GI Anatomy and Physiology · 5 min read
Stomach, Duodenum and Small Intestine
This chapter covers gastric regions and secretory cells, the four parts of the duodenum with the ampulla and sphincter of Oddi, and the absorptive specialization of the jejunum and ileum.
Gastric Regions
The stomach is divided into the cardia (just below the GE junction), the fundus (the dome above the GE junction, seen on retroflexion), the body (the largest portion, with prominent rugal folds along the greater curvature), the antrum (the smooth distal portion) and the pylorus, the muscular channel that regulates emptying into the duodenum. The angularis (incisura) on the lesser curvature is a common site of gastric ulcers.
During EGD, the endoscopist retroflexes the scope (bends the tip back on itself) in the stomach to inspect the cardia and fundus, where gastric varices, hernias and cardia cancers hide. Fluid naturally pools in the fundus when the patient lies left lateral, so suctioning the pool reduces aspiration risk and improves the view.
Gastric Cell Types and Secretions
| Cell | Location | Product and Function |
|---|---|---|
| Parietal cell | Fundus and body | Hydrochloric acid and intrinsic factor |
| Chief cell | Fundus and body | Pepsinogen, activated to pepsin by acid |
| G cell | Antrum | Gastrin, which stimulates acid secretion |
| D cell | Antrum and body | Somatostatin, which inhibits gastrin and acid |
| Mucous neck and surface cells | Throughout | Mucus and bicarbonate barrier |
| Enterochromaffin-like cell | Body | Histamine, which stimulates parietal cells |
Parietal cells secrete acid through the hydrogen-potassium ATPase (the proton pump), which is the target of proton pump inhibitors. Acid secretion is driven by three stimulants: acetylcholine (vagal), gastrin and histamine (acting on H2 receptors, the target of H2 blockers). Intrinsic factor from parietal cells is required for vitamin B12 absorption in the terminal ileum. Loss of parietal cells, as in autoimmune atrophic gastritis (pernicious anemia) or after total gastrectomy, therefore causes B12 deficiency with macrocytic anemia and neurologic symptoms such as paresthesias, ataxia and memory changes.
The mucus-bicarbonate layer and prostaglandin-driven mucosal blood flow protect the stomach from its own acid. NSAIDs block cyclooxygenase and reduce protective prostaglandins, which explains NSAID-induced ulcers. Long-term acid suppression is associated with enteric infections, including C. difficile.
Duodenum, Ampulla and Sphincter of Oddi
The duodenum is about 25 cm long and C-shaped around the head of the pancreas. It has four parts. The first part (the bulb) is the most common site of duodenal ulcers. The second (descending) part contains the major duodenal papilla, where the ampulla of Vater delivers bile and pancreatic juice; the minor papilla, for the accessory pancreatic duct, sits slightly proximal. The third (horizontal) part crosses the aorta and inferior vena cava beneath the superior mesenteric vessels. The fourth (ascending) part ends at the duodenojejunal flexure, suspended by the ligament of Treitz.
The ampulla of Vater is the common channel formed where the common bile duct and main pancreatic duct join. The sphincter of Oddi, a ring of smooth muscle around this terminal segment, controls flow of bile and pancreatic juice and prevents reflux of duodenal contents into the ducts. During ERCP, a side-viewing duodenoscope is positioned in the second part of the duodenum to see the papilla face on. Biliary sphincterotomy cuts the sphincter to allow stone extraction and stent placement.
The ligament of Treitz is the anatomic boundary between upper and lower GI bleeding. Bleeding proximal to it is upper GI bleeding; bleeding distal to it is lower or small bowel bleeding.
Jejunum and Ileum
The small intestine is about 6 meters long in adults. The jejunum (roughly the proximal two-fifths) has a thicker wall, prominent circular folds (plicae circulares) and the greatest surface area for absorption. The ileum (the distal three-fifths) has fewer folds and abundant lymphoid tissue in Peyer patches. Villi and microvilli (the brush border) multiply surface area enormously; brush-border enzymes such as lactase complete carbohydrate digestion.
Absorption is site-specific, and the exam frequently tests this.
| Site | Main Nutrients Absorbed | Clinical Link |
|---|---|---|
| Duodenum | Iron, calcium, folate begins | Celiac disease causes iron deficiency anemia |
| Jejunum | Most carbohydrates, proteins, fats, folate, water-soluble vitamins | Largest absorptive surface |
| Terminal ileum | Vitamin B12 with intrinsic factor, bile salts | Crohn ileitis or resection causes B12 deficiency and bile acid diarrhea |
Bile salts are reabsorbed in the terminal ileum and returned to the liver through the portal vein in the enterohepatic circulation. When the terminal ileum is diseased or resected, unabsorbed bile salts reach the colon and cause a secretory, watery diarrhea (bile acid diarrhea), often treated with a bile acid binder such as cholestyramine. Larger resections deplete the bile salt pool enough to cause fat malabsorption and steatorrhea, with loss of fat-soluble vitamins A, D, E and K.
The ileocecal valve separates the ileum from the cecum. It slows passage of ileal contents and limits backflow of colonic bacteria into the small bowel; loss of the valve after surgery increases risk of small intestinal bacterial overgrowth.
Key Takeaways
- Parietal cells make acid and intrinsic factor; chief cells make pepsinogen; antral G cells make gastrin; D cells make somatostatin.
- Acid secretion responds to acetylcholine, gastrin and histamine; PPIs block the proton pump, and H2 blockers block histamine action.
- The major papilla is in the second part of the duodenum; the ligament of Treitz divides upper from lower GI bleeding.
- Iron is absorbed mainly in the duodenum; vitamin B12 and bile salts in the terminal ileum.
- Terminal ileal disease or resection causes B12 deficiency and bile acid diarrhea; loss of the ileocecal valve predisposes to bacterial overgrowth.
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