Acquired Megacolon: 1. Chaga s disease. 2. Organic obstruction by tumour or stricture. 3. Toxic megacolon in UC and CD. 4. Functional obstruction.

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1 GIT DISEASES : Small And Large Intestines: Meckel s Diverticulum: It results form failure of involution of omphalo-mesentric duct. It is a blind ended tubular protrusion up to 6 cm long, usually seen in the ileum about 2 feet of the cecum composed of all layers of the normal small intestine. Rarely pancreatic rests are found. About half of the cases there are heterotopic gastric mucosa. Hirschsprung s Disease (Congenital Megacolon): Is dilatation of the colon greater than 6-7 cm in diameter due to functional obstruction caused by absence of Meissner s submucosal and Auerbach s myenteric plexuses. Male:Female ratio is 4:1. Acquired Megacolon: 1. Chaga s disease. 2. Organic obstruction by tumour or stricture. 3. Toxic megacolon in UC and CD. 4. Functional obstruction. Ischaemic Bowel Disease: 1. Arterial Thrombosis: a. Severe atherosclerosis. b. systemic vasculitis. c. dissecting aneurysm. d. angiographic procedures. e. aortic surgeries. f. Hypercoagulable states. g. oral contraceptives. 2. Arterial Embolism. 3. Venous thrombosis: a. oral contraceptives. b. antithrombin III deficiency. c. Intraperitoneal sepsis. d. postoperative states. e. vascular invasive neoplasms. f. cirrhosis. g. abdominal trauma. 4. Nonocclusive ischemia: HF, shock, dehydration, vasoconstrictive drugs. 5. Radiation injury, volvulus, hernias. Three histological types seen: 1. transmural. 2. Mural. 3. Mucosal. Angiodysplasia: Is tortuous dilatation of submucosal and mucosal blood vessels, seen most often in the cecum or right colon usually after the sixth decade of life, accounting to 20% of lower intestinal bleeding. Diarrheal Diseases: May be classified into: 1. Secretory diarrhea: a. infectious; by direct damage of surface epithelium or enterotoxin mediated. b. Neoplastic; elaboration of peptides or serotonin. c. Excess use of laxatives. 2. Osmotic Diarrhea: a. Lactulose therapy. b. Gut lavage. c. Antacids. 3. Exudative diseases: a. Infectious. b. Idiopathic inflammatory bowel diseases. 1

2 4. Malabsorption. 5. Deranged motility Malabsorption Syndromes: Is characterized by suboptimal absorption of fats, fat-soluble vitamins, proteins, carbohydrates, electrolytes and minerals and water. It may be caused by: 1. Defective intraluminal digestion. 2. Defective terminal digestion by enzymes. 3. Defective transepithelial transport. Classification: I. Defective Intraluminal Digestion: - Pancreatic insufficiency. - Zollinger-Ellison Syndrome: Inactivation of pancreatic enzymes by excess acids. - Ileal dysfunction or resection. - Biliary obstruction or hepatic dysfunction. II. Primary Mucosal Cell Abnormalities: - Disaccharidase deficiency (lactose intolerance). - Bacterial overgrowth with brush border damage. - Abetalipoproteinaemia. III. Reduced Small Intestinal Surface: - Celiac disease. - Short gut syndrome. - Crohn s disease. IV. Lymphatic Obstruction: - Lymphoma - TB and TB lymphadenitis. V. Infection: - Acute enteritis. - Parasitic infestation. - Tropical sprue. - Whipple s disease. VI. Iatrogenic: -Subtotal or total gastrectomy. - Distal ileal resection or bypass. Celiac Disease (Gluten-Sensitive enteropathy): The basic disorder of celiac disease is sensitivity to gluten present in wheat, oat, barley and rye that contains the water insoluble protein, gliadin. The small intestinal mucosa when exposed to gluten, accumulates a large number of B cells and plasma cells, crossing to the epithelial cells resulting in their damage and total flattening of mucosal villi with loss of surface area. It is thought that celiac disease arises after exposure to adenovirus, because gliadin cross reacts with E1b protein of type 12 adenovirus. There is an increased rate of intestinal lymphomas in celiac disease. 2

3 Idiopathic Inflammatory Bowel Diseases: Crohn s disease (CD) and Ulcerative colitis (UC) are chronic relapsing disorders of unknown origin. Aetiology: Both diseases remain obscure (idiopathic). Some factors are implicated: 1. Genetic predisposition. 2. Abnormal structure of intestinal mucosa. 3. Infectious causes: Measles, Chlamydia, atypical bacteria and mycobacteria. 4. Abnormal host immunoreactivity. Crohn s Disease (Terminal Ileitis, Regional Enteritis): Is a granulomatous disease that may affect any portion of the GIT from the esophagus to the anus, but most often involves the small intestine and colon. May be accompanied by iritis and uveitis, sacroiliitis, migratory polyarthritis, erythema nodosum, sclerosing cholangitis, nephrolithiasis and UTI. Systemic amyloidosis is a rare late event. CD is more prevalent in the US, UK and Scandinavia, and rare in Asia and Africa. It occurs at any age, but the peak incidence is between the second and third decades of life, with a slight female sex predilection. Gross involvement of the small intestine alone in 40%, small intestine and colon in 30%, the colon alone in 30%. There is sharply delimited transmural involvement of the bowel by an inflammatory process with mucosal damage. The involved intestinal wall becomes rubbery and thick with narrowing of the lumen. There is sharp demarcation between the diseased segment and the uninvolved area (skip lesion). Early disease exhibits mucosal ulcers, edema and loss of normal mucosal texture, then ulcers coalesce into long linear ulcers oriented along the axis of the bowel. The intervening normal mucosa acquire a cobblestone appearance. Narrow fissures develop between mucosal folds with the formation of fistulae and sinuses. Microscopically: 1. Inflammation with neutrophilic infiltration into the epithelial layer and formation of crypt abscess. 2. Ulceration. 3. Chronic mucosal damage: architectural distortion, atrophy and metaplasia. 4. Granulomas; inconstant finding, found even in uninvolved segments. 5. Dysplastic changes, increase the risk of colonic carcinoma. Ulcerative Colitis: Is a nongranulomatous ulcero-inflammatoty disease affecting the colon, limited to the mucosa and submucosa, except in the most severe cases. It begins in the rectum extending proximally in a continuous fashion, sometimes involving the whole colon. Some patients are associated with migratory polyarthritis, sacroiliitis, ankylosing spondylitis, uveitis, pericholangitis and sclerosing cholangitis and skin lesions. UC is more common than CD, seen commonly in western countries, with no sex predilection. Grossly: 1.UC involves the rectum and rectosigmoid areas in about 80%, extending proximally. Pancolitis in 10%. 2. In active inflammation there is mucosal hyperemia, edema and granularity with easy bleeding. 3. In severe disease there is extensive broad based ulcers aligned with the long axis of the bowel. 4. Regenerating mucosa bulge 3

4 upward to create pseudopolyps. 5. Adjacent ulcers interconnect by tunnels covered by attenuated mucosa. 6. Exposure of the submucous neural plexus to fecal material leads to shut down of neuromuscular function and the formation of toxic megacolon. 7. Progressive mucosal atrophy leads to flattened and attenuated mucosal surface. Microscopically: 1. Diffuse mononuclear inflammatory cell infiltrate in the lamina propria with neutrophilic infiltration of crypts (crypt abscess), inflammation is unaccompanied by granulomas. 2. Ulceration extending into the submucosa. 3. On remission, granulation tissue fills the ulcer crater with regeneration of mucosal epithelium, with consequent mucosal atrophy, fibrosis and architectural disarray. 4. Colonic carcinomas develop: 2% after 20 years of left colonic involvement, 10% after 20 years of pancolitis and 25% after 30 years. Differences Between UC And CD: FEATURES ULCERATIVE COLITIS CROHN DISEASE Clinical 1.Rectal bleeding Common Inconspicuous 2.Abdominal mass Practically never present 3.Abdominal pain Usually left-sided Usually right-sided 4.Sigmoidoscopy Abnormal in 95% Abnormal in less than 50% 5.Colon carcinoma 5 10% Very rare 6.Anal complications 7.Response to steroid therapy Rare; minor 75% 25% 8.Results of surgery Very good Fair Radiographic 1.Sparing of rectum Exceptional 90% 75%; fissures, fistulas, ulceration 2.Involvement of ileum Rare; dilated ( backwash ileitis ) Common; constricted 3.Strictures Absent Often present 4.Skip areas Absent Common 5.Internal fistulas Absent May be present 6.Longitudinal and transverse ulcers Exceptional Common 7.Fissuring Absent Common Morphologic 1.Distribution of 2.involvement 3.Mucosal atrophy and regeneration Diffuse; predominantly left-sided; mucosal and submucosal Marked Focal; predominantly rightsided transmural Minimal 4

5 FEATURES ULCERATIVE COLITIS CROHN DISEASE 4.Cytoplasmic mucin Diminished Preserved 5.Lymphoid aggregates Rare Common 6.Edema Minimal Marked 7.Hyperemia May be extreme Minimal 8.Granulomas Absent Present in 60% 9.Fissuring Absent Present 10.Crypt abscesses Common Rare 11.Rectal involvement Practically always 50% 12.Ileal involvement Minimal; dilated not more than 10 cm 50%; constricted; transmural inflammation 13.Lymph nodes Reactive hyperplasia May contain granulomas Colonic Divericulosis: Are blind pouches connected with the lumen of the colon. It is common in western countries in adults over the age of 60 with a prevalence of 50%. It is related to the intake of low fiber diet. Diverticula are small flask like or spherical, usually cm in diameter, 95% in the sigmoid colon. Muscular hypertrophy is usually seen in the affected segment. Most diverticulae are seen adjacent to the mesentery and lateral taeniae. The walls are usually very thin made up of mucosa and submucosa. Inflammation produce diverticulitis and peridiverticulitis. Polyps: Include: 1. Hyprplastic polyps (benign). 2. Hamartomatous polyps: Juvenile polyps, Peutz-Jegher polyps. 3. Inflammatory polyps. 4. Lymphoid polyps. 5. Adenomatous polyps: - Villous Adenomas: 1%, are sessile, may predispose to colonic carcinoma in 40% of the cases. - Tubular Adenomas: 89-94% are small and pedunculated. - Tubulovillous Adenomas: 5-10% Familial Polyposis Syndrome (FAP): Is an autosomal dominant disorder characterized by the development of colonic adenomas. A minimum number of 100 is required for the diagnosis. Most polyps are tubular adenomas, occasional polyps have villous features, most become evident in adolescence, the risk of colonic carcinoma is almost 100%, unless a prophylactic colectomy is done. The FAP gene is localized on chromosome 5q21. Colorectal Carcinomas: 98% are adenocarcinomas, almost always arise on adenomatous polyps. The peak incidence is between years, males are affected about 20% more often than 5

6 females. It is a worldwide disease, its incidence is 30 folds lower in Africa, South America and India. Dietary factors contribute to the development of carcinomas are: 1. Low contents of fibers. 2. High contents of refined carbohydrates. 3. High fat content. 4. a decreased intake of protective nutrients (Vit. A, C and E). It occurs in: -Cecum and Ascending colon: 25% - Rectum: 25% - Descending colon and sigmoid: 25% - Scattered: 25% 1-3% of carcinomas occur in patients with FAP or inflammatory bowel disease. Grossly: Tumours of the proximal colon tend to grow as fungating masses, obstruction is uncommon. Carcinomas of the distal colon are annular encircling lesions. Both deeply invade the muscle layer reaching the serosa. The majority of carcinomas are adenocarcinomas with different grades of differentiation, some exhibit extracellular mucin production. Cancers of the anal canal are squamous cell carcinomas. Duke s Staging System: Carcinoid Tumours: Are tumours arising from neuroendocrine cells distributed all over the small and large bowel mucosa, they normally function in the secretion of peptide and nonpeptide hormones. Although all carcinoid tumours are potentially malignant, the tendancy of aggressive behavior correlates with: 1. the site of origin. 2. Depth of penetration. 3. Size of tumour. Some tumours are referred by its major product (gastrinoma, somatostatinoma, insulinoma). The appenidix is the most common site, followed by small intestine, rectum, stomach and colon. In the appendix they appear as a swelling of the tip. APPENDIX : Acute Appendicitis: Appendiceal inflammation is associated with obstruction in 50% to 80% of cases, usually in the form of a fecalith and, less commonly, a gallstone, tumor, or ball of worms (oxyuriasis vermicularis). Morphology : neutrophilic exudate may be found throughout the mucosa, submucosa, and muscularis propria. Subserosal vessels are congested, and often there is a modest perivascular neutrophilic infiltrate. 6

7 Tumors of the Appendix The most common appendiceal tumor is the carcinoid usually discovered incidentally at the time of surgery.this neoplasm most frequently involves the distal tip of the appendix, where it produces a solid bulbous swelling up to 2 to 3 cm in diameter. nodal metastases are very infrequent, and distant spread is rare. the neoplastic cells may form discrete islands, trabeculae, or stands, the tumor cells are monotonously similar, having a scant, pink granular cytoplasm and a round to oval stippled nucleus. In most tumors there is minimal variation in cell and nuclear size and mitoses are infrequent or absent. Anal canal : Inflammatory diseases: Anal fissure is a single linear separation of the tissues of the anal canal extending through the mucosa Anal ulcer is a chronic process, usually of oval shape, that extends into the muscular layer. Anal fistula is an abnormal tract having an internal opening within the anal canal. The fistulous tract may lead to the skin, or it may end blindly in the perianal soft tissues. Hemorrhoids are the result of ectasia of the hemorrhoidal vascular plexus. They are divided into external (outside the anal verge, in the territory of the inferior rectal vessels) and internal (inside the rectum, in the territory of the superior rectal vessels). Stasis of blood in the veins of the hemorrhoidal plexus is usually caused simply by dependency. However, pathologic processes in the drainage path of those veins may cause secondary engorgement such as cirrhosis of the liver with portal hypertension, carcinoma of the rectum, leiomyoma of the uterus, or pregnancy. Tumors condyloma acuminatum is caused by HPV(human papilloma virus type 6, 11). Anal carcinoma is increasing in both males and females, HPV 16 being the specific subtype in 82% of cases, classified as squamous cell carcinomas 7

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