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Gi Study Guide

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There are several factors that increase the risk of developing pigmented gallstones,

including hemolysis (black),infection (brown) of gallbladder/biliary tree by E.


coli or Clonorchis sinesis, receiving TPN, alcoholic cirrhosis, and Crohn's disease.

In critically ill patients, acalculous cholecystitis can be caused by biliary stasis,


hypoperfusion, or infection.

Ascending cholangitis describes an infection of the biliary tree secondary to stasis or


obstruction. It can present with Charcot's triad of jaundice, fever, and RUQ pain. It can
then progress to Reynold's pentad, which also includes altered mental status and
shock.

Gallstone ileus classically presents with Rigler's triad of pneumobilia (air in the biliary
tree due to fistula), small bowel obstruction, and visualized gallstone in the bowels
on imaging.

HCC is strongly associated with hepatitis B infection and is most


common where hepatitis B virus (HBV) is endemic (eg, China).
Chronic HBV infection is a strong risk factor for developing HCC, even
in the absence of cirrhosis.

 Whipple disease may present with abdominal pain, diarrhea,


weight loss, and migratory arthritis, with biopsy findings of foamy
macrophages containing partially digested bacteria in the lamina
propria of the small intestine.
 Whipple disease is caused by infection with T. whipplei, a rod-
shaped, gram-positive bacterium.

Primary sclerosing cholangitis (PSC) is an inflammatory condition


of the bile ducts resulting in bile duct stenosis. PSC typically presents
with jaundice and abnormal levels of liver enzymes (especially alkaline
phosphatase). Imaging may show biliary strictures and rarefaction of
intrahepatic bile ducts. Patients with PSC also have an increased risk
of developing cholangiocarcinoma. Approximately 70% of patients with
PSC also have ulcerative colitis.
psc

 Alcoholic hepatitis presents in patients who heavily consume


alcohol with fatigue, malaise, and right-upper-quadrant pain.
 Moderate elevations of aminotransferases, an aspartate
aminotransferase:alanine aminotransferase ratio of >2:1,
and hyperbilirubinemia are common findings in
alcoholic hepatitis.

 Left-lower-quadrant pain, fever,


and leukocytosis suggest diverticulitis, a diagnosis that can be
confirmed by CT.
 Diverticulitis occurs when a diverticulum, caused by chronically
increased intraluminal pressure, becomes infected, leading to
a microperforation.

Amebic dysentery is caused by Entamoeba


histolytica, a parasite prevalent in tropical countries with poor
sanitation and transmitted via the fecal-oral route. Diagnosis is
confirmed by the detection of amoebas or E histolytica antigen in a stool
sample or liver abscess aspirate.

 Enterocolitis due to Campylobacter causes loose, watery, or bloody stools; fever; and
abdominal pain.
 Enterocolitis due to Yersinia may cause bloody diarrhea, typically in children aged 1 to
4 years in daycare settings.
 Salmonellosis due to Salmonella can cause bloody diarrhea and abdominal pain.
 Dysentery due to Shigella can cause abrupt-onset diarrhea containing blood
and mucus with tenesmus.
 Enterocolitis due to Necator americanus causes abdominal pain, diarrhea (sometimes
bloody), and iron-deficiency anemia.

 Celiac disease classically presents with steatorrhea, abdominal


pain, and bloating in association with eating foods containing
gluten.
 Confirmation of celiac disease requires biopsy of the duodenum,
which classically shows villous blunting and crypt hyperplasia.

signs of inflammation in acute cholecystitis


Ultrasound
include gallbladder wall thickening (≥3 mm)

 Cirrhosis is characterized pathologically by regenerative nodules


with thick, collagenous septae.
 Progression to fibrosis is mediated by persistent stellate cell
activation.

 Acute right-upper-quadrant pain and jaundice and


direct hyperbilirubinemia suggest an acute obstruction of
the common bile duct, most commonly due to gallstones,
or choledocholithiasis.

 Intestinal atresia and malrotation are the most common causes


of intestinal obstruction in the neonate. In the setting of trisomy
21, duodenal atresia is a more common cause of obstruction.
 Duodenal atresia is caused by a failure of recanalization of
the GI tract during embryogenesis and presents quickly after
birth with intractable emesis. “double bubble” sign

 Hirschsprung disease is caused by the failure of neural


crest cells to migrate and presents within a few days to 1 week
after birth with marked abdominal distension, failure to
pass meconium, and bilious emesis.
 Pyloric stenosis is associated
with hypertrophy and hyperplasia of muscle and presents
with nonbilious emesis and a scaphoid abdomen at 2 to 6 weeks
of age.
 Intestinal necrosis with bacterial overgrowth, or necrotizing
enterocolitis, is a severe infection typically affecting preterm
newborns around 10 to 12 days of age. It is characterized by
bilious vomiting, abdominal distension, bloody
stools, hypothermia, hypotension, and bradycardia.
 Meconium ileus is a common cause of GI obstruction in
neonates with cystic fibrosis. Dysfunction
of chloride secretion and consequent fluid secretion into the GI
tract leads to sticky meconium that is difficult to pass.

 Duodenal ulcers are chronic lesions that occur in gastroduodenal


mucosa exposed to injury from acidic peptic juices.
 Risk factors associated with the worsening of peptic ulcer
disease and H pylori–induced ulcers include nonsteroidal
antiinflammatory drug use, tobacco use, alcohol use, and genetic
predisposition.

 Symptoms of small bowel obstruction include bilious vomiting,


lack of appetite, abdominal pain, and dilated loops of small
intestine.
 The main risk factor for small bowel obstruction in the United
States is adhesions arising from abdominal surgery, followed by
hernias and intraluminal cancers of the small intestine.

 Bilateral, mucin-secreting “signet-ring” cells in the ovaries are


diagnostic of Krukenberg tumors, which are indicative
of stomach adenocarcinoma metastasis.
 A classic sign of metastatic gastric cancer is left
supraclavicular lymphadenopathy involving the Virchow lymph
node.

 Hyperbilirubinemia in newborns may cause an altered mental


state.
 Increased destruction of RBCs, lack of conjugation, and
increased enterohepatic circulation at birth are important causes
of hyperbilirubinemia in newborns.

 Fatty changes (macro- and microvesicular), Mallory bodies, and


a neutrophilic infiltrate are most commonly associated with
alcohol-associated hepatitis.

 Patients with achalasia often present with difficulty swallowing


both solids and liquids.
 Achalasia is characterized by a loss of ganglion cells in the
myenteric (Auerbach) plexus.
 Medical treatments for achalasia include calcium channel
blockers, nitroglycerin, and botulinum toxin injection, which help
to relax the lower esophageal sphincter

, Sudan III staining. A quantitative 72-hour fecal collection that


measures the amount of fecal fat could be performed subsequently to
quantify the daily fecal fat loss. Oily, foul-smelling stools
suggest steatorrhea, caused by fat malabsorption. Weight loss occurs
because macronutrients are being lost in the stool rather than
absorbed. This patient’s history of excessive alcohol use and multiple
bouts of acute pancreatitis is most suggestive of exocrine pancreatic
insufficiency caused by chronic pancreatitis.

 Biliary colic often presents with postprandial abdominal


discomfort.
 Hemolytic anemia may occur secondary to mechanical shearing
of RBCs caused by aortic valve disease.
 Unconjugated bilirubin is a major component of pigmented
gallstones, which are radiopaque on x-ray.

 Diverticulitis often manifests with left lower quadrant abdominal


pain and is usually caused by blockage of a diverticulum.
 The characteristic histopathologic finding of diverticulosis is focal
areas of weakness in the muscularis propria.
 Nonselective NSAIDs, such as naproxen and ibuprofen,
significantly increase the risk for gastritis, peptic ulcer disease,
and upper GI bleeding. This risk is increased by adding
glucocorticoids in the treatment.
 Inhibition of COX-1 by nonselective NSAIDs reduces the
production of prostaglandins in the GI tract, which compromises
the protective gastric mucosal layer and can lead to ulceration
and gastritis.

Direct hyperbilirubinemia in a child or teenager


without transaminase elevations, symptoms of liver disease, or signs of
biliary obstruction (eg, normal alkaline phosphatase) suggests a diagnosis
of Dubin-Johnson syndrome, an autosomal-recessive inherited form
of conjugated (direct) hyperbilirubinemia that presents with
mild jaundice or scleral icterus. The disorder is caused by an impairment
of the hepatocyte transport system for the removal of conjugated anions
into bile.

 Crigler-Najjar syndrome is caused by an absence of glucuronyl


transferase and presents as severe elevations of unconjugated
bilirubin without hemolysis in newborns.
 Gilbert syndrome causes an elevation of
unconjugated bilirubin resulting from a mild deficiency of
glucuronyl transferase.

 Patients with gallstones present with postprandial pain in the


upper right quadrant.
 Cholecystokinin stimulates gallbladder contraction and increases
pain in patients with gallstones.
 Postprandial right-upper-quadrant (RUQ) pain is most suggestive
of biliary colic due to gallstones. An ultrasound of the upper right
quadrant can confirm the presence of gallstones. Risk factors for
gallstones include obesity, female sex, and multiple pregnancies.
 Hepatocellular carcinoma is common in patients with
chronic liver disease.
 α-Fetoprotein is a marker for hepatocellular carcinoma.
 α-Fetoprotein is also elevated in patients with germ cell tumors,
such as yolk sac carcinoma.

This patient demonstrates weight loss; a palpable, enlarged,


nontender gallbladder (aka Courvoisier sign); and evidence of obstructive
jaundice (increased direct bilirubin and alkaline phosphatase). These findings are
concerning for pancreatic cancer.

 Esophageal varices are dilated veins in the esophagus caused


by portal hypertension and are usually asymptomatic until they
rupture. They are not associated with dysphagia.
 Adenocarcinoma of the esophagus most often presents with
dysphagia and unintentional weight loss in patients with a history
of gastroesophageal reflux disease.
 Achalasia causes dysphagia to both solids and liquids and
regurgitation.
 Plummer-Vinson syndrome is a triad of dysphagia, iron-
deficiency anemia, and esophageal webs.

PVS predisposes patients to squamous cell carcinoma of the


upper gastrointestinal tract including the hypopharynx and, more
commonly, the esophagus.

 A combination of abdominal pain, bilious vomiting, bowel


obstruction, and pneumobilia (ie, air in the biliary tree) is
suggestive of gallstone ileus.
 Forceful, postprandial, nonbilious vomiting in the first 2 months of
life suggests congenital pyloric stenosis.
 Pyloric stenosis can be diagnosed based on a thickened pylorus,
which is detectable by ultrasonography.

 Duodenal atresia, presenting with a "double-bubble" sign on abdominal plain


film, shows symptoms within the first 24 hours of life.
 Meckel diverticulum, showing a bright spot in the right lower quadrant on a
technetium-99m pertechnetate scan, commonly presents with painless
rectal bleeding before the age of 2 years.
 A corkscrew appearance of the distal duodenum and jejunum on upper
gastrointestinal series describes midgut volvulus, appearing within the first year of life.
Small bowel obstruction will be present.
 A target sign on ultrasound is indicative of intussusception, which typically presents in
children age 6 months to 3 years. Small bowel obstruction will be present.
 Acute calculous cholecystitis classically manifests with RUQ
pain, nausea, vomiting, and fever, with a positive Murphy sign on
examination.
 Acute calculous cholecystitis involves inflammation of
the gallbladder, most commonly from obstruction of the cystic
duct or gallbladder neck by a gallstone.

Slow waves are rhythmic depolarizations and repolarizations of


the smooth muscle cells within the muscularis propria of
the stomach and intestines; they synchronize contractions of the GI
tract.

 Fatigue, constipation, heme-positive stools, and a barium image


showing an “apple core” lesion suggest a tumor in the colon.
 Over time, chronic blood loss leads to iron-deficiency anemia,
which is typically a microcytic, hypochromic anemia.

 Splenic infarction presents with left upper quadrant abdominal


pain, left shoulder pain, and vomiting in a patient with a history of
embolic disorders or hypercoagulability.
 The spleen is supplied by the splenic artery, a branch of
the celiac trunk.

his patient’s early satiety, postprandial discomfort, and bloating, as well


as a history of type 2 diabetes mellitus, suggest a diagnosis
of gastroparesis, caused by impaired neural control of gastric
function. The most appropriate treatment for this condition
is metoclopramide, an antiemetic that functions by increasing
gastric motility. This prokinetic medication acts as a dopamine antagonist,
causing contraction of the lower esophageal sphincter, relaxation of
the pylorus, increased gastric contractions, and increased peristalsis in
the duodenum and jejunum.

 Pancreatic cancer can present with jaundice and nonspecific


symptoms such as fever, night sweats, and anorexia.
 Trousseau syndrome is a migratory thrombophlebitis sometimes
seen in pancreatic and other upper gastrointestinal cancers.
 Trousseau syndrome results from liberation of tissue factor by
advanced pancreatic tumors.
 Pernicious anemia causes vitamin B12 deficiency, resulting
in macrocytic anemia and peripheral neuropathy.
 Pernicious anemia is caused by autoimmune destruction of
parietal cells, leading to decreased production of intrinsic factor,
which is required for vitamin B12 absorption.

 Because ghrelin and neuropeptide Y are two proteins


responsible for stimulating appetite, they will decrease in a fed
state; however, leptin is the major hormone responsible for
decreasing hunger and appetite but is subject to long-term
changes, so it will remain the same.

 Right-upper-quadrant pain with a positive Murphy sign suggests


acute cholecystitis.
 Crohn disease affecting the terminal ileum can lead to
decreased bile acid reabsorption, increased cholesterol content
of the bile, and the formation of cholesterol stones, thereby
predisposing patients to acute cholecystitis. dilated gallbladder with
a thickened wall.

 Respiratory distress and bowel sounds in the thorax of


a neonate are indicative of a congenital diaphragmatic hernia,
which can lead to pulmonary hypoplasia.
 Congenital diaphragmatic hernias most commonly result from
failure of the pleuroperitoneal folds to fuse.
 Iron-deficiency anemia is characterized by shortness of breath,
weakness, fatigue, pale mucous membranes, low mean
corpuscular volume, and high RBC distribution due to reduced
oxygen delivery to the body.
 Iron is predominantly absorbed in the duodenum, and damage to
the duodenal enterocytes can lead to malabsorption of iron and
iron-deficiency anemia.

 Ondansetron is among the strongest antiemetics available and is


used as first-line therapy for chemotherapy-induced nausea and
vomiting; the ECG must be monitored during use because
ondansetron may prolong the QT interval.
 Ondansetron acts by blocking serotonin 5-HT3 receptors.

 Irritable bowel syndrome is a chronic functional gastrointestinal


disorder characterized by altered bowel habits and abdominal
pain in the absence of demonstrable organic findings.
 A specimen of the small bowel or colon obtained from a person
with irritable bowel syndrome shows normal
intestinal biopsy findings.

 Congenital aganglionic megacolon (Hirschsprung disease) is the


most common cause of lower intestinal obstruction in newborns.
 Hirschsprung disease is caused by an absence of ganglion cells
in the bowel wall, most commonly in the rectum and sigmoid
colon. Consequently, the proximal large bowel is often distended
above the constricted aganglionic distal region.

In Dubin-Johnson syndrome, the liver takes on a


grossly blackened appearance caused by pigmented granules that
accumulate within hepatocytes.

 Tracheoesophageal fistula is typically associated


with esophageal atresia, whose symptoms include vomiting,
choking, coughing, and cyanosis with feeding.
 Esophageal atresia causes polyhydramnios during pregnancy
because the fetus is unable to swallow amniotic fluid.
 Tracheoesophageal fistula with esophageal atresia in infants
manifests with choking and coughing with feeding and is
frequently associated with vertebral anomalies, anal atresia,
cardiac defects, tracheoesophageal fistulas, renal/genitourinary
anomalies, and limb defects.
 An air bubble in the stomach is often seen on an x-ray of the
chest of infants with a tracheoesophageal fistula.
 Acute hepatitis E is associated with fulminant hepatitis in
pregnant women, presenting with nausea, vomiting, and
watery diarrhea, with potentially rapid mortality.
 Hepatitis E is associated with hepatic tissue necrosis, which can
be seen on histologic examination as massive necrosis of
hepatocytes in all zones of the liver with reticulin collapse.

 Midgut volvulus presents with acute onset of vomiting, abdominal


pain, or fussiness in young children and is caused by congenital
intestinal malrotation.
 The midgut normally undergoes a 270° counterclockwise rotation
around the superior mesenteric artery during herniation and
returns to the abdominal cavity by the 10th week of embryonic
development.

 Enterokinase (enteropeptidase) allows the activation of several


digestive enzymes responsible for degrading proteins and
complex lipids.

 Indirect inguinal hernias are the most common type of hernia,


especially in boys in the first year of life.
 These hernias are the result of a congenital defect of the
processus vaginalis when it fails to close.

 Celiac disease, an autoimmune disorder with intolerance to


gluten, presents with foul-smelling diarrhea, steatorrhea, weight
loss, fatigue, and abdominal pain.
 Celiac disease is associated with dermatitis herpetiformis, a skin
disorder with clusters of pruritic, papular, and sometimes bullous
lesions that often appear in a symmetric pattern.

 Overuse of calcium carbonate for long periods can lead to milk-


alkali syndrome, characterized
by hypercalcemia (depression, constipation, weakness,
fatigue), metabolic alkalosis, and renal insufficiency.
 Calcium carbonate, an over-the-counter antacid, is a common
cause of hypercalcemia and milk-alkali syndrome.

 Perianal pain with a palpable lump suggests external


hemorrhoids, often caused by constipation or the compression of
pelvic veins in pregnancy.
 External hemorrhoids drain via the inferior rectal vein to
the inferior vena cava.
 Caused by infection with T. whipplei, Whipple disease manifests
via weight loss, diarrhea, and arthralgias; in
addition, histology reveals PAS-positive macrophages in
the lamina propria of the small intestine.

 Classic symptoms of appendicitis include abdominal pain that


starts diffusely and then localizes to the McBurney
point, fever, nausea, and lack of appetite.
 The most common cause of appendicitis is obstruction of the
appendiceal lumen, often due to lymphoid hyperplasia or fecalith
impaction leading to obstruction.

The pain can be localized to the McBurney point, a landmark that is


located two-thirds of the way from the umbilicus to the anterior
superior iliac spine.

 Cirrhosis coupled with evidence of a large lesion in the caudate


lobe suggests a diagnosis of hepatocellular carcinoma.
 Cirrhosis can cause a deficiency in vitamin K–dependent clotting
factors, leading to an increased prothrombin
time and coagulopathy.

Jaundice, ascites, splenomegaly, low-grade fever, and CT findings


of a nodular and shrunken liver are clinical signs of cirrhosis.

 Laboratory test abnormalities commonly seen in chronic liver


disease include elevated levels of aminotransferases
and bilirubin; hematologic abnormalities, such as
low platelet count (thrombocytopenia) from hypersplenism; and
prolonged prothrombin time and partial thromboplastin
time caused by decreased clotting factors.

 Levodopa can cause autoimmune hemolytic anemia, which


leads to an increase in unconjugated (indirect) bilirubin.

 Congenital diaphragmatic hernia presents


with dyspnea, cyanosis, and respiratory distress (intercostal
retractions) immediately after birth. Patients will
have scaphoid abdomen, and bowel sounds may be heard on
auscultation.
 Congenital diaphragmatic hernia is due to the failure of the
pleuroperitoneal canal to close completely, potentially leading to
herniation of abdominal viscera into the chest.

Hepatic hemangiomas are the most common benign lesion of


the liver and are often found incidentally on imaging. They are
characteristically hyperechoic on ultrasound, and color Doppler
ultrasonography may show peripheral feeding vessels. Although often
asymptomatic, this common, benign tumor can potentially
cause hemorrhage and, if severe, hypovolemic shock. driven by vascular endothelial
growth factor (VEGF) and fibroblast growth factor (FGF).

 Patients with diabetes may have GI symptoms such as


diabetic gastroparesis, which slows gastric emptying time, which
can cause nausea, vomiting, and abdominal pain.
 Metoclopramide is a D2-receptor antagonist used as a GI
prokinetic agent and antiemetic. Antagonism of centrally
located dopamine receptors can result in Parkinson-like adverse
effects.

 Somatostatinomas, which are usually found in the pancreas, are


characterized by high levels of somatostatin, an
inhibitory hormone. Somatostatinomas usually present with a
triad of steatorrhea, gallstones, and diabetes mellitus.
 Somatostatin is normally produced by δ cells of the pancreatic
islets.

 In a patient with cirrhosis, upper GI bleeding is often caused by


ruptured esophageal or gastric varices.
 The left gastric vein is the portal branch most directly involved
in the formation of esophageal and gastric varices.

 The IMA branches off the aorta at a site commonly affected by


AAAs. It can be compromised during AAA repair, potentially
leading to ischemia of the sigmoid colon. The duodenum (distal
part), jejunum, ileum, and ascending colon receive their blood supply from the superior
mesenteric artery. Because the superior mesenteric artery is located superior to the renal
arteries, it would not be affected by an AAA repair.

crohn

 Crohn disease can present with abdominal pain, diarrhea, weight


loss, and penetrating complications such as fistulas.
 Microscopy findings of transmural inflammation and
noncaseating granulomas are indicative of Crohn disease.

 Acute pancreatitis is characterized by nausea, vomiting, and


upper abdominal pain that may radiate to the back or
left shoulder.
 Hypocalcemia is a complication of severe acute pancreatitis and
may result from sequestration of calcium secondary to
intraperitoneal saponification.
 The Chvostek sign, a facial muscle twitch that occurs when
tapping over cranial nerve VII on the cheek, is a specific finding
associated with hypocalcemia.

 Ulcerative colitis often presents with bloody diarrhea and


abdominal pain.
 Ulcerative colitis is associated with HLA-B27.
 HLA-B27 is associated
with Psoriasis, Ankylosing spondylitis, Inflammatory bowel
disease, and Reactive arthritis (remember PAIR).

This patient has likely Budd-Chiari syndrome (BCS), based on the


blockage of the hepatic vein flow seen on ultrasound, along with the
sudden onset of abdominal pain, jaundice (icterus), and altered
mental status. BCS occurs when there is obstruction of blood flow
in the hepatic veins or in the inferior vena cava by an acute clot or
by malignant compression of the veins.It is most often associated
with a hypercoagulable state.

 Acute pancreatitis presents with acute-onset abdominal


pain, nausea, and systemic inflammatory response syndrome.
 Inappropriate conversion of trypsinogen to the
pancreatic enzyme trypsin causes autolysis
and necrosis in pancreatitis.

Bevacizumab is a monoclonal antibody that inhibits VEGF. It is


used in the treatment of colon cancer and wet AMD.
 VEGF is a cellular factor that promotes blood vessel proliferation
and expansion, and overexpression of VEGF
enables tumor growth.

 Abdominal symptoms and elevated liver enzymes in the context


of presumptive acetaminophen ingestion are suggestive
of acetaminophen poisoning.
 An acetaminophen overdose overwhelms normal metabolic
systems, leading to metabolism by the CYP450 enzyme pathway
and generation of toxic metabolites, resulting in centrilobular
(zone 3) necrosis.

 A VIPoma is a pancreatic tumor that secretes VIP and results in


Verner-Morrison syndrome, with the mnemonic WDHA.
 Normal functions of VIP include increased secretion of water and
electrolytes into the intestinal lumen and relaxation of
intestinal smooth muscle and sphincters.
WDHA: Watery Diarrhea, Hypokalemia, and Achlorhydria.

 Crohn disease is a type of inflammatory bowel disease and most


commonly presents with abdominal pain, fever, weight
loss, diarrhea (bloody or nonbloody), fistulas, abscesses,
and malabsorption.
 Crohn disease is characterized by transmural inflammation of the
bowel wall and cobblestone mucosa, with skip lesions occurring
anywhere along the digestive tract.

 Mucosal and submucosal inflammation describes ulcerative


colitis, a form of inflammatory bowel disease that presents with
bloody diarrhea.
 Irritable bowel syndrome presents with recurrent abdominal pain
and altered habits (constipation, diarrhea, or
both). Colonoscopy would show normal mucosa.

 Direct inguinal hernias are most common in middle-aged and


older men.
 Direct inguinal hernias protrude medial to the inferior epigastric
vessels and superior to the inguinal ligament within
the Hesselbach triangle.
 Lateral to the inferior epigastric artery and superior to the
inguinal ligament describes the relative location of indirect
inguinal hernias, which typically occur in infants.
 Inferior and lateral to the pubic tubercle or inferior to the
inguinal ligament and medial to the common femoral
vein describes the relative location of femoral hernias, which are
most common in older women.

An x-ray of the abdomen of a patient with Hirschsprung disease will


show dilated loops of bowel and an absence of gas in the rectum.

 Histamine H2-receptor antagonists, such as ranitidine,


famotidine, and cimetidine, bind to and inhibit Gs-coupled
histamine H2-receptors, thereby decreasing hydrogen
ion secretion by parietal cells and relieving the symptoms
of heartburn and reflux.

 When a patient with heavy alcohol use or other risk factors


for portal hypertension experiences bleeding in the
upper gastrointestinal tract, the bleeding most likely comes from
esophageal varices.
 Esophageal varices develop because of increased pressure in
the portal system, specifically the left gastric vein; high pressure
leads to portal-systemic collaterals that are fragile and prone to
bleeding.

 Hereditary hemochromatosis is an autosomal-recessive disorder


leading to hepatic cirrhosis.
 Hereditary hemochromatosis is a disorder of the HFE gene,
resulting in excess absorption of iron, which leads to elevated
saturation of transferrin with iron.
 Opioid medications cause constipation by activating μ-receptors
in the gut, which slow peristalsis.
 Constipation is often managed with a bowel regimen consisting
of a stool softener in combination with a stimulant laxative, such
as senna glycoside, which stimulates peristaltic activity in
the intestine.

 The classic clinical presentation of carcinoid syndrome includes


shortness of breath, chronic diarrhea, flushing, and a right-
sided heart murmur (most likely tricuspid regurgitation).
 Carcinoid tumors secrete large amounts of serotonin; if
extraintestinal metastasis is present, carcinoid syndrome can
develop.
 Selective serotonin reuptake inhibitors benefit patients with
depression by increasing the concentration of serotonin in the
neuronal synapses.

 UC may present with chronic bloody diarrhea and abdominal


pain.
 Patients with UC have an increased risk for the development of
PSC, which presents with an elevated alkaline
phosphatase level, jaundice, fatigue, and pruritus.

 Physical indicators of lactose intolerance include intermittent


postprandial diarrhea, bloating, flatulence, and abdominal pain;
an elevated stool osmotic gap essentially confirms the diagnosis.

 Irritable bowel syndrome tends to present with persistent,
rather than intermittent, symptoms. Patients typically have a
normal osmotic gap.
 Peptic ulcer disease most commonly stems from use
of nonsteroidal anti-inflammatory drugs or infection
with Helicobacter pylori. It leads to ulcers in either
the stomach or the duodenum and tends to present with
epigastric pain.
 Crohn disease may show bloody diarrhea with a low osmotic
gap.
 Escherichia coli enteritis would present with a secretory
diarrhea (low osmotic gap).

 Crohn disease may present with intermittent chronic abdominal


pain and diarrhea and often affects the terminal ileum.
 Vitamin B12 deficiency, a cause of megaloblastic anemia, is
associated with a number of clinical and laboratory
abnormalities, including fatigue and peripheral neuropathy.
 Vitamin B12 deficiency is characterized by elevated levels of
methylmalonic acid and homocysteine.

 Orlistat is used in the management of weight loss for individuals


with a BMI >30 kg/m2 or a BMI >27 kg/m2 and comorbidities.
Adverse effects include abdominal pain, flatulence, frequent
bowel movements, bowel urgency, steatorrhea, and decreased
absorption of fat-soluble vitamins.

 Biliary atresia manifests with elevated levels of direct bilirubin,


pale stools, and dark urine, and patients become jaundiced
several weeks after birth but have no associated congenital
anomalies.
 Biliary atresia results in obliteration of extrahepatic bile ducts.

 Nonselective NSAIDs, such as naproxen and ibuprofen,


significantly increase the risk for gastritis, peptic ulcer disease,
and upper GI bleeding. This risk is increased by adding
glucocorticoids in the treatment.
 Inhibition of COX-1 by nonselective NSAIDs reduces the
production of prostaglandins in the GI tract, which compromises
the protective gastric mucosal layer and can lead to ulceration
and gastritis.
 Glucocorticoids activate intracellular glucocorticoid receptors and
suppress the immune system response.

 GI bleeding in a child, particularly with evidence


of intussusception and/or obstructive symptoms, suggests
a Meckel diverticulum.
 Meckel diverticulum contains ectopic gastric mucosa from
which bleeding can occur.
 Because Meckel diverticulum arises from the midgut, ectopic
gastric tissue can be visualized in the distribution of the superior
mesenteric artery, which is the blood supply for structures arising
from the midgut.

 Acute cholecystitis commonly causes acute right-upper-quadrant


pain.
 Sonography shows thickening of the gallbladder lining due to
obstruction of the biliary duct system.

Crigler-Najjar syndrome is characterized by the body's inability to conjugate bilirubin


due to the complete absence of UDP-glucuronosyltransferase. Unconjugated
bilirubin accumulates, leading to severe jaundice and kernicterus (bilirubin deposition
in the basal ganglia).
Gilbert syndrome is characterized by mild jaundice following a period of stress,
fasting, or illness. This occurs as a result of decreased UDP-glucuronosyltransferase
activity, leading to the buildup of unconjugated bilirubin.
When symptoms are present, painless hematochezia (red blood in stool) is the most
common presentation of Meckel's diverticulum. It can also present with right lower
quadrant (RLQ) pain and melena, or as in this case, with a complication such
as obstruction, which is causing the patient to vomit.

This obstruction could be due to:


 Intussusception: proximal bowel invagination into the distal bowel.
 Volvulus: twisting of a loop of bowel around its mesentery.

A pertechnetate (99mTc) study is the preferred investigation for diagnosing Meckel's


diverticula in children.
Lynch syndrome, also known as hereditary nonpolyposis colon cancer (HNPCC), is a
familial cancer syndrome caused by an autosomal dominant mutation in mismatch
repair (MMR) genes resulting in microsatellite instability.

Risk factors for the development of colorectal cancer include:


 Low-fiber diet
 IBD
 Tobacco
 Age >50

In an individual with colorectal carcinoma, barium enema x-ray will often show a
sharply defined circumferential "apple-core" constriction of the colon.
 Whipple disease → fat malabsorption → vitamin D deficiency → increased PTH →
increased MSH → skin hyperpigmentation.

Psyllium, a bulk-forming laxative, soaks up water, swells, and forms a bulky stool in the
intestine. This can help both constipation and mild diarrhea by producing stool that's
easier to pass and reducing free water in the lumen.

[Choices A and B]: Famotidine (an H2 receptor blocker) and omeprazole (a proton
pump inhibitor) are both used to treat GERD.

[Choice C]: Ondansetron is a serotonin (5HT-3) receptor antagonist used to treat


nausea symptoms.

Lubiprostone, a chloride channel activator, helps bring water into the lumen of the
intestine. This softens the stool and makes it easier to pass, relieving constipation.

 Secretin normally inhibits gastrin release.


 For patients with gastrinomas, secretin stimulation will actually further increase
gastrin levels.
Cholangiocarcinoma is diagnosed with endoscopic retrograde
cholangiopancreatography (ERCP) + biopsy. The biopsy will show glands and
mucin on histology:

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