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Figure 9-1 Gastric anatomy.

stomach is glandular and there are three distinct histologic zones.2 The region of the cardia is a small area around the entrance of the esophagus where there is a preponderance of mucous-secreting glands. The fundus and body contain the bulk of gastric glands which synthesize and secrete gastric juice. Gastric juice is a watery secretion containing hydrochloric acid and pepsin. Pepsin is a digestive enzyme which hydrolyses protein into polypeptide fragments. The glands of the fundus and body contain three populations of cells. Mucous neck cells secrete mucous to protect the gastric mucosa from autodigestion by acid and pepsin. Parietal cells secrete hydrochloric acid and intrinsic factor which binds vitamin B12 facilitating its absorption in the ileum, and pepsin-secreting chief cells. Finally, the glands of the pyloric region secrete mucous and associated endocrine cells, G cells, and the hormone gastrin.

Parietal cells have receptors for acetylcholine, gastrin, and histamine. As a result, gastric secretion is regulated by acetylcholine, gastrin, and his-tamine which bind their receptor leading to stimulation of acid secretion. Stimulation of gastric secretion has been divided into three separate phases: the cephalic phase, gastric phase, and intestinal phase.3 The cephalic phase originates with sight, smell, thought, and taste of food and is initiated in the cerebral cortex. The afferent impulse is delivered through the vagal nerve fibers innervating the stomach. The vagus acts directly on the parietal cells through acetylcholine and indirectly through the release of gastrin-releasing peptide to stimulate gastrin release. The gastric phase originates with food entering the stomach and subsequently stimulating the release of acetyl-choline from vagal and local nerves, gastrin from G cells, and histamine from enterochromaffin-like cells. Finally, the intestinal phase of gastric secretion is stimulated by food entering the duodenum and contributes only a small portion of the stimulation to gastric secretion. Paradoxically, the intestinal phase of gastric secretion is predominantly an inhibitory signal which inhibits ongoing gastric secretion. During this phase, several intestinal hormones (e.g., secretin, cholecystokinin [CCK], somatostatin, and gastric inhibitory peptide [GIP]) are released which serve to inhibit gastric secretion.

Symptoms of burning or pain in the upper abdomen, usually occurring about an hour or so after meals or even during the night, are classic in patients with gastric ulcers. These symptoms are relieved temporarily by antacids, milk, or medications that reduce stomach acid production. Gastric ulcers4,5 are classified by location (Fig. 9-2) and whether acid hypersecretion is involved in their pathogenesis (Table 9-1). Type I ulcers are the most common representing approximately 60 percent of all ulcers. Type I ulcers are commonly found along the lesser curvature, where the lesser curvature acutely angles to the right marking the end of the body and the beginning of the antrum, near the incisura angularis. Ulcers that arise coincident with duodenal ulcers and are associated with high acid production are classified as type II ulcers and represent about 20 percent of ulcers. Ulcers in the prepyloric and pyloric region are classified as type III gastric ulcers and constitute about 20 percent of all ulcers, and because of their common association with

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