Gastrointestinal bleeding is classified as upper (proximal to the ligament of Treitz at the duodenojejunal junction) or lower, with differing etiologies, hemodynamic consequences, and management. Upper GI bleeding from peptic ulcer disease occurs when mucosal defense mechanisms (mucus-bicarbonate barrier, prostaglandin-mediated mucosal blood flow, epithelial cell renewal) are overwhelmed by aggressive factors -- Helicobacter pylori infection (present in 60-80% of peptic ulcers) disrupts the mucus layer through urease-mediated ammonia production and vacuolating cytotoxin (VacA), while NSAIDs inhibit cyclooxygenase-1 (COX-1), reducing protective prostaglandin E2 synthesis and impairing mucosal blood flow. When ulceration erodes into submucosal arteries, brisk hemorrhage produces hematemesis (bright red or coffee-ground emesis depending on contact time with gastric acid converting hemoglobin to acid hematin) and melena (black, tarry stool from degradation of hemoglobin by intestinal bacteria). Variceal bleeding from portal hypertension (portal pressure gradient exceeding 12 mmHg) causes massive hemorrhage when thin-walled submucosal veins in the esophagus or gastric fundus rupture under high transmural pressure, with mortality rates of 15-20% per episode. Lower GI bleeding originates distal to the ligament of Treitz, most commonly from diverticulosis (arterial bleeding from...