Robbins Chapter 17

Clinical features of ulcerative colitis.

A relapsing disorder bloody diarrhea with stringy, mucoid material, lower abdominal pain, and cramps that are temporarily relieved by defecaPon. Colonic dilaPon and toxic megacolon: (Inflammation and inflammatory mediators can damage the muscularis propria and disturb neuromuscular function) may lead to perforation.

Celiac Disease

Also known as celiac sprue or gluten-sensitive enteropathy, nontropical sprue) • Hypersensitivity to gluten (gliadin), • Resulting in loss of small bowel villi • and malabsorption.

Predict the clinical consequences of celiac disease.

Anemia, chronic diarrhea, bloating, or chronic fatigue. Although there is no gender preference, celiac disease is detected two-to-three fold more commonly in women. Pediatric celiac disease: irritability, abdominal distention, anorexia, chronic diarrhea, failure to thrive, weight loss, or muscle wasting. Diagnosis: IgA antibodies to tissue transglutaminase or IgA or IgG antibodies to deamidated gliadin. Anti-endomysial antibodies are highly specific but less sensitive than other antibodies.

Volvulus

Complete twisting of a loop of bowel about its mesenteric base of attachment is called volvulus and produces both luminal and vascular compromise. Consequence: obstruction and infarction.

Clinical features of Crohn disease.

Extremely variable: diarrhea, fever, abdominal pain, iron-deficiency anemia, generalized nutrient malabsorption, fibrosing strictures, may lead to colonic adenocarcinoma.

Describe the morphological features of ulcerative colitis.

FIGURE 17-37B Microscopic pathology of ulceraPve coliPs. A, Crypt abscess. B, Pseudopyloric metaplasia (boMom). architectural crypt distorPon, and epithelial metaplasia

Explain the pathogenesis of Crohn disease.

Haphazard crypt organization results from repeated injury and regeneration. (Distortion of mucosal architecture).

Hernias

Hernia sac. Acquired hernias most commonly occur anteriorly or at sites of surgical scars. Consequence: Impair venous drainage of the viscus; The resultant stasis and edema increase the bulk of the herniated loop, leading to permanent entrapment, or incarceration, and, over time, arterial and venous compromise (strangulation) develops that can result in infarction.

Identify the causes of of Ischemic Bowel Disease.

Ischemic Bowel Disease • Hypoperfusion may cause mucosal or mural infarctions; • Acute vascular obstruction may lead to chronic, transmural infarction. Acute arterial obstruction include • severe atherosclerosis; • hypercoagulable states, • embolizaPon of cardiac vegetaPons or • aortic atheromas.

Identify the various intestinal causes of malabsorption syndrome.

Malabsorption presents most commonly as chronic diarrhea. Defective absorption of nutrients in one of the four phases of nutrient absorption: 1. intraluminal digestion; 2. terminal digestion, which involves the hydrolysis of carbohydrates and peptides by disaccharidases and peptidases, respectively, in the brush border of the small intesPnal mucosa; 3. transepithelial transport, in which nutrients, fluid, and electrolytes are transported across and processed within the small intesPnal epithelium; 4. lymphatic transport of absorbed lipids • A hall mark of malabsorption is steatorrhea; • Most commonly encountered in the United States are pancreatic insufficiency, celiac disease, and Crohn disease

Predict the clinical consequences of Ischemic Bowel Disease.

Sudden, severe abdominal pain and tenderness, sometimes accompanied by nausea, vomiting, bloody diarrhea, or grossly melanotic stool. Shock and vascular collapse. Peristaltic sounds diminish or disappear, and muscular spasm creates board-like rigidity of the abdominal wall. As the mucosal barrier breaks down, bacteria enter the circulation and sepsis can develop; mortality may exceed 50%. Bloody diarrhea.

Describe the morphology of Crohn's disease.

The intestinal wall is thickened and rubbery as a consequence of transmural edema, inflammation, submucosal fibrosis, and hypertrophy of the muscularis propria, all of which contribute to stricture formation. Microscopy: Distortion of mucosal architecture. Epithelial metaplasia (Paneth cell metaplasia may also occur in the left colon). Noncaseating granulomas.

Pathogenesis of celiac disease.

Unknown etiology • But, almost all people with celiac disease carry the class II HLA-DQ2 or HLA-DQ8 allele

Predict the consequences of Meckel's diverticulum

What are the symptoms of Meckel's diverticulum? • Gastrointestinal bleeding (which can be seen in the stool) • Abdominal pain and cramping • Tenderness near the navel (belly button) • Obstruction of the bowels, a blockage that keeps the contents of the intestines from passing. This can cause pain, bloating, diarrhea, constipation, and vomiting. • Diverticulitis (swelling of the intestinal wall) • The most common symptom in children under five is bleeding, which is caused by ulcers that develop in the small intestine when the diverticulum secretes stomach acid.

Explain the pathogenesis of ulcerative colitis.

limited to the colon and rectum. FIGURE 17-36A Gross pathology of ulceraPve coliPs. A, Total colectomy with pancoliPs showing acPve disease, with red, granular mucosa in the cecum (leL) and smooth, atrophic mucosa distally (right). B, Sharp demarcaPon between acPve ulceraPve coliPs (right) and normal (leL). C, Disease is limited to the mucosa. Granulomas are not present in ulceraPve coliPs.

Identify the various causes of intestinal obstruction and predict the clinical characteristics of each.

Mechanical obstructions are the most common. Tumors and infarction account for only about 10% to 15% of small bowel obstructions.

Intussusception

Occurs when a segment of the intestine, constricted by a wave of peristalsis, telescopes into the immediately distal segment. Once trapped, the invaginated segment is propelled by peristalsis and pulls the mesentery along. Consequence: intestinal obstruction, compression of mesenteric vessels, and infarction.