Small Intestine Anatomy & Physiology

Background/orientation content from a textbook reference chapter (Sabiston Ch50 - Small Bowel Anatomy, Physiology, Obstruction & Crohn Disease), not critically-appraised primary literature. Filed as foundational reference for the small-bowel disease and procedure pages that build on it.

Embryology

The small intestine derives from the embryonic midgut, which also gives rise to the cecum, appendix, ascending colon, and proximal two-thirds of the transverse colon. The duodenum has a dual origin — distal foregut and proximal midgut — which explains its dual (celiac + superior mesenteric) blood supply. The midgut undergoes physiologic herniation into the umbilical cord, 270° of counterclockwise rotation, and retraction back into the abdominal cavity during weeks 6–10 of gestation; errors in this process produce malrotation and related anomalies.

Gross anatomy

The small intestine spans roughly 3–6 m in the adult and is divided into duodenum, jejunum, and ileum:

• Duodenum — retroperitoneal (except the first ~2 cm), C-shaped around the pancreatic head, four parts (superior/descending/horizontal/ascending); receives the common bile duct and pancreatic duct at the ampulla of Vater.
• Jejunum — begins at the ligament of Treitz; thicker wall, larger/taller circular folds (plicae circulares), larger caliber, and a less complex mesenteric vascular arcade (longer vasa recta) than ileum.
• Ileum — thinner wall, shorter/fewer plicae circulares, smaller caliber, more complex mesenteric arcades (shorter vasa recta), and contains Peyer patches concentrated in the antimesenteric wall of the distal ileum. No sharp anatomic boundary separates jejunum from ileum — the distinction is gradual.

Neurovascular and lymphatic supply

• Arterial: superior mesenteric artery (SMA) supplies the entire jejunoileum via a series of arcades and vasa recta; the duodenum additionally receives supply from the celiac axis (superior pancreaticoduodenal artery) as well as the SMA (inferior pancreaticoduodenal artery).
• Venous: parallels the arterial supply, draining to the superior mesenteric vein, which joins the splenic vein to form the portal vein.
• Lymphatic: lacteals within intestinal villi drain to mesenteric lymph nodes along the vascular arcades, then centrally toward the cisterna chyli and thoracic duct; lymphatic drainage is also the route for absorbed long-chain fat (as chylomicrons).
• Innervation: dual autonomic supply — sympathetic (via splanchnic nerves/celiac and superior mesenteric ganglia, generally inhibitory to motility) and parasympathetic (via the vagus, generally stimulatory), plus an intrinsic enteric nervous system (myenteric/Auerbach’s plexus between the muscle layers, submucosal/Meissner’s plexus) capable of independent reflex activity.

Microscopic anatomy

Four wall layers, as elsewhere in the GI tract: mucosa (epithelium + lamina propria + muscularis mucosae), submucosa, muscularis propria (inner circular, outer longitudinal), and serosa. The mucosa is thrown into villi (absorptive, project into the lumen) and crypts of Lieberkühn (secretory/regenerative, at the villus base); this architecture massively amplifies absorptive surface area. Epithelial cell types include absorptive enterocytes, mucus-secreting goblet cells, hormone-secreting enteroendocrine cells, antimicrobial-peptide-secreting Paneth cells (concentrated at the crypt base), and stem cells that continuously repopulate the epithelium (turnover roughly every 3–5 days).

Digestion and absorption

• Carbohydrates: salivary and pancreatic amylase break starches down to oligosaccharides/ disaccharides; brush-border enzymes (lactase, sucrase-isomaltase, maltase-glucoamylase) complete digestion to monosaccharides, which are absorbed via SGLT1 (glucose/galactose, sodium-coupled) and GLUT5 (fructose, facilitated diffusion).
• Protein: gastric pepsin begins digestion; pancreatic proteases (trypsin, chymotrypsin, carboxypeptidases — secreted as zymogens and activated by enterokinase at the brush border) and brush-border peptidases complete it to amino acids and small peptides, absorbed via multiple sodium-coupled amino acid transporters and peptide transporters (e.g., PepT1).
• Fat: pancreatic lipase (aided by colipase) and bile salts (which emulsify fat and form micelles) digest triglycerides to monoglycerides and free fatty acids; these diffuse into enterocytes, are re-esterified to triglycerides, packaged with apolipoproteins into chylomicrons, and exit via the lymphatics (lacteals) rather than the portal vein — unlike carbohydrate and protein absorption products, which go directly to the portal circulation.
• Water and electrolytes: the small intestine absorbs several liters of fluid daily (dietary intake plus salivary/gastric/biliary/pancreatic/intestinal secretions), following osmotic gradients generated by solute (especially sodium-coupled nutrient) absorption; sodium absorption occurs via multiple coupled mechanisms (with glucose/amino acids, sodium-hydrogen exchange, sodium-chloride cotransport).
• Vitamins: fat-soluble vitamins (A, D, E, K) follow the fat-absorption/micelle pathway; most water-soluble vitamins are absorbed by specific carrier-mediated mechanisms throughout the small bowel; vitamin B12 is the exception, requiring intrinsic factor (from gastric parietal cells) and absorption specifically in the terminal ileum — the anatomic basis for B12 deficiency after terminal ileal resection or in terminal ileal Crohn disease.

Motility

Small bowel motility is organized into fasting and fed patterns. In the fasting state, the migrating motor complex (MMC) is the dominant pattern — a cyclical wave of activity (phases I–III, with phase III being an intense burst of peristalsis) that sweeps from stomach to terminal ileum roughly every 90–120 minutes, functioning as an interdigestive “housekeeper” that clears residual luminal debris and limits bacterial overgrowth. Feeding disrupts the MMC and produces a fed pattern of irregular, segmenting contractions that mix and slowly propel chyme.

Endocrine function

The small intestine is the body’s largest endocrine organ by cell number, with enteroendocrine cells distributed throughout the mucosa secreting hormones that regulate digestion, motility, and appetite — including secretin (stimulates pancreatic bicarbonate secretion, released in response to duodenal acid), cholecystokinin (CCK) (stimulates gallbladder contraction and pancreatic enzyme secretion, released in response to luminal fat/protein), motilin (triggers the MMC phase III), gastric inhibitory peptide/glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) (incretins, augment insulin release), and others. These hormones act via specific G-protein-coupled receptors on target tissues.

Immune function

The small intestine hosts the majority of the body’s gut-associated lymphoid tissue (GALT), concentrated in Peyer patches (aggregated lymphoid follicles, most dense in the distal ileum), which sample luminal antigen via specialized M cells overlying the follicle. This drives differentiation of B cells into plasma cells producing secretory IgA, which is transported across the epithelium into the lumen and provides the dominant humoral defense against enteric pathogens without triggering a full inflammatory response — a mechanism of “tolerance” toward the normal luminal microbiota and dietary antigens that, when dysregulated, is implicated in the pathogenesis of inflammatory bowel disease (see Crohn Disease, Inflammatory Bowel Disease).

Open items / gaps

• No detail yet in the wiki on malrotation/volvulus as a distinct congenital entity — this chunk covers only normal embryology.
• MMC/motility disorders (e.g., chronic intestinal pseudo-obstruction of the small bowel) not yet covered as their own topic.