A major causative factor (60% of gastric and 90% of duodenal<unk> s) is chronic inflammation due to Helicobacter pylori that colonize the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis known as type B gastritis. This results in a defect in gastrin production leading to increasedgastrin secretion. Gastrin stimulates the production of gastric acid by the parietal cells. The acid erodes the mucosa and causes the<unk> . Another major cause of<unk><unk>  disease is the chronic use of NSAIDs  The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins.
Peptic ulcer pathophysiology
Gastritis pathophysiology
Stomatitis pathophysiology
H.pylori gastritis pathophysiology
Dyspepsia pathophysiology
Diverticulosis pathophysiology
Carcinoid syndrome pathophysiology
Nausea and vomiting pathophysiology