Meckel Diverticulum Etiology and Derived from remnant of vitelline duet (yolk stalk) Epidemiology Occurs in 2% of population. pop 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 anastomosisCeliac 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. 98Crohn 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 occurAdenomatous 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 cancerColorectal 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.