened walls); children
have less abdominal fat making CT less valuable for visualization o MRI may be used
in pregnancy if pt is obese or ultrasound is unavailable o Abdominal X-ray is not
often useful; may show calcified fecalith, but not routinely ordered Management
does pain occur based on gut level? *?Surgical appendectomy o Laprascopic approach
� longer surgery, higher cost, high incidence of abscess; faster recovered, lower
overall complication/infection rate, smaller scar o Open approach �
shorter/cheaper/less abscess; slower recovery/higher complications/big scar *?If
you get in there and you have a normal appendix o Remove it anyway; this leads to
effective ??rule out?? in future presentations of RLQ pain o Don??t remove it if
cecal Crohn??s disease; high chance of fistula formationo Also look for other
causes of symptoms * *?�Non-operative approach with abx and supportive care only
has been used but is controversial; not gold standard; you won??t typically do
this. * *?�Preoperative Abx are always recommended * *?�Postop Abx-->non-perforated
(24hr); perforated (till fever/leukocytosis resolve; usually 3-5 days) Problems
that can come up o *?�Pyuria does not necessarily mean cystitis! Don??t jump to
that conclusion. o *?�If there??s pus in the abdomen...but the appendix is intact;
diagnosis is peri-appendicitis and careful abdominal exploration is needed to find
source of infection/peritonitis o *?�If pt has pseudo-appendicitis (Yersinia
Enterolitica); often will present with all the signs of appendicitis but will also
have bloody or watery diarrhea. Typically transmitted by contaminated water or
pork. Classically a child in day-care or a daycare worker. o More common in pt with
hereditary hemochromatosis (Y.entero loves iron)o Self-limited; but
Immunosuppressed patients may die from dissemination-->sepsis o Tx: doxycycline *
*?�Ruptured appendix may be misdiagnosed as PID as both cause cervical motion
tenderness and adnexal tenderness. Often PID = bilateral pain since onset; pain
lower in pelvis; additional signs of vaginal infection, risk factors, or history
of untreated STI * *?�Acute appendicitis is considered ??urgent?? not ??emergent??
as risk of rupture increases 5% every 12hr * *?�>5 day Hx of RLQ pain usually means
the appendix is ruptured and often a local abscess has formed o Small abscess �
treatment with IV abx and admission-->appendectomy o Large abscess � percutaneous
drainage, abx, and admission-->appendectomy Populations Special*?Pregnant Women:
acute appendicitis is the most common surgical emergency in pregnancy! While
abdominal contents shift up...RLQ pain is still presented even in 3rd trimester.
Appendix rupture AND appendectomy can cause significant morbidity and mortality to
the fetus, thus diagnosis with imaging (ultrasound or MRI) is critical before
treatment * *?�Children <5yr: harder to get H&P and higher risk of early rupture
(45% present with it) * *?�Elderly: more prone to rupture (50%) and microcytic
anemia should prompt workup for perforated colon cancer (can mimic appendicitis!)
Chapter 21: Pencil Thin Stools and Intermittent Constipation � Colorectal Cancer
Screening Guidelines for Colorectal Cancer *?Normal Risk:o Age 50-75yr �
colonoscopy every 10yr -OR- FOBT or Flexible Sigmoidoscopy every 3-5yr -OR- annual
FOBT (any (+) test that isn??t colonoscopy needs to be followed-up by colonoscopy)
o Age 76-85yr � if never screened or if clinically indicated, pt may benefit *?1st
degree Family Member with Colorectal Cancero Age 40yr or 10 years prior to family
member diagnosis (whichever comes first) o Repeat colonoscopies every 5 years *?
High Risk Patients: o Family Hx of polyps or CRC: colonoscopy every 2-3 years
starting 10 years before first familial diagnosis or age 40 (if the 10 years prior
puts you lower than age 40) o Inflammatory Bowel Disease (Crohn??s or UC): every 1-
2 years starting 8 years post-diagnosis ??Can start 12-15yr post-diagnosis if
disease restricted to left colon o FAP: colonoscopy every year starting at age 10 o
Lynch syndrome (HNPCC): colonoscopy every 1-2 years starting age 20Risk Factors:
older age (>50), African American, IBD, family Hx, low-fiber/high-fat diet,
sedentary lifestyle, obesity, smoking, EtOH, Type 2DM, Hx of radiation therapy to
the abdomenEpidemiology: 3rd most common and 3rd most fatal cancer in men & women
Presentation * *?�Common symptoms: Unintended weight loss (cachexia from TNF-a),
anemia * *?�Left sided cancer: more common, at rectosigmoid junction, changes in
bowel habits (constipation or diarrhea), obstructive symptoms, pencil thin stools
(circumfrential growth-->narrowed lumen), abdominal distention, colicky pain,
hematochezia * *?�Right sided cancer: insidious iron deficiency anemia, melena, RLQ
pain with mass (rare) * *?�Note that digital rectal exam is very important as you
may be able to palpate a mass if it??s in the distal ends of the colon. If palpable
you may be able to assess the characteristics of the mass, allowing for better
surgical planning Pathophysiology *?Three major types of colon polyps:o
Hyperplastic: most common non-neoplastic polyp; no need for further workupo
Hamartomatous: juvenile/Peutz-Jegher (hyperpigmentation of lips/genitals
polyps...benign) o Adenomatous: most common overall with potential malignancy -->?
further workup, but less than 1% of these will actually be malignant!*?Adenomatous
polyps MUST be further assessed as this will determine its risk for malignancy: o
Morphology: sessile [more malignant] or pedunculated [more benign]o Histology:
[more benign] tubular < tubulovillous < villous [more malignant]o Size: [low risk
of invasion] (<1.5cm) < (1.5-2.5cm) < (>2.5cm) [high risk of invasion] *?Adenoma
-->?Carcinoma sequence is the typical mechanism for developing colorectal cancero
Step 1: APC tumor suppression gene loss -->?increased proliferationo Step 2: KRAS
mutation -->?unregulated intracellular signaling = growth -->?adenoma formation o
Step 3: p53 mutation -->?loss of genetic regulation, accumulation of mutations -->?
carcinoma o This sequence is thought to take about 10yr...thus the screening
recommendations *?Common metastatic sites of colorectal cancero Regional lymph
nodes & liver (distal mets from portal system) are most commono Rectal cancer may
disseminate via either portal or systemic veins thus lungs (internal iliac-->?SVC),
spine/brain (sacral veins), or iliac lymph nodes are common sites as well as liver
& peritoneumGenetic Syndromes Associated with Colorectal Cancer *?Lynch Syndrome
(Hereditary Non-polyposis colorectal cancer [HNPCC]) o Two major types: * ??�Lynch
syndrome I: only colon cancer * ??�Lynch syndrome II: colon and extra-colonic
cancer (endometrial carcinoma most common) o Dx: Modified Amsterdam Criteria (3-2-
1-0 rule!) ??3 or more relatives with colon cancer (one must be first degree to the
other two) ??2 or more generations affected??1 familial case before age 50 ??0
change of Familial Adenomatous Polyposis excluded (APC gene mutation excluded) *?
Familial Adenomatous Polyposis (FAP) o Familial deletion of one APC gene (chrom.
5), resulting in 100s-1000s of polyps o 100% chance to progress to colonic
adenocarcinoma before ageo Tx: prophylactic colon and rectum removal + increased
CRC screening *?Gardner Syndromeo FAP + fibromatosis + osteomas (often on forehead)
o May also have retinal pigment hypertrophy or impacted/supernumery teeth *?Turcot
Syndrome ??TURcot like a TURban on your head??o FAP + CNS tumors (medulloblastoma
or glial tumors) + caf� au lait spots *?Juvenile polyposis syndromeo Benign
hamertomatous polyp arising in children <5 y/o - rectal polyp can prolapse & bleed
o Commonly SMAD4 gene recognized mutationo Dilated glands with mucin and surface
erosion on histology *?Peutz-Jeghers Syndromeo Auto dominant mutation in STK11 gene
o Benign hamertomatous polyps anywhere in GI tracto Mucocutaneous hyperpigmentation
(lips, oral mucosa, genital skin) o Increased risk of colorectal, breast, and
gynecological cancero ??Arborizing??, pedunculated polyps with bands of smooth
muscle Workup * *?�FOBT � useless for the most part. If positive, you proceed with
work-up, if negative you don??t have enough negative predictive value to rule
anything out...and proceed with workup * *?�Colonoscopy- the first step with
clinical suspicion of CRC. Visualization and biopsy of any suspicious lesions is
key for diagnosis and treatment plan management * *?�Labs: CBC, Carcinoembryonic
Antigen (CEA; post diagnosis, nice to help follow treatment response as many things
mal elevate CEA), LFTs (looking for liver mets) * *?�Imaging: o Colon Cancer: CT
c/a/p (check for mets; 20% of pts present with metastatic disease); PET scan may be
used but is not routinely needed o Rectal Cancer: trans-rectal ultrasound & MRI a/p
to better characterize/stage disease. The goal is to preserve the sphincters
surgically and assess the need for neoadjuvant chemotherapy Staging * *?�0 � only
involvement mucosa * *?�I � invades mucosa and submucosa * *?�II � invades through
muscle layers and nearby tissues/organs * *?�III � lymph node involvement * *?�IV �
distant metastatic spread Management o *?�Bowel prep � oral polyethelene glycol +/-
non-absorbable Abx to clear stool and decrease bacteria from the gut. Helps with
visualization and minimizes stool spillage in colon surgery o *?�Polyps �
polypectomy or segmental resection with surveillance from 1-5 years o *?�Colonic
Resection + Lymph Node dissection � depends on location of cancer o Right-sided
cancer � right colectomy + ligation of ileocolic arteryo Transverse colon �
transverse colectomy or extended right colectomy + ileocolic/middle colic artery
ligationo Left-sided colon � left colectomy with ligation of the IMA o Sigmoid
colon � left colectomy with ligation of the IMA o A minimum of 12 lymph nodes must
be resected for accurate staging * *?�Neoadjuvant Chemotherapy � often used in
rectal cancer in hopes of sphincter-sparing surgery as well as later stage colon
cancers (rarely in early stages) * *?�Radiation � used only in rectal cancer as it
can be administered locally; colon cancer would require whole pelvis radiation
(which causes radiation enteritis and increased risk for further cancer!)
Complications of Colon Surgery * *?�Injury to the ureter/duodenum/spleen � often
avoided with careful dissection * *?�Anastomotic leak � POD 1-7 with fever,
abdominal pain/tenderness, ileus, and leukocytosis; if confirmed, re-operation for
resection/washout/ostomy diversion are required Chapter 22: Chronic Constipation +
Severe Abdominal Pain � Large Bowel ObstructionDifferential Diagnosis: colon
cancer, diverticulitis, stricture, volvulus, fecal impaction, Ogilvie??s syndrome
(pseudo-obstruction), toxic megacolon o *?�Constipation � low frequency of stools
(<3/week) o *?�Obstipation � complete lack of gas or stool per rectum (big
suggestion of bowel obstruction) Presentation * *?�Vital signs: fever/tachycardia
(inflammation from bowel ischemia), & tachypnea (enlarged bowel making it hard for
diaphragmatic excursion) * *?�Abdominal Exam: little/no tenderness, distention,
tympani; possible signs of irreducible hernia * *?�Rectal Exam: often empty, but
may be with palpable mass (impacted stool, neoplasm, stricture) * *?�Often less or
later onset vomiting (vs SBO) and decreased bowel sounds (vs SBO) What causes
abdominal distention? (5 Fs) *?Fat (big belly), feces (impaction), fetus (pregnancy
belly), flatus (ileus/obstruction), and fluid (ascites) Pathophysiology * *?�Most
common causes � malignancy (CRC) is #1, then diverticulitis/stricture, then
volvulus * *?�Left sided CRC is most likely to cause obstruction due to smaller
diameter of the descending colon * *?�Ogilvie??s Syndrome � ??pseudo obstruction??
which will present nearly
identical to LBO, but occurs in debilitated hospitalized patients. Pt will often
develop while in their hospital stay for something else (most classically in the
post-operative setting!)-->neostigmine is Tx of choice * *?�Malrotation of the Gut
� congenital condition where gut formation has not undergone proper rotation during
development. This puts the bowel and its mesentery out of normal position and often
without proper attachment. * *?�Volvulus � actual twisting of the gut to cause
obstruction. It may be a result of malrotation! o Cecal Volvulus � occurs due to
congenital malrotation, cecum/right colon not properly attached to peritoneal wall,
thus allowing them to freely twist o Sigmoid Volvulus � acquired condition where
progressive stretching can cause twisting of the sigmoid around it??s small
mesentery. Risk factors all include things that can cause constipation (anti-
cholinergic drugs, stool retention, CF, Chagas?? disease, high fiber diet, etc.) o
Complicated volvulus � the result of volvulus causing ischemia and eventually
gangrenous bowel/sepsis! Severe abdominal pain, fever, tachycardia, altered mental
status, and marked tenderness (peritoneal signs) can all point to this Work up*?
Labs: CBC (leukocytosis), serum lactate (lactic acidosis), CMP (electrolyte
imbalance/dehydration) *?Imaging: o 1st imaging study = Abdominal (upright and
supine) & chest (upright) X-rays * ??�Distended large bowel can be indicative of
obstruction * ??�Mesentery twisted around the center (??coffee bean sign?? or ??
bent inner tube sign??) indicates large bowel volvulus as the cause o Additional
imaging = CT with oral/IV contrast OR Contrast enema??Can show ??whirl sign?? of
volvulus??Enema can be diagnostic and therapeutic as the enema may unblock the
bowel Management * *?�1st step: IV fluids + foley catheter placement + NG tube
placement for decompression of gut * *?�Uncomplicated sigmoid volvulus: De-torsion
via endoscopy (preferred) or barium enema o If successful: semi-elective sigmoid
resection after acute event is over. The recurrence rate is high, so the best way
to stop recurrence is to take out the damn thing. Poor surgical patients have the
option of medical management o If unsuccessful: go to the OR for surgical de-
torsion * *?�Complicated sigmoid volvulus: due to worry/evidence of bowel
ischemia/perforation, colon resection is mandated without attempts for de-torsion.
Intraoperatively, the volvulus portion is removed without de-torsion and the
proximal end is brought out with a colostomy * *?�Cecal volvulus: surgery is 1st
line due to high incidence of bowel necrosis and de-torsion failure * *?�Ogilvie??s
Syndrome: neostigmine + colonic decompression * *?�Pregnancy + LBO: volvulus is the
2nd leading cause of LBO in pregnancy! Immediate de-torsion with delayed resection
until after birth (if possible) Chapter 23: Left Lower Quadrant Pain �
DiverticulitisRisk Factors: obesity, low fiber diet, high fat/red meat diet,
advanced age Pathophysiology *?Diverticula o Most common location for diverticula =
sigmoid colono Most common site of infection of diverticula = left & sigmoid colono
Rectal diverticula are very rare, as the tenia coli coalesce into a circumferential
band of muscle in the rectum, which is thought to eliminate weak points in this
portion of bowel o True diverticulum � all layers (mucosa, submucosa, muscularis)
are involvedo False diverticulum � only mucosa/submucosa are involved *?Fistulaso
Main causes = diverticulitis (most common), colon cancer, IBD, bladder cancer,
radiation injury, trauma, foreign bodyo Cause of failure to close (FRIEND) �
Foreign body present, Radiation, Inflammation/Infection, Epithelialization,
Neoplasm, and Distal Obstructiono Colovesicular fistula � feces/air in urine,
recurrent/refractory/atypical UTI (multiple bugs or anaerobes) due to recurrent
seeding with stool o Colovaginal fistula � feces in the vaginal vault Presentation
* *?�LLQ pain, nausea, anorexia, low-grade fever, absent bowel sounds * *?�RLQ pain
may present if patient has especially redundant sigmoid colon, which can run into
the RLQ Diagnosis/Workup * *?�Largely clinical from presentation * *?�Imaging � CT
scan showing diverticular outpouchings * *?�Note that barium enema and colonoscopy
are CONTRAINDICATED as they may exacerbate inflammation and result in
perforation/fistula formation * *?�Staging (Hinchey Staging system) o Hinchey I -
localized abscess (para-colonic)o Hinchey II - pelvic abscesso Hinchey III -
purulent peritonitis (pus in the abdominal cavity) o Hinchey IV - feculent
peritonitis. o Stage I-III can be managed surgically with laparoscopic approach and
washout Management *?First Step: determine if patient has evidence of SIRS (any two
of the following) o Temperature >100.4 or <96.8o HR>90o RR >20 or PaCO2 <32mmHg
(hyperventillatory hypocapnea) o WBC >12,000, <4000, or >10% band forms * *?�If no
SIRS -->?send home with Abx/clear fluid diet; if SIRS -->?admit and give IV
abx/fluids/analgesia * *?�Uncomplicated Diverticulitis: it??s only the diverticula
and inflammation o IV abx/fluids/analgesia/NPO; if failure to improve then CT scan
for abscess search or movement to the OR for colon resection! o 6-8 weeks after
resolution -->?colonoscopy is recommended to search for other disease processes
that might have caused presentation! *?Complicated Diverticulitis: abscess,
obstruction, peritonitis or fistula makes for complication!o Free perforation +
diffuse peritonitis � emergent colectomy/colostomy (reversal in 12wk; distal end of
resection is rectum w/loss of taenia coli), proximal end is healthy bowel...not
necessarily parts free of diverticula)o Large bowel obstruction � urgent
colectomy/colostomyo Large (>4cm) local abscess � CT-guided drainage with elective
colectomy o Small (<4cm) local abscess � IV abx with elective colectomyo
Colovesical fistula � IV abx with elective bladder repair/colectomy * *?�Note that
non-emergent surgery can be repaired with primary anastomoses (you remove part of
the colon, then simply re-attach the two other portions and you??re done (no
colostomy for later reversal!) * *?�Note that a bowel prep has not been shown to
reduce infections in these surgeries * *?�Patients may be medically managed
(without elective colectomy) as long as it remains effective. Recurrences can
occur, as long as they??re able to recover medically! Chapter 24: Neck Pain and
Paralysis Following Surgery � Anterior Spinal Artery Syndrome Differential for
Spinal Injury *?Complete spinal cord injury � complete loss of motor/sensory
function below level of lesion o Often penetrating trauma that transects the major
tracts of the spinal cordo Corticospinal tract (motor), posterior columns
(proprioception, deep touch/pressure), spinothalamic tracts (pain/temperature)*?
Brown-Sequard syndrome (Cord Hemisection) � ipsilateral motor weakness, UMN signs,
& loss of touch/proprioception + contralateral loss of pain/temperature sensation
starting 1-2 dermatomes below the lesion o Often penetrating injury to only part of
the spinal cord o Best prognosis for recovery of neurologic function, Bowel/Bladder
function, and Ambulation*?Central Cord syndrome � weakness/sensory loss of upper
extremity & proximal lower extremity. Distal lower extremity unaffected
(topographic layout of spine lays the lower extremity toward the lateral portions &
upper extremity in the central portions!) o Classic is injury from severe extension
injury (elderly with cervical subluxation)*?Anterior spinal artery (anterior cord)
syndrome � paraplegia/loss of pain & temperature sensation; preserved deep
touch/pressure, vibration, and proprioception (posterior columns preserved)o
Classic is patient undergoing AAA repair with damage to the artery of Adamkiewicz;
may also occur with severe flexion injuryo Worst prognosis for recovery of
ambulation (10%) H&P * *?�Most common cervical spinal levels damaged in trauma-->C2
(33%) > C6 > C7 * *?�Most common cervical spinal level suffering subluxation damage
-->?C5-C6 interspine (most mobility) * *?�Upper Motor Neuron Signs � weakness,
increased tone, spasticity, hyperreflexia, clonus, (+)Babinski, & (+)Hoffmann (no
fasciculation, no atrophy) * *?�Lower Motor Neuron Signs � weakness, fasciculation,
atrophy, decreased tone, loss of reflex, diminished sensation along dermatomes (no
clonus/special reflexes) * *?�Radiculopathy � damaged nerve root; burning/tingling
pain radiating down the limb and LMN signs * *?�Myelopathy � damaged to spinal
cord; radiating pain at level of lesion and UMN signs * *?�Some Classic Dermatomes
� C4 (Shoulder), T4 (nipples), T10 (umbilicus), L4 (knees), S4-S5 (perianal) o When
examining the chest, note that dermatome levels will jump from C4-->T1 with the
other cervical dermatomes covering the upper extremity *?Deep Tendon Reflexeso
Classics: C5/6 (biceps), C6 (brachioradialis), C7 (triceps), L4 (patella), S1
(achilles) o Grading: 0 (none), +1 (sluggish), +2 (normal), +3 (brisk), +4 (clonus)
*?Quick Factso Complete spinal cord lesion at or above C3 may cause diaphragmatic
paralysis (thus death) and paralysis of all four limbso Differentiating a complete
vs incomplete spinal cord section is as simple is seeing if there is no function
(complete) or some residual function (incomplete)o Babinski Sign is NORMAL in a
child <2yr, but may occur in UMN lesions Pathophysiology*?Spinal Shock � temporary
syndrome resulting in flaccid paralysis, loss of all reflexes, and loss of
urinary/rectal tone below the level of the lesiono Sacral sparing occurs when the
sacral nerves (perianal sensation/anal sphincter tone) are preserved and is a good
sign of recovery in pts with spinal shock * *?�Neurogenic Shock � shock due to loss
of sympathetic outflow from the spinal cord (vasodilation,
bradycardia, hypotension) * *?�Neck injury is commonly due to flexion, extension,
axial loading (vertical compression), or rotation o Thoracic spine is much more
rarely injured; this is due to their better fixation of the thoracic vertebrae from
high facets/rib fixation as well as no anterior herniation of the T-spine *?
Atlanto-Occipital Dislocation � dis-articulation of the atlas facets from the
occipital condyles of the head, causing severe instability in the cervical spine
(quadraplegia, diaphragm paralysis) o Kids with trisomy 21 have a heightened risk
for this and should be screened prior to sports participation (classic is before
the special Olympics) Work-Up * *?�Neurologic exam � elucidates deficits allowing
for neurologic diagnosis * *?�X-ray/CT/MRI � used to correlate with neurologic exam
findings to confirm suspicions * *?�NEXUS Criteria � criteria to clinically ??
clear?? patient of a C-spine fracture. If they have any of the following criteria,
the should have a 3-way cervical spine X-ray o ??NSAID??: Neurologic deficit
(focal), Spinal Midline Tenderness, Altered Mental Status, Intoxication,
Distracting injuryo 3-way cervical spinal X-ray: anteroposterior (AP, lateral, and
open mouth (odontoid) * *?�Cervical CT � used to investigate anything abnormal seen
on X-ray; allows good evaluation of fractures/hematomas/disc fragments & clearance
for surgery in a comatose patient * *?�Cervical MRI � best used in assessing
lesions to the spinal cord to better characterize neurologic deficits & best for
ant soft tissue damage o Necessary to evaluate patients with SCIWORA *?Spinal Cord
Injury Without Radiographic Abnormality (SCIWORA) � typically occurs due to
contusion or stretching of the spinal cord, so no overt injury has occurred. o Most
common in pt age <3yr & at the C2 level spinal column o Can only be evaluated
properly by MRI imaging Management *?General Idea for Tx of Cervical Spinal Injury
� immobilize patients with rigid cervical collar/spine board o Maintain BP
(fluids/pressors), insert Foley (monitor urine output, prevent bladder distention),
give stool softeners to prevent severe constipation, prevent DVT with
compression/anticoag. o External orthoses may be used to provide additional
stability support * *?�Neurogenic shock is managed by IV fluids + pressors (for BP)
+ inotropes (for bradycardia) * *?�Complete/high spinal cord injury is managed by
spinal stabilization, surgical decompression in still- intact spinal cord, physical
rehab, prevention of decubitus ulcers, bowel/bladder management, and prevention of
DVT and pneumonia * *?�Incomplete spinal cord injury is treated essentially the
same as complete/high, but decompression is typically more aggressive in as there
is a higher chance for regain of function in the partially sectioned spinal cord *
*?�Emergent Surgery in Spinal Cord Injury is warranted with unstable vertebral
fracture, non-reducible spinal cord compression with deficits or ligamentous injury
with facet instability Complications *?When exposing the anterior cervical spine
for decompression, the recurrent laryngeal nerve may be inadvertently cut leading
to hoarse voice (unilateral) or dyspnea/increased aspiration risk (bilateral)
Chapter 25: Loss of Consciousness Following Head Trauma � Traumatic Brain Injury
Differential Dx (Pt GCS <8 with TBI) *?Epidural Hematoma � MMA laceration by
temporal bone fracture resulting in blood accumulation between the dura mater and
the skull o Classically blunt head trauma causing a brief loss of consciousness
(brainstem arousal center disruption)/fracture-->lucid interval-->loss of
consciousness with rapid decline (blood accumulation/herniation from hematoma mass
effect) o ??Lens-shaped?? bleed on CT head o Often rapidly expanding due to
arterial source and may need emergent evaluation*?Subdural Hematoma � bridging vein
rupture causing bleed between dura/subarachnoid layers o Classically in old
folks/alcoholics/anti-coagulated pt with mild trauma (fall from standing) ??Regular
brain atrophy in elderly puts tension on bridging veins increasing risk! o ??
Crescent-shaped?? bleed on CT heado Acute SDH � occurs within 72hr of insult, often
in younger pt or very bad injurieso Chronic ADH � often in the elderly with
insidious onset of abnormal gait, decreased consciousness, aphasia, cognitive
dysfunction, memory loss, and personality changes * *?�Intraparenchymal Hematoma �
bleeding within brain parenchyma often from aneurysm rupture or AV malformation
bleeding due to hypertensive hemorrhage. Rarely caused by primary brain contusion.
* *?�Subarachnoid hemorrhage � bleeding into the normally CSF-filled subarachnoid
spaces. Due to either trauma or vascular rupture o ??Worst headache of my life??
(??thunderclap headache??) is a classic complaint*?Diffuse Axonal Injury �
acceleration/deceleration injury resulting in axonal stretching between grey &
white matter causing injuryo Pathology of ??shaken baby syndrome?? or other
traumatic event without obvious bleed H&P * *?�Traumatic Brain Injury (TBI) �
injury to the brain that results in function (loss of consciousness, loss of memory
surrounding accident, altered mental status, or focal neurologic deficit) * *?
�Glasgow Coma Scale (GCS) � exam designed to quickly evaluated head trauma patients
and monitor improvement or deterioration. Add up your three categories and that??s
your number! o Eye Opening � 1(none), 2(pain), 3(voice), 4(spontaneous)o Verbal �
1(none), 2(nonsense), 3(inappropriate), 4(confusion), 5(oriented), T1(intubated)o
Motor � 1(none), 2(decerebrate), 3(decorticate), 4(pain withdraw), 5(local pain),
6(commands) o GCS <8 is considered a ??coma?? and should be intubatedo Note that
GCS may be skewed by alcohol/drugs, sedative, hypoxia, shock, & hypothermia *?Signs
of Basilar Skull fractureo Battle??s Sign � retroauricular ecchymosiso Raccoon eyes
� bilateral periorbital ecchymosis * *?�Localizing the brain lesion on physical
exam is as easy as looking for contralateral paralysis (disruption of neural
tracts) and ipsilateral abnormal pupillary findings (uncal herniation compressing
CNIII). Thus right side paralysis + left side abnormal pupil points to the TBI
being on the right side * *?�Kernohan syndrome � paralysis and pupil abnormalities
occur on the same side. This is due to an abnormal herniation of the cerebral
parenchyma making paralysis a ??false localizing sign?? * *?�Decorticate posturing
- abnormal UL flexion with abnormal LL extension (loss of cortical input) * *?
�Decerebrate posturing � abnormal extension of UL/LL (loss of cerebral input)
Pathophysiology * *?�Concussion � mild TBI causing problems with memory, balance,
coordination, & concentration. Headaches, dizziness, confusion, personality
changes, and irritability may also occur * *?�Uncal Herniation � herniation of the
uncus; results in compression of ipsilateral CNIII (ipsilateral blown pupil) and
ipsilateral cerebral peduncle (contralateral hemiparesis) * *?�Cerebral Perfusion
Pressure = mean arterial pressure (MAP) � intracranial pressure (ICP) o ICP is
controlled by brain tissue, CSF, and blood within the cranial vault; to keep ICP
constant these three things will attempt to offset each other as a neural auto-
regulatory responseo Knowing this, intracranial bleeds will increase ICP,
subsequently decreasing cerebral perfusion o Also, CO2 levels are the greatest
drive of cerebral perfusion (more CO2 = more perfusion); thus hyperventilation to
blow off CO2 can have temporary benefit by decreasing ICP and allow for longer time
of effective cerebral perfusiono Also note, that a patient will NOT spontaneously
start breathing if they??ve been on high vent settings (low CO2) as there is not
enough CO2 drive for respiration on the brain. So don??t be surprised if a patient
is apneic if you try to take them off the vent after hyperventilating them *?
Cushing??s Triad � hypertension, bradycardia, and irregular respiratory rate with
increased ICP o Hypertension � reflexive effort to maintain CPP with increased ICP
(via vasoconstriction)o Bradycardia � reflexive response to elevated BP from
vasoconstriction set off by ICPo Irregular respiratory rate � the combination of
severe bradycardia and ICP not being offset by BP results in medullary dysfunction
(breathing center) * *?�Coup � direct brain injury sustained at the point of impact
* *?�Countrecoup � brain injury sustained at the opposite side of the coup from the
brain sloshing back and striking the inside of the skull in response to the coup
Initial Management * *?�Assess and address the ABCs, neurologic exam, and
assessment of injuries * *?�Intubation warranted with GCS <8 * *?�Correction of any
coagulopathy to aid in minimizing new/ongoing bleeding * *?�Imaging o Initial: Non-
contrast CT of the head is warranted with anyone GCS <12 or with risk factors
(elderly, anti-coaglated, alcohol abuse) o Repeat: new neurologic signs, continued
vomiting, worsening headache, loss of >2 on GCS, signs of increasing ICP *?
Intracranial Pressure Monitoring is warranted when:o TBI (GCS<8) with abnormal CTo
TBI (GCS<8) with normal CT + any of two of these (hypotension, abnormal posturing,
age >40) o Monitored via ventriculostomy tube (may also be used to drain CSF if
pressure is too high) *?Increased ICP (>20mmHg) Treatmento Intubate/paralyze �
rocuronium/etomidate preferred as succinylcholine/ketamine increase ICP o Mild
hyperventilation � goal of PaCO2 30-35mmHg; <30 causes decreased cerebral bloodflow
o Elevate head of the bed (30-45o) � allow for better venous drainageo Loosen
cervical collar if restricting venous flow � buildup of venous pressure isn??t
good!o Mannitol � doesn??t cross BBB, allowing for shift of fluid from intracranial
vault to peripheral vessels, and diuresis. Avoid in patients with
hypotension/hypovolemia
(duresis will worsen this) and pts with kidney failure (can??t handle the mannitol
diuresis) ??Hypertonic saline may also be used for a similar effecto Barbiturate
coma may be induced if the above treatments are not working well enough *?
Craniotomy Indicationso Drilling holes into the skull cranium to relieve pressureo
Epidural hematoma >30mL in volume OR causing >10mm midline shift o Acute subdural
hematoma >5mm thick or causing >10mm midline shift *?Decompressive craniotomy
indicationso Removing parts of temporal skull to relieve even more pressure o
Failure of medical management *?Brain Death Criteriao Testing warranted only if pt
has GCS of 3; pt must be euthermic (>32.2C), PaO2 >90mmHg, systolic BP >100mmHg, &
cannot be paralyzed/sedated (proven with serum/blood testing) o 1. Absence of
Brainstem Reflexes (corneal, gag, oculocephalic, and oculovestibular)o 2. No
response to deep, central paino 3. Agreement of Two physicianso 4. Apnea Test (no
spontaneous respirations with PaCO2 >60mmHg Chapter 26: Multiple Extremity Injuries
After Motorcycle Accident � READ ONLY Chapter 27: Immediate Swelling After Trauma
to the Knee � READ ONLY Chapter 28: Right Groin Pain/Limp � READ ONLYChapter 29:
Chronic Right Hand Pain � READ ONLY Chapter 30: Full Term Male Infant with
Respiratory Distress � Congenital Diaphragmatic Hernia Differential Dx: *?Transient
Tachypnea of Newborn: most common cause of respiratory distress in term babies;
residual pulmonary fluid remains in lungs after birth o Benign and should only last
hours-days o CXR: diffuse pulmonary infiltrates + ??wet silhouette?? around the
heart*?Hyaline membrane disease (Respiratory distress syndrome): most common cause
in premies o Poor surfactant production in premature Type II alveolar cells o CXR:
homogenous pulmonary infiltrates + ??air bronchograms??*?Meconium aspiration
syndrome: meconium stained amniotic fluid will be noted at birth *?Persistent
pulmonary HTN, bronchial atresia, pulmonary agenesis, pneumonia, and non-pulmonary
etiologies are less common but possible Presentation * *?�Prenatal Screening: will
be picked up at the latest around 24wk gestation on ultrasound (bowel loops in
thoracic cavity, contralateral displacement of heart/mediastinum) * *?�Displaced
heartbeat: loops of bowel is moving the heart/mediastinum away from hernia * *?
�Tachypnea/tachycardia/absent breath sounds/bowel sounds in chest:
displacement/poor development of lung tissue from infiltrating bowel causing
respiratory distress/poor formed lung tissue * *?�Scaphoid abdomen/ Barrel shaped
chest: loops of bowel moving out of abdomen and into the chest * *?�Supracostal
retractions/grunting: sign of severe respiratory distress/impending cardiovascular
collapse. Baby should be intubated and placed on mechanical ventilation.
Pathophysiology o *?�Failure of the septum transversum to divide the pleural &
coelomic cavities during development (typically finished by week 12) allows for
bowel herniation during critical lung development resulting in lung hypoplasia. o
*?�Mediastinal shifting also causes compression of the contralateral lung o *?�When
the baby takes their first breath; normally pulmonary circuit pressure goes from
high resistance -->low resistance, allowing for pressure changes in the heart to
allow for adult circulation to be established (closure of foramen ovale, ductus
arteriosis, etc.) o *?�Lung hypoplasia + contralateral lung compression keeps
pulmonary vasculature resistance high. Resultant hypoxemia/acidosis/hypotension
cause pulmonary vasoconstriction, further worsening flow into the pulmonary circuit
o *?�The poor pulmonary flow results in acute respiratory
distress/hypoxemia/retention of CO2 Anatomy * *?�Side of defect: Left side most
common (85%), right side (10%), and bilateral (5%) is most rare. * *?�Portion of
diaphragm affected: o Bochdalek hernia: posteriolateral defect (most common; cause
classic symptoms)o Morgagni hernia: parasternal or retrostenal (rare; often no
pulmonary problems, but symptoms of bowel obstruction)o Diaphragmatic eventration:
thinning of intact diaphragm due to poor muscularization (rare!) o Diaphragmatic
agenesis: no diaphragm; very severe *?Many children have additional accompanying
anatomical defects (malrotation/non-rotation, ASD/VSD, horseshoe kidney,
polydactyly, NTDs, hydrocephalus, Trisomeies, etc.) Workup * *?�Child unstable -->?
immediate intubation * *?�Child stable or recently intubated -->?undergo NGT/OGT
tube placement * *?�NGT tube placement where NGT fails to pass -->?Choanal atresia
* *?�NGT/OGT passes past pharynx + CXR o Tube won??t pass through esophagus + gas
in abdomen-->esophageal atresia + TEFo Tube won??t pass through esophagus & no gas
in abdomen-->esophageal atresia & no TEFo Tube in stomach but abdominal contents in
thorax -->?CDHo Tube in stomach with normal abdomen -->?cystic lung lesion or
bronchopulmonary sequester Prognosis*?Survival rate between 60-80% and directly
correlates with degree of hypoplasia Management*?First Step: intubate if in
respiratory distress o Best to intubate immediately without bag-mask oxygen
delivery, as the air rush of the bag-mask can cause significant barotrauma to the
already poorly functioning lung tissue * *?�Second Step: placement of NGT/OGT with
suction to decompress stomach (open up more space for compressed lungs) & search
for atresias * *?�Third step: admission to NICU with proper blood
pressure/ventilator support o FiO2 100%; PEEP at 3-5cmH2O; permissive hypercarbia
(PCO2 <60mmHg) and O2 saturation levels between 80-95% are acceptable to minimize
barotrauma of aggressive ventillationo Nitric oxide inhalation may be used to
decreased pulmonary HTNo Extracorporeal membrane oxygenation (ECMO) may be used if
child is refractory to these things * *?�Surgical Repair of Defect: delayed until
evidence of lung maturation in NICU (simply with time and support). Whenever pt is
being weened down on vent settings, surgery can be considered. * *?�Work-up for
further congenital anomalies is also warranted Chapter 31: Newborn with Bilious
Emesis � Duodenal Atresia Presentation *?Bilious Vomiting: yellow/green stained
vomit proves that the GI tract is patient past the Ampulla of Vater (rules out
pyloric stenosis). Typically, this type of vomiting indicates a surgical problem o
Note that 20% of pts with duodenal atresia will have it before the Ampulla of
Vater; this will lead to non-bileous vomiting. Thus, just because it??s non-
bileous, doesn??t mean it??s not duodenal atresia. * *?�Polyhydraminos: too much
amniotic fluid; can be an indicator impaired swallowing (which includes GI
obstruction) or urine overproduction (maternal diabetes, twin pregnancy) * *?
�Passage of meconium: yes, even with bowel obstruction, the infant may still pass
meconium. Lanugo, amniotic fluid, bile will not be able to form it, but mucus is
shed throughout the GI tract (even with an obstruction) thus can form meconium * *?
�??Double Bubble?? sign on CXR: two pouches of gas (stomach and proximal duodenum)
seen due to gas filling the stomach, a stricture point at the pyloric sphincter,
then gas filling duodenum proximal to the atresia point. Pathophysiology * *?�Bowel
obstruction may in intrinsic (duodenal atresia) or extrinsic (annular pancreas,
adhesive Ladd??s bands); but gas throughout the bowel with signs of obstruction
points to partial obstruction vs total * *?�Duodenal development involves lumen
obliteration around week 8, with subsequent re-canalization afterward. Failure of
recanalization results in obstruction * *?�Jejunal/Ileal development does not
undergo this obliteration/recanalization process and obstruction is the result of
poor bloodflow causing segmental ischemia-->segmental obstruction * *?�There are
several associated abnormalities with duodenal atresia with the top 4 being Down??s
syndrome, Annual pancreas, Malrotation of the gut, and congenital heart disease.
Workup * *?�First Step: IV access, fluid resuscitation, NGT placement for stomach
decompression * *?�If unstable: suspect malrotation/volvulus -->?prophylactic ABX +
exploratory laparotomy * *?�If stable: AP/lateral CXR o No dilated loops of bowel
(proximal obstruction) + Double bubble + no distal bowel gas = duodenal atresia o
No dilated loops of bowel (proximal obstruction) + Double bubble + distal bowel
gas-->Upper GI contrast study o Dilated loops of bowel (distal obstruction)--
>contrast enema to assess Lower GI tract Management o Workup as indicated aboveo
Surgery should be delayed for thorough workup if patient is stable; but clinical
instability warrants emergent trip to the OR for exploratory laparotomy for repair
of malformed gut Areas to Get in Troubleo Inadequate resuscitation before emergent
surgery-->hypovolemia can result in hypotension that??s exacerbated by anesthesia,
which may lead to shock!o Not working up cardiac defects-->nearly 20% of babies
with duodenal atresia will have cardiac defects due to comorbidity with Down??s
Syndrome! These may take precedence over the GI problem and should be addressed
first.o Damage to annular pancreas-->this is another common co-malformation with
duodenal atresia. In surgery care must be taken to not damage the pancreas as it
may lead to pancreatic enzyme leak! Chapter 32: Infant with Bilious Emesis �
Malrotation with Midgut Volvulus Bilious Emesis Differential Based on Age * *?�Any
age � Adhesions, Hirschprung??s disease, incarcerated inguinal hernia, malrotation
w/volvulus * *?�Neonate (0-1mo) � annular pancreas, duodenal atresia, imperforate
anus, jejunoileal/colonic atresia, meconium ileus, meconium plug, necrotizing
enterocolitis * *?�Infant (1-24mo) � intussusception * *?�Child (2-12hr) � ileus
2nd to appendicitis, intussusception Presentation o *?�Bilious or nonbilious
vomiting (depends on part that has undergone volvulus) should always prompt a
search for midgut volvulus, as it can be a life threatening condition! o *?
�Basically any developmental defect (esp of the gut) puts a patient at risk for
volvulus Pathophysiology * *?�The midgut is defined by receiving blood from the
superior mesenteric artery (starting at the Ligament of Treitz) and includes the
2nd part of the duodenum through the proximal 2/3 of transverse colon * *?
�Development of the midgut occurs in the 6th week of gestation with rapid
elongation and herniation into the umbilicus. Ultimately this section of bowel
undergoes 270o of counterclockwise rotation, finally finding it??s final resting
spot around week 12. * *?�Malrotation occurs when midgut starts to take it??s first
90o angle turn and return from it??s herniated position back to the abdominal
cavity. Improper fixation causes the remaining 180o of turning to occur around the
midgut mesentery, giving the classic ??corkscrew?? appearance. * *?�Problems occur
when this bowel becomes kinked, resulting in obstruction and strangulation -->?
bowel ischemia and eventually death/perforation * *?�While acute volvulus is an
emergent surgical event, malrotation doesn??t necessarily cause volvulus AND
volvulus may ??kink and un-kink?? causing colicky symptoms chronically. Workup o *?
�If patient is hemodynamically unstable, skip imaging and go to the OR o *?
�Abdominal X-ray: exclude perforation (free air under diaphragm) o *?�Upper GI
series with contrast: show the course of the gut and will be diagnostic for
volvulus o Most commonly, this is a normal study o Classically shows ??corkscrew??
gut from improper rotation around mesentery Management * *?�If free air under
diaphragm or hemodynamically unstable proceed to surgery without more imaging * *?
�Surgical fixation is necessary for resolution of malrotation/volvulus o IV fluid
resuscitation + ABx + NGT for stomach decompression + emergent laparotomyo If bowel
is not infarcted-->Ladd??s Procedure (un-twisting, division of Ladd??s bands,
fixation + prophylactic appendectomy to avoid confusing symptoms later in life
should appendicitis occur) o If bowel is infarcted -->?bowel resection with Ladd??s
Procedure *?During surgery; large bore NGT should be passed through the end part of
the duodenum to rule out atresia or other malformations of the gut *?If pt is found
to have asymptomatic malrotation, surgery the the earliest convenience should be
done Chapter 33: Infant with Non-Bilious Emesis � Hypertrophic Pyloric Stenosis
Differential Dx * *?�Surgically managed: antral web, pyoric atresia, pyloric
stenosis, GERD from anatomic defect * *?�Medically managed: acute gastroenteritis,
GERD, metabolic disorders, pylorospasm Presentation *?Healthy baby with progressive
non-bilious, projectile vomiting immediately following meals; baby will always seem
hungry despite vomiting (??hungry baby!??) o Vomiting only food/mother??s milk
directly after or during feeding sessionso Olive shaped mass can be palpated and
visible peristalsis can be seen in upper abdomen o Sunken fontanelles from
dehydration *?Risk factors: first-born child, erythromycin administration, formula
feeding (late presentation at 3-5wk) Pathophysiology * *?�Poorly understood; but
histologic evidence points to immature/absent ganglia resulting in inability of
pylorus to relax, resulting in hypertrophy/hyperplasia and obstruction * *?�Stomach
muscle hypertrophy/dilation occurs due to vigorous peristalsis in attempts to pass
chyme through the obstructing pylorus * *?�As stomach peristalsis strength grows,
it becomes so intense that is overwhelms the lower esophageal (cardiac) sphincter,
resulting in projectile vomiting Workup o *?�If palpable ??olive?? is appreciated
-->?this is diagnostic, no further workup needed o *?�If no ??olive?? is
appreciated -->?abdominal ultrasound showing pyloric thickness >3mm & length >15mm
are typically diagnostic (although this number can change with age!) o *?�If still
uncertain or negative ultrasound with high suspicion -->?upper GI series with
contrast showing delayed emptying, retrograde peristalsis, and ??string sign??/??
tit sign?? at the pylorus is diagnostic o Major concern for aspiration of contrast
fluid (as the child will surely vomit anything in it??s stomach; thus this test
should be done only if needed!)*?CMP may show a hypochloremic, hypokalemic
metabolic alkalosis from protracted vomiting o Hypochloremia � loss of Cl- ions
from HCl in vomito Hypokalemia � dehydration from vomiting results in aldosterone
activation to restore intravascular volume with subsequent Na+ retention and K+
wastingo Alkalosis � with decreasing K+, but still demand for Na+ resorption, the
kidney is less able to used the Na+/K+-antiporter. Na+ traveling more distally in
the nephron results in more activation of the Na+/H+ antiporter, wasting H+ to save
Na+ resulting in paradoxical aciduria. Management*?First Step: IV access with fluid
resuscitation for protracted vomiting in this order: o 1st - Isotonic normal saline
bolus at 20mL/kgo 2nd � D5 with 1�2NS at 1.5x normal infusion rateo Once child
urinates � add 20mEq/L KCl to the already running fluid o Electrolyte abnormalities
should be corrected before surgery *?Ramstedt pyloromyotomy � small incision into
pylorus with spreading and fixation of the muscle to relieve the obstruction; air
or methylene blue are introduced via NGT to prove patency/lack of leak. o Should be
delayed until proper fluid resuscitation/electrolyte balancing has occurredo
Optimal fluid status shows normal urine output, serum bicarb <30mmol/L and normal
K+ o Pt should be able to eat a few hours following surgery, although post-op
vomiting isn??t uncommon. Vomiting 3-4 days following surgery indicated
complication Areas of Trouble * *?�Inadequate fluid resuscitation may lead to
anesthesia induced hypotension/death * *?�Leak � fever, tachycardia -->?feeding
intolerance, leukocytosis -->?peritonitis, sepsis; must be re- operated on to fix
the leak Chapter 34: Infant Born with Abdominal Wall Defect �
Omphalocele/Gastroschisis Differential Dx * *?�Gastroschisis � discussed below * *?
�Omphalocele � midline abdominal wall defect with herniation of gut contents;
amnioperitoneal membrane covering gut contents, umbilical cord insertion into this
membrane; heightened risk for abnormal formation of other systems; liver herniation
may allow for earlier detection * *?�Bladder/Cloacal Exstrophy � exstrophy of sac
filled with hemi-bladder/urethra/kidney/intestine; typically occurs inferior to
umbilical stalk, often sac partially divides two hemi-bladders (inside and
outside), often extensive associated developmental defects * *?�Prune Belly
Syndrome � abdominal wall hyposplasia, gut contents held within collagenous wall
(making it ??pruned??), 95% males, associated with UG system underdevelopment
(hypoplastic prostate, bilateral undescended testes, infertility, bladder outlet
obstruction) * *?�Urachal Abnormality � communication between bladder/anterior
abdominal wall from poor/absent ablation of the urachus. May be fistula/cystic
sac/small outpouching. Associated with NTDs and omphalocele Gastroschisis o *?�Risk
Factors: <20yr, white race, single pregnancy, low BMI, frequent UTIs, cigarette
smoking, drug or alcohol use o *?�Presentation: Paraumbilical (right sided), small
(<5cm) abdominal wall defect with evisceration of gut contents and sometimes
associated evisceration of gonads, bladder, & stomach o Lacks membrane covering cut
contents (gut exposed to open air)o Cord insertion is normal at the umbilicuso
Causes matting, dilation, and thickening of bowels; malrotation is common; Ileus is
common o Rarely associated with other developmental abnormalities; intestinal
atresia rarely (10-25%) o Maternal AFP may be mildly elevated *?Pathophysiology:
not totally clear, but thought to be due to vascular accident in the umbilical ring
resulting in poor development and defect development. Right sided defect is thought
to be more common due to involution of the right umbilical vein o Bowel
abnormalities are due to extended exposure to amniotic fluid causing inflammation *
*?�Workup: Covering/Peds Surgery consult, blood labs, IV fluids, urine output
monitoring, Full body X-ray for anatomic survey/implanted device location check *
*?�Management: o Initial: stabilize airway, Central/Peripheral IV access, IV
fluids, cover with sterile plastic wrap, warming lamp, OG-tube decompression,
urinary catheter, broad spectrum Abx o Place viscera in sterile dacron-silastic
silo to allow for gradual reduction as inflammation slows o Attempt reduction &
schedule for surgical reduction when abdominal laxity will facilitate repair o
Ventilation/fluid & nutrition support with intra-abdominal monitoring for healing
Omphalocele * *?�Risk Factors: <20 or >40yr, high BMI, SSRI use/family Hx * *?
�Presentation: Umbilical/epigastric/or hypogastric variable sized (but often large)
abdominal wall defect with herniation of gut and sometimes the liver into a
membrane sac o Covered in amnioperiotneal membrane (10-20% will rupture)o Cord
insertion is into the amnioperiotneal membraneo Bowl is typically normal appearing;
malrotation often present; bowel function normal o Commonly associated with other
developmental disorders (Beckwith-Wiedemann, Trisomy 13/18, Pentology of Cantrell,
various defects of the gut o Maternal AFP severely elevated*?Pathophysiology:
results from arrest of lateral-body fold migration and body wall closure during
organogenesis. When normal gut herniation occurs around week 5, development
arrests, leaving the herniated gut in place until birth. This is thought to be due
to a failure of cell migration, thus the higher association with concomitant
developmental
defects. o Note that liver herniation (giant defect) is rarely associated with
chromosomal abnormality! *?Workup: Peds Surgery consult, blood labs, IV fluids,
urine output monitoring, Full body X-ray for anatomic survey/implanted device
location checko Echocardiography for assessment of heart defects & genetic testing
also recommended *?Management:o Initial: stabilize airway, Central/Peripheral IV
access, IV fluids, cover with sterile plastic wrap (if sac is ruptured), warming
lamp, OG-tube decompression, urinary catheter, broad spectrum Abx o If ruptured �
follow gastroschesis algorithmo <2cm defect � immediate surgical reduction -->?
support for healingo 2-9cm defect � place viscera into sterile dacron-silastic silo
for reduction -->?surgery/supporto >9cm defect � apply sclerosant to
sac/cardiopulmonary stabilization -->?sterile dacron-silastic silo for reduction--
>surgery/support Which is More Urgent? Why? * *?�Short Term � Gastroschisis. The
exposed, inflamed, nonfunctional bowel requires immediate protection and surgical
correction. The child also has increased insensible fluid losses which can also
cause problems * *?�Long Term � Omphalocele. The child has a protected, functional
bowel. However, the high association with other developmental defects makes the
child??s future development very difficult and sometimes, not viable. Areas to Get
in Trouble o *?�Remember to note respiratory distress and intubate as necessary o
*?�Remember to carefully check for bowel ischemia/necrosis and address as needed o
*?�Remember to wrap bowel in plastic wrap & warm with lamp immediately. Moist gauze
is avoided as it is not water-tight and will cause significant loss of insensible
fluids o *?�TPN should be provided to patients with slow return of bowel function.
Matted/inflamed bowels are likely to be non-functioning. o *?�Post-reduction,
abdominal compartment syndrome (low urine output, insufficient ventilation,
positive fluid balance) may occur. It should be monitored with intra-abdominal
pressure monitoring. Chapter 35: Excessive Drooling in a Newborn � Esophageal
Atresia with Tracheo-Esophageal Fistula Presentation * *?�Excessive drooling with
white/frothy mucus buildup in mouth/nose * *?�Cannot tolerate feedings with
immediate gagging/choking and vomiting of food * *?�Oxygen desaturation with
feeding � often implies severe abnormality in tracheo-bronchial anatomy (some of
feedings go into the lungs!) o May result in respiratory distress/pneumonia
development *?EA may manifest via polyhydramnios (failure of swallow) on prenatal
ultrasound Pathophysiology *?Esophageal Atresia: Abnormal development of trachea-
esophageal fold which normally separates the caudal primitive foregut into the
esophagus and trachea *?TEF: thought to be due to defective epithelial-mesenchymal
interactions in a lung bud that fails to develop. This lung bud wants to hang out
with the esophagus and the fistula is formed. Types of TEF * *?�Many types with
different combinations of defect/TEF * *?�Type C (proximal esophageal pouch with
distal TEF) is most common (85%) with Type A (pure EA without TEF) being next most
common (8%) Associated Abnormalities o *?�VACTERL, CHARGE, or Trisomy syndromes are
often diagnosed o *?�VACTERL = vertebral, anorectal, cardiovascular,
tracheoesophageal, renal, and limb abnormalities o *?�CHARGE = coloboma, heart
defect, atresia choane, retarded growth, genital defects, and ear defects Workup *?
First Step: Placement of NG-tube with CXR (AP and lateral) o Gastric bubble
presence = some connection between air and stomach (no EA or EA + TEF)o EA = shows
NG-tube coiled in the esophagus/mediastinum or going into the tracheao Checks for
abnormal lungs = pneumonia, primary lung lesions, congenital diaphragmatic hernia *
*?�Contrast esophagram may be used in equivocal findings; however, the concern of
aspiration pneumonitis should reserve this test only if truly necessary * *?
�Diagnosis can be made simply with history and radiologic findings consistent with
disease Management * *?�First Steps: intubate if signs of respiratory distress,
place NG-tube into esophageal pouch/elevate child?? s head (minimize vomiting thus
aspiration). * *?�If pneumonia: broad spectrum Abx & gastrotomy tube for
decompression should be placed * *?�Surgical repair: able to undergo repair surgery
as soon as patient is stable/able to tolerate surgery o Physical exam,
cardiac/renal ultrasound, ECG, and X-rays for anatomic survey must be done prior to
surgery to ensure anesthesia tolerance/find all defects for repair *?Complications:
o Esophageal anastamotic leak (15%) � often heal with stricture needing surgical
revision o Strictures (80%) � need esophagostomy and balloon dilationo GERD (100%)
with increased risk of Barrett??s esophagus *?Prognosis: 100% survival rates, but
often with significant GI complications that will be addressed Areas of Trouble *
*?�Interrupted IVC (IVC drains into the azygous vein to get to heart) � the azygous
vein is typically divided during EA/TEF repair. If interrupted IVC is present, this
will cause cutoff of lower extremity venous drainage & death of the patient * *?
�Right-sided aortic arch � rare, but possible (esp. with developmental defects!).
Right thoracotomy is the typical approach for repair, thus right-sided AA would
result in disaster. If present, a left thoracotomy is the proper approach. * *?
�Avoid intubation/ventilation if possible as the abnormal connections between the
trachea and GI tract may result in pumping air into the GI tract-->abdominal
distention. This distention will compress lung volumes, leading to worsening lung
function (the opposite of what you want!) Chapter 36: Recently Changed Skin Lesion
� Cutaneous Cancers Pathophys: UV light exposure (esp. UVB) resulting in DNA damage
Risk Factors: o *?�UV light exposure � ask about childhood blistering/peeling
sunburns, use of tanning salons, & overall sun exposure. All of these can result in
double the risk for skin cancers. o *?�Immunosuppression � difficulty in repairing
damage to DNA o *?�Fair-skinner/blue eyes � less pigmentation to protect from UV
rays * *?�Certain occupations are predisposed to high sun exposure like farmers,
lifeguards, construction workers, gardener, field worker, etc. * *?�Chronic Skin
inflammation (SCC only) � chronic venous ulcers, burns, long-standing infections,
hiradrenitis suppurativa, HPV, etc. 2762/2603: Basal Cell Carcinoma *?Most common,
often an excellent prognosis. Correlates with cumulative sun exposure o Worst
subtype is morpheaform (characterized by collagenase production) o Classically the
upper lip will be this type of skin cancer * *?�Presentation: pearly/rolled edge
nodule with keratinized or ulcerated center. Sometimes featuring spider angiomata
on the lesion, oozing or crusting * *?�Dx: clinical picture and biopsy * *?�Tx: o
Superficial � excision (3-5mm margin) or local destruction
(cryotherapy/electrodessication) o Deep � MOHS surgery 2604/4033/4319: Squamous
Cell Carcinoma * *?�Intermediate incidence with intermediate prognosis, typically
not metastatic when found, but will invade if left untreated. Correlates with # of
severe sun exposure events (burns, tanning beds, etc.) * *?�Presentation: rough
scaly plaque/nodule with possible hyperkeratosis/ulceration/bleeding. Classically
can cause neurologic damage due to perineural invasion (numbness/parastheisa) o
Sunburns, radiation, immunosuppression, burns, scars, and warts are all risk
factorso Note that if you??ve a lesion on the lower lip (more sunlight exposure) is
SCCo Note that a Marjolin ulcer is an SCC arising from the site of a
scar/burn/previous injury and has an increased risk of metastaseso Bowen??s Disease
is a SCC in-situ appearing as an erythematous plaque with adherent yellow crust.
While is may become SCC, it has no metastatic potential * *?�Dx: skin biopsy that
includes the deep reticular dermis (assess depth of invasion) showing
dysplastic/anaplastic keratinocytes/keratin pearls * *?�Tx: o Low risk: excision
(5-10mm margin) or local destruction (cryotherapy/electrodessication) o High risk
or cosmetic areas: Mohs micrographic surgery 2767/2765/4312: Malignant Melanoma *
*?�Arises from melanocytes (neural crest derivatives) either pre-existing or new-
onset lesion * *?�Least common skin cancer, but most deadly o Considered the most
common malignancy of women age 25-29o Women typically get it on the legs while men
get it on the backo Sites of Metastases: other parts of skin > lung > liver > brain
> bone > small bowel o Most common cancer to metastasize to the small bowelo
Digital melanoma is most commonly on the great toe *?Risk Factors:o UV light
exposure � ask about childhood blistering/peeling sunburns, use of tanning salons,
& overall sun exposure. All of these can result in double the risk for skin
cancers.o Immunosuppression � difficulty in repairing damage to DNAo Fair-
skinner/blue eyes � less pigmentation to protect from UV rayso Certain occupations
are predisposed to high sun exposure like farmers, lifeguards, construction
workers, gardener, field worker, etc. *?Subtypes:o Superficial Spreading � most
common & good prognosis due to long horizontal growth phase occurring before a
vertical growth phaseo Lentigo maligna � best prognosis; appears as a group of
freckles growing as a unito Acral lentiginous � most common in dark-skinned
individuals & poor prognosis likely due to difficulty in detection. Often subungal,
mucous membranes, or on palms/soles. NOT related to UV light exposureo Nodular �
worst prognosis (rapid vertical growth), much more variable presentation that other
subtypes making it harder to catch in early stages*?Presentation: new or existing
melanotic skin lesion demonstrating o o ABCDEs (Asymmetry, Raggy Border,
verigated Color, Diameter >6mm, Enlargement or new symptoms)Ugly Ducking Sign
(suspected melanoma simply looks out of place next to other benign nevi on the
patient??s skin) Metastatic Disease may show palpable lymph nodes or other signs*?
Dx: Incisional/punch or excisional biopsy down to dermis to show depth of invasion
o Shave biopsy is inappropriateo Breslow Thickness will determine severity of
disease o Labs are taken to check for signs of metastatic disease ??If no palpable
lymph nodes: CBC, LFTs, LDH, and CXR??If palpable lymph nodes or signs of
metastatic dx: CBC, LFTs, LDH, CT C/A/P & PET scan ??If signs of central neurologic
Dx: MRI of brain *?Tx: surgical excision with wide margins (1-2cm)o Margins will
depend on Breslow Thicknesso Sentinel Lymph node biopsy is indicated in patients
with depth >0.75mmo Lymph node dissection indicated in patient with palpableo
Adjuvant therapy is of questionable benefit and isn??t always usedo MOHS surgery is
considered a poor option for melanoma due to difficulty in obtaining stained
histologic slides during the surgery necessary for visualizationo If fingernail
melanoma: amputation of finger at joint just proximal to the lesion *?Follow-up:
every 3-6mo for the next 3yr; regional lymph node disease is most common recurrence
2764: Seborrheic Keratoses*?Benign lesion that tends to favor the face/trunk/old
people and is often consider unsightly o May be indicative of underlying GI
malignancy as the Sign of Leser-Tr�lat where many of these lesions appear rapidly.
* *?�Presentation: waxy/greasy, ??stuck-on??, well circumscribed lesion that may be
flat or raised with normal surrounding skin. Can vary from pink/white to pale to
brown/black. Typically, slowly enlarging. * *?�Dx: clinical * *?�Tx: none needed
except for cosmetic reasons 4410: Actinic Keratosis * *?�Presentation:
hyperkeratosis causing ??sand-paper like?? papules in areas of sun exposure. Often
begin small/flat but may accumulate becoming ??cutaneous horns??. Pre-malignant for
SCC * *?�Dx: shave biopsy with light microscopy showing characteristic cell
proliferation * *?�Tx: electrodessication or cryotherapy o Chapter 37: Right Leg
Pain, Swelling, and Erythema for Two Days � Necrotizing Soft Tissue Infection
(NSTI) With a presentation like this, many infectious and cutaneous problems can be
on the differential. It??s important to know how to have some quick
differentiators: * *?�NSTI � will be discussed in detail below * *?�Cellulitis �
often redness and swelling of the skin, but without major tissue destruction * *?
�Cutaneous anthrax � painless/itchy black eschar with edema/erythema * *?�DVT �
unilateral (often leg) swelling/erythema/pain, with history of hypercoagulability,
immobility, or some inflammatory state * *?�Hypersensitivity � Redness/swelling
with no fever/leukocytosis. Ask about plant/animal exposure. * *?�Stasis dermatitis
� fibrosis and ??brawny?? discoloration secondary to venous insufficiency. May
become inflamed/crusted with exudate. Hx of DVT and cardiovascular problems is
common. * *?�Sweet??s Syndrome � acute eruption of plaques/vesicles with erythema,
fever, and neutrophilia. Associated with G-CSF administration, pregnancy, and
malignancy. Pathophysiology o *?�May involve skin (necrotizing cellulitis), fascia
(necrotizing faciitis), or muscle (necrotizing myositis) o *?�Organisms responsible
help organize the ??typing?? of infection: Type I (polymicrobial), Type II (Group A
Strep) and Type III (Clostridium perfringens or ??gas gangrene??) o *?�Note that
infection with Clostridium septicum is associated with occult malignancy, esp.
colon cancer! o *?�Fournier??s gangrene is NSTI of the scrotum/perineum
Presentation o *?�Vitals: Fever, tachycardia, hypotension, leukocytosis, low serum
sodium o *?�Skin: Acute painful area of erythema/swelling/bullae (tissue
destruction and fluid accumulation/ violacous skin (ischemia to dermis/epidermis).
Classically ??pain out of proportion to appearance?? o *?�Creptius and gas bubbles
on X-ray indicate necrosis of tissue with gas-forming organisms (Clostridia sp)
Risk Factors * *?�Anything that may depress immunity or tissue perfusion (diabetes,
IV drug use, alcohol abuse, obesity, WBC cancers, chronic steroid use, renal
failure, liver cirrhosis, etc.) * *?�Recent wound or surgery (introduction of
bacteria into the area) Diagnosis * *?�Often diagnosed clinically, but important to
distinguish from cellulitis as management is total different * *?�Definitive
diagnosis is based on surgical debridement pathologic examination (murky fluid,
grey fascia, lack of bleeding from fascia) * *?�If you are highly suspicious but
not sure of diagnosis o X-ray showing bubbles in soft tissue can help reassure the
diagnosis o Surgical debridement for definitive diagnosis can be undertaken on high
suspicion alone Management * *?�First Step � IV fluids, broad spectrum Abx, and
aggressive surgical debridement * *?�When debriding, you go until you find viable
soft tissue without evidence of infection. o Typically, dead tissue is liquefied
(grey, ??dishwater?? fluid). Fascia can appear grey with little bleeding and may
separate from muscle too easily on digital exploration o It is unacceptable to
leave borderline-looking tissue, thus you must go until obviously healthy tissue is
visualized * *?�If extensive muscle necrosis is present, amputation may be the best
option to save patient??s life * *?�A second-look operation should be scheduled for
24hr post-initial debridement to ensure that more tissue has not become infected.
Further debridement is necessary if dead tissue is found. * *?�Hyperbaric oxygen
may be used adjectively along standard fluid/Abx/debridement care * *?�Sadly,
mortality is around 25% for these patients Chapter 38: Post-Operative Bleeding �
Congenital & Acquired Bleeding Disorders Pre-Op History * *?�Important to ask about
history of excessive bleeding from gums, epistaxis, bleeding into muscles/joints,
excessive menstrual bleeding, & bleeding after minor procedures (tooth extraction,
skin biopsy, etc.) * *?�Ask about family history of bleeding (hints at congenital
bleeding disorders) * *?�Ask about liver/kidney disease and malabsorption syndrome
(short gut syndrome, cystic fibrosis) which may potentially limit production of
clotting factors (either directly or via Vit.K malabsorbtion) * *?�Ask about heart
disease (pt may be in anti-platelet or anti-coagulant medication) Pathophysiology o
*?�Primary Hemostatic Disorder � disorder of platelet function (quantitative or
qualitative), thus the initial clot cannot be formed properly (primary hemostasis)
o *?�Secondary Hemostatic Disorder � disorder of coagulation cascade (locking up
the platelet plug with conversion of fibrinogen-->fibrin by factor VIII) o *?
�Coagulopathy � anything impairing the body??s ability to clot blood. Note that
hypothermia and metabolic acidosis can exacerbate coagulopathies! o *?�Medical
post-op bleed � diffused bleeding caused by underlying coagulopathy. Because it??s
diffuse, these bleeds will not benefit from re-operation, but rather medical
management/support o *?�Surgical post-op bleed � focal bleeding from an artery or
vein that was not properly ligated during surgery. Re-operation and proper ligation
of bleed is the best treatment o *?�Fibrinolysis � normal process which limits
coagulation to only the area of damage. Plasmin binds to fibrin, and breaks it up,
breaking up the cross-linked platelets o *?�Hyper-Fibrinolysis � excess plasmin
production that counteracts clotting and leads to bleeding o Primary � increase in
circulating tPA (poor clearance, loss of anti-tPA mechs) o Secondary � systemic
hypercoagulable state, leading to physiology tPA increase (DIC, etc.) *?
Thrombocytopenia � <150,000 platelets causing in primary hemostatic disorder o
Symptoms are based on how low the count is??>100,000 � asymptomatic??50,000-100,000
� occasional petechiae??10,000-50,000 � purpura after minor trauma-->Plt infusion
if invasive procedure ??<10,000 � spontaneous bruising/bleeding gums -->?everyone
gets Plt transfusion o Many causes (below), but most common cause is alcohol abuse
* *?�Vitamin K dependent clotting factors are factors II, VII, IX, X, protein C,
and protein S * *?�INR � measures extrinsic (VII, X)/common pathways (I, II, V);
monitors Warfarin * *?�PTT � intrinsic (VIII, XI, X, XI, XII)/common pathways (I,
II, V); monitors Heparin Specific Disease Processes[Congenital
Coagulopathies]--------------------------------------------------------------------
----------------------------------------- 2256/4412: Anti-phospholipid syndrome *?
Presentation: typically, a woman with recurrent fetal loss or arterial/venous
clots. Elevated PTT despite hypercoagulable state is due to the responsible
antibodies interfering with lipid components of the PTT test itself. PTT will not
correct with 1:1 dilution of normal plasma. o Diluted Russel viper venom test OR
kaolin clotting time tests may also be used o Occurs in approx. 30% of women with
SLEo Will have a (+)VRDL/(-)FTA-ABS *?Dx: must meet 1 clinical criterion and 1 lab
criterion o Clinical: ????????o Lab: ??????Arterial/venous thrombosis>3 unexpected
fetal losses before the 10th week gestation>1 unexpected fetal loss after the 10th
week gestation>1 premature, normal birth before 34 weeks due to pre-eclampsia,
eclampsia, or placental insufficiency Lupus anticoagulant (pro-coag in-vivo and
anti-coag in-vitro) Anti-cardiolipin antibody (IgG or IgM with medium to high
titer) Anti-b2GP1 antibody (IgG or IgM with high titer) anticoagulation with LMWH
(even before testing) *?Tx: immediateo Note that corticosteroids are not the
current standard of care 4861: Hemophilia * *?�X-linked recessive disorder causing
lack of clotting factors (A =
factor VIII def; B = factor IX def) * *?�Presentation: delayed/prolonged bleeding
after minor trauma/procedure o Hemarthroses (bleed into joint), intramuscular
hematomas, GI bleeding, hematuria (without kidney damage), and spontaneous bruising
are all common signs o Labs: Prolonged aPTT with normal platelet count, bleed time,
and PT * *?�Dx: decreased amount of either factor VIII or factor XI * *?�Tx:
Administration of missing factor through injection o Desmopressin can promote
Factor VIII production and be used in mild Hemophilia A Von Willebrand Disease*?
Presentation: often pts unaware, as symptoms are mild. Hx of prolonged bleeding
after minor procedures (tooth extraction/skin biopsy) or excessive menses with
eventual clotting is classic. o Intra-op: diffused oozing of blood within operated
on tissueo Post-op: continued bleeding or post-op hematoma formation *?
Pathophysiology: von Willebrand Factor (vWF) is a protein that binds sub-
endothelial collagen when it?? s exposed after damage to tissue. vWF provides a
link between the collagen and the GP1b receptor on platelets, allowing for primary
hemostasis of be achieved. o A lack of vWF causes difficulty in primary hemostasis
due to poor platelet plug formation o vWF is also a co-factor for factor VIII, thus
low wVF can decrease factor VIII levels * *?�Labs: normal to prolonged PTT
(decreased factor VIII), normal INR (coagulation cascade intact) increased bleed
time (BT; poor platelet plug formation) * *?�Subtypes: o Type 1 (AD): quantitative
decrease in vWF levels; mild symptomso Type 2 (AD): quantitative decrease and
qualitative dysfunction; 4 subtypes with 2A being the most common; all cause
moderate symptomso Type 3 (AR): severe quantitative decrease, rare, most severe
symptoms * *?�Dx: ??? * *?�Tx: ??? [Acquired
Coagulopathies]--------------------------------------------------------------------
------------------------------------------- Liver Failure o *?�Coagulation factor
production is a job of the liver, thus dysfunction of the liver results in poor
factor production-->coagulopathy (increase PT/INR) o *?�Note that Factor VIII is
not exclusively produced in the liver...thus all other coagulation factors will
drop, but Factor VII will be at normal or elevated levels! *?Tx: FFP,
cryoprecipitate, coagulation factor infusion, platelet transfusion Renal Failure *
*?�Failure to eliminate uremic toxins from the blood results in uremia-->platelet
dysfunction * *?�Will likely cause an anion-gap metabolic acidosis and can be
initially managed with emergent dialysis (definitive) & administration of
desmopressin (symptomatic) Malnutrition4112: Vitamin K Deficiency o *?�Vit K is a
critical co-factor for enzymatic carboxylation of clotting factors II, VII, IX, X.
Typically vitamin K stores can last 30 days but in sick folks only last about 1
week! o *?�Presentation: bleeding diathesis with evidence of pathologic
anticoagulation o Classically lack of supplementation at birth, malabsorption for
any reason, or liver disease will lead to Vit.K deficiency * *?�Dx: clinical
presentation * *?�Tx: Fresh Frozen Plasma administration with vitamin K injection
Acquired FVIIII (Factor XIII) inhibitors *?Some funky autoimmune destruction of
factor VIII either post-partum, in rheumatic disease, or in malignancy presenting
with new purpura/soft tissue bleeding
[Thombocytopenia]------------------------------------------------------------------
------------------------------------------------------ Impaired Production of
Platelets * *?�Occurs due to medications/infection/alcohol (most
common)/nutritional deficiency * *?�Decreased megakaryocytes in bone marrow biopsy
is diagnostic * *?�Treatment is based on underlying disorder (treat disease, stop
medication, etc) Platelet Pooling o *?�Sequestration in the spleen; can happen for
various reasons o *?�Tx: splenectomy if symptomatic 4316/4859/4616/2250: Heparin-
Induced Thrombocytopenia (HIT) *?Type 1 � mild thrombocytopenia (<100,000) usually
within 2 days of starting Heparin o Does not cause any ill effects, nor warrants
intervention. o Not immune mediated and will resolve within a few days after
stopping heparin*?Type 2 � immune mediated platelet activation by HIT antibody (IgG
against PF4, which is exposed with platelet exposure to heparin)o Presentation:
worsening thrombosis in response to heparin (usually 5-10 days, may be earlier if
prior exposure to heparin), skin necrosis in injection site (belly, periumbilical)
or gangrene distally (blue/darkening toe can be a confusing, but classic symptom!)
* ??�Thrombocytopenia � destruction of platelet-HIT complexes by spleen and on-
going thrombus formation * ??�Thrombus formation � HIT antibodies activate
platelets with promote aggregation and activation of coagulation cascade, promoting
arterial/venous thrombus formation o Dx: serotonin release assay (gold standard) or
immunoassay (only high titers)o Tx: immediate cessation of heparin with initiation
direct thrombin inhibitor (fondiparinux or argatroban) � start treatment
immediately before confirmatory testing 4338/4339: Thrombotic Thrombocytopenic
Purpura (TTP) * *?�Autoimmune or hereditary decrease in ADAMTS13 enzyme (cleaves
vWF multimers) resulting in extra- long vWF which promotes intravascular platelet
thrombus formation, which can shear passing RBCs * *?�Presentation:
Thombocytopenia, Microangiopathic hemolytic anemia, renal insufficiency, neurologic
changes (headache, confusion, stroke, coma), and fever. Sometimes scleral icterus.
o Labs: normal PT/PTT (no activation of coagulation cascade!),
anemia/thrombocytopenia, elevated creatinine (kidney damage from clots), o Smear:
fragmented RBCs (schistocytes) * *?�Dx: presentation with labs/smear * *?�Tx:
emergent plasmapheresis (replenishes ADAMTS13/removes possible autoantibody),
corticosteroids, FFP for support, +/- splenectomy 4383/4860: Immune
Thrombocytopenia (ITP) * *?�Platelet destruction/inhibition of megakaryocyte
production by IgG anti-platelet membrane glycoprotein antibodies * *?�Presentation:
asymptomatic petechiae/ecchymosis, mucutaneous bleeding, possible recent viral inf.
o Labs: isolated thrombocytopenia (<100,000)o Smear: megakaryocytes wit no other
abnormalities * *?�Dx: clinical presentation, CBC, Labs with HIV/HCV testing (may
be cause of disease) * *?�Tx: o Kids: Skin only = observe | bleeding = IVIG or
glucocorticoidso Adults: Plt >30k + no bleed = observe | Plt <30k or bleed =
Glucocorticoids-->IVIG, dapsone, or danazol-->splenectomy (in that order of
escalation) DIC * *?�Presentation: severe deterioration in the setting of some
other disease process; often diffused bleeding/evidence of clotting, diffuse end-
organ dysfunction, and shock are present * *?�Etiology: o Delivery (of a baby):
amniotic fluid enters the blood, activating the coagulation cascade (tissue
thromboplastin present in fluid) o Infection: sepsis causing wide-spread
endothelial cell production of tissue factor OR gram(-) rod sepsis results in
widespread TNF-a production o Cancer: Auer rods in AML active the coagulation
cascade; mucin with adenocarcinoma activating the coagulation cascade * *?
�Pathophysiology: initial coagulopathy that leads to widespread
clotting/consumption of platelets & clotting factors causing clotting and bleeding
diffusely throughout the body * *?�Labs: increased INR, increased PTT, decreased
fibrinogen, increased fibrinogen split productions/D- dimer, decrease hemoblobin,
deceased hematocrit * *?�Dx: presentation/labs * *?�Tx: treatment of underlying
problem; platelet/FFP/cryoprecipitate infusion may be used as support 4796: HELLP
syndrome o *?�Presentation: pre-eclampsia, nausea/vomiting, RUQ pain; o *?�Labs:
Hemolysis (low hemoglobin, low haptoglobin, schistocytes), Elevated LFTs, and Low
Platelets o *?�Pathophysiology: Unclear, may have to do with aberrant placental
development o *?�Dx: clinical presentation with agreeing labs o *?�Tx:
stabilization with IV fluids/MgSO4, Methyldopa to reduce BP, corticosteroids to
speed fetal lung development with immediate delivery of the fetus (best if >34wk
gestation) Common Anti-platelet/Anti-coagulant Medications * *?�Aspirin (non-rev) �
COX-inhibitor decreasing PGE2/TXA2 formation to inhibit platelet activation * *?
�Clopidogrel (non-rev) � blocks ADP receptors stopping platelet-fibrinogen binding
* *?�GPIIb/IIIa (abciximab; non-rev) � stops GPIIb/IIIa receptors on platlets to
stop plt-plt aggregation * *?�Heparin (protamine sulfate) � activates AT-III -->?
inactivates thrombin/factor Xa * *?�LMWH (enoxaparin; protamine sulfate) � binds
factor Xa to inactivate * *?�Direct thombin inhibitor (agatroban; hemodialysis) �
inhibits thrombin to stop clot cross-linking * *?�Warfarin (FFP or Vit.K) �
inhibits Vit.K-epoxide reductase -->?stops II,VII,IX,X production Work-up *?
Clinical history, PTT/INR are the best way to workup a bleeding disorder of any
kind post-op Management * *?�First Step: ABCs, adequate IV access, assess H&P for
bleeding disorder, order a type-and-cross, CBC, INR, and PTT * *?�Re-exploration
surgery should only be done if medical bleed has been effectively ruled out and the
patient fails to stop bleeding/becomes hemodynamically unstable Complications of
Blood Transfusion4160/4671/4672: Transfusion Reactions and Special Situations with
Blood Transfusion *?There are several adverse reactions that can occur with blood
transfusion, however more common ones have fairly specific time frames where they??
ll appear, giving you a clue to the problem o Seconds-Minutes � anaphylactic
reactiono Within 1hr � acute hemolytic reaction (poor type matching)o 1-6 hrs �
Transfusion-related acute lung injury (TRALI) or Febrile Non-hemolytic reactions o
2-10 days � delayed hemolytic reaction *?Anaphylactic reactiono Rapid shock,
angioedema/urticaria, and respiratory distress within minutes of transfusiono
Caused by Anti-IgA antibodies in recipient reacting to IgA in the donor blood
(occurs classically in patients with select IgA-deficiency)o Tx: stop transfusion;
epinephrine, intubation, fluid resuscitation *?Acute Hemolytic Reactiono Occurs due
to poor type matching (clerical error) within the 1st hour of infusion o
Presentation: fever, chill, flank pain, hemoglobinuria -->?DIC/renal failureo Dx:
(+)direct Coombs test or pink plasma (due to hemolysis)o Tx: immediate cessation of
transfusion and fluids for supportive therapy *?Febrile Non-Hemolytic Transfusion
reactiono Most common adverse reaction to a blood transfusiono Because small bits
of leukocytes/plasma cells are present even in packed RBC transfusions, WBCs can
release cytokines in storage that will trigger transient fever, chills, and malaise
without hemolysis in responseo Leukoreduction is necessary to limit these reactions
� reduces number of WBCs via various methods, decreasing released cytokines AND
decreasing cytomegalovirus transmission (often resides in WBCs)o Tx: Stop
transfusion, administer anti-pyretics, and only use leukoreduced products for
future transfusions??Premedication with anti-pyretics/anti-histmaines NOT EFFECTIVE
*?Transfusion Related Acute Lung Injury (TRALI)o Respiratory distress/non-
cardiogenic pulmonary edema 6 hours after transfusion o Anti-leukocyte antibodies
in the donor??s serum cause this reaction; Antibody-WBC complex aggregates in the
lung vasculature causing inflammation and pulmonary edema o Tx: fluid
resuscitation, vasopressors, aggressive respiratory support *?Delayed hemolytic
reaction o Mild fever/hemolytic anemia 2-10 days post transfusion caused by
amnestic antibody response (antibody was previously formed, but only in low titers.
The transfusion jacked those titers up) o Dx: (+)direct Coombs or (+)new antibody
screen o Tx: supportive care Areas to Get in Trouble *?Not stopping blood thinners
early enough before surgery: Aspirin (4 days), clopidogrel (7-10 days), warfarin
(2-3 days for INR<2.0, and 4-6 days for INR at 1.0...below 1.5 is safe for
surgery!) Chapter 39: Post-operative Decreased Urine Output � Post-op AKI
Differential Dx * *?�Pre-renal � poor perfusion of a normal kidney (hypovolemia for
any reason, or CHF) * *?�Intra-renal � kidney damage causing poor function
(ischemia, toxic damage from drugs, etc.) * *?�Post-renal � obstruction in the
ureter/bladder/urethra causing backup pressure and nephron damage Presentation * *?
�Rarely physical signs of AKI; signs may be of underlying cause resulting in AKI
(oliguria with concentrated urine, signs low volume, etc.) * *?�Labs:
BUN/Creatinine (>20:1 = pre-renal azotemia, thus poor perfusion!) * *?�Urine output
o Normal Adult is 0.5mL/kg/hro Normal Child is 1.0mL/kg/hro Oliguria � less than
normal urine output for 2 consecutive hours...but not absence of output o Anuria �
lack of urine output...typically defined at 50-100mL urine over 24hr period. There
should never be 0mL urine output (this is a technical error if you see it) * *?
�Common nephrotoxic medications � contrast agents, aminoglycosides, amphotericin B,
cisplatin, cyclosporine and NSAIDs * *?�Contrast induced nephropathy � absolute
increase in Cr >0.5mg/dL or relative increase of 25% from baseline 48-72hr
following contrast administration o Prehydration with normal saline � helps ward
this off by helping flush out the contrast media o N-acetylcystine, bicarbonate,
and normal saline hydration with contrast media help prevent renal damage as well
Pathophysiology *?Kidney filtration is driven by high filtration pressure in
glomerular capillaries pushing fluid into Bowmann??s space. o Pre-renal � not much
fluid passing through overall...thus less urineo Intra-renal � glomeruli not
working properly, may not be able to accept filtrate at all o Post-renal � pressure
buildup in Bowmann??s space stops filtrate from the capillaries *?Non-renal of
increased BUN/Cr ratioo Upper GI bleed � breakdown and absorption of RBC
nitrogenous components raises BUN, but creatinine is left unchanged leading to
ratio changeso Increased urea production � often due to steroids (similar mech to
Upper GI bleed) o Low muscle mass � poor creatinine production from regular muscle
breakdown *?Unilateral kidney obstruction will NOT lead to renal failure, as the
other kidney should normally compensate for the poor-functioning kidney (unless
there??s only 1 kidney present) *?Post-Op Oliguria is a common thing as the HPA
axis under acute stress/blood loss will release Aldosterone/ADH to replete
intravascular fluid o Poor urine output is expected within 24hr post-op; any longer
than 24hr should be assessed for renal injury/hypovolemia o Post-op bleeding may
also present as oliguria (even with a normal H&H). The blood loss causes
hypovolemia, and fluids have yet to redistribute into the intravascular space,
meaning that blood total volume is low, but concentration is normal (normal H&H
with oliguria). H&H will drop over the next 8-10 hrs, revealing the bleeding * *?
�Prolonged pre-renal AKI can result in intra-renal AKI due to poor perfusion of
kidney parenchyma, which may eventually result in Acute Tubular Necrosis--
>prolonged oliguria with proper resuscitation! * *?�General anesthesia effect
causes loss of sympathetic tone o Cardiovascular function � slowed heart rate,
vasodilation, drop in BP -->?poor organ perfusiono Renal function � lack of
perfusion -->?acute insult -->?kidney damage in pt with pre-existing renal problems
(healthy folks can likely tolerate it!) Work-Up * *?�Examine for signs of
hypovolemia/hypoperfusion * *?�Labs: o BUN/Cr (allows for some identification of
renal dysfunction and may clue a pre-renal azotemia) o Fractional Excretion of
Sodium (FENa) -->?FENa = (UNa/PNa)/(UCr/PCr) * ??�Pre-renal � FENa (<1%); UOsm
(>500); UCr/PCr (>40); UNa (<20) � sodium/water being retained because of low
volume resulting in very concentrated urine (kidney works well) * ??�Intra-renal �
FENa (>1%); UOsm (<350); UCr/PCr (<20); UNa (>40) � intravascular volume is fine,
but glomeruli are being damaged, leading to wasting of Na/water * ??�Post-renal �
FENa (>4%); UOsm (<50); UCr/PCr (<20); UNa (>40); intravascular volume is fine, but
kidney is quickly being damaged by back-up of urine causing more severe features
* ??�Note that diuretics will alter these levels, making FENa useless o FEurea may
be a more useful measure to delineate different levels of renal damage when a
diuretic is in useo Urinalysis � allows for microscopic evaluation of urine for
clues to renal damage ??High specific gravity � volume depletion??Hematuria � renal
stones/damage to renal collecting system??Muddy Brown cast � acute tubular necrosis
??RBC cast � glomerulonephritis??WBC casts � interstitial nephritis or
pyelonephritis (inflammation in the kidney) ??Fatty casts � nephrotic syndrome??
Broad casts or waxy casts � chronic renal failure * *?�Imaging � ultrasound of
bladder/ureter/kidney (hydronephrosis) or Doppler ultrasonography to assess renal
perfusion are both worthwhile studies for assessment * *?�RIFLE criteria � grading
system of renal dysfunction based on Serum Cr, GFR, and urine output o Risk of
Injury � Cr (1.5x inc.), GFR (25% dec.), Urine (<0.5mL/kg/hr for 6h)o Renal Injury
� Cr (2.0x inc.), GFR (50% dec.), Urine (<0.5mL/kg/hr for 12h)o Renal Failure � Cr
(3.0x inc.), GFR (75% dec.), Urine (<0.5mL/kg/hr for 24h or anuria) o Loss of Renal
Function � total loss of renal function for >1mo o End-Stage Renal Function � total
loss of renal function for >3mo Management * *?�First Step: rule out is obstructed
urinary catheter (easy to assess and fix just by flushing the catheter) * *?�Next
Step: order labs, review nephrotoxic medications, dose-adjust all renal-excreted
drugs * *?�Fluid Challenge: infusion of 500mL saline over 30min to see if oliguria
resolves o Pre-renal AKI from hypovolemia should resolve with fluid challenges o If
no response-->obtain CVP-->if low, continue challenges, if normal consider renal
pathology * *?�Post-renal obstruction: always check he catheter first; then undergo
further evaluation * *?�10776: Indications for Immediate Dialysis o Acidosis � if
metabolic acidosis with pH <7.1 refractory to therapyo Electrolyte Abnormalities �
symptomatic or severe (>6.5) hyperkalemiao Ingestion � methanol, ethylene glycol,
salicylate, lithium, valproic acid, or carbamazepine o Overload � if volume
overload is refractory to diureticso Uremia � typically if its symptomatic
(encephalopathy, pericarditis, or bleeding) * *?�Diuretics in oliguria will only be
beneficial if decompensating heart failure is the cause (less overfilling of the
heart to help improved cardiac output, thus perfusion to kidney) * *?�Dopamine in
oliguria theoretically would work (helps increase cardiac output and promote
naturesis) but actually causes worsening of AKI insult -->?don??t use it. Remember
to NEVER order anything with contrast (MRI, CT with con, etc.) on a patient with
AKI unless you want to kill their kidneys Chapter 40: Shortness of Breath 5 Days
Post-op � Pulmonary Embolism Risk Factors for DVT/PE (Virchow??s Triad) * *?�Stasis
� immobilization * *?�Endothelial injury � surgery, trauma, central line within
past 3mo, or Hx of DVT/PE * *?�Hypercoagulability � smoking, OCPs, Hx DVT/PE,
cancer, congenital thrombophilias * *?�Note if pt with DVT/PE lacks these risk
factors, even with careful history, workup for underlying malignancy or hereditary
hypercoagulable state should be undertaken Presentation o *?�Recent history of at
least one of Virchow??s Triad o *?�Symptoms: Acute onset SOB, unilateral pleuritic
chest pain worsening with inspiration, hemoptysis, tachycardia,
tachypnea/hypocapnea/respiratory
alkalosis (pH>7.4), hypoxemia (poor perfusion) o *?�Massive Pulmonary Embolus
(saddle embolus) will present with additional hypotension, elevated JVP/central
venous pressure, right ventricular heart failure, elevated BNP/troponins, new onset
arrhythmia (RBBB), more centralized chest pain, and sometimes instant death o *?
�Signs of DVT (unilateral leg swelling, calf pain, leg
warmth/erythema/tenderness/Homan??s sign) should be assessed as this may be the
underlying cause for the PE o May-Thurner syndrome � syndrome of left iliac vein
compression due to anatomy of the left iliac artery. Causes a 2x increase in DVT of
the left leg vs the right Anatomy*?Area of occasion is Peripheral Artery (10%),
Proximal Artery (90%), Pulmonary artery (rare) Pathophysiology*?Hereditary
Thrombophilias - Any patient with young age of PE/DVT (<45 y/o), recurrent PE/DVT,
or unusual sites of PE/DVT (cerebral artery, mesenteric artery, portal veins)
should be testedo Factor V Leiden � a classic of white women and the most common
overall. Autosomal dominant mutation of the gene for Factor V in coagulation
cascade, making it resistant to Protein C cleavage/inactivation. Thus it induces a
hypercoagulable state.o Prothrombin 20210A � 2nd most common causing increased
prothrombin levelso Anti-thrombin III deficiency � decreased anti-thrombin III
levels, often acquired during DIC, cirrhosis, or nephrotic syndrome (peeing out all
you??re anti-coagulation proteins)o Protein C/Protein S deficiency. � if one isn??t
present, there??s decreased inactivation of Factors V/VIII. Protein C deficiency
classically causes Warfarin induced skin necrosis. o Homocysteinemia � not well
understood; pts benefit from B6 (pyridoxine) and B12 (cobalamin) supplementation to
aid conversion of homocysteine-->methionine or cysteine *?Acquired Thrombophilias �
advanced age, pregnancy, cancer, OCPs, HRT, smoking, obesity, nephrotic syndrome,
and HIT are all ones to consider Workup*?Wells criteria � help determine what the
pre-test probability of PE is present o +3 � signs of DVTo +1.5 � previous PE/DVT |
Heart Rate +100 | recent surgery/immobilization o +1 � hemoptysis | cancero
Interpretation: <2 low risk | 2-7 moderate risk | >7 high risk *?First Stepo If low
risk � obtain a D-dimer assay (<500 ng/mL is negative and PE is ruled out;
>500ng/mL is positive and workup should continue as PE has not been ruled out)o If
intermediate risk � you can go either way...but the safe side the to bet on high
risk o If high risk or (+)D-dimer � immediately start heparin & order CT angiogram
of chest (remember Heparin halts propagation of clot, allowing intrinsic
fibrinolytic system to start working slowly on breaking up the clot) *?Labs o ABG �
acute respiratory alkalosis, hypoxemia, increased A-a gradient ??Normal A-a
gradient is calculated via [(Age/4) + 4] o ECG � sinus tachycardia; sometimes
arrhythmias if saddle PE??SI/QIII/TIII (20%) � sign of right ventricular strain; S-
wave in Lead I is huge; Q wave in Lead III is huge, and T-wave is inverted in Lead
IIIo V/Q scan � multiple areas of perfusion deficit with normal ventilation ??
Reported as High, Intermediate, Low, Very low probability of PE??Not the best test
(not readily available, not great predictive value), but a ??Very Low?? score has a
high negative predictive value *?Imagingo CTa chest � will show a filling defect in
the pulmonary arterial system & sometimes will show peripheral infarction of tissue
(Hampton??s hump!)o CXR � typically normal, but sometimes with unusual features: ??
Westermark??s sign � area of hyper-lucency representing collapse of distal blood
vessels where the PE is lodged ??Hampton??s hump � wedge-shaped hyperdense region
at peripheral lung representing area of ischemia/infarction ??Fleischer??s sign �
prominent central pulmonary artery (only seen in saddle embolus)o Echocardiogram �
may be used to quickly assess for right heart strain (indirect sign of PE)o Lower
Extremity Doppler ultrasound � may be used to quickly assess for evidence of DVT
(may show signs of embolic disease, thus raising chance of PE) Management*?
Anticoagulation o Normal renal function: any anticoagulant will be fine, factor Xa
inhibitors preferredo Poor renal function (GFR <30): limited to un-fractioned
heparin (until PTT 1.5x normal) followed by warfarin. Any inhibition of renal
function can cause accumulation of the really cleared factor Xa inhibitors--
>uncontrolled anticoagulation.o If Hx of HIT: direct thrombin inhibitor should be
used (argartroban, lepirudin, or bivalirudin) o If ongoing
bleeding/contraindication to anticoag: placement of IVC filter and stabilization *?
Subsequent Treatments o Low risk (no sign of R. heart strain) � heparin alone (body
will dissolve clot)o Sub-massive (evidence of R.heart strain but not hypotension) �
consider tPAo Massive (R.heart strain and sustained hypotension) � tPA or pulmonary
embolectomy (if pt is not candidate for tPA) *?Long Term Treatment o First PE � 3
months anticoagulation & minimize risk factorso Subsequent PE � 6 months
anticoagulation & minimize risk factorso If malignancy -->?LMWH is preferred over
warfarin these ptso If pregnant -->?unfractioned or LMWH cannot cross placenta
(warfarin is a teratogen!) Chapter 41: Abdominal Pain Following MVA � Traumatic
Bleeding and Hemorrhagic ShockShock defined as ??inadequate perfusion for aerobic
metabolism, leading to hemodynamic instability, and end- organ dysfunction?? Types
of Shock typical for trauma settings * *?�Hypovolemic/Hemorrhagic � trauma causing
hemorrhage or burns typically cause decreased blood/plasma volume leading to this
type of shock * *?�Cardiogenic � blunt heart trauma (arrhythmia, tamponade,
contusion) or tension pneumothorax result systolic (pump doesn??t work) or
diastolic (blood can??t fill the heart) failure * *?�Neurogenic � high-cervical
spinal trauma results in loss of sympathetic tone-->peripheral vasodilation and
leakage of blood plasma. Differs from classic presentation of shock featuring warm
extremities and normal-low heart rates * *?�Anaphylactic shock and septic shock
typically aren??t part of acute traumatic settings Presentation: tachycardia,
hypotension, pale/cool extremities, weak pulses, prolonged capillary refill, low
urinary output, and altered mental status; often signs of trauma and internal
bleeding present *?Note that young patients often can maintain blood pressures due
to strong vascular tone, despite significant blood loss from trauma
Pathophysiology: the 5 main ??cavities?? for hemorrhage are the chest, abdomen,
pelvis/retroperitoneum, long bones, and the ??floor?? (outside the body) *?Blood
loss is classified based on % of blood lost and accompanying signs/symptomso Class
I (0-750mL; <15%) � all vitals normalo Class II (750-1500mL; 15-30%) � normal BP;
tachycardia, decreased pulse pressure, tachypnea o Class III (1500-2000mL; 30-40%)
� decreased BP/tachycardia/dec. pulse pressure/tachypnea o Class IV (>2000mL; >40%)
� same as III with severely decreased pulse pressure (<25mmHg) *?Common hemorrhagic
injuries based on ??cavity?? injuredo Chest � lung laceration, rib
fracture/intercostal artery tear; rarely aortic transection (distal to ligamentum
arteriosum) from deceleration injuryo Abdomen � liver laceration (most common organ
injured) or spleen laceration (most common cause of bleeding)o
Pelvis/retroperitoneum � pelvic fracture (internal iliac artery or pelvic veins),
renal trauma; very rarely aortic or IVC ruptureo Long bones � bilateral femur
fractureso ??Floor?? � any major trauma communicating with outside the body can
have this; although large scalp lacerations are often an overlooked cause of
massive bleeding*?Closed head injury and bleeding into the cranial vault will NEVER
cause hemorrhagic shock (not enough space to bleed into!) o Cushing reflex �
increased ICP (from intracranial bleed) -->?vasoconstriction to maintain brain
perfusion-->baroreceptor sensation of intense BP-->profound bradycardia Initial
Management *?ABCDE??s of Trauma (??Primary Survey??)o Airway (with C-spine
precaution) � is the patient breathing spontaneously? Is the airway patient? If
not, check for C-spine injury/disease. Intubate with C-spine in mind.o Breathing �
after establishing the airway; look for symmetric chest wall expansion, auscultate
both lung fields for breath sounds, palpate the chest for crepitus/deformityo
Circulation � check peripheral pulses (radial pulse = at least 80mmHg systolic;
femoral/carotid pulse = at least 60mmHg systolic); place two large bore (16 gauge
or higher) needles/start fluids o Disability (neurologic evaluation) � GCS with
focused neurologic exam based on complainto Exposure/Environmental Control � cut
away clothes for full exposure for survey. After survey, cover in warm blankets to
minimize temperature changes *?AMPLE Secondary Survey o If patient is able to
speak/respond to questions, the AMPLE survey can get more info o Allergy,
Medications, Past Medical history, Last Meal, Events Preceding the Injuryo Careful
head-to-toe physical exam if time Basics of Trauma Airway Management (the A & B in
ABCDE) * *?�Remember that establishing the airway is the 1st task of any trauma
setting * *?�Rapid Sequence Intubation (RSI) � two man technique where 1someone
sedates the pt using weight- based calculated doses of sedative (etomidate)/NMJ
blocking agents-->performs orotracheal intubation & 2someone holds the C-spine
neutral as spinal injury is there until proven otherwise in trauma o Nasotracheal
intubation is NOT recommended in acute trauma as basilar skull fractures may be
present. The tube may pass into and damage the intracranial space/contents! * *?
�Surgical Airways result in surgical creation of an airway to bypass damaged normal
airwayso Cricothyrotomy
� airway of choice in acute trauma (fast/few complications); incision through
cricothyroid membrane (between thyroid cartilage/cricoid cartilage). Works well for
short term, but sub-glottic stenosis makes this a poor long-term optiono
Tracheostomy � less preferred in acute setting (longer time/more difficult);
incision is made through tracheal rings; good for long-term airway management * *?
�Proper intubation is confirmed clinically (misting of tube, auscultation of breath
sounds), CO2 detection strip test in exhaled air, CXR confirming placement of tube
Basics of Trauma Circulatory Management (the C in ABCDE) o *?�After placement of
large bore needles (16 gauge or greater)-->draw blood for labs & type/cross o *?
�Placement of IV lines are preferred in the antecubital fossa; but access in other
places is fine if this is not available (like with significant arm trauma) o Note
that interosseous IV access may be needed in children <6yr due to small vessels *?
Central Line placement is indicated if peripheral lines cannot be obtained or if
patient is hemodynamically unstable and close BP monitoring is required. Femoral
access is preferred during acute event due to ease of placement. Fluid
Resuscitation in Acute Trauma * *?�Crystaloids � standard fluids featuring only
osmotic ions (normal saline, lactated ringers, etc.) * *?�Colloids � standard
fluids that have additional large molecules (like albumin) in them to,
theoretically, help retain intravascular volume by bolstering plasma oncotic
pressure. They??re not really used, as they??re more expensive & studies have not
shown clear benefit vs normal fluids * *?�First Step: Rapid infusion of 2 liters
normal saline or lactated Ringers o Normal Saline � 154meq/L Na, 154meq/L Cl o
Lactated Ringers � 130meq/L Na, 109meq/L Cl, 28meq/L lactate, 4meq/L K, 3meq/L Ca2+
??Lactate is converted to bicarb in the liver; helps with buffering with academia??
Hypotonic in regards to sodium; infusion may cause hyponatremia (cerebral swelling)
??Name is from the presence of lactate & original inventor, Dr. Sydney Ringer o 5%
Dextrose (D5W) � 278mmol/L glucose; usually added to normal saline to add some
nutrition; not typically indicated in traumatic setting o Large amounts of K+ are
NOT given as decreased renal perfusion in shock decreases K+ excretion & traumatic
injury may release K+ into the serum from intracellular space *?Next Step (if 2
Liter fluid challenge fails): Massive Transfusion Protocol o [1:1] ratio of [Packed
RBCs:Fresh Frozen Plasma (FFP)] ??1:1 � PRBCs-->FFP-->PRBCs-->FFP-->(up to 10 units
PRBCs every 24hr) ??Start with O-type blood and convert to specific blood with
cross/typeo [1:1:1] ratio of [PRBCs:FFP:Platelets] has come into recent favor and
may be used *?After Starting Fluid resuscitation: identify the bleed and try to
stop ito Determine bleeding compartment (Chest/Abdomen/Pelvis/Retroperitoneum/Long
Bone/Floor) with a FAST scan/CXR/Pelvic X-rayo Chest � insertion of chest tube for
drainageo Abdomen � immediate exploratory laparotomyo Pelvis � assess need for
pelvic stabilization & plan for embolization of bleeding artery *?Diagnostic
Peritoneal Lavage � local anesthesia with small abdominal incision with placement
of catheter. Withdrawal of more than 20cc blood is confirmatory. Lavage with 1L NS
yielding 100,000 RBCs/mm3 is confirmatory. Often done if FAST is equivocal.
Subsequent Management*?Liver Injury � most commonly injured organ after blunt
abdominal trauma o Hemodymanically stable = medical management + selective liver
embolizationo Unstable = exploratory laparotomy (Ex-Lap) to stop bleeding (usually
perihepatic packing with laparotomy pads, cauterization, & suturing with pad
removal 48hr after bleeding control)o Note the pringle maneuver may be used to
temporarily control bleeds intra-op. If this fails to control bleed, it??s
concluded that bleeding if from hepatic veins*?Splenic Injury � the most common
cause of abdominal bleeding after blunt abdominal trauma o Hemodymanically stable
with clean FAST = selective splenic embolization to control injuryo Henodynamically
unstable or FAST(+) = splenectomy or spleen repair + immunization against
encapsulated organisms 2wk later (H.flu, N.meningititis, S.pneumoniae, etc.)o
Kehr??s Sign � referred left-shoulder pain due to splenic injury irritation of the
diaphragm *?Pelvic Fracture � stabilization of fractures and placement of pelvic
binders across the femoral greater trochanters is best to control ongoing bleeding.
o If ruled out other sites of bleeding, Selective embolization of bleeding pelvic
vessels should be done to control the bleeding Areas of Trouble * *?�Free fluid in
the peritoneum without solid organ damage is NOT a sign that everything is OK. It
means that some occult leak (intestinal leak, intestinal bleed, bladder rupture,
etc.) has occurred. * *?�Using vasopressors in hypovolemic shock will only lead to
worsening end organ damage. The peripheral arteries are already constricting to
maintain BP, thus further alpha-adrenergic stimulation will only worsen end organ
ischemia and have limited effect on blood pressure * *?�Hypotension definition
varies with age o Age 20-49 -->?systolic <100 mmHg o Age 50-69 -->?systolic <120
mmHg o Age 70+ -->?systolic <140 mmHg Chapter 42: Penetrating Abdominal Trauma
Presentation * *?�Pre-hospital report (from EMTs/etc.) is Mechanism, Injuries,
Vitals, Treatment (MIVT) * *?�Two most common penetrating abdominal traumas: o Stab
wound = low velocity/kinetic energy, damage only to area of penetration o Gun shot
= high velocity/kinetic energy, remote damage from fragmentation/blast can occur *
*?�Two most common organs injured in penetrating abdominal trauma: small intestine
and liver * *?�Three physical exam findings mandating immediate surgical
intervention in PAT: o Hypotension, peritonitis, & evisceration-->2 out of 3
mandate surgery o Often X-rays are taken to help quickly characterize the
path/extent of injury*?Tangential gunshot wound � PAT where path of the bullet has
clear entry and exit wounds & penetrated no internal organs/deeper structureso
Don??t forget that blast injury and fragmentation can still occuro X-ray and CT
assessment should be done to assess for internal injuries Anatomy*?Border
Definitions of Body areas o Anterior abdomen � xiphoid/costal margins, anterior
mid-axillary lines, and inguinal ligaments/public symphysis o Flank �
anterior/posterior mid-axillary lines from 6th intercostal space to iliac crest o
Back � tips of the scapula, posterior axillary lines, and iliac crests * *?�Three
Distinct regions of the internal abdomen � peritoneal cavity, pelvis, &
retroperitoneum * *?�Retroperitoneum o Organs � 2nd-4th parts of duodenum,
ascending/descending colon (posterior wall), rectum (distal), pancreas, kidney,
ureter, bladder o Retroperitoneal hemorrhage is difficult to diagnose as normal
signs of peritonitis are not there, FAST exam, and peritoneal lavage will not show
hemorrhage. o Retroperitoneal hematomas are divided into Zones, which aids in
remembering what organs are present in each zone and directs surgical intervention
o Zone 1: upper midline/central (ICV, SMV, aorta & branches) -->?always explore
surgicallyo Zone 2: upper lateral (renal artery/vein) -->?BAT (selective), PAT
(explore surgically)o Zone 3: lower midline/pelvic (common/internal/external iliac
A & V) -->?BAT (DO NOT explore), PAT (explore surgically)*?Transpelvic gunshot
wound is concerning for damage to ureters, bladder, iliac vessels, rectum, &
vagina. CT scan of abdomen & pelvis with rectal/vaginal exam (if woman) should be
done. Workup * *?�Immediate Surgery indicated with hypotension, peritonitis, or
evisceration * *?�In absence on Immediate Surgical indication-->CT
chest/abdomen/pelvis o FAST exam and DPL are of limited utility due to poor
assessment of retroperitoneal structures o Local wound exploration should only be
attempted by an experienced physician; allows for assessment of anterior fascia
(penetrated or not)-->if penetrated, surgery indicated; if not penetrated, no
surgery needed Initial Management * *?�1st step: ABCDEs with careful survey for
injuries (make sure to check axilla & perenium) * *?�2nd step: draw labs,
fluid/blood product resuscitation/any steps to address specific problems * *?
�Permissive hypotension: less aggressive fluid resuscitation to avoid ??popping the
clot?? and creating a dilution coagulopathy. Used in the setting of penetrating
torso trauma only (not blunt/head trauma) * *?�ABx/Analgesia: not recommended
unless pt has indication for immediate surgery (may mask signs/symptoms needed for
assessment if not going to surgery!) * *?�Tetanus prophylaxis: no if up to date
with tetanus shot; if immunization status unknown, then only tetanus-prone injuries
should get prophylaxis (soil contaminated, >6hr old wound, rusty nail, etc.) * *?
�Impalement: same trauma assessment WITHOUT attempt to remove penetrating object
until 1proper imaging can be done to assess anatomic effects, 2pt can be taken to
the OR for removal. Subsequent Management o *?�Trauma patients are draped from chin
to knees in the OR for immediate access to any portion of the chest/abdomen/pelvis
if needed during surgery o *?�Exploratory laparotomy is the mainstay of surgical
management for PAT o *?�Laparoscopic approach may be used if surgical assessment of
peritoneal penetration is needed, but immediate laparotomy is not indicated (no
peritonitis, hypotension, or evisceration). o *?�Lethal Triad �
Acidosis/Hypothermia/Coagulopathy o These are three major killers seen in trauma
patients which, if not corrected, will lead to death o Should be watched and
corrected immediately should they pop up*?Damage control surgery � due to concern
intra-op of the ??lethal triad??, this approach
takes patients for a limited time in the OR to correct life-threatening
hemorrhage, limit bowel contamination, and temporary closure with prompt ICU
transport for resuscitation o After adequate resuscitation, pt may return to the OR
for further work * *?�Non-operative management � appropriate in patients who are
hemodynamically stable, without peritonitis, with normal mental status, and CT scan
showing no intra-abdominal injury * *?�Prophylactic Abx should be given for 24hr
post-trauma admission; even with evidence of bowel perforation, increased duration
does NOT provide benefit Complications *?Abdominal Compartment Syndrome � clinical
deterioration due to heightened intra-abdominal pressure; often decreased urine
output, increasing peak pressures on ventilator, and increasing vasopressor support
will be symptoms o Bladder pressure measurement increase may help make Dxo Tx:
decompressive laparotomy w/ re-opening of abdominal fascia and leaving it open to
allow for pressure relief Chapter 43: Pedestrian Struck by Motor Vehicle �
Traumatic Extremity Injury Presentation * *?�6Ps of Ischemic Limb Injury � pain,
pallor, polar, pulselessness, paresthsias, paralysis (the final two are signs of
critical ischemic injury and require emergent intervention if present!) * *?�Signs
of vascular injury to limb o ??Hard Signs?? of limb damage � bleeding, expanding
pulsatile hematoma, palpable thrill, audible bruit, absent pulseo ??Soft signs?? of
limb damage � Hx of hemorrhage, small/stable hematoma, unexplained hypotension,
penetrating wounds without hitting major vessels, nerve deficit, abnormal pulses *?
Examination of Injured Limb o Vascular � pulses, perfusion (temp, color, capillary
refill), hard/soft signs of injuryo Neurologic � sensation, strength, reflexeso MSK
� fracture/gross deformity, joint exam (active/passive range, instability,
effusions) o Soft tissue � intact, degree of contamination Pathophysiology * *?
�Popliteal Artery � due to it??s course (tethered above/below the knee with
anastomotic network as it passes behind the knee), forceful traction (posterior
knee dislocation)/transection (medial tibial plateau fracture) injuries are most
damaging. Typically presents with popliteal artery thrombosis & distal limb
ischemia. * *?�Axillary artery � most commonly from anterior dislocation of
shoulder girdle. Posterior dislocation more often injures the axillary nerve * *?
�Subclavian artery � classically from clavicle fracture (subclavian runs just
between the clavicle and 1st rib). May present with associated
pneumothorax/hemothorax * *?�Brachial artery � supracondylar fractures; most common
in children because of their thinner humeral supracondylar region. Lack of
treatment may result in Volkmann??s contracture (hand flexure) * *?�Superior
Gluteal (posterior)/Inferior Pudendal (anterior) (internal iliac branches) � pelvic
fractures (depending on posterior/anterior) could damage either one. Often major
blood loss! * *?�Femoral artery � anterior hip dislocations (external
rotation/abduction) more often injure the artery; posterior dislocation (internal
rotation/adduction) more likely sciatic nerve. Always concern with avascular
necrosis if femoral head fracture is also present. Workup * *?�If ??hard signs??
present � no further workup, go to OR for hemorrhage control/injury repair * *?�If
no ??hard signs?? present o Ankle-Brachial Index (ABI) � allows for possible
identification of vascular injuryo If ABI is <0.9 (abnormal; evidence of injury),
vascular imaging must be done to assess injury ??CT angiography
(rapid/non�invasive, requires contrast) � test of choice??Duplex ultrasonography
(accurate/noninvasive, not quickly available, operator dep.) ??Contrast
arteriography (very sensitive/specific, but invasive/expensive) o If penetrating
trauma is close to an artery, but not causing symptoms/normal ABI, no further
workup is needed *?Posterior knee dislocations should also have:o Pre-reduction a
plain film X-ray (assess damage to surrounding structures)o Post-reduction plain
film X-ray (assess for fractures and success of reduction)o Post-reduction clinical
assessment (check for neuro/vascular damage & joint function) *?Mangled Extremity
Severity Score (MESS) � scoring system used to evaluate whether a severely injured
limb should be attempted to be salvaged or not. o Ischemia >6hr, older patients,
severe shock, high-energy wounds, and presence of arterial/nerve injury are all
criteria that would point to amputation rather than salvage o Even if a limb is
technically salvageable, if function is completely lost & leads to a worse quality
of life, it may be better to amputate Management * *?�First Step � Primary survey
(ABCDEs) and secondary survey (H&P) with aggressive control of bleeding * *?
�Tourniquets � early application and proper placement with limb exsanguination have
been shown to result in better outcomes. Make sure to minimize application time to
as little as possible. * *?�Posterior Knee Dislocation o Immediate reduction (good
to have X-ray beforehand) with exam focused on restoring circulation and assessing
neurologic function/ligamentous injury/open fractures o After reduction, re-check
vascular status (ABI -->?CTa if ABI is still <0.9 -->?if abnormal go to OR) o If
ABI is normal, resume medical management and close watch*?Surgical management is
best achieved within 6hr with goal of restoring distal perfusion o Typically
resection-->anastomosis/grafting is basis for restoring bloodflow o If autologous
vein graft is needed for popliteal artery repair the greater saphenous vein from
uninjured leg is the best choice (preserves collateral flow; remember to reverse
orientation so venous valves don??t impede bloodflow) o If popliteal vein also
injured � every attempt should be made to repair the vein, but if it is not
salvageable, the ipsilateral saphenous vein flow should be ensured (collateral
bypass). o If orthopedic repair also needed � if ischemia is severe, vascular
intervention takes precedence, and often a temporary shunt is placed. Orthopedic
manipulation in surgery may cause damage to an arterial repair, so the shunt is
helpful here. After ortho is done, definitive vascular repair can be achieved. o
Heparin � helps reduce rate of amputation in the affected limb as long as patient
isn??t contraindicated to it??s use o Post-op complications �
thrombosis/compartment syndrome following re-establishment of flow are the two
biggest concerns Areas of Trouble*?Just because the patient has a palpable pulse
does NOT mean there is not arterial injury! Retrograde flow from collateral
arteries and inherent unreliability of physical vascular exam make a palpable pulse
less conclusive. ABI + pulse exam is always the best course! Chapter 44: Gunshot
Wound to the Left Neck Important Signs to Look for in Pt with Neck Injury * *?
�Stridor � compression of the upper airway; often intubation or surgical airway
will be needed * *?�Odynophagia � pain with swallowing; oropharyngeal/esophageal
injury likely causes this * *?�Horner??s Syndrome � ptosis/myosis/anhydrosis;
damage to cervical sympathetic chain nerve fibers, which travel along the
internal/external carotids. May indicate injury to these vessels * *?�Bruit �
arterial damage (carotid/subclavian) may result in fistula formation with adjacent
veins resulting in a bruit (result of venous vibration from arterial pressure flow)
* *?�Crepitus � air under the soft tissue; indicates damage to lungs/airways with
release of air * *?�Hoarse voice � vocal cord dysfunction due to vagus nerve or
recurrent laryngeal nerve damage Anatomy * *?�Neck Zone 1 [clavicles/sternal notch
-->?cricoid cartilage] � great vessels, common carotids, vertebral arteries, lung
apicies, thymus, thoracic duct, distal trachea, esophagus, cervical spine, brachial
plexus * *?�Neck Zone 2 [cricoid cartilage-->angle of the mandible] � mid-
carotids/vertebral arteries, jugular veins, esophagus, vagus/recurrent laryngeal
nerves, phrenic nerve, cervical spine, larynx, trachea * *?�Neck Zone 3 [angle of
the mandible -->?base of skull] � proximal internal/external carotids, vertebral
arteries, proximal jugular veins, oropharynx, cervical spine Pathophysiology o *?
�Penetration of the Platysma is how a penetrating neck injury is defined. If it has
not been penetrated, then no further workup for neck trauma is needed. o *?
�Pseudoaneurysm � may develop when an artery has a focal full-thickness injury that
gets tamponaded by local soft tissue. The vessel is not exsanguinating, but the
space is filled with blood, generating an enclosed pulsatile mass o Classically a
pulsatile mass following trauma is either A-V fistula, aneurysm, or pseudoaneurysm
*?Arterial intimal injury � concussion/blast damage may injure only the arterial
intima. If small, this may be insignificant. If large, it may occlude the lumen or
generate a false lumen for dissection.o Larger intimal injuries will likely need
surgical correctiono If large intima injury extends high into intracranial carotid,
you may be forced to manage medically, due to lack of access*?Two major nerve
lesions from neck trauma: o Recurrent laryngeal nerve � vocalis paralysis = hoarse
voice (unilateral)o Phrenic nerve � hemidiaphragm paralysis = difficulty breathing,
elevation of diaphragm on affected side Workup/Management * *?�Algorithmo Standard
Primary & Secondary Survey of Trauma (intubate, transfuse, etc. as necessary)o If
hard signs of vascular injury present -->?prep for ORo If hard signs absent -->?
helical CT angiography (characterize extent/location/nature of injury) ??No concern
for injury-->observation??Zone 1 or 3 injury -->?catheter angiography (arterial
damage) or triple endoscopy (aerodigestive tract damage)??Zone 2 injury (most
common) -->?surgical exploration (arterio-venous
damage) or triple endoscopy (aerodigestive tract damage) * *?�Zone 1 Injuries
should always be assessed for pneumothorax * *?�Zone 2 surgical threshold is lower
as this zone is easily accessible via incision anterior to the sternocleidomastoid
muscle * *?�Management of Vascular injuries o First gain proximal, then distal
control of the injured artery (cut off bleed at it??s source!)o If arterial
bleeding that cannot be controlled by direct pressure-->passage of Foley catheter
into wound with balloon inflation to tamponade the vessel may be done!o Carotid
Injury � gain proximal/distal control & start heparin. Resect any portions of
damaged carotid. If <2cm resected do primary anastomosis; if >2cm, then take
greater saphenous vein to use as an autologous graft anastomosis ??Always prep
drape both thighs with vascular injury, just in case you need the greater saphenous
vein for autologous graft! o Internal Jugular Injury � primary repair (venorrhaphy)
or end-to-end repair should be attempted. If not possible, ligation of
proximal/distal vein is accepted/well-tolerated o Pseudoanaeurysm � surgical
resection/repair; unstable and may enlarge/ruptureo AV fistula � stable, but rarely
closes. Needs surgical resectiono Intimal injury � stable, with either medical
management (small) or repair (large or complex) Areas of Trouble * *?�Because
bullets (and bullet fragments!) may cross multiple zones of the neck, it??s
important to evaluate with helical CT to make sure of damage, instead of simply
using entry/exit wounds * *?�Not addressing airway first can be a costly mistake.
There is NOT much space for an expanding hematoma, thus tissue displacement may
easily impede the airway, esp in a patient who started with a normal patent airway.
* *?�Blunt Carotid Injury � often hard to diagnose and clinically occult; high
index of suspicion needed. o Presentation: MVA with focal neurologic deficit not
obvious on CT head.o Pathophys: stretching of the vessel or direct trauma causing
dysfunction/damage o Dx: CTa of the neck to assess vesselso Tx: anticoagulation
only (prevent clot formation) Chapter 45: Stab Wound to the Chest � Thoracic Trauma
??Lethal Six?? Thoracic Trauma Injuries * *?�Airway obstruction � stridor/gurgling
following trauma/foreign body aspiration/expanding hematoma * *?�Tension
pneumothorax � one-way valve to an injured lung o Presentation: Hypotension,
dyspnea, tachypnea, JVD, unilateral absent breath sounds (damaged side), deviation
of trachea to unaffected side o Pathophysiology: trauma generates a one way valve
(tissue being the valve) which causes buildup of air within the chest cavity. As
this increases, compression of the heart/IVC/SVC result in poor preload filling and
eventually loss of cardiac output due to diminished preload. o Imaging: enlarged ??
water-bottle?? heart; may be normal in acute settings * *?�Open pneumothorax � open
chest all injury with air entry into pleura from outside world * *?�Massive
hemothorax � total whiteout of lung field & muffled lung sounds, typically from
lung parynchymal injury or intercostal artery injury * *?�Flail Chest � paradoxical
motion of chest wall, often with underlying lung contusion. Result of trauma
fracturing two or more consecutive ribs-->free wall that stays in place during
respiration * *?�Cardiac tamponade � fluid filling the pericardium (trauma often
causes hemopericardium) o Presentation: Beck??s triad (hypotension, JVD, muffled
heart sounds), narrowed stroke volume, hepatojugular reflex, pulsus paradoxus, &
electrical alterans ??Trauma to the cardiac box (clavicles superior, nipples
lateral, and subcostal margin inferior) can cause this o Pathophys: pericardial
pressure begins to exceed left ventricular diastolic pressure, resulting in septum
infiltration of the left ventricle. This reduces preload, thus causing hypotension
and narrowed stroke volume (<30mmHg) ??Rapid accumulation of pericardial fluid is
the most important factor in tamponade; at rapid pace, only 200-300mL of fluid can
result in full manifestation ??Slowly evolving tamponade may allow for up to 1000-
2000mL because it gives time for the pericardium to stretch/adjust to the new
pressures o Dx: made with FAST scan in trauma setting (fluid surrounding the
heart!) ??Hidden Six?? Thoracic Trauma Injuries * *?�Blunt aortic injury �
deceleration injury; widened mediastinum/tracheal deviation to the right * *?
�Esophageal injury � subcutaneous air surrounding esophagus; typically penetrating
trauma * *?�Tracheobronchial injury � massive subQ emphysema; either deceleration
or penetrating injury * *?�Diaphragmatic rupture � sudden rise in intra-abdominal
pressure or penetrating injury to the diaphragm itself; may be asymptomatic
(delayed Dx); herniation of stomach/colon may occur * *?�Blunt cardiac injury �
spectrum from unexplained tachycardia, BBB, cardiac rupture, to cardiogenic shock;
typically has accompanying sternal fracture * *?�Pulmonary contusion � rarely seen
initially on CXR, but develops within 24hr of injury H&P/Pathophysiology o *?
�Combative trauma patients may have ??air-hunger?? (hypoxia), hypovolemia,
cardiogenic shock, hypoglycemia, EtOH intoxication, drug intoxication. (acting
funny doesn??t always mean high/drunk!) o *?�Penetrating injury above the nipple =
likely thoracic injury o *?�Penetrating injury below the nipple = may be thoracic,
diaphragmatic, or abdominal injury (due to diaphragmatic excursion during
respiration cycle!) o *?�Type of weapon causing injury should be noted, as
ballistic course may be predictable (knife) or may change upon entry (bullet).
Bullets have even been seen entering an artery and embolizing! o *?�Narrowed pulse
pressure (systolic � diastolic = <30mmHg) � indicates some form of systolic
dysfunction (tamponade, hypovolemic shock, or cardiogenic shock) o *?�Rolling the
patient over and checking axilla/perineum are very important for checking entire
body for trauma wounds. Done only in situations where neck/spinal damage is very
unlikely. o *?�??Sucking Chest Wound?? � air bubbling from a chest wound due to
open pneumothorax large enough that inspired air takes the path of least resistance
into the chest cavity... through the wound (>2/3 diameter of the trachea), not the
trachea! Bubbling is ??expiration?? during diaphragm relaxation. o *?�Subcutaneous
emphysema = pneumothorax until proven otherwise. Typically causes crepitus! o *?
�Air embolism � entry of large amounts of air into the bloodflow, significantly
disrupting it o Presentation: cardio (chest pain, arrhythmia, right heart failure),
pulm (dyspnea, hypoxemia, hypercarbia), CNS (confusion, paradoxical cerebral
embolism) o Pathophysiology: most commonly from damage around the lung hilum,
causing a fistula between a bronchus & the pulmonary vein ??Air will disrupt normal
bloodflow long enough to cause ischemic damage*?Note that a normal abdominal exam
does NOT rule out abdominal injury. Peritonitis may more slowly develop, only to
show a smaller injury that??s been there the whole time. Initial Management *?First
Step: Primary and Secondary surveyo If cardiac tamponade is suspected, DO NOT
INTUBATE a patient, as positive pressure ventilation will increase pulmonary
pressure, further decreasing preload and worsening cardiac output *?
Airway/Breathing (Concern for pneumothorax was in this patient) o Breath
sounds/Obtain CXR to rule in/out pneumothoraxo Needle Thoracostomy � immediate
decompression of thoracic cavity with pneumothorax. Needle is placed in 2nd or 3rd
midclavicular intercostal space on affected side (minimal risk to heart and
collapsed lung tissue) above the rib (minimial risk to intercostal neurovascular
bundle). Needle is advanced till a rush of air is noted o Tube Thoracostomy (chest
tube) � definitive management of pneumothorax/hemothorax; placement of a hollow
plastic tube between the 4th/5th intercostal space to allow drainage. o Thoracotomy
� indicated for massive hemothorax (>1.5L immediately or >150-200mL/h for 3hr) in
order to gain acute hemorrhage control. ??Allows for hemorrhage control,
decompression of tamponade, cross-clamping of descending aorta, cardiac massage,
prevention of air embolism, and repair of cardio- pulmonary injury ??Indications:
penetrating trauma with <15min pre-hospital CPR; blunt trauma with <5min of pre-
hospital CPR; persistent post-penetrating trauma hypotension (SBP <60mmHg) ??
Contraindications: pt has no signs of life *?Circulation (concern for
hemorrhage/tamponade) o Palpate pulses, start 1L fluid bolus, send type/cross,
apply pressure to external injury o FAST scan should be able to show fluid
surrounding the pericardiumo Continue IV fluids (increases pre-load to maintain
cardiac output)o Do NOT use pressors (increases afterload, decreasing cardiac
output) o Subxiphoid (pericardial) window: surgical procedure that opens a small
portion of the chest to view the pericardium for blood. Only used in stable pts
with equivocal FAST suspected of tamponade. If negative, you??ve avoided a median
sternotomy; if positive, undergo sternotomy for definitive treatment. o Definitive
Tx: go to the OR for median sternotomy for release of tamponade & repair of injury;
note that pericardiocentesis is NOT recommended in trauma patients (likely clotting
blood, less effective with the needle; may be used in situations where surgical
intervention is not readily available to buy time until OR can be reached)
Subsequent Management * *?�Combative Pt: order blood glucose finger-stick, pulse
Ox, and vitals (altered mentation may be due to non-intoxicant reasons!) * *?�Chest
Tube Management: must be monitored for eventual removal o Collection � collects
fluid/blood/pus & measures amounts; connects water seal to chest tubeo Water seal �
one-way valve allowing air to be removed from
pleural space but doesn??t allow air to enter pleural cavity; connects suction-
control chamber to collection chamber??If air bubbles are passing through, then a
large pneumothorax is decompressing ??If no air bubbles, disconnect suction and ask
pt to cough or kink the chest tube for a bit then release. If bubbles, then the
pneumothorax has not healed. If nothing, then chest tube may be removed. o Suction
control � controls the amount of suction; connects wall suction and water seal o
[Wall suction<--water seal<--collection chamber<--chest tube<--pleural cavity] * *?
�100% oxygen (vs normal 21% oxygen room air) has been shown to speed pneumothorax
healing. This is because more O2 enters the vasculature and increases the pressure
within them, somehow leading to increase rate of resorption of the damaged tissue.
* *?�Sucking chest wound management � initially placement of occlusive dressing to
stop airflow; definitive treatment is occlusive dressing + tube thoracostomy (chest
tube) placement * *?�Flail Chest management � give analgesia to maximize comfort
with respiration (allowing for breath = atelectasis not happening) &
oxygenation/PEEP if ventilation is compromised. The role of Rib fixation apparently
has yet to be established. Complications * *?�Laceration of a coronary vessel may
occur with pericardiocentesis; worsening tamponade! * *?�The Left phrenic nerve
passes over the posterior left ventricular pericardium and is at risk when opening
the pericardium. * *?�If chest tube fails to drain a hemothorax properly;
thoracotomy/drainage (if unstable) or VATS procedure (if stable) are recommended *
*?�If a chest tube fails to fix a pneumothorax, first check to see the tube isn??t
occluded or kinked. If it??s proper, major airway damage has occurred and the
patient requires immediate intubation, bronchocscopy to assess injury, and
immediate thoracotomy for repair. Chapter 46: Burns to the Face, Trunk, and
Extremities � Acute Burns Presentation *?Risk factors for burn injury: extremes of
age, alcohol/drub abuse, smoking, violence, low SES o Children and elderly =
highest morbidity risk for burns *?Degrees of Burnso 1st degree (superficial) �
epidermis only; like sunburn (painful, dry, blanching, red, NO blisters) o 2nd
degree (superficial partial thickness) � epidermis and part of dermis (painful,
swollen, warm, mottled areas, YES blisters)o 2nd degree (deep partial thickness) �
epidermis and part of dermis (painless, warm, white, mottled areas, YES blisters
often with weeping surfaces)o 3rd degree (full thickness) � epidermis and dermis
(painless, white, dry, leathery, no blanch) o 4th degree (oh shit) � skin,
underlying bone, tendon, adipose, or muscle (bad news and disfiguring. If the burn
has gone through more than the skin, you??re at this level)*?Estimating Total Body
Surface Area (TBSA) affected by burn: o Rule of 9s: the body can be divided into
sections that are easily divisible by 9 as an estimate for surface area-->?Head (9
a/p), Each arm (9 a/p), Anterior torso (18), posterior torso (18), each leg (9
a/p), genitals (1) o Handprint estimate � adult size palm estimates about 1% of
body surface area burned. Best when estimating patchy areas of burn o Non-
superficial burns >40% of TBSA = higher mortality *?When to transfer to a burn
center o 2nd/3rd degree >10% TBSA (<10yr or >50yr) o 2nd/3rd degree >20% TBSA (any
age)o 2nd/3rd degree involving hands, face, feet, genitals, perineum, or skin on
major jointso Electrical or chemical burns (additional associated problems to be
addressed with these) o Concomitant inhalational injury (classic for people in
building fires)o Significant pre-existing medical conditionso Suspected child
abuse/neglect *?Inhalational Injury � smoke/heat causing damage to oropharynx/lungs
o High concern in patients with burn injuries occurring in enclosed areas/facial
burnso Upper airway edema � stridor or failure of upper respiratory system. Often
burn of the oropharynx will swell while in the hospital; best to prophylactically
intubate if concerned. o Acute respiratory failure (chemical pneumonitis) � low pO2
with high pCO2, chest pain, respiratory acidosis, tachypnea w/ shallow breathingo
CO poisoning (house fires/gas heaters/car exhaust) � headache, nausea/vomiting,
cherry-red skin, deceptively high pO2-->seizure, coma, death (anoxia)o Cyanide (CN)
poisoning � may be considered in any patient with burn injury (discussed below) o
Carbonaceous Sputum � dark sputum from inhalation of smoke; indicator of
inhalational injury o Changes in voice quality & singed nasal hairs (signs of burns
to face) *?Burn Wound Sepsis � 2nd degree -->?3rd degree burn while in the hospital
(skin necrosis), discolored burn, eschar with green hue, black/necrotic skin, skin
separation, signs of sepsis o Fever isn??t accurate here as the skin (the body??s
primary temp regulator) is compromised o Dx: finding >105 bacteria/g of tissue on
quantitative analysis*?Circumferential, Full Thickness Burns � concerning as the
forming eschar can compromise venous, but not arterial bloodflow via
circumferential swelling (acts as tourniquet).o Extremity � compartment syndrome
from high pressure blood pooling o Chest � difficulty with chest wall
expansion/respirationo Tx: escharotomy (remove the restricting band of tissue)
Pathophysiology * *?�Thermal Burns � caused by extreme heat, most common is
scalding from boiling water * *?�Chemical Burns � caused by caustic substances;
alkali burns (basic) are often more severe due to the substances to penetrate
tissues & cause liquefactive necrosis; acidic burns are less damaging and cause
coagulation necrosis * *?�Electrical Burns � external burn may be deceivingly
small, as electrical current can run through underling tissue causing damage
(muscle necrosis, shoulder dislocations, myoglobinuria/renal failure o Arrhythmias
are an immediate life-threatening cause of death due to disruption of the hearts
electrical conduction system. Direct current (DC) = asystole & Alternating current
(AC) = V-fib o Cataracts are (somehow) a long term complication of electrical
injury * *?�First 24hr � elevated glucose (catecholamine release), Decrease in
cardiac output 50% (decreased plasma volume via dehydration & increased vascular
resistance from vasoconstriction), decreased CVP (dehydration), decreased in
#circulating erythrocytes from direct damage in injured tissue. * *?�Dehydration �
because the skin plays a large role in maintaining a fluid barrier (keeps water in)
disruption with burn can quickly lead to evaporative losses-->hypovolemic ??burn??
shock o GI (Curling) ulcers � loss of fluid leading to decreased GI perfusion can
cause GI mucosal ischemic necrosis-->ulceration (classically in duodenum) *?Burn
Wound Infections � delay healing, encourage scarring, and may result in wound
infection/sepsis. Systemic Abx are NOT recommended for burn infection prevention
but topicals are. o Bacterial most common [Pseudomonas (Gram -) >> S.aureus >
Strep. pyogenes]o Fungal infections (C. albicans) typically occurs later in course
as topical Abx eliminate all bacteria from the wound, allowing fro real-estate to
be taken over by fungus o Viral infections are less common but most common is
Herpes Simplex Virus if occurring Workup * *?�1st step � primary & secondary
survey; if signs of inhalation injury present, then immediate intubation is
essential as worsening edema may make later intubation impossible. * *?
�Inhalational Injury o Clinical signs (mentioned about) should prompt immediate
intubation and further workupo Fiberoptic bronchoscopy (gold stnrd) - visualize
carbon deposition & damage/necrosis of tissue o High probability V/Q scan � can
show low V/Q ratio noting impaired ventilationo Labs � >10% carboxyhemoglobin, <90%
oxygen saturationo CXR � rarely positive early in injury; little value in diagnosis
*?Carbon monoxide poisoningo Carbon monoxide pulse oximetry � will show elevated CO
presence in bloodo Standard ABGs � show normal pO2 with decreased SaO2 (CO bound to
Hb causing elevated partial pressure, but tissue saturation will be low) Management
* *?�Inhalational Injury � early intubation to prevent loss of airway from
worsening edema * *?�Fluid Management o Parkland Formula [Total Fluid Volume =
(4cc/kg)(weight in kg)(%TBSA burned)] * ??�Used with 2nd degree burns or worse with
>20% TBSA covered * ??�Infuse half of total fluid in 1st 8hr from time of injury
(thus if you got them 7hr after injury, you need to haul ass to get it all in
within 1 hr!) * ??�2nd half of fluid infused over next 16hr following 1st half * ??
�Some concerns due to lack of account/adjustment for compartmental fluid shifts;
may lead to electrolyte abnormalities if not monitored o Urine Output can be used;
titrate fluid infusion to 0.5mL/hg/hr (adults) or 3mL/kg/hr (children) o Lactated
Ringer??s is preferred as it??s closer to physiologic ion concentrations and may
aid with resolving possible metabolic acidosis from hypovolemia??Colloid solutions
are more expensive and linked with pulmonary complications in burns ??Normal saline
(due to high Cl- content) can lead to hyperchloremic metabolic acidosis (wasting of
HCO3-) due to high amounts of fluid needed to resuscitate burn pts*?Wound
management � regular cleansing and debridement with application of topical
antimicrobial ointments & dressing.o Prophylactic IV abx � contraindicated; no
benefit and selection for resistance organisms o Topical Agents ??Silver
sulfadiazine � antimicrobial; may result in neutropenia or thrombocytopenia, poor
deep penetration, ineffective against Pseudomonas ??Silver nitrate � antimicrobial;
poor deep penetration, ineffective against Pseudomonas, may stain skin brown, and
rarely causes methemoglobinemia ??Sulfamylon (madenide acetate) � antimicrobial;
good deep penetration and kills Pseudomonas; carbonic anhydrase inhibitor
(metabolic acidosis can occur) and painful to apply to burns o Skin graft � used if
wound bed is deemed ??clean??; do not do if signs of infection * *?�CO poisoning �
100% O2 via non-rebreather face mask * *?�Circumferential Chest burn � chest
escharotomy should be done, as the restricting band of tissue can lead to
respiratory decline * *?�Circumferential extremity burn � escharotomy (concern for
compartment syndrome) * *?�Curling Ulcer prevention � PPI or H2 blocker should be
given prophylactically * *?�Nutrition � enteral route is preferred but TPN may be
used if pt cannot tolerate these. Oral feedings are not recommended due to likely
damage/swelling to the oropharynx * *?�Chemical Burn considerations � copious
irrigation/removal of caustic substance is extremely important; also protection of
others/removal of patient from area of exposure are critical * *?�Electrical Burn
considerations � cardiac monitoring for 12-24hr (concern for arrhythmias) Areas of
Trouble * *?�Child Abuse � may be represented by burn injury (cigarette burn is
classic) with inconsistent/conflicting histories by parents. All child abuse is
reported to proper authorities by mandate. * *?�Chronic non-healing burn wounds are
concerning Marjolin??s Ulcer (SCC arising from the site of a scar/burn/previous
injury and has an increased risk of metastases) Tips from UWorld 4446: Carbon
Monoxide Poisoning o *?�Carbon monoxide has better steric interactions with heme as
a molecule. Thus is tightly binds heme, shifting the oxygen dissociation curve to
the left-->holds on to oxygen and won??t deliver o *?�Presentation: headache,
confusion, malaise/dizziness, red cheeks -->?syncope, seizure, coma,
arythmia/myocardial ischemia. May be intermittent if patient exposure is
intermittent (like works at a traffic stop) o Labs: secondary polycythemia
(reactive EPO production from tissue hypoxia)o Smokers are more sensitive to
external CO as they have a low level (3%) of carboxyhemoglobin at any given time*?
Dx: elevated carboxyhemoglobin level on arterial blood gas o Note that pulse
oximetry does NOT differentiate between normal/carboxyhemoglobin *?Tx: 100% oxygen
until labs normalize 11566: Cyanide Toxicity*?Presentation: CNS (headache, altered
mental status, seizure, coma), cardio (arrhythmias), respiratory (tachypnea turning
into respiratory depression), GI (abdominal pain, nausea, vomiting), renal
(metabolic acidosis from lactic acid, and renal failure) o Etiology: prolonged
sodium nitroprusside infusion (metabolized to CN-), combustion of wool/silk
(contain CN-), or industrial exposures * *?�Dx: clinical presentation * *?�Tx:
sodium thiosulfate or hydroxycobalamine infusion to remove CN- from blood Chapter
47: Severe Right Leg Pain following Tibia Fracture � Compartment Syndrome
Presentation *?5Ps � early (pain on passive motion/out of proportion to exam),
nerve compression (paresthesia, paralysis), vascular compromise (pallor, polar,
pulselessness, increased capillary refill time) o Similar to acute limb ischemia,
but vascular compromise is a LATE symptom (vs as an early sign) o Failure to
recognize (like assuming pain is from fracture) may lead to ischemic necrosis!
Anatomy * *?�Thigh compartments (3) � anterior, medial, posterior * *?�Lower leg
compartments (4) � anterior, lateral, superficial posterior, deep posterior o
Anterior compartment most susceptible to compartment syndrome; the deep peroneal
nerve runs through this compartment and compression can cause 1st web interspace
foot numbness (sensory fibers) & foot drop (extensor digitorum brevis & extensor
halluces brevis) * *?�Upper arm (2) � anterior, posterior * *?�Forearm (3) �
dorsal, volar, mobile wad Etiologies * *?�Decreased compartment size � plaster
cast, circumferential 3rd degree burn, external compression, splints, or anti-shock
garments * *?�Increased compartment volume � vascular/blast/crush injury, fracture,
electrical burn, hematoma, ischemia reperfusion syndrome, SIRS/sepsis
Pathophysiology *?Compression syndrome occurs when limb compartment pressure begins
to rise due to any etiology. Normal compartment pressure is 5-10mmHg. When
pressures rise upwards of 20mmHg, veins/venules are compressed and venous outflow
is impaired. Increased pressure backs up into the capillaries, resulting is halt of
capillary flow, loss of O2 delivery to tissue, and ischemic necrosis! o
Circumferential burn � eschar forms contraction band, blocking venous outflow.
Capillary pressure increase causes leakage and edema o Ischemia/reperfusion �
inflammation from reperfusion injury causes capillary leako Large-volume
resuscitation � in situations where this is necessary, often extensive damage or
infection/shock are occurring. High volume + elevated capillary leak = edema.o
Severe exertion � muscle breakdown causes inflammation -->?capillary leako
Prolonged surgery/immobilization � may result in a crush injury (constant pressure
on one area) resulting in inflammation/edema * *?�Acute extremity compartment
syndrome � classic syndrome that was described in ??presentation?? * *?�Chronic
extremity compartment syndrome � less common syndrome where syndromes occur
chronically with muscle exertion. Transient tissue edema with activity causes
pain/swelling, that is relieved with cessation and rest. Dx made with clinical
history & presentation. NOT an emergency. * *?�Abdominal compartment syndrome �
occurs with increased intra-abdominal pressures causing compression and
dysfunction/damage of internal organs of the abdominal/thoracic cavities o Impaired
respiration � compression of diaphragm/thoracic cavity -->?hypoxemia/hypercarbia o
Compressed IVC � decreased preload -->?decreased cardiac output/stroke volume -->?
ischemia o Compressed kidney � impaired renal perfusion/diminished urine output and
AKIo Often can lead to multi-organ failure and high risk of mortality * *?
�Pulselessness � only occurs in extremely high compartment pressures; sign of
serious damage and concern for irreversible ischemic damage should be raised * *?
�Volkmann??s Contracture � fixed, intense wrist/hand flexion due to fibrosis of
damaged forearm muscles following forearm compartment syndrome o Classically occurs
in children following supracondylar fracture; brachial artery injury results in
ischemic inflammation in forearm-->muscle damage -->?fibrosis/contracture Workup *
*?�Clinical Dx: tense, swollen compartment with pain on passive motion + clinical
Hx suggestion * *?�Compartment pressure measurement: contraindicated strong
clinical suspicion (delay in treatment & risk of false negative); best used as a
rule-out or if clinical exam cannot be performed o 5-10mmHg (normal) with >20mmHg
diagnostic *?Bladder pressure measurement: used to diagnose abdominal compartment
syndrome. Physical exam isn??t reliable for diagnosis; thus measurement is
necessary every time. >20mmHg is diagnostic Management*?Extremity compartment
syndrome: Immediate decompressive fasciotomy of all compartments of affected limb
section. It??s hard to rule out specific compartments, thus the risk is not worth
reward. o Fasciotomy should be generous, as swelling can continue to increase. Open
that thing up!o The deep posterior compartment is the most difficult to decompress
(lower leg); but vital as it contains both the posterior tibial nerve, tibial
nerve, and peroneal arteries (foot function!) *?Abdominal compartment syndrome:
urgent decompressive laparotomy with maintenance of open abdomen wound + wound vac.
Closure can be done with decreased edema/intra-abdominal pressure. Chapter 48:
Bloody Emesis � Upper GI BleedDifferential Dx: Gastritis (pernicious anemia,
H.pylori), PUD (gastric or duodenal), erosive esophagitis, Mallory- weiss tear,
Esophageal varicies, gastric cancer, Curling/Cushing ulcers (Stress ulcer),
Aortoenteric fistula, Osler- Weber-Rendu syndrome Characteristics of Emesis or
Stools can give insight to upper/lower GI bleeding * *?�Upper GI � bright-red
bloody or coffee-ground emesis * *?�Upper > Lower � melena or maroon stools
(digestive enzymes -->?oxidation -->?RBC darkening) * *?�Lower > Upper �
hematochezia (less digestive enzymes, thus blood is red; massive upper GI bleed can
overwhelm the GI enzymes action, resulting in this presentation, although this is
more rare) Pathophysiology *?Esophageal Variceso Proximal 2/3 of esophagus mucosa
is drained by the esophageal veins -->?SVCo Distal 1/3 of esophagus mucosa is
drained by the left gastric vein (coronary vein) -->?portal vein o When liver
cirrhosis occurs, the portal venous drainage is backed up, resulting in portal
venous high pressure/distention, thus distention of all the veins feeding ito The
distal esophagus is then prone to bleeding with these torturous veins (risk of
upper GI) *?Acute Gastritiso Erosive, superficial inflammation of the gastric
mucosa due to impaired defenses allowing damage by normally produced HClo Normal
defenses include prostaglandins (minimize inflammation from HCl), bicarbonate
(neutralize HCl), and somatostatin (turn off hormonal stimulation of HCl
production)o Impairment can occur from small amounts of alcohol (increase HCl
secretion), chronic NSAID use (limit COX-1/COX-2 prostaglandins), or consuming
corrosive materials *?Chronic Gastritis o Non-erosive inflammation of the gastric
mucosa due to various inflammatory states o Type A � fundus-dominant, associated
with pernicious anemiao Type B � antrum-dominant, associated with H.pylori
infection (most common) *?Dieulafoy??s Lesiono Rare vascular malformation where a
large, torturous artery runs along the gastric sub-mucosa (typically along the
lesser curvature of the stomach), which can be damaged and bleed o Endoscopy � pin-
point defect in gastric mucosae
with active bleeding, with subsequent identification of arterial malformation NOT
associated with ulceration Anatomy*?Remember that the stomach has a fairly
extensive blood supply, and bleeding at different areas will result in different
involvement of gastric blood supplies o Gastric ulcers (posterior stomach wall)
-->?splenic artery o Gastric ulcers (lesser curvature) -->?left gastric arteryo
Duodenal ulcer -->?gastroduodenal artery *?The ??upper GI tract?? is considered
from the [oropharynx-->distal duodenum at the Ligament of Treitz] as this spot is
the transition from retro to intraperiotoneal Work-up * *?�??Occult GI bleed?? �
bleed isn??t known to the patient (no obvious bleed) but signs (FOBT or anemia)
point to a bleed occurring. These tend to be lower GI bleeds. * *?�??Obscure GI
bleed?? � bleed is known (often obvious bleeding) but the source cannot be
identified on endoscopy. These tend to be upper GI bleeds. * *?�Fluid resuscitation
� (two large-bore needles) restores blood volume and will reveal extent of bleeding
* *?�Placement of NG tube � suction out blood for better GI tract visualization,
using this for lavage is great way to confirm bleeds (use only room temp fluid;
cold fluid may cause increased Vagus stimulation) o Bloody/coffee grounds suctioned
-->?confirmed upper GI bleed o Clear fluid suctioned -->?no stomach bleed, but
cannot rule out duodenal bleed o Bilious fluid suctioned -->?confirmed no upper GI
bleed * *?�Coagulation studies � may show evidence for bleed & need for transfusion
* *?�Blood type/cross � get some blood ready just in case infusion is needed o Type
& screen-->just get pt blood characteristics, likely won??t need the bloodo Type &
cross-->blood is suspected to be necessary; actually crosses pt with donor blood o
Immediate transfusion -->?give O negative blood as it won??t cause a reaction * *?
�Hemoglobin/Hematocrit � may be totally normal early on, and may not even change
until patient has lost 30-40% of their blood volume! Remember that whole blood is
being lost (thus the proportions are all the same!). H&H only begins to change once
the kidneys start conserving sodium/H20 (12-24hr) or IV fluids are administered.
Hypovolemic shock (tachycardia, decreased urine output, drop in BP) may be an
earlier sign than changes on H&H! * *?�BUN/Creatinine - RBC proteins will be broken
down increasing intestinal urea production/absorption (>20 is considered
increased). If the kidneys are hypoperfused due to bleeding, they may reabsorb more
urea to increase blood volume. The increased absorption in both the
intestines/kidney raises the BUN increasing the BUN:Creatinine ratio! * *?
�Endoscopic study � either upper or lower depending on suspected etiology; the only
time you won??t have an endoscopy is with massive GI bleed making endoscopy unable
to visualize anything. This done after pt is stabilized and best done within 12hr
of admission Treatment *?If endoscopy is negative � further studies to figure out
problem o Capsule endoscopy/Further endoscopic studies/Tagged RBCs � for less
energetic bleeds o Angiography � typically used in brisk bleeds (1cc/min) & may
allow for therapeutic embolization * *?�If endoscopy is positive � found etiology
must be treated accordingly * *?�If pt actively vomiting blood, they should be
upright at 30o unless contraindicated * *?�Conservative management should be done
if pt is stable o Mallory-weiss -->?observe (spontaneous resolution occurs often)o
Gastritis -->?H2/PPI + d/c EtOH + H.pylori workupo Esophageal Varices -->?
octreotide (venoconstriction) + endoscopy/banding o Peptic ulcer -->?gastric level
+ H2/PPI + H.pylori workupo Dieulafoy??s lesion -->?endoscopic banding *?Surgical
management is reserved for unstable patients, those who fail conservative therapy,
or to exclude esophageal varicies Further Information on Etiologies 2596: MALT
lymphoma (MALToma) * *?�Gastric cancer often the result of H.pylori infection;
looks like a heaped up ulcer * *?�Dx: endoscopy with biopsy showing MALT-lymphoma *
*?�Tx: o Eradication of H.pylori ([omeprazole, clarithromycin, amoxicillin] or
[bismuth, omeprazole, a tetracycline, an aminoglycoside] o Chemotherapy ([CHOP] or
[CHOP + bleomycin]) can still play a role should H.pylori eradication fail to cure
the cancer Chapter 49: Severe Epigastric Pain � Peptic Ulcer Disease/Perforated
Viscus PUD Presentation *???Burning??, non-radiating epigastric pain with onset
depending on region of damageo Gastric ulcer � pain with eating (HCl production =
further erosion) & weight loss (avoid eating) o Duodenal ulcer � relief with eating
(Bicarb from pancreatic juices) & weight gain (yay eating!), but pain re-starts 2-
3hr post-prandially * *?�Nausea, vomiting, abdominal distention, melena, tenderness
to palpation of epigastrum * *?�History of GERD, chronic NSAID use, smoking, Family
Hx of ulcers Perforated PUD Presentation *?Presentation: chronic epigastric pain
that suddenly worsens with an initial sharp pain which quickly radiates; rebound
tenderness/guarding (peritonitis due to gastric contents in peritoneal cavity), &
air under the diaphragm on CXR (indicates perforation) o Pt often lays very still
because of abdominal pain with movement; exquisite pain with palpation with
guarding/rigidity. o Shoulder pain may be present (diaphragm irritation, referred
pain via phrenic nerve) o Septic shock & hypovolemia may be initial presentation
depending on duration of condition *?Dx: immediate CXR, as diagnosis and prompt
treatment (<12hr) is critical to limit mortality o Serum amylase/lipase should be
ordered to rule out acute pancreatitis o Labs will often be normal outside an
elevated WBC with left shift *?Tx: immediate surgical repair Pathophysiology * *?
�Remember that ulceration results from either acid hyper-secretion or decreased
mucosal barriers (NSAIDs, lack of somatostatin, lack of bicarb) * *?�H. pylori
infection (90% of duodenal ulcers & 80% of gastric ulcers) result in ulceration by
provoking gastrin hypersecretion-->HCl hypersecretion-->antral gastritis--
>ulceration * *?�Chronic NSAID use (including aspirin) inhibits COX-1/COX-2 -->?
inhibits prostaglandin/thromboxane production. These typically regulate
inflammation & HCl secretion, thus their absence causes damage! * *?�Cigarette
smoking (x2 risk of PUD) results in decreased prostaglandins and mucus
proliferation as well as throwing off he apoptosis/proliferation balance in the
stomach. * *?�Cushing Ulcer � increased intracranial pressure resulting in Vagal
hyperstimulation -->?HCl hypersecretion-->mucosal damage; high perforation risk *
*?�Curling ulcer � severe burns cause hypovolemia -->?mucosal ischemia -->?mucosal
damage -->?ulceration Classification of Peptic Ulcers o *?�Type I � lesser
curvature at the incisura (most common type) � mucosal barrier disruption etiology
o *?�Type II � lesser curvature/duodenum � HCl hypersecretion o *?�Type III �
prepyloric antrum � HCl hypersecretion o *?�Type IV � cardia of the stomach near
gastroduodenal junction (very painful!) � barrier disruption o *?�Type V �
Anywhere, but associated with NSAID use � barrier disruption Work-Up * *?�Making
the diagnosis is largely clinical (no lab tests are really going to help you here;
remember that most of your labs are going to be normal!) * *?�Labs: CBC (is there
bleeding?), CMP (contraction alkalosis? Loss of HCl?), amylase/lipase (rule out
acute pancreatitis), LFTs (help rule out choledocolithaisis/cholecystitis) * *?
�Imaging: abdominal series OR upright CXR (look for pneumoperitoneum; absence
doesn??t rule out perforation); thickened viscera may also be seen o If perforation
is suspected barium UGI series (causes barium peritonitis) and upper endoscopy
(insufflation can make perforation worse!) are contraindicatedo CT abdomen with
gastrografin contrast may be used to confirm diagnosis; may also show that
perforation has sealed itself, allowing for non-operative management Management of
Perforated PUD * *?�ICU admission with close observation * *?�Volume resuscitation
� likely inflammation, leakage of fluid, and vomiting need replacement * *?�NG tube
placement � stomach decompression (decrease leakage into abdominal cavity) * *?
�Broad spectrum IV ABx � only if sepsis if noted * *?�Initiation of PPI + Testing
for H.pylori-->triple therapy for H.pylori if (+) Surgical Management of Perforated
PUD o *?�Excision of perforated ulcer with patching + PPI therapy o *?�Laprascopic
approach is preferred and outcome are similar in surgeons with experience o *?
�Surgery is ALWAYS indicated unless the ulcer has spontaneously healed (40-80% of
perforations). Consider a conservative approach if: (1) It??s been <12hr since
onset of symptoms, (2) Pt is hemodynamically stable, (3) Pt is <70yr old, (4) Pt
doesn??t have any history of peptic ulcer treatment failure, (5) Pt is high risk
for surgery due to co-morbidities, (6) Radiologic evidence points to spontaneous
sealing of the perforation Chapter 50: Chest Pain and Early Satiety � Gastric
Cancer Epidemiology * *?�4th most common cancer in the world; more common in the
Far East, less common in USA * *?�Typically occurs in 70-80 y/o patients * *?�Rate
in USA is very low due to H.pylori treatment & widespread use of refrigerators
(less salting, pickling, etc. for food storage) Risk Factors o *?�Typically,
several risk factors come together for gastric cancer o *?�Common ones: Family Hx,
Diet high in nitrates/salt/fat, H.pylori infection, tobacco use o *?�Genetic:
BRCA1/2, HER2 overexpression, Peutz-Jegher syn., HNPCC, Type A blood Screening * *?
�Most common type is gastric adenocarcinoma (90%), typically with metastatic spread
at time of dx * *?�Typically, only 50% have local disease at dx with only 50% of
local disease being resectable! o Though to
be due to vague, non-specific symptoms associated with these diseases *?Because
it??s much rarer in the US, screening is not routinely recommended Anatomy*?Blood
supply to the stomach o Celiac Trunk -->?left gastric arteryo Celiac Trunk -->?
common hepatic -->?right gastric arteryo Celiac Trunk -->?common hepatic or right
gastric -->?right gastroepiploic artery o Celiac Trunk -->?splenic -->?left
gastroepiploic artery o Celiac Trunk -->?splenic -->?short gastric artery History &
Physical * *?�Common Symptoms: Vague abdominal pain, weight loss, fatigue,
dyspepsia, melena/anemia * *?�Specific Symptoms: Virchow??s nodes, Sister Mary
Joseph nodule, Irish??s node (left axillary node) * *?�Less Common Symptoms:
Dysphagia/early satiety (cardia involvement), acute upper GI bleed, palpable mass,
obstructive jaundice/elevated LFTs (growth into hepaticoduodenal ligament)
Pathophysiology * *?�Intestinal Type Gastric Adenocarcinoma: well-differentiated
type arising from gastric mucosa, typically occurring due to chronic inflammation
in the stomach (H.pylori, poor diet, smoking, etc.). Most commonly found in the
distal stomach (where all that ingested crap lies!) * *?�Diffuse Type Gastric
Adenocarcinoma: poorly-differentiated tumor asiring from lamina propria; grows in a
diffuse, sub-mucosal pattern resulting in gastric thickening (not a discreet mass);
typically occurs due to congenital disorders (younger pts); Most commonly found in
the proximal stomach. o Linitis Plastica: formation of the gastric wall into a
thickened ??plastic?? wall due to thickening *?GI Stromal Tumors (GIST; 1%):
mesenchymal tumors arising from the interstitial cells of Cajal (GI pacemaker
cells) appearing as smooth masses with regular borders. Express c-KIT & CD117
universially. o Neoadjuvant/maintainence therapy with Imatinib (Tyr-kinase
inhibitor)o Resection of mass through wedge resection (gastrectomies are only
rarely needed) * *?�Gastric Carcinoid Tumors (1%): rare to arise in the stomach;
often small and treated endoscopically or only observed unless functional) * *?
�Gastric Lymphoma: typically occur as a MALT-oma (H.pylori infection; treatment of
bacterium causes regression of tumor) or as a diffuse B-cell lymphoma (CHOP
chemotherapy followed by radiation) o CHOP-->cyclophosphamide, doxorubicin,
vincristine, & prednisone Workup * *?�Diagnosis-->Upper endoscopy allows for
visualization and biopsy. Multiple biopsies have a sensitivity around 98% (gold
standard) * *?�Staging-->endoscopic ultrasound (assess size, depth, and local lymph
nodes) + CT CAP (identify distant metastatic disease. PET scan also very good at
assessing lymph node involvement o At least 15 nodes must be resected and analyzed
for proper staging of gastric adenocarcinoma o D1 dissection � perigastric lymph
node dissection for stagingo D2 dissection � hepatic, left gastric, celiac, and
splenic lymph node dissection for staging (preferred for completeness but higher
rate of morbidity) Management * *?�No invasion of mucosa/lamina propria � mucosal
resection with 5mm margins (met. risk is LOW!) * *?�Distal invasive cancers �
subtotal gastrectomy with Bilroth II or Roux-en-Y reconstruction * *?�Proximal
invasive cancers � proximal gastrectomy or total gastrectomy with reconstruction *
*?�With proper staging of gastric adenocarcinoma: o Operable T1N0 � limited
resection is goodo Operable >T1N0 � Neoadjuvant chemo -->?surgical resection -->?
post-op ??Neoadjuvant care MAY be skipped, but not preferredo Inoperable or
metastatic disease -->?palliative chemo with re-assessment following treatment
Complications ??HER-2 (-)-->classic chemo drugs??HER-2 (+)-->trastuzumab + classic
chemo drugs??If not a candidate for chemo (can??t handle it) then just initiate
palliative care * *?�Dumping Syndrome � syndrome of high-osmolar food entry into
the small intestine (loss of pyloric sphincter due to gastrectomy) resulting in
diarrhea, stomach cramps, & hypotension 20-30 minutes following eating * *?
�Anastomotic Leak � leakage of the abdominal tract due to incomplete healing. Often
presents with abdominal pain, peritonitis, fever/tachycardia/leukocytosis-->sepsis
if untreated. o Upper GI CT with gastrografin � use if unsure about diagnosis �
(+)if showing a leak!o First line: source control with operation to fix leak with
subsequent bowel wash-out; keep pt NPO and place on TPN post-op with NG tube
placement to minimize gastric contents o 2nd line: complete resection of leaking
area Chapter 51: Chest Pain After Vomiting � Boerhaave Syndrome (Spontaneous
Esophageal Rupture) Risk Factors * *?�Alcoholism/overeating/bulemia (all can cause
forceful vomiting/wretching) * *?�Most common in pts 50-70yr Presentation *?
Mackler??s Triad: vomiting, thoracic pain (radiation to back/flank/abdomen,
aggravated by swallowing), subcutaneous emphysema (crepitus on sternal palpation;
pathognomonic for syndrome) o Dyspnea & dysphagia are often common signs as well*?
Note that early Dx is critical! Boerhaave??s has high mortality (40%) which
increases higher after 24hr Pathophysiology * *?�Esophageal perforation is not
typically spontaneous. 60% are iatrogenic (upper endoscopy). Trauma, foreign body
ingestion, or malignancy are all more common causes. Only about 10% are
spontaneous. * *?�Forceful vomiting causes intense intragastric pressure. This
pressure is transmitted through the esophagus, which normally propels vomitus out
the mouth. If the cricopharyngeus muscle fails to relax the upper GI tract to allow
passage of vomitus, the pressure is retained in the esophagus-->rupture! * *?
�Sepsis occurs due to contamination of the mediastinum by GI bacteria o Pleural
effusions may also occur due to erosion of the pleural membrane from gastric
contents in the mediastinum. This may also lead to pleuritis-->sepsis *?The most
common place for rupture is the left, posterolateral aspect of the esophagus, 2-3cm
proximal to the GE-junction-->this is why left-sided pleural effusion/atelectasis
is most often seen Work up*?First step: chest X-ray o Look for pneumomediastinum
(air in mediastinum) and left-sided pleural effusion/atelectasis o Up to 1/3 of pts
will have normal CXR and air in mediastinum is best seen 1hr post-perforation *?If
X-ray is questionable: CT with water-soluble oral contrast o High sensitivity for
diagnosis & allows for evaluation of surrounding structures (a huge advantage over
an esophagram with contrast) aiding surgical planning/approach o Also, it allows
for assessment of other diagnoses if Boerhaave??s isn??t what??s going ono Water-
soluble oral contrast is critical...barium can cause a huge inflammatory rxn if it
leaks into mediastinum/surrounding structures*?Endoscopy is NOT used as
insufflation runs the risk of enlarging the perforation Management * *?�Initial:
Aggressive IV fluids (2 large-bores; if septic, monitor with central venous
catheter), NPO, broad spectrum Abx for mouth/gut bacteria, anti-fungal, H2 blocker
or PPI, if hemodynamically unstable place arterial line and start vasopressors * *?
�Conservative: accepted in pts with low co-morbidities, no sepsis/shock, and a
small perforation that??s <24hr old or healed already o All initial treatments +
nasogastric suction + parenteral nutrition o Repeat imaging at hospital day 7 o If
perforation seems to be healed, resume oral intake and continue Abx for 6-8wk *?
Surgical: preferred treatment for everyone else o Perforation closure: preferred in
pts with smaller perfso Esophageal resection: preferred for larger perfs. Often
resected, then re-constructed with colon or jejunum at a later date (after they
recover!)o Both procedures require debridement of de-vitalized tissue in the
esophagus, mediastinum, and pleura (pleural decortication) Chapter 52: Scrotal Pain
� Testicular Torsion Presentation *?Classic symptoms: nausea/vomiting, sudden onset
testicular pain >24hr, superiorly displaced testicle, absent cremaster reflex o
Cremaster reflex: ipsilateral testicular elevation due to cremaster muscle
contraction with stroking of the inner thigh (genitofemoral nerve; L1-L2) *?Other
causes of acute unilateral testicular pain & some differentiating signso Trauma �
85% blunt, often due to sporting injury; this should be in the history ??May cause
rupture & hematoceleo Torsion of epididymal appendage (appendix testis) � gradual
onset unilateral pain (most common reason in child), cremaster reflex present??Blue
dot sign: palpation of small, firm tender nodule on epididymal head, that has a
blue discoloration on examination??Tx: NSAIDs, ice packs, and scrotal support;
surgical excision for refractory symptoms o Epididymitis � scrotal pain relieved
with support (Prehn??s sign), fever, dysuria, induration Pathophysiology * *?�Bell-
Clapper deformity � congenital defect of the processus vaginalis resulting in
failure of the gubernaculum/testis/epididymis posterior anchoring to the inner
scrotum. Both testes are allowed to swing freely (like the ball inside a bell),
predisposing to torsion later in life! * *?�Most common age 12-18yr * *?�Prior
torsion puts the other testicle at risk for torsion! Work-Up o *?�Scrotal exam
should ALWAYS be performed in adolescent male with nausea/vomiting o *?�Labs: o If
high clinical suspicion, none are needed. This would delay surgical intervention. o
If low clinical suspicion: urinanalysis/CBC (rule out infectious causes)*?Imaging:
Doppler ultrasound of testes (high sensitivity/specificity for torsion & rule
in/out other things) o Confirm adequate bloodflow, look for blood in testis (new =
hyperechoic; old = hypoechoic) o Trauma and torsion often occur in sporting events,
which can muddy the waters here! Management * *?�Torsion <6hr (100% viability):
attempt at ED manual de-torsion (lateral rotation of testis) with elective
bilateral
orchiopexy. If manual de-torsion not possible, surgical de-torsion/orchiopexy is
needed * *?�Torsion >6hr: immediate surgical de-torsion/orchiopexy is needed o If
testicle is necrotic, orchiectomy is warranted * *?�Minor trauma (no significant
swelling/pain/breaks in scrotum): scrotal support, ice packs, NSAIDs, rest * *?
�Major trauma (penetrating, lack of bloodflow, rapidly expanding hematoma,
avulsion, scrotal de- gloving, or violation of tunica albuginea): go to OR for
exploration and repair Prognosis *?Torsion timing: <6hr (100% viability), 12hr (20%
viability), 24hr (0-10% viability) *?Fertility is often not affected significantly
with unilateral loss of a testicle. However, risk of anti-sperm antibodies (loss of
immunologically privileged site) may occur with trauma/necrosis of testicle
decreasing sperm count Chapter 53: Scrotal Mass � Testicular Cancer Differential
Based on Anatomic Location of Mass * *?�Scrotal Skin: epidermoid/pilar cyst,
squamous cell carcinoma * *?�Spermatic cord: indirect inguinal hernia, hydrocele,
varicocele * *?�Epididymis: epididymitits, spermatocele, torsion of testicular
epididymal appendate (appendix testis) * *?�Testis: orchitis, testicular torsion,
testicular cancer Risk Factors � cryptorchidism (biggest), personal/family Hx of
testicular cancer, Klinefelter??s Synndrome, white race, male 20-35yr (most common
age range)Presentation o *?�Painless mass within the testicle (cancer until proven
otherwise!) o *?�Constitutional signs suggest metastatic disease o Retroperitoneal
lymph nodes: back/abdominal pain, weight loss, nausea o Pulmonary mets: cough, SOB
* *?�Gynecomastia: may be present in hormonally active tumors secreting B-hCG
(choriocarcinoma) * *?�Hyperthyroidism symptoms: alpha unit of B-hCG similar to
TSH; thus choriocarcinoma may cause this Pathophysiology o *?�When Cryptorchidism
results in testicular cancer, the distribution is undescended testicle (75%) and
descended testicle (25%); thus an underlying problem with the tissue may be
present, not just the problem of lack of descent o *?�Seminomatous germ cell tumors
(35%) o Seminoma � most common in adults; high response to radiation; rarely
metastasizes with good prognosis, rarely B-hCG production *?Nonseminomatous germ
cell tumors (65%)o Embryonal carcinoma � malignant/aggressive hematogenous spread,
often necrosis, B-hCG or AFP production is commono Yolk sac tumor � most common
children, malignant, AFP productiono Choriocarcinoma � malignant, early
hematogenous spread, B-hCG production common o Teratoma � derived from >2 embryonic
layers, may be benign or malignant, AFP or B-hCG o Mixed germ cell tumor � multiple
components of the above *?Sex-Cord stroma tumorso Leydig cell � benign,
paraneoplastic syndromes due to testosterone production o Sertoli cell � benign,
often clinically silent *?Othero Lymphoma � older men, diffuse large B-cell, often
bilateral/malignant Workup * *?�Labs: B-hCG, AFP, LDH (used for staging/response
tracking/prognosis) * *?�Imaging: o Ultrasound: solid mass within the testicle
(cystic/fluid mass is less likely)o CT abdomen/pelvis: used to assess lymph nodes
for stagingo CXR: used to assess lungs for stagingo CT chest: done only if signs of
metastatic disease is found on CT a/p or CXR o CT head or MRI brain: done only if
neurologic symptoms present *?Biopsy is contraindicated due to high risk of seeding
Management *?Radical inguinal orchiectomy: allows for removal of testicle and
spermatic cord up to internal ring o Approach preferred as it allows for removal of
more spermatic cord = less local recurrence *?Post-surgical treatments may be
utilized based on tumor type/clinical situation o Radiation: often used in
seminomaso Chemotherapy: may be used in most testicular cancerso Retroperitoneal
lymph node dissection: often used in non-seminomas *?Complicationso Unilateral
orchiectomy will NOT lead to infertility or erectile dysfunction o RPLND may injure
nerves leading to erectile dysfunction Chapter 54: Blood in UrineDifferential
Diagnosis: Acute cystitis, bladder cancer, nephrolithiasis, prostatitis, renal
cancer, pyelonephritis, PKD, prostate cancer, BPH, trauma, urethral stricture,
vigorous exercise, IgA nephropathy, intense exercise Differential By Age: * *?
�<20yr � Acute (UTI, Foley trauma, exercise); Chronic (IgA nephropathy) * *?�20-
50yr � Acute (UTI, Foley trauma, nephrolithiasis); Chronic (PKD,
prostate/bladder/kidney cancer) * *?�>50yr � Acute (UTI, Foley, nephrolithiasis);
Chronic (BPH, PDK, prostate/bladder/kidney cancer) Presentation o *?�Gross
Hematuria � visible urine color change to pink (mild active bleed), red (moderate-
severe active bleed), brown (old blood/glomerular bleed), or passage of clots o *?
�Microscopic Hematuria � grossly normal urine with RBCs or heme seen on
urinanalysis o >3RBCs/HPF on only one urine specimen warrants complete hematuria
workup *?Pseudohematuria � pink/orange/red/brown discoloration not due to RBCs in
urine o Foods (beets/rhubarb/artificial dyes)o Drugs (rifampin, sulfonimides,
phenazopyridine, nitrofurantoin, phenytoin, levodopa, methyldopa, quinine,
choloquine, Adriamycin, metronidazole) o Rhabdomyolysis (huge amount of myoglobin)o
Conjugated bilirubinemia (conj. bili is water soluble) * *?�Pain + Hematuria �
likely indicates infection/urinary obstruction/urinary trauma * *?�Nephrolithiasis
� colicky flank/groin pain, pt will move/shift body weight relieving pain due to
shifting of stone (as opposed to peritonitis where pts stay very still) o Risk
Factors - Hx, fHx, high protein diet, male, low fluid intake, dehydration,
recurrent UTI, diabetes, gout, RTA, hypercalcemia, some medications*?Renal Cancer �
incidental discovery of mass on imaging most common; may have flank pain, abdominal
mass, and hematuria triad (10-15% all three)o Risk factors � smoking, male, older,
obesity, fHx, heavy metal/chemical exposure * *?�Bladder Cancer � painless gross
hematuria, rarely with urinary symptoms * *?�Prostate Cancer � incidental discovery
with PSA or DRE most common; may have urinary obstruction symptoms similar to BPH o
Metastatic disease can present as bone pain, obstructive renal failure, weight loss
Anatomy * *?�Upper UG tract � kidney-->end of ureter * *?�Lower UG tract �
bladder-->exit of urethra Pathophysiology *?Kidney Stones � typically form in the
kidney/renal pelvis and often pass freely through the UG tract iif <5mm.
Obstruction commonly occurs ureteropelvic junction, pelvic brim, or ureterovesical
junction. o Calcium oxalate stones � most common stones; radiopaque;
HyperCa2+/Chrohn??s risk factors o Struvite (magnesium ammonium phosphate) stones �
classically occur secondary to urease(+) UTI bugs (Proteus, Klebsiella), staghorn
calculi, radioopaque o Calcium phosphate stones � form well in alkaline urine,
radiopaque; RTA/hyperaparthroidism o Uric acid stones � form poorly in alkaline
urine, so best to alkalinze urine to treat; radiolucent; risk factors (low urine
pH, gout, chemotherapy, ileostomy patients, high protein diet) *?Renal Cancer o
Renal Cell carcinoma (most common) arises from renal tubular cellso Histologic
Subtypes � Clear Cell (70%), papillary (15%), and chromophobe (5%)o 33% metastatic
at Dx � most commonly to lungs, but may go many placeso Genetic syndromes
associated with RCC are von Hippel-Lindau (AD; chrom 3p), tuberous sclerosis (AD,
chrom 9), or Birt-Hogg-Dube (AD, chrom 17)o Paraneoplastic syndromes associated �
polycythemia (EPO production), hypercalcemia (PTHrP production), hypertension
(renin production), Cushing??s syndrome (cortisol production), or Stauffer??s
syndrome (liver dysfunction/hepatosplenomegaly, unknown mechanism) *?Bladder Cancer
o Urothelial cell carcinoma (transitional cell carcinoma; most common type) o
Graded low or high + staged based on local invasion depth *?Prostate Cancer o
Prostatic adenocarcinoma (most common) Workup*?First Step: urine dipstick (beware
of false positives with myoglobinuria, or iodine solution cross-rx) o Even if
negative, pt should probably have a urinanlysis*?Second step: urinalysis with urine
microscopy (RBCs/HPF, WBCs, bacteria, crystals, dysmorphic RBCs, casts) to further
determine presence/source of bleedingo Casts, proteinuria, dysmorphic RBCs, brown
urine-->glomerular source and should be referred to nephrologist for further workup
*?Labs: CBC (anemia, infection, thrombocytopenia), CMP (BUN/Cr), PT/PTT/INR (rule
out coagulopathy), PSA (prostate screening, some false positives with
instrumentation/infection), urine culture (infection), urine cytology (malignancy)
o Negative cytology does NOT rule out malignancy; low-grade tumors sensitivity of
50% and large amount of urine RBCs can result in false-negative *?Concern for
nephrolithiasis: non-contrast helical CT (CT-KUB) is most sensitive for imaging;
ultrasound should be used in pregnancy women/women of childbearing age o In HIV
patients, anti-retroviral drugs can crystalize in the UG tract forming small
radiolucent stones. CT-KUB will not show anything! So this is the one situation
where contrast CT is useful for stones to show a filling defect *?Typically, any
further workup will be based on suspected etiology Management * *?�Remember that
the 1st thing to do is to find and address the underlying cause. The below are
common causes and should be easily recalled. * *?�Renal Stones � based on estimated
size of stone and likelihood of passing spontaneously o <5mm � likely to pass;
supportive care + tamsulosin (alpha blocker, relax ureteral wall) unless
septic/solitary kidney/uncontrolled paino 5-9mm � intermediate; clinical judgement
should be your guideo >9mm � unlikely to pass, invasive treatment (shock wave
lithotripsy, percutaneous nephrostomy, or nephrolithotomy)o Emergent Surgery �
urosepsis, intractable
pain, progressive renal damage, or solitary kidney. Need to relieve obstruction
with ureteral stent or nephrostomy tube placement. *?Renal Masses � depend on size
and health of patiento Surveillance + thermal/cryoablation � small masses or poor
surgical candidateso Partial/Radial nephrectomy � recommended for masses with any
concern of RCCo Radical nephrectomy removes kidney/perinephric fat/Gerota
Fascia/ureter/lymph nodes and sometimes the ipsilateral adrenal gland *?Bladder
Cancer o Dx/Staging � transurethral resectiono Small/superficial mass � complete
transurethral resection + intravesicluar mitomycin (chemotherapy) or bCG infusion
(immunotherapy) + close monitoringo Invasive to detrussor/non-metastatic - Radical
cystectomy with urinary diversiono Radical cystectomy removes entire bladder,
pelvic lymph nodes, [prostate, seminal vesicles] for male and [cervix, uterus,
fallopian tubes, and part of vagina] for women *?Prostate Cancer o Disease
contained in prostate + >10yr life expectancy � removal of prostate/seminal
vesicles o Poor surgical candidate/reduced life expectancy � noninvasive therapy
(external beam, brachytherapy, or androgen deprivation) + surveillance Situations
Special*?Persistent bleeding despite Foley/Manual Irrigation o 3-way catheter
placement for continuous irrigation � allows for drainage alongside stopping
urokinase exposure (stops regular coagulation cascade) o If continued bleeding � go
to OR for cystoscopy for clot evacuation, pathologic assessment and fulguration
(cauterization of bleeding sites) *?Admission for gross hematuria is warranted by
(1) bleeding despite adequate bladder irrigation or (2) symptomatic anemia Areas to
Get You in Trouble * *?�Assuming hematuria is due to UTI and not doing a full
workup (don??t be a dumbass) * *?�Not placing a Foley in the setting for
significant gross hematuria (you need to irrigate clots out) * *?�Placing a Foley
with trauma/blood at the urethra (worry of urethral transection) may lead to a full
transection and worsening damage Chapter 55: Transient Loss of Vision in the Right
Eye � Carotid Artery Embolization Differential Dx: * *?�Circulatory � embolus to
ophthalmic artery; central retinal artery occlusion (cherry red spot), retinal vein
occlusion (??cloudy vision?? with cotton wool spots, edema, retinal hemorrhage);
giant cell arteritis (jaw claudication, headaches, ^ESR), or severe orthostatic
hypotension * *?�Ocular � retinal detachment (floaters), or open angle glaucoma
(peripheral-->central vision loss) * *?�Neurologic � papilledema, optic neuritis,
retinal migraine Risk Factors *?Older age, male gender, HTN, smoking,
hypercholesterolemia, diabetes, obesity Presentation * *?�Amaurosis Fugax (Greek
� ??darkness??; Latin ??fleeting??) � transient vision loss (??shade coming down??)
resulting from atherosclerotic debris breaking from a plaque in the internal
carotid, and transiently lodging in the ophthalmic artery (1st branch of ICA) * *?
�Hollenhorst Plaques � bright yellow, refractory spots seen on ophthalmic
indicative of cholesterol microemboli breaking off and lodging into the eye
arteries * *?�Carotid Bruit � indicative of a carotid plaque. Must rule out heart
murmur (can be transmitted up carotids), external carotid bruit (benign), and
subclavian bruit (possibly subclavian steal syndrome!) Signs of Other Problems
Mimicking Carotid Embolization *?Motor weakness/paralysis & Sensory loss �
indicative of a TIA or stroke! While a patient may have transient vision loss,
additional symptoms suggesting brain involvement are not ok! o ACA stroke � leg
weakness, hemiplegia, urinary incontinence (contralateral; lower > upper) � medial
surface of frontal/parietal lobes o MCA stroke � aphasia, hemi-neglect,
hemiparesis, gaze preference (contralateral; most common form of anterior
circulation stroke) � lateral surface of frontal/parietal lobes o PCA stroke �
homonymous hemianopia; note that posterior circulation strokes are NOT from carotid
embolism; thus a carotid endarterectomy is NOT useful *?Dizziness, Syncope,
Headaches � most commonly due to vertebral artery disease, but rarely may be caused
by bilateral carotid stenosis Anatomy*?Internal Carotid branches � no branches in
the neck (easy to identify on scans!) o Intracranially, the Ophthalmic Artery is
the 1st branch of the internal carotid*?External Carotid branches � Superior
Thyroid, Ascending Pharyngeal, Lingual, Facial, Occipital, Posterior Auricular,
Maxillary, and Superficial temporal (??some attendings like freaking out potential
medial students??) Pathophysiology *?Stroke stuff � consult neuro block noteso
Typically, the size of the embolus is the critical factor in determining stroke vs
TIA. Larger emboli (like from the left atrium) are harder to dissolve via the
fibrinolytic system, thus making for longer interruptions in bloodflowo Recurrent
TIAs are likely from carotid artery plaques (consistent course when breaking off) o
Multiple TIAs/strokes in different parts of more likely from atrial plaques (longer
distance allows for greater variability when breaking off) * *?�Atherosclerotic
Plaque Formation � endothelial damage -->?thrombin/ADP/cytokine release -->?
platelet migration/fatty streak formation-->ultimately smooth muscle
infiltration/calcification/fibrosis * *?�Carotid artery bifurcation is a classic
place for atherosclerotic plaque formation due to alteration of shear stresses on
the intimal walls of the artery o High shear stress � good for the intima, kind of
like how mechanical stress promotes bones to grow. The Inner wall of the
bifurcation is blasted with blood and rarely has plaque buildup.o Low shear stress
� makes favorable conditions for plaque formation (blood isn??t blowing away the
atherosclerotic plaques). The outer walls have transient reversal of blood flow due
to the diverting flow of medial blood (hitting the bifurcation) getting blasted out
toward the outer walls. These slower flow states favor formation of plaques. *?
Typically, carotid stenosis symptoms are due to cholesterol emboli (NOT significant
stenosis). Collateral blood flow to the circle of Willis will provide adequate
bloodflow. o This is also why amarosis fugax is typically NOT accompanied by stroke
symptomso Larger plaques are more unstable, thus more likely for cholesterol emboli
to break off Workup * *?�Auscultation for bruits: not bad but not the most
sensitive/specific test. May be helpful as a nice correlate but won??t make or
break the diagnosis * *?�First diagnostic test: carotid duplex scan � ultrasound
scan that shows the plaque and estimates degree of stenosis based off of post-
plaque bloodflow velocity (higher velocity = more stenosis; 0-49%, 50-69%, 70-99%,
or occluded) * *?�Confirmatory tests: either CTa or MRa (allows for actual
measurement of stenosis Treatment o *?�Distinguishing degree of stenosis is
critical for treatment decision making o *?�In symptomatic patients: o <49% -
aspirin + statin +/- clopidogrelo 50-69% - carotid endarterectomy (CEA) is
considered (men/brain symptoms/ Increasing % stenosis more benefit; women/amaurosis
fugax/lower & stenosis less beneficial) ??Risk reduction at 5 years � 22%-->16% o
70-99% - CEA for both men and women (within 2 weeks; stops risk of further
embolization) ??Risk reduction at 2 years � 26%-->9% o 100% - aspirin + statin +/-
clopidogrel (control risk factors; no risk of embolization due to no bloodflow in
the artery!) *?In asymptomatic patientso <59% - aspirin + statin +/- clopidogrelo
60-99% - CEA for men; aspirin + statin +/- clopidogrel for women ??Risk reduction
at 2 years-->11% - 5% o 100% - aspirin + statin +/- clopidogrel * *?�CEA is always
followed by medical initiation of aspirin and a statin * *?�CEA has no benefit in a
person with previous stroke causing severe neurologic deficit; the point of CEA is
to stop any further embolization to protect perfused tissue. If that tissue is
dead, then there??s no benefit to the risks of the procedure. * *?�Women are
treated more conservatively due to data showing worse post-op outcomes. Smaller
caliber vessels are thought to be the culprit (more likely for recurrent stenosis!)
* *?�Blood pressure control prior to CEA is critical. Concern of perioperative
cerebral hyperperfusion syndrome (severe headache, neurologic deficits, seizure, or
cerebral hemorrhage) due to carotid body manipulation. Pts with high BP have a
higher incidence of this syndrome. * *?�Acceptable stroke/death rate after CEA is
<3% (asymptomatic) and <6% (symptomatic) * *?�Cranial Nerves that are at risk with
CEA o CN VII (marginal mandibular branch) � drooping at the corner of the moutho CN
IX (glossopharnyngeal nerve) � difficulty swallowingo CN X (recurrent laryngeal
nerve branch) � hoarsenesso CN XI (spinal accessory nerve) �
sternocleidomastoid/trapezius muscle weakness o CN XII (hypoglossal nerve) � tongue
deviation toward injured side *?Note that carotid artery stenting (CAS) may be
considered in symptomatic patients with high perioperative risk (previous surgery,
neck irradiation, lesion high in the neck) Chapter 56: Right Calf Pain with Walking
� Peripheral Artery Disease/Claudication Risk Factors *?Smoking, diabetes,
hypertension, hypercholesterolemia, old age, male gender, obesity, sedentary
lifestyle, family Hx of vascular disease, heart attack, or stroke Presentation * *?
�Claudication: triad of 1pain in the leg with walking, 2relief with a few minutes
of rest, 3reproduction of the pain with walking the same distance each time * *?
�Peripheral Artery Disease: buildup of atherosclerotic plaques which limit arterial
flow, resulting in ischemia to leg muscles and pain with use o Severity is based on
the Rutherford rating scale (0 � asymptomatic; 1 � mild claudication; 2 � moderate;
3 � severe; 4 � ischemic
rest pain; 5 � minor tissue loss; 6 � major tissue loss)o Ischemic Rest Pain
(Rutherford 4) � classically occurs at the toes (hardest to get blood to) and at
night (bloodflow is gravity dependent); pt will describe pain in the feet that
wakes him up at night, where he must get up or dangle his legs till it passes. This
sign is considered limb threatening ischemia * *?�Buerger??s Sign (dependent rubor)
� elevation of the foot (1-2min) causes them to become pale. When putting the feet
back down, they become very red like lobsters (arteriolar vasodilation!). If this
sign is absent, it??s very unlikely to have ischemic rest pain. * *?�Pulse deficit
� can give a clue as to level of atherosclerotic stenosis o When examining pulses,
which ones do you check? (17 total!) ??Bilateral: superficial temporal, carotid,
brachial, radial, femoral, popliteal, posterior tibial, dorsalis pedis ??
Unilateral: abdominal aorta (just above umbilicus)o Calf muscle atrophy, hair loss
(follicle death), dry scaly skin (sweat glands death), shiny skin (thinning skin),
ulceration, and increased capillary refill time (<2 sec is normal) Anatomy*?Which
muscle groups are commonly noticed with PAD/claudication? o Calf muscles
(superficial femoral artery) � travels through the Hunter/Adductor canal; it??s the
most common site for atherosclerotic plaques, thus the most commonly affected! o
Buttock (internal iliac artery) � the aorta/common iliacs provide flow the to
internal iliac, thus compromise of either of these palpable sites will affect the
butt! o Hamstrings are NOT often affected � they are not utilized heavily in normal
walking, thus pain here is more likely to be some some other pathology o Feet
muscles (rare; tibial artery) � usually from some isolated disease process! * *?
�Hunter/Adductor Canal � lies within the femoral triangle (inguinal ligament,
adductor longus, and Sartorius) and allows passage of the SFA down the leg. * *?
�Note! That while the SFA is the most common site of atherosclerosis, the common
femoral artery is the most common site of arterial emboli! Pathophysiology * *?
�Dependent Rubor � the distal arterioles are so poorly perfused that they are
constantly vasodilated, allowing for intense pooling of arterial blood in the feet
when gravity is allowed to pull it down. * *?�Pain onset � often occurs at a
consistent distance (fixed deficit of blood flow), but this distance may shorten
with increased effort in walking (walking up a hill, etc.) * *?�Claudication of
certain muscles � shows the level at which claudication is occurs (referenced
above) Named Syndromes *?Subclavian Steal Syndrome � atherosclerotic disease of one
subclavian artery proximal to the vertebral artery. In higher demand situations,
the diseased subclavian cannot provide perfusion...thus the vertebral artery
reverses flow from the vertebral to perfuse the arm. o Transient vertigo,
dizziness, & syncope during upper body exercise * *?�Buerger??s Disease
(thromboangiitis obliterans) � classically occurs in young, male, heavy smokers;
smoking through to cause inflammatory occlusion of distal arteries in the
hands/below the knees. Smoking cessation is the only effective treatment! * *?
�Leriche Syndrome � occlusion of the intrarenal aorta, often seen in smokers. o
Triad: buttock/thigh claudication, absent femoral pulses, erectile dysfunctiono
E.D. from [aorta -->?internal iliacs -->?internal pudendal arteries]o Often slow
developing, thus collaterals enlarge and allow for only claudication, not ischemia
Workup*?Ankle-Brachial Index � blood pressure is measured in the ankles (dorsalis
pedis & posterior tibial) and the arms (brachial arteries); the highest ankle &
highest arm systolic pressures are used. o Normal � 1.2 � 1.0o Mild PAD � 0.9 � 0.7
(claudication)o Moderate PAD � 0.7 � 0.4 (claudication) o Severe PAD - <0.4
(ischemic rest pain) * *?�Arterial Duplex scan � Doppler ultrasound is used to
search for evidence of atherosclerosis and estimates % stenosis based on flow
velocity after the plaque * *?�If interventions are being planned, better
visualization of the plaques should be gotten via CTa or MRa * *?�Screening of
asymptomatic PAD patients does not provide any benefit; thus is not indicated!
Prognosis o *?�Risk of limb loss with only claudication is 5% at 5 years o *?�Risk
of limb loss with ischemic rest pain is 50% at 1 year o *?�Ischemic rest pain, non-
healing ulcer, and gangrene are poor prognostic signs and warrant more aggressive
interventional planning Management * *?�First Step: smoking cessation, diet change,
supervised exercise program, control chronic diseases (HTN, dyslipidemia, diabetes,
etc.) * *?�Symptomatic management: o Cilostazol � vasodilator, thrombin inhibitor,
inc. HDL, dec. TAGs; useful for symptom control but contraindicated in patients
with heart failureo Pentoxifylline � FDA approved but no better than placebo
(decreases blood viscosity) *?Drugs for medical managemento Statins � typically
given to PAD patients, even with normal cholesterol levels (stabilize plaques).
Goal is an LDL <100, or <70 if cardiovascular risk factors. Doesn??t increase
walking distance. o Aspirin � indicated (less platelet aggregation), but doesn??t
increase walking distances.o Clopidogrel �indicated (irreversible platelet
inhibitor); doesn??t increase walking distances. o Heparin/Warfarin � no role; the
problem is atherosclerosis, not blood clots/emboli *?Invasive Managemento
Endovascular angioplasty/stenting or open endarterectomy/bypass are optionso
Rutherford Class 0 or 1 � not indicatedo Rutherford class 2 or 3 � indicated if 1pt
is a good candidate for surgery and 2claudication significantly interferes with
lifestyleo Rutherford class 4, 5 or 6 � indicated as limb loss is distinct
possibility Areas of Trouble/Controversy * *?�Note that diabetic patients may have
falsely normal ABIs due to Monckeberg??s arteriosclerosis (intense medial layer
calcification of the artery; often in vessels below the knee) making arteries
incompressible by your blood pressure cuff. The ABI cannot adequately assess these
arteries! * *?�If a patient refuses to quit smoking it??s your call whether or not
to do an invasive procedure. It typically has worse outcomes, thus they??re often
refused. * *?�Endovascular and open approaches have similar outcomes in class 5/6
disease. Chapter 57: Sudden Onset Severe Abdominal Pain � Ruptured AAA Risk Factors
* *?�Classics: Smoking (strongest risk factor!), age >60yr, white race, male sex *
*?�Others: Hx of extra-abdominal aneurysm/ coronary artery
disease/atherosclerosis/HTN, family Hx AAA * *?�Note that diabetes is NOT a risk
factor...and is actually protective against AAA Presentation *?Un-Ruptured AAA �
often asymptomatic and often undetected...only revealing itself when it ruptures. o
Abdominal/lower back pain (interface with surrounding tissue) or thrombus formation
with distal embolization causing symptoms can, but rarely, occur *?Ruptured AAA �
acute abdominal pain radiating to the left flank, palpable pulsatile abdominal
mass, hemorrhagic shock (hypovolemia, tachycardia, pallor, diaphoresis), weakened
LE pulses Screening * *?�Physical exam � deep palpation of the abdomen for aortic
pulse with diameter estimation * *?�Duplex Ultrasound � one-time screen for men 65-
75yr with (+)smoking history o If relative with AAA -->?screen at age 60o If found
to have AAA between 3-4cm -->?annual ultrasound monitoringo If found to have AAA
between 4-4.5cm -->?biannual ultrasound monitoring Pathophysiology*?Normal AA size
� 1.8cm (women) to 2.0 (men) o By definition, aneurysm is 1.5x larger in diameter
than average sizeo Thus an infrarenal aortic aneurysm would have to be >3cm at
minimumo Aneurysm expansion is typically 2-4mm/year; but can grow >5mm/6month
(rapid expanding) *?Medial layer breakdown through elastin & collagen degradation
of the AA results in aneurysm o Thought to be driven by matrix metalloproteinase
(MMP) activity (increased in AAA pts) o Note that statin drugs and having diabetes
have been shown to DECREASE MMP activity! *?Rupture risk increases with increasing
sizeo Typically rupture occurs into the retro-peritoneum to the left (vena cava is
on the right!)o While rare, peritoneal rupture would like cause instant death, as
there??s no ability to compress this rupture point Work-up*?First step: ABC
management (intubation if unstable; two large bore needles with limited fluids) o
IV fluids are limited as permissive hypotension (goal of 70mmHg systolic) as
aggressive resuscitation tends to exacerbate bleeding (increased BP/dilution of
coagulation factors) o <1L of crystalloids, then packed blood products are
recommended * *?�If hemodynamically stable: get CT angiogram w/ contrast of abdomen
(confirms Dx, area of rupture, and if endovascular approach can be used) * *?�If
hemodynamically unstable: imaging is NOT needed with confirmatory exam findings.
Bedside abdominal ultrasound may be used to confirm large AAA presence (likely
won??t show hemorrhage as bleeding is typically retroperitoneal) Management *?Non-
ruptured Asymptomatic AAAo < 5.5cm diameter - you simply watched it based on
guidelines. The risk of surgical repair outweighs the risk of rupture in this size
aneurysmo > 5.5cm diameter or Enlarging >1cm/year � elective repair (either
approach) *?Ruptured AAAo Emergent repair (open preferred) *?AAA elective repairo
Open repair � cheaper, faster, lower rate of re-operation; higher risk and longer
recover o Endovascular aneurysm repair (EVAR) � (opposite characteristics than open
repair) ??AAAs with short ??aortic neck?? (length between renal artery branch and
aneurysm) are not suitable for this repair ??Concern of persistent ??endoleak?? due
to incomplete resolution of aneurysm sac ??Requires lifetime follow-up for
endoleak surveillance (CTa at 1month-->yearly) o Most common cause of post-op
death is heart attack *?Endoleak � persistent high pressure flow into aneurysm sac
following surgeryo Type 1 � most worrisome; persistent high-pressure aortic/ iliac
vessel flowo Type 2 � most common; persistent low-pressure retrograde flow from
visceral branches o Type 3 � flow between junctions of multiple stents at
aortic/iliac vesselso Type 4 � flow through stent pores Pearls of Wisdom * *?�AAAs
can rupture and temporarily seal, leading to no contrast leakage on CTa. However,
these CTa scans can also retroperitoneal fluid adjacent to the AAA. This is
considered ruptured AAA until proven otherwise and should be treated as such! * *?
�Early onset diarrhea after AAA repair is high sign of post-op ischemic colitis,
classically due to ligation of the inferior mesenteric artery. Proper medical or
surgical management is warranted! * *?�GI bleed after AAA repair could be several
things however, aortoenteric fistula is a CLASSIC reason why this might happen
months to years following repair. o Typically occurs at the 4th part of duodenum
(rests next to the aorta)o Upper endoscopy is typically NEGATIVE, but fluid/air
around the graft can be seen on CT o Management � excision of graft + bypass
surgical repair + long-term abx Chapter 58: Cold, Painful, Right Lower Extremity �
Acute Limb Ischemia Presentation *???6 Ps?? � pain (typically calf), pallor,
pulselessness (defining feature), paresthesia, paralysis, and poikilothermia (cold
limb) o Acute � sudden decrease in perfusion lasting <2 weeks o Chronic � lasts >2
weeks * *?�A good cardiac history is essential as 80% of emboli causing ALI come
from the heart (Atrial fibrillation (most common, hypomobility); recent MI
(hypomobility), valvular disease (vegetation), left atrial myxoma (tumor breaks off
and embolizes) * *?�Palpation of the abdominal aorta, femoral artery, or popliteal
artery may revel a stiff mass present * *?�Always examine the contralateral limb to
compare for polkiothermia/pallor/etc.; if the other leg is totally normal, embolic
may be more likely vs systemic signs of atherosclerosis (ischemic) * *?�Past
interventions for PAD are a common cause (grafts or iatrogenic trauma are
classics!) Etiology o *?�Thrombotic (50% of cases)� arterial thrombosis,
hypercoagulable disorder, arterial trauma o *?�Embolic (40% of cases)�
cardioembolic (a-fib, CHF, recent MI, myxoma), popliteal/aortic aneurysm embolism,
paradoxical embolism (signs of DVT) o *?�Other (10% of cases) � acute aortic
dissection, systemic shock (late manifestation) Pathophysiology *?Thrombotic ALI is
the result of two mechanisms: o Plaque buildup � progressive narrowing of the
arterial lumen resulting in low-flow to limbso Intraplaque rupture � local
hemorrhage/clot formation can seal off an already narrowed artery resulting in an
acute manifestation and total limb ischemia*?The most common place for an embolus
to lodge is at arterial bifurcations (the sudden decrease in diameter from
supplying artery-->two smaller arteries means the embolus will stop as soon as it
hits a new artery that??s too small for it to pass through) o Aortic bifurcation �
bilateral femoral pulses (and below), 5Ps distal to the umbilicus bilaterally o
Common femoral bifurcation � unilateral symptoms of affected limbo Popliteal
bifurcation � pedal +/- popliteal pulses absent, 5Ps of foot +/- calf *?Muscle
shows irreversible cell damage after 3 hr with total cell death occurring after 6hr
Some Imaging Modalities Used to Assess Arterial Bloowflow *?Ultrasound Doppler �
measures bloodflow based on ultrasound waves bouncing off moving blood; often more
sensitive than palpating for pulses; reported in several different ways o Triphasic
� normal flow; [initial high flow systolic phase -->?brief retrograde diastolic
phase -->?final diastolic low flow phase] � ALI may be present but other processes
should be considered o Biphasic � often normal, but may represent early disease �
ALI maybe present, consider others o Monophasic � abnormal, severe reduction in
flow � ALI likely present o Absent � typical of affected vasculature in acute limb
ischemia � ALI likely present*?Duplex Ultrasound � combined Traditional + Doppler
ultrasound (the ??duplex??), with display superimposed on each other to allow for
structure identification and bloodflow assessment o Often used to locate area
disease and characterize the lesions; very useful in planning for surgical
intervention *?Ankle-Brachial Index � compares systolic pressure of ankle arteries
and brachial arteries; with chronic limb ischemia (like intermittent claudication)
this is essential. However, as lower extremity flow is often severely reduced in
ALI it??s less valuable in that situation. Work-up * *?�Good history/physical
exam/vital signs can never be replaced, always start with these. * *?�Determining
severity of ALI is CLINICAL o Stage I (viable) � no sensory or muscle weakness �
good prognosiso Stage IIa (marginal threat) � minimal sensory weakness (restricted
to the toes), no muscle weakness � salvageable with prompt treatmento Stage IIb
(immediate threat) � sensory loss more than the toes with mild-moderate muscle loss
� salvageable with immediate re-vascularizationo Stage III (irreversible) �
profound sensory loss with paralysis/rigor � permanent irreversible damage has been
done *?Imaging o Duplex ultrasonography � good initial assessment to rule out ALI.
Can show problems in the affected limb but not the proximal arterial tree, limiting
it??s use to a degree o CTa � gold standard; allows for full visualization of
arterial tree (proximal disease as well as distal disease causing symptoms)
allowing for surgical planning o Femoral contrast angiography � former gold
standard; invasive and contrast expose has led it to be replaced by CTa ??Still can
be used intra-operatively in emergent situations where immediate re-
vascularization is necessary (like presentation after a few hours of symptoms) o
Transthoracic Echocardiography??May be used to assess the heart if cardioembolic
disease is suspected??May be use used to assess for atrial septal defect with a
bubble study in suspected paradoxical embolus (bubbles passing from RA-->LA isn??t
OK!)o Venous duplex ultrasonography � if paradoxical embolus is suspected; use to
assess venous thrombosis as source of embolus Management*?Initial Steps: o
Immediate anti-coagulation � clinical suspicion is only thing necessary; stops
propagation of clot so the body can work on dissolving it with the fibrinolytic
system) o Placement of limb in dependent position � increase bloodflow to area of
ischemia) o IV fluids � optimize fluids to allow for optimal perfusion in
collateral vessels * *?�2nd step: Doppler/Duplex ultrasound � used as a ??rule
out?? * *?�Treatment is Based on Stage o Stage I � imaging (CTa) -->?thrombolysis
or surgery if proximal embolus suspectedo Stage IIa � imaging (CTa) -->?
thrombolysis or surgery if proximal embolus suspectedo Stage IIb � immediate
surgical intervention (femoral contrast angiography used intra-op) o Stage III �
amputation to save healthy tissue *?Surgical Modalities of Txo Endovascular
approaches (catheter tPA thrombolysis, percutaneous aspiration thrombectomy, or
percutaneous mechanical thrombectomy) o Surgical approaches (embolectomy,
endarterectomy, distal bypass) * *?�Often patients with cardioemblolic disease
should be on systemic anticoagulation * *?�Reperfusion syndrome � systemization of
toxic metabolites released by dead cells during ischemia o Check CPK/myoglobinuria
(rhamdomyolysis can occur from ischemia and systemization can result in acute
kidney injury due to heme pigments precipitating in high-solute parts of the renal
tubules resulting in toxic injury from cast formation in proximal tubules!) ??50%
of pts with CPK >5000 will have AKIo Monitor electrolytes � hyperkalemia (K+ high
intracellularly) may result (discussed below) Monitoring should be done with ANY
re-vascularization procedure (not just Stage II or III!)o Prevent it from happening
with with IV fluids (more fluid for dissolving) & bicarbonate infusion (alkaline
urine for dissolving) Areas To Get You in Trouble *?Diagnosing ALI as a neurologic
condition � parestethsias and weakness are common in nerve problems, but the key is
checking pulses/proper imaging. If these are normal, then ALI is much less likely!
Extra info from UWorld 3648/2167/4760/4422/4288/8331: Hyperkalemia *?Presentation:
confusion, lethargyo EKG changes: peaked T-waves, QRS widening, bradycardia, and
ventricular arrhythmias with sine wave pattern *?Etiologies:o Recent stroke (high
neuronal activity means lots of K+ getting into the blood) o Drugs (non-selective
B-blockers, ACE inhibitors, ARBs, K-sparing diuretics
[spirononlactone/eplerenone/amiloride/triamterene], digoxin, NSAIDs, TMP-SMX as it
can block aldostone, apparently) * *?�Dx: high K+ (>5.0) on basic metabolic panel
or fast rise in K level * *?�Tx: o Emergent treatment � Ca2+ carbonate or Ca2+
gluconate infusion (stabilize cardiac myocyte) o Fast-acting treatments � IV
insulin + glucose AND/OR albuterol inhalation (activate Na/K+ ATPases and pull K+
into the cells, lowing blood concentration)o Long-term treatments � aim to reduce
total body potassium after stabilization by other tx * ??�IV fluids � dilute blood
and promote diuresis for K removal * ??�Diuretics � promote diuresis to promote K
removal * ??�Exchange resins (sodium polystyrene sulfonate) � pull K from the body
via the GI tract (takes hours for effect) * ??�Hemodialysis � remove K directly via
hemodialysis *?Note that any of these treatments (esp. albuterol for
bronchodilation) may result in hypokalemia