Peptic Ulcer

Peptic ulcer disease results from an imbalance between aggressive factors (hydrochloric acid, pepsin, H. pylori virulence factors, NSAIDs) and protective mechanisms (mucus-bicarbonate barrier, prostaglandin-mediated mucosal blood flow, epithelial cell renewal). H. pylori colonizes the gastric antrum, produces urease to create an alkaline microenvironment, and releases virulence factors (CagA, VacA) that disrupt tight junctions, induce epithelial apoptosis, and trigger chronic inflammation. NSAIDs inhibit COX-1, reducing prostaglandin E2 and I2 synthesis, which decreases mucosal blood flow, bicarbonate secretion, and epithelial cell proliferation. Duodenal ulcers result from H. pylori-induced antral gastritis causing excessive gastrin release and acid hypersecretion, while gastric ulcers involve direct mucosal injury with normal or reduced acid output.