Small intestine

The small intestine achieves its enormous absorptive surface area of approximately 32 square meters—about the size of a studio apartment—through three levels of structural amplification: circular folds (plicae circulares) are large permanent folds of mucosa and submucosa visible to the naked eye; villi are finger-like projections of mucosa that increase surface area about 10-fold; and microvilli cover each enterocyte, forming the brush border that increases surface area a further 20-fold.

The small intestine is divided into the duodenum, jejunum, and ileum. The duodenum (approximately 25 cm) receives chyme from the stomach along with pancreatic enzymes and bile, and is where most chemical digestion begins. The jejunum (~2.5 m) is the primary site of nutrient absorption. The ileum (~3.5 m) absorbs vitamin B12 (bound to intrinsic factor), bile salts, and any remaining nutrients, and contains Peyer's patches for immune surveillance.

Celiac disease is an immune-mediated condition in which ingestion of gluten—a protein in wheat, barley, and rye—triggers an autoimmune response that damages the intestinal villi of the small intestine. Villous atrophy reduces the absorptive surface area dramatically, causing malabsorption of fat, carbohydrates, proteins, and micronutrients. Symptoms include diarrhea, bloating, weight loss, and nutritional deficiencies. Treatment is strict lifelong gluten avoidance.

Duodenal ulcers are more common because the duodenum is exposed to highly acidic gastric chyme and is less protected than the stomach. The duodenal mucosa relies on bicarbonate secretion from Brunner's glands and pancreatic secretions to neutralize acid. Helicobacter pylori infection—the leading cause of peptic ulcer disease—is particularly prevalent in the duodenal bulb, where it disrupts the mucosal defense mechanisms.

Crohn's disease is a chronic inflammatory bowel disease that can affect any part of the gastrointestinal tract but most commonly involves the terminal ileum. Unlike ulcerative colitis, Crohn's disease causes transmural (full-thickness) inflammation, skip lesions (alternating areas of disease and normal bowel), and granuloma formation. Complications include strictures, fistulas, abscesses, and malabsorption—particularly of vitamin B12 and fat-soluble vitamins if the terminal ileum is severely affected.