Gastrointestinal Diseases Overview

Crohn's Disease

• Gross Appearance: Cobblestone appearance of the mucosa, adherent creeping mesenteric fat, deep fissures, fistula tracts and fibrosis
• Microscopic Features: Chronic active inflammation with deep ulcers, fissures, & neutrophils. All wall layers are affected (transmural) with fibrosis, granulomas (35% non-caseating), and no dysplasia.
• Complications: Thrombosis or embolism of mesenteric artery leading to infarction of a segment, septic peritonitis, and gangrene.

Chronic Intestinal Obstruction

• Definition: Gradual incomplete obstruction of the intestinal lumen.
• Causes: Functional (Hirschsprung disease) or organic (adhesions, endophytic tumor, fibrous stricture)
• Gross Appearance: Proximal segment markedly dilated and hypertrophic, distal segment collapsed.

Diverticular Disease of The Colon

• Definition: Acquired herniations of mucosa and submucosa into the intestinal wall.
• Complications: Diverticulitis or abscess, bleeding, perforation & septic peritonitis, fibrosis & stricture.

Acute Diffuse Suppurative Appendicitis

• Etiology: Obstruction with fecolith & seeds (adults), lymphoid hyperplasia (children), or carcinoid tumor. Organisms include Staphylococci and E. coli.
• Complications: Perforation & septic peritonitis, peri-appendicular inflammatory mass/ abscess, gangrene, portal pyemia, mucocele (mucus-filled bag), empyema (pus-filled bag), and chronic appendicitis.

Malabsorption

• Definition: Defective absorption of fats, proteins, carbohydrates, water, electrolytes, minerals, and vitamins.
• Etiology: Celiac disease (gluten-induced enteropathy), tropical sprue, Giardiasis, secondary malabsorption due to various factors (inflammation, tumors, post-surgical resections). Patients generally present with chronic diarrhea, steatorrhea, and weight loss.

Typhoid Fever

• Definition: Systemic infective disease of the small intestine and other organs caused by Salmonella typhi, predominantly affecting children and adolescents.
• Route of infection: Ingestion of contaminated water or food.
• Pathogenesis: Pathological features include enlarged and swollen Peyer's patches, oval longitudinal ulcers in the intestinal mucosa, and enlarged spleen.
• Complications: Hemorrhage, perforation, secondary amyloidosis, and dysplasia/adenocarcinoma.

Primary Intestinal Tuberculosis

• Mode of infection: Swallowing of human or bovine tubercle bacilli.
• Pathology: Primary complex includes an initial lesion with a group of tubercles in Peyer's patches forming a small nodule and minimal ulceration of the covering mucosa, tuberculous lymphangitis, and tuberculous lymphadenitis (Tabes Mesenterica).
• Fate and Complications: With good body resistance, the disease localizes. With low body resistance, the disease spreads. Direct spread leads to TB peritonitis, while lymphatic spread leads to TB lymphadenitis. Other complications include hemorrhage, fissures, fistulae, fibrosis with strictures, secondary amyloidosis, and malabsorption.

Secondary Intestinal Tuberculosis

• Mode of infection: Ingestion of infected sputum from patients with pulmonary TB.
• Pathology: Lesions typically occur in the terminal ileum and caecum, with bacilli reaching Peyer's patches and solitary follicles, leading to caseous necrosis and erosion of the covering mucosa. Multiple tuberculous ulcers result, located in the terminal ileum, transversely (girdle), and undermined edges with a caseous floor. Mesenteric lymph nodes show minimal lesions.
• Fate and Complications: Spread can occur directly, leading to TB peritonitis, or lymphatically, leading to TB lymphadenitis. Other complications include hemorrhage, perforation, secondary amyloidosis, dysplasia/adenocarcinoma, and liver damage (associated with primary sclerosing cholangitis).

Intestinal Polyps and Tumors

• Non Neoplastic Polyps: Bilharzial polyps, pseudopolyps (in ulcerative colitis), hyperplastic polyps, and hamartomatous polyps (including juvenile polyps and Peutz-Jeghers polyps).
• Neoplastic Polyps (Adenomas): Tubular adenoma (pedunculated, small), villous adenoma (sessile, large), tubulo-villous adenoma (combined). Adenomas are very common, their incidence increases with age, and they are considered precursors to colorectal cancers. The risk of malignancy is correlated to the size of the adenoma and the degree of dysplasia.
• Familial Adenomatous Polyposis (FAP): Autosomal dominant hereditary disease characterized by numerous colorectal adenomas during teenage years, caused by mutations in the APC gene. Diagnosis requires at least 100 polyps. Colorectal carcinoma develops in 100% of patients before age 30. Prophylactic colectomy is standard therapy for patients carrying APC mutations.