UGIB can be defined as bleeding from any site along the gastrointestinal tract (GIT) that is above the

ligament of treitz

etiology

Peptic ulcer

In most people H. pylori causes antral gastritis associated with depletion of somatostatin (from D cells) and increased gastrin release from G cells. Most duodenal ulcer patients have exaggerated acid secretion in response to stimulation by gastrin, and H. pylori exacerbates this by stimulating gastrin production.

 Traditional NSAIDs reduce the integrity of the duodenal mucosa but are probably responsible for only a small proportion of duodenal ulcers. They greatly increase the risk of bleeding or perforation from preexisting gastric and duodenal ulcers.

Gastric erosions
Unlike ulcers, erosion shows no evidence of fibrosis. Erosions do not penetrate the muscularis mucosae. Alcoholic beverages with low ethanol content (beer and wine) are strong stimulants of gastric acid secretion and gastrin release (S. Chari et al, 1993)

Varices
extremely dilated sub-mucosal veins in the lower third of the esophagus and usually due to portal hypertension Cirrhosis - cirrhosis can cause them to become irregular and tortuous with accompanying increased resistance to flow Portal vein thrombosis

oesophagitis

GERD and Barretts oesophagus Alcohol Cigarette smoking infection

Mallory-Weiss Syndrome
Vomitting Bulimia Trauma Severe hiccups Severe coughing Gastritis Hiatus hernia

vascular lesions

hereditary haemorrhagic telengectasias(OslerWeber-Rendu) gastric antral vascular ectasia (Water- melon stomach)

neoplasms
Squamous cell ca of the oesophagus Adenocarcinoma of oesophagus Gastric adenocarcinoma

 Uncommon causes; they include

Erosive duodenitis, aortoenteric fistulas, Dieulafoys lesion (in which an aberrant vessel in the mucosa bleeds from a pinpoint mucosal defect), prolapse gastropathy, haemobilia hemosuccus pancreaticus