Clinical meaning
GI bleeding pathophysiology differs fundamentally by anatomical location relative to the ligament of Treitz. Upper GI bleeding (UGIB) originates proximal to this landmark and most commonly results from peptic ulcer disease, where acid-pepsin erosion through the muscularis mucosae damages submucosal arteries — posterior duodenal ulcers erode into the gastroduodenal artery, while lesser curvature gastric ulcers may erode into the left gastric artery, both capable of producing massive arterial hemorrhage. Variceal bleeding occurs when portal hypertension (hepatic venous pressure gradient >12 mmHg) forces blood through portosystemic collaterals, particularly the submucosal veins of the distal esophagus, which dilate under high pressure with thin walls susceptible to rupture. Lower GI bleeding (LGIB) most commonly results from diverticular bleeding, where the vasa recta (arterial branches in the colonic wall) are mechanically eroded by diverticula, producing painless, brisk hematochezia that typically self-resolves but can be massive. Hemorrhagic shock follows a predictable physiological cascade: initial compensatory sympathetic activation produces tachycardia (earliest sign) and peripheral vasoconstriction (cool, clammy skin) before hypotension manifests at approximately 30% blood volume loss (Class III shock). The BUN-to-creatinine ratio >20:1 is a...