Pathology of Intestines PDF

Pathology of Intestines Ahmed Almobarak  Topics to be covered The following topics will be discussed: 1- Diverticula of the intestine. 2- Congenital mega colon (Hirschsprung’s disease) 3- Mal-absorption syndromes: – Celiac disease. – Tropical sprue. – Lactose intoleran...

Pathology of Intestines Ahmed Almobarak  Topics to be covered The following topics will be discussed: 1- Diverticula of the intestine. 2- Congenital mega colon (Hirschsprung’s disease) 3- Mal-absorption syndromes: – Celiac disease. – Tropical sprue. – Lactose intolerance. – Whipple’s disease.  Inflammatory Bowe Diseases Also known as Idiopathic intestinal inflammations: Include the following diseases: – Regional enteritis “ Crohn’s disease”. – Ulcerative colitis.  IBDs I- Regional enteritis: “Crohn’s disease” CD: Definition: it is a chronic non specific granulomatous disease. Cause: – Unknown. Sites: – Typically it affects the terminal part of the ileum. – The colon or any part can be affected.  IBDs: Chron’s Disease Gross appearance: – It is a segmental (skip) lesion. – The mucosa is swollen and protruded (cobble- stone appearance) with deep linear or fissure ulcers run along the axis of the bowel. – The wall of the intestine is greatly thickened, the lumen is narrow (string sign in x-ray) & there is serosal extension of mesenteric fat.  Crohn’s disease, gross Part of small intestine Cobblestone  Crohn’s disease Microscopic: – There is diffuse infiltration of all layers of the intestinal wall by mononuclear cells with hyperemia and edema. – The characteristic lesion is submucosal tubercles, formed of epithelioid and giant cells without caseation necrosis. – Fibrosis in late stages. Crohn’s disease, microscopic submucosal tubercles  Crohn’s Disease Clinical features: – Recurrent episodes of diarrhea. – Abdominal cramps. – Fever which lasts days to weeks. – Age: two peaks: 10-30, 50-70.  Crohn’s Disease Complications of CD: – Intestinal obstruction (due to narrowing). – Perforation of fissuring ulcers, leading to peritonitis or fistula formation. – Mal-absorption syndrome. – Bleeding and anemia. – Mucosal dysplastic changes which increase risk for malignancy five-fold to six-fold.  Ulcerative Colitis Ulcerative colitis (UC): Definition: it is an inflammatory condition of the colon and rectum, initially it is acute but becomes chronic with periods of remission. The inflammation is limited to the mucosa and submucosa except in severe cases. Cause: – Unknown.  Ulcerative Colitis Gross appearance: – Continuous lesion in the whole colon. – Congested velvety mucosa. – Shallow ulcers. – Pseudopolyps (intact mucosa).  Ulcerative colitis, gross ulcers: red color, intact mucosa: pink  Ulcerative Colitis Microscopic: – In the acute phase: There is severe congestion of the mucosa and presence of “crypt abscess”. Formation of large mucosal ulcers. – In the chronic phase: Distruction of glandular epithelium. Infiltration by chronic inflammatory cells, mainly plasma cells. Epithelial hyperplasia, & may be dysplasia.  Ulcerative colitis, microscopic crypt abscess, infiltration by plasma cells  Ulcerative Colitis Clinical features: – Attacks of diarrhea with mucus and blood in the stool. – May persist for days or weeks or months. – Then subside to recur after a varying period. – Age: peaks at 20-30.  Ulcerative Colitis Complications of UC: – Rectal hemorrhage which leads to anemia. – Diarrhea and weight loss. – Perforation (rare). – Malignant change (after 10 ys of pancolitis). – Secondary amyloidosis. – Toxic mega-colon (massive dilatation of the colon with loss of motility).  Comparison between CD & UC Crohn’s disease Ulcerative colitis Site: terminal ileum, colon Colon only. Gross: cobble stone with Velvety superficial mucosa, fissuring ulcers, thick wall, ulcers, and pseudopolyps. narrow lumen. Microscopic: transmural infl Crypt abscess, ulcers, no with non caseating tubercles tubercles, minimal fibrosis. and fibrosis. Malignant change: may Occurs (after 10 years). occur.  Acute Appendicitis Acute appendicitis: The most common cause of acute abdomen. Occurs in children and young adults of both sexes. Cause: – Obstruction of the lumen leading to ischemia of the wall and secondary bacterial infection (E coli). – Obstruction is usually due to: fecoliths, hyperplastic lymphoid tissue, worms, or tumors.  Acute Appendicitis Gross appearance: – The appendix is swollen, – Congested, – Fibrin may be seen on the serosal surface. Acute appendicitis, gross  Acute Appendicitis Microscopic: – Inflammatory exudate in the lumen. – Infiltration of the wall by acute inflammatory cells (PNLs) especially the muscle layer. – Ulceration and necrosis of mucosa. – Congestion of blood vessels and edema of the wall. – Gangrenous necrosis in severe cases.  Acute appendicitis, microscopic, mucosal inflammation and necrosis  Acute Appendicitis Clinical features: – Peri-umbilical pain migrating to the right lower quadrant. – Anorexia. – Vomiting. – Mild fever. – Leucocytosis (> 15000/cmm).  Acute Appendicitis Complications of acute appendicitis: 1- Perforation and peritonitis which may lead to toxemia and death (2%). 2- Portal pyemia. 3- Chronic appendicitis.  Diverticular Disease Diverticula of the intestine: Defined as out pouching of the wall of the intestine. Calssification: It may be: – Congenital (Meckel’s diverticulum) or – Acquired (colonic diverticulosis).  Diverticular Disease Meckel’s diverticulum: – Remnant of the vitelline (omphalo-mesentric) duct. – Rule of 2s: Occurs in 2% of population. Usually diagnosed at 2 years of age. 2 feet (60 cm) from the ileo-cecal valve. 2 cm in length. 2% of carcinoid tumor occur in Meckel diverticulum. Meckel’s diverticulum  Diverticular Disease Complications: – Inflammation (diverticulitis). – Peptic ulcer if there is ectopic gastric mucosa. – Carcinoid tumor. – Intestinal obstruction.  Diverticular Disease Colonic diverticula (acquired): – Occurs in the sigmoid colon in old patients due to chronic constipation. – Gross appearance: Usually multiple, formed of mucosa and submucosa, protruding through weak points in the musculosa. Located at the line of mesenteric attachment to the intestine. Diverticulosis, sigmoid colon sacs bluish in color  Diverticular Disease Complications of colonic diverticulum: 1- Inflammation. 2- Fistulous communication with other abdominal viscera. 3- Perforation and peritonitis.  Hurschsprung Disease Congenital megacolon (Hirschsprung disease): Genetic disorder leads to lack of ganglion cells in a segment of the colon. There is dilatation of the colon above this part. Gross: – The affected segment (rectum or sigmoid colon) is narrow. – The part above shows dilatation.  Congenital mega colon the affected lower part is narrow  Hurschsprung Disease Microscopic: – Absence of ganglion cells in Auerbach’s and Meissner’s plexuses in the submucosa.  Hurschsprung Disease Clinical features: – Occurs in infancy. – More in females (4:1). – Constipation – Abdominal distention – Vomiting. Complications: – Enterocolitis (life threatening). – Perforation (rare).  Malabsorption Syndromes Mal-absorption syndromes: Causes: I- Mal-digestion: due to Diseases of pancreas, Diseases of biliary tree, or Overgrowth of bacteria in stomach or intestine. II- Reduced absorptive capacity: Celiac disease. Crohn disease. Surgical resection.  MAS: Classification III- Transport abnormalities: due to lymphatic obstruction: Lymphomas. Tuberculosis.  Malabsorption Syndrome Clinical manifestations of mal-absorption: – Diarrhea. – Bulky stools. – Weight loss. – Fatigue. – Evidence of vitamin deficiencies.  Celiac Disease Mal-absorption diseases: Celiac disease (gluten-sensitive enteropathy, non-tropical sprue): Characterized by: – Flat small bowel mucosa. – Prompt clinical improvement after withdrawal of foods that contain gluten.  Celiac Disease Pathogenesis: – It is an immunologic disorder in which reactivity to gliadin (glycoprotein in gluten) results in damage of the epithelial cells lining the villus. – Anti-gliadin, anti-reticulin and anti-endomysial antibodies are present in the serum of the patients.  Celiac Disease Gross appearance: – The atrophic changes are most severe in the proximal small bowel. Microscopic: – Loss of villi. – Increased intra-epithelial lymphocytes. – The lamina propria shows increased plasma cells. Celiac disease compared to normal Loss of villi.  Celiac Disease Clinical manifestations: – Presents in childhood with mal-absorption. – Abdominal distension, and flatulence. – Diarrhea, steatorrhea, weight loss. Treatment: dietary restriction of gluten.  Tropical Sprue Defining Features: Found chiefly in tropical areas. Mal-absorption with steatorrhea, most likely secondary to bacterial infection (E coli). Microscopic: variable degree of villous atrophy is found. Patients respond dramatically to broad spectrum antibiotics.  Disaccharidase Deficincy Lactose intolerance disease (disaccharidase deficiency): Lactase enzyme deficiency. The enzyme is localized to the small intestinal brush border and digests lactose. Absence of the enzyme leads to sugar fermentation in the lumen.  Lactose intolerance disease Clinical manifestations: – Abdominal cramps. – Diarrhea. – Flatulence. – Weight loss.  Whipple disease Whipple’s disease: Rare infectious disease involving may organs including small intestine, joints, lung, heart, liver, spleen and CNS. Occurs in adult males (30-50 years). Clinical manifestations: – Mal-absorption. – Weight loss. – Diarrhea.  Whipple disease Pathogenesis: – It is due to special type of bacteria named Tropheryma whippelii. – The patient’s macrophages have lysosomal defect that prevents the ingested bacteria from destruction by the usual way.  Whipple disease Microscopic: – The lamina propria of the small bowel is filled with macrophages stuffed by PAS positive rod-shaped bacilli. Treatment: antibiotics.  Whipple disease Low power, H&E stain High power, PAS stain