I.

Disease Process (6 questions)

A. Inflammation and repair
1. 4 stages of inflammatory response
-Histamine released and blood flow increases as does permeability
-Neutrophil exudation
-Monocyte exudation
-Repair/Restoration
2. Cell types involved in inflammatory response
White Blood Cells: PMNs /Polymorphonuclear Leukocytes
Neutrophils
- Largest quantity of the WBCs
-Perform phagocytosis
Eosinophils
-Number increases with allergy
Basophils
-Contain histamine
-Migrate out of the blood and become mast cells
White Blood Cells: Mononuclear
Monocytes
-Largest in size of WBCs
-Perform phagocytosis
-Called Macrophagesor Histiocytes when they migrate out of blood
Lymphocytes
-Second largest in quantity
-Release lymphotoxin and lymphokine
-More active in the immune process
Leukocytes
B. Neoplasia
1. Comparison of benign and malignant neoplasms
Benign = relatively harmless unless a vital area is involved
Malignant cancerous ! They grow and then spread throughout the body
2. Characteristic behavior of malignant neoplasms
-Very invasive with vague borders
-Dedifferentiated appear to be very immature version of cell of origin
-Metastasis spreads via blood or lymph to other tissues/organs
-Rapid growth
-High fatality rate
3. Nomenclature of neoplasms

Benign tissue of origin + suffix oma

-Benign tumor in glandular tissue = adenoma
-Benign tumor in bone =osteoma
-Benign tumor in fatty tissue =Lipoma
Malignant:
If tissue of origin is epithelial, than add suffixcarcinoma
Malignancy in glandular tissue =Adenocarcinoma
If tissue of origin is bone, muscle, cartilage, or connective tissue, add suffix sarcoma
Malignancy in bone =Osteosarcoma
EXCEPTIONS
-Melanoma or Lymphoma usually malignant! Need to see adjective in front of term (benign or
malignant)
-Glioma highly fatal malignancy of glial cells in the CNS
4. etiologies of Malignant neoplasms
HORMONES
VIRUSES
GENETIC PREDISPOSITION
RADIATION
SMOKING
CHEMICALS
ENVIRONMENT
C. Inherited diseases
1. Chromosome aberrations
a. Cause: missing, extra or irregular portion of chromosome
b. Three examples: turners(Xo), klinefelters(XXY), downs(trisomy 21)
2. Genetic diseases
a. Autosomal inheritance
(1) How it occurs: Occur when heterozygotes (carriers) mate
(2) Three examples
-Cystic Fibrosis: Recessive gene causes thick exocrine secretions which impair lung and
pancreatic function
-Sickle Cell Anemia: Hemolytic anemia caused by fragile and abnormally shaped RBCs
-Phenylketonuria (PKU): Missing enzyme prevents metabolization phenylalanine;Causes CNS
damage to the newborn
b. Sex linked
(1) How it occurs: Usually the defective allele is transmitted from
mother to son on the X of the 23rd chromosome
(2) One example: hemophilia
D. Immune response
1. Antigen-antibody reaction
-Antigen is rendered harmless by one or a combination of the following:
Precipitation, Agglutination, Opsonization, Neutralization
-A series of protein enzymes that attach to antigen-antibody complexes involving IgG and IgM
2. Three types of allergic reactions:

asthma, hay fever, hives (urticaria), GI/food allergy

3. AIDS: too much shit to copy and paste, look it up on the slides
II. Heart Diseases (12 questions)
A. Coronary artery disease: buildup of fatty plaque in the coronary arteries
1. Risk factors: Smoking, High cholesterol (especially LDL), Obesity, High fat
diet, Lack of exercise, Hypertension, Diabetes, Stress, Age, Gender Heredity
2. Pathological changes: Atherosclerosis and the tendency to form clots may cause
significant myocardial ischemia
B. Myocardial infarction
1. Definition: Ischemia that is severe enough and lasts long enough to cause death
of myocardium cells
2. Three zones of damage: Zone 3 (outer):ischemia, Zone #2 (middle): injury,
Zone #1 (inner): necrosis
3. Pathological changes and repair
-Phagocytosing necrotic tissue
--in the heart this tissue is replaced with scar tissue (fibrosis)
-Generating collateral circulation
--May not occur quickly enough or effectively enough to sustain life
4. Manifestations: check signs and symptoms
5. Treatment: Analgesic for pain (usually morphine)
Oxygen
Clot dissolving drugs: TPA (Activase)
C. Arrhythmias recognize:
1. Premature ventricular contractions

2. Ventricular Tachycardia

3.Ventricular fibrillation

D. Congestive heart failure

1. Definition:
Failure of the heart to pump adequate amount of blood to the tissues
2. Pathology of fluid retention:
-Decreased blood flow to kidney causes release of rennin
-This is converted to angiotensin
-Angiotensin makes the adrenals secrete aldosterone
-Aldosterone causes the kidney to retain sodium and fluid while releasing potassium
into the urine

3. Manifestations and treatment

Manifestiations
-Enlarged ventricle
-Pulmonary and/or systemic edema:
Gurgling breath sounds Swollen feet and
ankles

-Increased sodium and lowered

potassium

Treatment
-Oxygen
-Diuretics for excess fluid
-Cardiotonic drugs to improve pumping
-efficiency

Digitalis and its derivatives

-Low sodium diet;possibly supplemental

potassium

E. Cardiogenic shock
1. Definition: systolic blood pressure less than 90 mmhg and signs of
impaired tissue perfusion

2. Etiologies:

-Severe damage to the left ventricle

and/or:
-Aneurysm forms on damaged ventricular wall
and/or:
-Ventricle ruptures

F. Congenital defects description of abnormalities, direction of blood flow and

whether cyanosis exists for:

Atrial septal defect

-Heart murmurs, hole in septum
-Overload and enlargement of right
ventricle

Ventricular septal defect

-Heart murmurs, hole in septum

Patent ductus arteriosus

-Ductus arteriosus remains open
-blood for the body flows from aorta to
lungs, overloads pulmonary artery

Coarctation of the aorta

-Congenital narrowing of aorta
-Increase in resistance to left
ventricle and can eventually lead to
heart failure

-Increased blood flow to lungs

Tetralogy of Fallot (cyanotic)

1. Ventricular septal defect
2. Narrowing pulmonary
outflow channel
3. Misplaced aorta
4. Hypertrophy of right
ventricle
Decreased blood flow to lungs

G. Rheumatic heart disease

1. Etiology complication of a strep infection
2. Pathology: reaction to strep immune complex causes vegetations to form on
valves (usually mitral or aortic)
H. Infectious endocarditis
1. Pathology:Vegetations form and not only cause stenosis or insufficiency, but
may break off and become emboli

2. Difference between subacute and acute

Sub-acute caused by strep
Acute caused by staph

III. Blood and Lymph Diseases (6 questions)

A. Anemias
1. Pernicious anemia
a. Cause: Decreased vitamin B-12 in blood

May be due to heredity or chronic atrophic gastritis

b. Appearance of RBCs: macrocytic

c. Treatment: b-12 injections
2. Irondeficiency anemia
a. Cause chronic, low-grade blood loss in adults; poor dietary intake in
pregnant women and young children

b. Appearance of RBCs: microcytic, hypochromic

c. Treatment oral or IV supplement, control blood loss

3. Hemolytic anemias
a. Hereditary
Pathology and
Manifestations
-Fragile RBCs rupture and the
fragments cause organ
dysfunction as well as anemia

Three types
-Sickle Cell Anemia: abnormally shaped and
fragile RBCs seen in blacks
- Congenital Spherocytic Anemia: fragile RBC
membrane that takes in too much fluid
-Thalassemia (Cooleys Anemia): fragile RBCs
and decreased hemoglobin usually seen in
persons with Mediterranean ancestry

S.O.B/easy fatigue
Pallor
Increased reticulocytes
Enlarged spleen
Increased Bilirubin levels and possibly
jaundice
Organ dysfunction
due to fragmented
b. Acquired
examples
cells
acting as emboli: abdominal pain, fever,
swollen & painful joints, neurologic
dysfunction
Treated by: removal of spleen, steroids

B. Polycythemia
1. Definition: too many RBCs ( 6 MILL, 18g, 54%)
Polycythemia Vera
For unknown reason bone marrow
makes too
many RBCs (WBCs and platelets may
increase
also
Blood becomes very thick (increased
viscosity) and clots easily
Heart also has to work harder to pump
Patients are prone to thrombosis and
organ
infarction (including heart)

Secondary Polycythemia
A compensatory polycythemia
caused by chronic hypoxia
(usually due to high altitude or
chronic lung disease)
-treat chronic hypoxia

Spleen enlarges also

Treated by periodic phlebotomy

C. Hemophilia
1. Causes Sex-linked transmission most commonly passed from mother to son.
Causes absence of clotting factor VIII or IX

2. Manifestations
-Under the skin
Into joint capsules, deep tissues and cavities

Is very painful!

Platelets are usually OK

3. Treatment: administer missing clotting factors

D. Thrombocytopenia purpura reduced platelets (60k) causing purple lesions

Cause

Decreased platelet production

Bone marrow disease

Shift in platelet distribution

Chronic liver or spleen disease

Increased destruction of
platelets

Idiopathic; autoantibodies; drug

Treatment
Petechiae
Oozing of blood from mucosal surfaces
Excessive menstrual bleeding
Excessive bleeding during dental
procedures
No joint or deep tissue bleeding!

Treatment
-Steroids to decrease destruction
-Splenectomy
-Packed RBCs with platelets if bleeding
is life threatening

E. Leukemias

Acute or chronic

In acute, the tumor cells are more

dedifferentiated and the disease
progresses more rapidly

Abnormal Cells:

Myelogenous if abnormal cells are

PMNs
Lymphocytic if abnormal WBCs are
lymphocytes

Pathology
Bone marrow is taken over by tumor cells
Increased production of useless WBCs and
decreased production of RBCs and platelets
Reduced immune function
Severe and refractory infections
Organ enlargement
Lymph nodes, spleen, some bones (usually cranial)
CNS dysfunction due to increased intracranial pressure
Death is usually due to complications caused by pathology
Sepsis, bleeding, anemia, organ dysfunction from
metastasis

2. Etiologic factors : radiation, viral infection, heredity

4. Treatment : Initially chemotherapy and radiation, bone marrow transplant
F. Lymphomas: A malignancy in lymph nodes or lymphoid tissue
-The primary symptom, prior to metastasis is lymph node enlargement
-Disease responds well to chemotherapy and radiation therapy

Kidney Diseases (5 questions)

A. Hypertension
1. Normal mechanism for compensation for reduced blood volume: Decreased pressure
sensed by JG cells activates the renin-angiotensin-aldosterone mechanism
2. Ways mechanism backfires: artheroscelerosis, prevents J-G cells from not sensing
proper pressure in renal blood flow

B. Pyelonephritis: Inflammation of the renal pelvis and interstitial tissue of the kidney
Pathology
-Intense inflammation causes abscesses to
from in renal pelvis and interstitial tissue
-If severe enough, the kidneys may fail
-Can be acute or chronic
Fibrosis will be present if chronic

Etiology:
Bacterial infection that often spreads
retrograde from the bladder (cystitis)
Common agents: E-Coli, Strep, and
Staph

Manifestations
-Fever
- Flank Pain
-U.A. shows pyuria and bacteriuria
-Urinary signs: frequency, urgency, and
burning

C. GlomerulonephritiS: Inflammation of the glomerulus caused by a reaction to immune

complexes and complement
ETIOLOGY
Usually caused by a strep infection
Strep throat
Strep skin lesion

MANIFESTATIONS
Initial strep infection
Urinary signs:
Hematuria, proteinuria, dark urine, &
decreased output
Facial and ankle edema
Due to hypoproteinemia and sodium and
fluid retention
Hypertension
Possible renal failure

PATHOLOGY
Immune complexes and compliment damage glomerular
membrane and cause it to become more permeable
WBCs, RBCs , and plasma proteins pass into Bowmans
capsule

D. Acute and chronic renal failure: Failure of the kidney to adequately remove waste
products and maintain fluid and electrolytes.
ETIOLOGY
Damage due to disease processes, e.g.,
pyelonephritis , glomerulonephritis, etc
Reduced renal blood flow (shock)
Burns, trauma, dehydration
Toxins

MANIFESTATIONS
Decreased urine output
Increased BUN, uric acid,creatinine, and
ammonia
Decreased pH
Abnormal electrolyte levels
Anemia (if chronic) due to decreased
erythropoietin

TREATMENT: hemodialysis, kidney transplant

V. Lung Diseases (10 questions)
A. Infectious diseases
Croup affects larynx, trachea, main stem bronchi
Epiglotitis affects epiglottis
Acute bronchitis trachea, main stem, segmental bronchi
2. Which diseases are caused by bacteria, virus, fungi
Croup, epiglotitis, chronic bronchitis are viral
Coccidioidomycosis is fungal
Mycobacterium Tuberculosis is bacterial

B. Pulmonary edema
1. Three alterations causing pulmonary edema and one example of each
2. Manifestations of interstitial and alveolar edema
3. Treatment
1
Increased hydrostatic pressure
CHF, fluid overload
Decreased osmotic pressure
Loss of plasma proteins (albumin) due to
blood, loss, liver disease, kidney disease
Altered capillary permeability
Neurogenic , eg, head trauma, heroin OD,
triggers of ARDS

2
Dyspnea and S.O.B
crackles breath sounds indicating
alveoli and small airway collapse
If severe enough, audible gurgling sounds will
be heard

Hypoxia
Patient may cough up pink, frothy fluid
3
For increased hydrostatic pressure:
diuretics, eg Lasix
For decreased osmotic pressure: whole
blood or albumin
For altered capillary permeability: support
oxygenation and ventilation until condition
stabilizes
May require mechanical ventilation

C. Restrictive Lung Disease

1. Diagnosis by pulmonary function test
2. Pneumoconiosis: lung disease by inhalation of dust particles
a). Etiologies: occupational exposure to silicosis, asbestos, coal mines
b). General pathology: Prolonged inhalation of dust particlescausing chronic
inflammatory response in the alveoli
Results in fibrosis

E. Obstructive lung diseases

1. Diagnosis by pulmonary function test
2. Asthma
a). Pathology
-Trigger mechanism causes mast cells on airways to degranulate and release histamine
-Histamine causes inflammatory reaction in airways

b). Manifestations: dyspnea, wheezing, tachypnea, cough, cyanosis

c). Treatment: inhaled drugs, albuterol, oxygen therapy, steroids

3. COPD Pink Puffer

Emphysema/
-Hyperinflation of alveoli with destruction
of alveolar septa, pulmonary capillary bed,
and elastic tissue in alveolar wall
-Works hard enough to maintain acceptable
levels of O2 and CO2
-Good color
-Appears S.O.B most of time
-Minimal sputum
-Emaciated appearance
-Heart failure occurs late

Chronic Bronchitis/ Blue

Bloater
Productive cough for at least three
months of the year during a two year
period
Does not work as hard so has poor color
and does not appear to be as S.O.B. as the
pink puffer
Lots of sputum production
Minimal weight loss
Heart failure occurs early

d). Complications of COPD: cor pulmonale, heart failure due to lung

disease
F. Bronchogenic carcinoma: lung cancer
1. Pathology of two representative types
-Squamous cell carcinoma: tumor develops in large central airways
-adenocarcinoma: tumor arises from glandular cells in peripheral airways
Pathology Tumors spread not only through the lung but metastasize easily and early
because of vascular and lymphatic access
2. Manifestations
-Dyspnea/S.O.B on exertion that progresses to dyspnea/S.O.B. at rest
-Fatigue and unexplained weight loss
-Dry, persistent cough that may progress to hemoptysis

VI. Endocrine Diseases (4 questions)

Pituitary
secretes: growth hormone, stimulating hormones for
other glands
Hyperpituitarism/acromegaly (after puberty)
-excessive growth in long bones, hands, feet, and head
-Coarse facial features with thickened tongue and
curvature of thespine
Hypopituitarism/ pituitary dwarf(before puberty)/
Simmonds (*adult)
Small but proportional/causes premature aging and
senility
Diabetes Insipidus: decreased secretion of ADH
polydipsia, polyuria, weakness/fatigue

Adrenal
Cortex secretes mineral corticoids glucocorticoids and
sex hormones.
Medulla secretes norepinephrine and epinephrine
Hyperadrenalism (cushings): Excess levels of
glucocorticoids which alters metabolism of proteins,
glucose(carbohydrate), and lipids (fat). Truncal obesity
with thin limbs, fat shoulder pads
Hypoadrenalism (addisons): decreased
glucocorticoids and mineral corticoids Weight loss with
G.I.
Disturbances, Areas of excess pigmentation and/or
absent pigmentation

Thyroid
Secretes: thyroxin, regulates metabolic rate
Hyperthyroidism (graves) gland hypertrophy,
too much thyroxin. exophthalmos, enlargement of
thyroid
Hypothyroidism(myxedema) decreased
thyroxin, decreased metabolic rate. Puffy eyes
Neonatal hypothyroidism (cretinism) low
thyroxin, inhibits mental/physical development
nontoxic goiter: enlargement of thyroid without
affecting function

Parathyroid
Secretes parathormone which regulates
blood levels of calcium
HyperPARAthyroidism
Manifestations: muscle weakness, weak
bones that are painful and fracture easily,
kidney stones
hypoPARAthroidism low calcium blood
levels, muscle tetany and hyperexcitable
nervous system

VII. Reproductive System Diseases (5 questions)

A. Prostatitis: inflammation caused by STD
1. Types: chronic(swollen and hardened by fibrosis) and acute (swollen and
squishy)
2. Pathology: inflammation with abcesses
3. Manifestations: dysuria, nocturia, low back pain, pyuria, leukocytosis, fever
B. Cancer of the prostate and BPH
1. Growing characteristic and metastatic spread
Metastasizes throughout body, but preferentially to bone
S & S may not appear until it has metastasized to another location

2. Pathology and manifestations of both are similar: dysuria, cystitis,

pyelonephritis, urethral obstruction
3. Treatment: radiation or surgery, hormone therapy
C. Carcinoma of the cervix
1. Predisposing factors increased wear and tear on the cervix, Promiscuity, STD,
Papilloma virus, Maternal history of DES
2. Detection: pap smear
3.Spread: Spreads to adjacent structures (usually urethra/bladder and rectum)
Metastasizes via lymphatics

D. Carcinoma of the endometrium

1. Predisposing factors: Irregular menstrual, cycle history, Infertility/no childbirth, Delayed
menopause

2. Detection: pap smear, biopsy

3. Spread: Spreads through uterus, fallopian tubes, ovaries and out into peritoneal
Cavity. Metastasizes via blood and lymphatic system

E. Endometriosis
1. Definition: Presence of endometrial tissue outside of uterine lining
2. Pathology: Usually retrograde migration to ovary but may go anywhere in the abdominal cavity

3. Commonly affected organs: anywhere in the abdomen

F. Ovarian cyst/Ovarian cancer
Follicular Cyst
-Benign, nonneoplastic cyst
-May cause pain and possibility of
Cystadenocarcinoma
rupture
-Highly malignant adenocarcinoma
-May cause internal hemorrhage
-May
be primary
or spread
from
-Usually
regress on
their own
without
endometrial
treatment carcinoma
-Usually no symptoms until it has
metastasized

Cystadenoma
-Benign, neoplastic cyst filled with serous
fluid or mucus
-Can become very large and can be quite
painful
-Treatment is usually surgical resection

G. Fibrocystic disease of the breast

1. Etiology Caused by the stimulating effects of fluctuating estrogen levels
2. Pathology: Benign mixture of fibrotic, cystic lesions with ductal hyperplasia

H. Cancer of the breast

1. Predisposing factors:
Breast cancer genes BRCA1 and BRCA2 (heredity), prolonged treatment with
estrogenprogestin (menopause)
2. Pathology:
Adenocarcinoma replaces normal tissue in a glandular arrangement surrounded by
connective tissue and fibrosis
Because of proximity of axillary lymph nodes, it metastasizes early and easily
Most often to lung or bone

3. Manifestations: palpable painless mass, nipple discharge, discoloration,

ulcerative lesion
4. Treatment: surgery, chemo, hormone therapy
VIII. Nervous System Diseases (5 questions)
A. CVA
1. Two types define
TIA(causes symptoms but no damage to brain tissue but CVA does) and CVA
2. Etiologies: thrombosis and hemorrhage and atheroscelerosis
3. Pathologies: brain dies from lack of oxygen, dead cells phagocytosed, replaced
with scar tissure
4. Manifestations change in LOC, headache, hemiparesis, seizure, N&v,
INCONTINENCE, SPEECH/SENSORY DISTURBANCE
5. Treatment ocygen, thrombolytics, craniotomy, speech/physical therapy
6. Prevention: address risk factors for athero,
B. Meningitis
1. Pathology:
-Yellow-pus exudates forms in the meninges around the brain and spinal cord
-Causes brain dysfunction due to increased pressure
-Also interferes with drainage of CSF

2. Manifestations: stiff neck, rigidity even in LOC, hydrocephalus, headache

3. Invading bacterial species; tapeworms
C. Encephalitis
1. Etiology: Usually caused by a virus: herpes simplex, HIV, arboviruses, rabies
2. Manifestations: Fever, headache, agitation and delirium, seizures, coma/catatonic state

D. Multiple sclerosis:
1. Pathology: degeneration of the myelin sheath of nerve fibers in the brain and spinal cord,
build up of scar tissue

2. Manifestations: Paresthesia, weakness, visual problems, ataxia, tremors, incontinence,

with progression to total paralysis

E. Parkinsons disease

1. Pathology: Degeneration of the substantia nigra in the midbrain causing decreased

amounts of dopamine
2. Manifestations: Resting tremors, masklike expression, muscle rigidity, shuffling gait,
monotone speech, possibly dementia
3. Treatment: L-dopa, implanted substantia nigra cells, electrical stimulation of midbrain,
stem cells(?)

F. Neoplasms
1. Three types definitions and tissue of origin
2. Two types of symptoms
G. Epilepsy
1. Definition: condition of recurrent seizures
2. Pathology A sudden, transient alteration in electrical activity in the brain which may
cause sensory, motor, and psychic symptoms as well as impairment of consciousness

3. Types of seizures
Partial abnormal electrical discharge is
confined to a limited area of the brain at the
onset of the seizure
Simple partial no impairment of
consciousness. Symptoms depend on area of
brain involved
Complex partial may have some impairment
of consciousness. Obvious sensory and/or
motor symptoms

Generalized abnormal electrical activity occurs

throughout brain causing loss of consciousness
Absence (petit mal): common in kids, blank stares
Tonic Clonic (grand mal)
Tonic phase
-Loss of consciousness with tonic stiffening of all muscles
-Patient does not breathe and gets cyanotic
- Tonic phase may last 1 minute
Clonic phase synchronized jerking of extremities and
head
-Intense salivation and tongue biting
- May last 1-4 minutes

TREATMENT
Tonic phase help patient down to prevent them from hitting
their head
- Do NOT force anything in their mouth!
Clonic phase move things out of their way or put pads around
them
-May lay on side if jerking is not too intense
- Do not try to restrain or try to force anything in their mouth
Post Ictal open and clear airway and assist patient as needed

IX. Musculoskeletal Diseases (5 questions)

A. Fractures

Stabilization may be done through

external fixation (casts and splints)
or internal fixation (surgical reduction
with pins and rods)

B. Osteomyelitis
1. Cause: STAPH OR STREP
2. Pathology: Damages medullary canal and weakens bone and makes it prone to further
fracture and deformity

C. Osteoporosis
1. Definition: decrease in bone density due to calcium loss
2.Causes: Aging, menopause, steroid therapy, immobilization, low dietary calcium

D. Arthritis
1. Rheumatoid
a. Pathology: Autoantibodies attack the synovial lining of joint capsules causing
chronic damage and fibrosis
b. Diagnosis: autoimmune disease that affects ALL joints
c. Treatment: methotrexate, Exercises and physical therapy, pain meds, joint
replacement, alternative treatments, ie, shark cartilage
d. Complications: Patient may also develop skin nodules, lung fibrosis, and
inflammation and vasculitis in the heart

2. Osteoarthritis
a. Etiology: Caused by aging and increased wear and tear
b. Pathology: Degeneration of cartilage leading to roughening of the articular
surface of bones

E. Diseases of the back

1. Slipped disc (Herniated Nucleus Pulposus)
a. Etiologies: injury or degenerative disease
b. Pathology: Herniation of disk material puts pressure on nerve roots
c. Manifestations: pain and paresthesia on affected side and down affected leg
d. Treatment: Rest, muscle relaxants, analgesics Manipulation Various surgical
procedures

X. Digestive Tract Diseases (8 questions)

A. Hernias
1. Describe each type
Inguinal Hernia intestine protrudes through the abdominal wall in the groin or in the scrotum
Hiatal Hernia: Herniation of the stomach into the thorax at the esophageal hiatus
Umbilical Hernia: Herniation of umbilical stump in: young children
Omphalocele: Herniation of abdominal viscera due to congenital defect in abdominal wall closure in utero

2.Define strangulation and incarceration

-Incarcerated herniated tissue can not be pushed back into place

-Strangulated incarcerated hernia has had its blood supply cut off and the tissue becomes
necrotic

B. Diverticula
1. Definition: Saccular herniation of colon mucosa through the muscular wall of the colon
2. Pathology and Complications: Result is an outpouching of the intestinal wall. This
pouch acts as a pocket in which digestive material can become caught and cause inflammation of
the pouch leading to diverticulitis

C. Inflammatory diseases
1. Gastritis, inflammation of gastric mucosa
a. Definition: Inflammation of the gastric mucosa that can be chronic or acute
b. Etiologies and Pathology: infection from contaminated food/water, dietary
indiscretion, chemical irritation
Acute causes edema and some superficial erosion
Chronic may cause hypertrophy or atrophy of mucosa
Atrophy may lead to pernicious anemia and/or gastric cancer

2. Crohns disease: chronic inflammatory disease that occurs in patches in

ileum+colon
a. Pathology: patchy thickening of the intestinal
wall with possible erosion/ulceration
b. Complications: Bowel obstruction, Peritonitis, Fistulas
c. Manifestations: Fever, abdominal pain, diarrhea

3. Ulcerative Colitis
a. Pathology: Leads to abscesses, necrosis, and possible ulceration with
perforation

b. Complications: high risk at developing colon cancer

c. Manifestations: painful & bloody diarrhea, weight loss, anemia and shock
from internal blood loss, peritonitis

D. Ulcer: Circumscribed erosion of the mucus membrane that usually occurs in the lesser curvature of the
stomach and in the duodenum

1. Pathology acute, subacute, chronic

Acute: Red, swollen areas that may have blood in the center of the lesion
Subacute: Erosion is through mucosa and into muscle layer; Center of lesion usually has
pus in it
Chronic: Fibrous, scar tissue is present with the erosions
2. Complications: Perforation may lead to peritonitis and hemorrhage
3. Manifestations: Painful, gnawing sensation in stomach that is usually relieved by
intake of food; increased gastric acidity

4. Treatment: antibiotics, antacids, dietary control, no smoking, surgery for

perforations
E. Neoplasm
1. Leukoplakia
a. Definition: Hyperplastic cell growth of hard-white squamous tissue in the
mucus membrane of the oral cavity

b.Relationship to cancer: precancerous sign

2. Stomach carcinoma
a. Predisposing factors: unknown but chronic gastritis due to helicobacter
infection may be a cause
b. Manifestations: similar to ulcer, no specific symptoms until cancer has
metastasized
3. colo-rectal

a. Predisposing factors: heredity, high fat/low fiber diet,chronic ulcerative

colitis
b. Manifestations: unexplained weight loss, fatigue, blood in stool,
constipation, diarrhea
F. Malabsorption syndrome: failure to digest and/or absorb food
Impaired digestion:
Pancreatic disease
Liver disease
Altered continuity of
the GI tract
Injury
surgery

Impaired absorption:
Crohns disease
Ulcerative colitis
Celiac disease
Gluten intolerance
Causes atrophy of
intestinal
mucosa

Manifestations:

Weight loss
Cutaneous bruising
Abdominal distension
Anemia
Calcium deficiency
Fat-soluble vitaminsdeficiency
Large, bulky, foul smelling fecal material

XI. Liver, Gallbladder and Pancreas Diseases (7 questions)

A. Viral hepatitis
1. Etiologies types: biliary tract dysfunction, biliary artesia, substance abuse,
viral infection
2. Pathology: Acute or chronic inflammation of the liver that causes poor liver function due to
necrosis and the buildup of fatty cells in the liver

3. Manifestations
Flu like symptoms
Anorexia
Malaise
N&V
Sometimes B, C, D, E
and G will have no
symptoms
Large, palpable liver
Dark urine
Jaundice
Labs
Decreased liver function
Increased liver enzymes
In severe cases of
hepatitis, the patient may lapse into a coma

B. Cirrhosis: end stage liver failure caused by chronic inflammation

1. Etiologies: biliary tract problem, substance abuse, chronic infection
2. Pathologies
a. Liver changes
b. Vascular changes
3. Manifestations
a. Liver damage
b. Portal hypertension

 Weakness, malaise, anorexia and weight loss

Hemorrhage/shock due to esophageal varices
In males, hair loss, testicular atrophy, and gynecomastia
Ascites (due to hypoproteinemia and portal hypertension)
Jaundice
Spider angioma and Caput Medusae
Multi-organ system failure. Eg, renal failure, respiratory failure
Encephalopathy/hepatic coma due to accumulation of nitrogen-containing compounds
in blood

C. Cholecystitis: inflammation of gall bladder caused by cholelithasis

1. Etiology: cholelithasis
2. Pathology: Gallbladder becomes swollen and the wall starts to ooze calcium; This
facilitates more stone formation

D. Cholelithiasis
1. Definition: presence of stones in gallbladder
2. Etiology: obesity, pregnancy, stasis, drugs, heredity
3. Pathology: stones obstruct biliary tract leading to cholecystitis, hepatitis,
pancreatitis
E. Pancreatitis: Acute or chronic inflammation of the pancreas resulting in pancreatic necrosis
and possible hemorrhage

1. Etiologies: biliary tract disease from cholelithasis/cystitis or alcoholism

2. Pathology:
-Etiologic agent causes an increase in pressure in the pancreatic ducts which
allows pancreatic enzymes to be released into the pancreatic epithelium
-Besides poor pancreatic function, this can lead to necrosis of the pancreas and
allow it to start hemorrhaging and may also result in perforation
Peritonitis!
3. Manifestations
Severe LUQ pain
N&V
Fever
Signs of shock if hemorrhaging
Signs of peritonitis if perforation occurs
Labs show high levels of pancreatic enzymes in the blood
If chronic, malabsorption and possibly diabetes