Meckel Diverticulum
Etiology and Derived from remnant of vitelline duet (yolk stalk)
Epidemiology Occurs in 2% of population.
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Pathology Gross: Blind pouch on antimesenteric border of ileum within 2 feet of the ileocecal valve causing
tubular outpouching of small intestine
Microscopic: True diverticulum with all 3 layers of the bowel wall (mucosa, submucosa, muscularis
propria); may contain acid-secreting gastrie mucosa and/or pancreatic tissue
Clinical Presents in first 2 years of life. Usually asymptomatic, but can cause peptic ulcerations leading to
Manifestations a GI bleed, intussusception (invagination of a bowel segment into a more distal bowel segment),
or volvulus (twisting of one bowel portion around its own mesentery). Intussusception presents,
th red currant jelly stools owing to bowel ischemia, Volvulus presents with acute abdominal pain,
constipation, gas, and sigmoid distention.
Treatment Surgical excision
Notes Meckel diverticulum is the most common congenital abnormality of the GI tract,Acute Appendicitis
Etiology and Caused by obstruction of the appendix by a fecalith, inflammation, foreign body, or neoplasm
Epidemiology Peak incidence is between 10 and 30 years of age
Pathology Gross: Red, swollen appendix with fibrinous exudate
Microscopic: Neutrophilic infiltrate extending through to muscularis; abscess formation;
ulcerations: congested vasculature
Clinical Vague periumbilical pain that later localizes to RLQ pain; fevers anorexia; nausea: vomitings
Manifestations —_ psoas sign (pain on passive extension of right hip): obturator sign (pain with passive flexion and
internal rotation of right hip)
Complications include gangrene and perforation leading to peritonitis
Lab findings: Leukocytosis
Treatment Appendectomy
Notes Appendicitis is the most common abdominal surgical emergency, affecting 10% of population,Hirschsprung Disease
Etiology and Caused by failure of neural crest cell migration during embryogenesis
Epidemiology Occurs in 1 in 5000 births; affects boys more than girls; associated with Down syndrome
Pathology Gross: Dilation of colon proximal to aganglionic segment (megacolon); involvement of rectum
Microscopic: Absence of ganglion cells of Auerbach and Meissner plexuses
Clinical Presents as failure to pass meconium or chronic constipation with abdominal bloating early in life;
Manifestations may also present as acute enterocolitis with watery, foul-smelling stool, or perforation of colon
‘Treatment Surgery and anastomosisCeliac Sprue
Etiology and
Epidemiology
Autoimmune-mediated intolerance to gluten (present in wheat, oat, rye, and barley)
More common in people of northern European descent; also associated with HLA-DR3 and HLA-
DQw2
Pathology
Gross: Blunting and atrophy of small intestinal mucosal villi
Microscopic: Increased lymphocytes and plasma cells in the lamina propria; loss of brush border
Clinical
Manifestations
May become symptomatic in infaney with growth retardation and failure to thrive, but may present
in young adulthood, Also may see steatorrhea (pale, bulky, frothy, foul-smelling stool), abdominal
istention, weight loss, or dermatitis herpetiformis (symmetric, recurrent, pruritic, subepidermal
blisters usually occurring over extensor surfaces of the extremities or over the trunk, scalp, and
neck); 10%-15% of patients will develop enteropathy-type T-cell lymphoma.
jal and anti-TTG antibodies
Lab findings: Abnormal D-xylose tes
antigliadin and antiendom,
Treatment
Gluten-free diet; dapsone for dermatitis herpetiformis
‘Tropical sprue is a malabsorption syndrome caused by overgrowth of enterotoxigenic organisms
found in the tropics and is treated with broad-spectrum antibiotics.
Whipple disease is caused by a rare multisystemic infection with PAS-positive actinomycete,
Tropheryma whippeli. It presents with a malabsorption syndrome, arthralgias, and CNS, cardiac,
and ocular involvement.
98Crohn Disease
Etiology and
Epidemiology
Idiopathic, although infectious causes have been suggested
Occurs most frequently in women between the ages of 15 and 30
Pathology
Gross: Changes located to terminal ileum, small intestine, and colon; not found in rectum; ereeping
fat over bowel surface: thickened bowel wall leading to a narrow lumen; linear ulceration of the
mucosa; cobblestone mucosa (submucosal edema with elevation of surviving mucosa)
Microscopic: Transmural inflammation; skip lesions (areas of normal bowel interspersed with
diseased bowel); fissures; noncaseating granulomas; atrophy of crypts: mucosal metaplasia
Ginical
Manifestations
Intermittent bouts of low-grade fever, diarrhea (often with blood), and RLQ pain; may have
RLQ mass on physical examination
Extraintestinal manifestations: Oral aphthous ulcers, erythema nodosum, migratory polyarthritis,
uveitis, sacroiliitis, ankylosing spondylitis
Complications: Fibrous strictures causing intestinal obstruction or perforation, perianal fistulas,
and malabsorption syndrome
Imaging: String sign on x-ray after barium swallow (represents narrowed bowel lumen); evidence
of ulceration, stricturing, or fistulas of the small intestine or colon on endoscopy
Treatment
Antidiarrheals; glucocorticoids; sulfasalazine; immunosuppressants
Notes
Crohn disease is considered an inflammatory bowel disease along with ulcerative colitis.Ulcerative Colitis
Etiology and May be related to immune system dysfunction
Epidemiology Occurs most commonly in women between ages of 20 and 25, but affects all ages
oi ig ee
Pathology Gross: Continuous lesions of the colon with rectal involvement; friable mucosal pseudopolyps
ical
Manifestations
(mucosal remnants of previous ulcerations) with free-hanging mesentery
Microscopic: Mononuclear inflammatory infiltrate in lamina propria; erypt abscesses and ulcers
(neutrophilic infiltrate in crypt lumen); dysplastic changes in epithelial cells; submucosal fibrosis
and glandular atrophy results from healed disease
May present with tenesmus (urge to defecate with ineffectual straining) or chronic diarrhea with
blood and mucus. Extraintestinal manifestations: Pyoderma gangrenosum (painful ulcerating
boils) and primary sclerosing cholangitis (fibrosing chronic cholestasis that can lead to portal
hypertension).
Complications include severe colonic stenosis, toxic megacolon (inflammation of myenteric
plexuses leading to gangrene), and increased risk for colorectal adenocarcinoma
Imaging: Loss of haustrations causes lead-pipe appearance
‘Treatment
Antidiarrheals; sulfasalazine; glucocorticoids; immunosuppressants; proctocolectomy (with placement
of ileostomy) is curative
Notes
Ulcerative colitis is considered an inflammatory bowel disease along with Crohn disease.Diverticular Disease (Diverticulosis and Diverticulitis)
Os
Etiology and Diverticulosis: Development of diverticula is associated with increased pressure in the bowel and
Epidemiology bowel wall weakness; commonly seen in people > 60 years; associated with low-fiber diet
Diverticulitis: Caused by inflammation of diverticula, usually by impacted fecal material
Pathology Diverticula: Gross: blind pouches leading off the alimentary tract that communicate with gut
lumen; most commonly false (pulsion) diverticula resulting from herniation of mucosa through
defects in muscular layer; less commonly true (traction) diverticula consisting of mucosa, muscularis,
and serosa. Microscopic: atrophic mucosa with thin muscularis propria.
Diverticulosis: Presence of multiple diverticula most commonly in the sigmoid colon
Diverticulitis: Inflammation of diverticula with inflammatory infiltrate with edema
Clinical Diverticulosis: Usually asymptomatic, but can present with vague abdominal discomfort and frank
Manifestations blood in the stool with no leukocytes or epithelial cells
Diverticulitis: Presents with fever, a chronic colicky LLQ abdominal pain, and possibly bright
red blood in the stool; complications include perforation, abscess formation, peritonitis, and bowel
stenosis
Treatment erticulosis: High-fiber diet; psyllium fiber laxatives
Diverticulitis: Antibiotics; high-fiber diet; consider colonic resection if multiple episodes of
diverticulitis occurAdenomatous Polyps of the Colon
Etiology and
Epidemiology
Associated with familial predisposition (possible connection to mutation of tumor suppressor gene
on chromosome 5)
Present in 35% of adults > 50 years of age
Pathology
‘Tubular adenomas (75%): Usually found in colon, small and pedunculated with stalk; dysplastic
epithelium with hyperchromatic nuclei and loss of cell orientation
Tubulovillous adenomas (15%): Resemble tubular adenomas but surface is covered by fingerlike
villi, similar to villous adenomas
Villous adenomas (10%): Usually found in rectum or sigmoid colon; broad-based (sessile) polyps
with large numbers of fingerlike villi; villi have dysplastic columnar epithelium
Clinical
Manifestations
Usually asymptomatic but can result in rectal bleeding, which may cause an iron deficiency anemia,
Associated with inereased risk for colorectal adenocarcinoma (especially with villous adenomas).
‘Treatment
Colonoscopic removal of adenomatous polyps; primary surgical resection of large sessile lesions
Aspirin and NSAIDs used to decrease incidence of adenomas and colorectal cancerColorectal Adenocarcinoma
Etiology and Risk factors include adenomatous polyps, long-standing ulcerative colitis, low-fiber diet, old age,
Epidemiology positive family history, hereditary nonpolyposis colorectal cancer (HNPCC), and familial
adenomatous polyposis (FAP)
Most commonly occurs between the ages of 60 and 80
Pathology Gross: Appearance varies from polypoid mass (proximal colon) to lesions with ulcerated centers
and irregular margins that circumscribe bowel (distal colon)
Microscopic: Dysplastic columnar cells in glandular formation; may produce mucin, some tumors
may be anaplastic
Clinical Can be asymptomatic; if symptomatic, presents with pallor, weight loss, intermittent diarrhea,
Manifestations LQ pain, or obstruction
Lab findings: Positive stool guaiac test; increased serum CEA; microcytic, hypochromic anemia
(iron deficiency anemia secondary to GI bleed)
Treatment Surgical resection; chemotherapy (5-FU)
Notes Colorectal cancer is the second leading cause of death owing to malignancy in the United
States. Preventive measures include screening all patients > 50 years of age with colonoscopy
every 10 years.