Primary Causes & Pathophysiology
Mucosal breach (lining break) exposes vessels to acid and shear so clots fail. Ulcers and erosions (shallow lining sores) erode into submucosal arteries (deeper wall vessels). Portal hypertension (high liver-vein pressure) dilates varices (swollen veins) that rupture under strain. Diverticula (wall pouches) and angiodysplasia (fragile surface vessels) bleed from thin walls. Tumours and inflammation (immune gut injury) create friable (easily torn) tissue. Volume loss then cuts perfusion (organ blood flow) and drives shock.
Acid and Helicobacter pylori (stomach germ) erode mucosa (lining) into arteries causing brisk upper loss
High liver-vein pressure dilates collateral veins (bypass vessels) that rupture with massive vomiting of blood
NSAIDs, alcohol and reflux injure surface lining so diffuse oozing and melena (black stools) occur
Forceful vomiting shears mucosa (lining tear) causing arterial ooze after retching
Vasa recta (pouch wall vessels) stretch over domes and rupture into lumen (bowel channel) causing painless red loss
Degenerative dilated capillaries (tiny fragile vessels) leak or burst, often in older adults
Tumour neovessels (new fragile vessels) and ulcerated mass bleed chronically or acutely
Immune ulcers and friable mucosa (easily torn lining) ooze blood with diarrhoea and urgency