Peptic ulcer disease (PUD) results from an imbalance between mucosal aggressive factors (gastric acid, pepsin, H. pylori, NSAIDs) and mucosal defensive factors (mucus-bicarbonate barrier, prostaglandin-mediated mucosal blood flow, epithelial cell turnover). H. pylori, a gram-negative spiral bacterium, colonizes the gastric antral mucosa beneath the mucus layer, producing urease that converts urea to ammonia (alkalinizing its microenvironment for survival) and virulence factors (CagA, VacA) that damage epithelial cells, stimulate inflammatory cytokines, and disrupt the mucus-bicarbonate barrier. H. pylori infection causes 60-70% of gastric ulcers and 70-90% of duodenal ulcers. NSAIDs cause ulcers through dual mechanisms: systemic COX-1 inhibition reduces prostaglandin synthesis (decreasing mucosal blood flow, bicarbonate and mucus secretion), and topical acidic damage to the gastric epithelium. Duodenal ulcers result from H. pylori-driven gastric acid hypersecretion (antral predominant gastritis increases gastrin release), while gastric ulcers result from impaired mucosal defense with normal or low acid secretion. Zollinger-Ellison syndrome (gastrinoma) causes severe PUD through massive acid hypersecretion from a gastrin-secreting tumor. Complications include hemorrhage (most common), perforation (surgical emergency with pneumoperitoneum on upright CXR), gastric outlet obstruction, and penetration into adjacent organs...