Anatomy of stomach and duodenum.

Physiology of gastric secretion.

Pathophysiology of acute and chronic
ulcer
Anatomy of stomach
 Hollow, muscular organ
 The stomach is an intraperitoneal organ.
 First intra-abdominal part of the gastrointestinal tract,
situated between the esophagus (proximally) and the
duodenum (distally)
 Divided into the cardia, gastric fundus, body (stomach),
and pylorus
 Curvatures of the stomach lesser and greater
Anatomy of duodenum
 First and widest part of the small intestine
 C-shaped: surrounds the head of the pancreas
 Located mainly within the epigastric and umbilical
regions of the abdomen
 Divided into the 4 parts.
Only the 1st part of the duodenum is intraperitoneal. The
2nd–4th parts are retroperitoneal.
 Physiology of gastric secretion
The gastric mucosa is composed of numerous gastric glands that lie within the lamina
propria.
 Parietal cells (located in the middle of the glands)
Secrete hydrochloric acid (HCl) and intrinsic factor
Stimulated by acetylcholine, histamine, and gastrin
Inhibited by prostaglandins and somatostatin
 Mucosal cells (located at the neck of the gastric glands)
Secrete protective mucus
Stimulated by acetylcholine, prostaglandins (which inhibit HCl secretion), and secretin
 Chief cells (located at the base of the glands)
Secrete pepsinogen
Stimulated by acetylcholine, gastrin, secretin, and vasoactive intestinal polypeptide (VIP)
Pathophysiology of acute and chronic
ulcer
H. pylori
Gastric ulcers
 H. pylori secretes urease → conversion of urea to amonia → alkalinization of acidic environment → survival
of bacteria in gastric lumen
 Bacterial colonization and attachment to epithelial cells → release of cytotoxins (e.g., cagA toxin) →
disruption of the mucosal barrier and damage to underlying cells
Duodenal ulcers
 H. pylori inhibits somatostatin secretion → ↑ gastrin secretion → ↑ H+ secretion → excess H+ delivery to
the duodenum
 Direct spread of H. pylori to the duodenum → inhibition of duodenal HCO3- secretion→ acidification and
insufficient neutralization of duodenal contents
Pathophysiology of acute and chronic
ulcer
NSAIDs
 Inhibit COX-1 and COX-2 → decrease in prostaglandin production → erosion of the gastric mucosa
 Decrease mucosal blood flow
 Inhibit mucosal cell proliferation

Acid hypersecretion: (e.g., Zollinger-Ellison syndrome)

increased gastrin production → ↑ H+ secretion and parietal cell mass → delivery of excessive acid to the
duodenum