A Detailed Review on: Recent Advances, Pathophysiological Studies and Mechanism of Peptic Ulcer

Abstract

A peptic ulcer is a chronic disease in which involve the complication of the gastrointestinal tract by identifying the mucosal damage secondary to gastric acid secretion and pepsin. It generally occurs the proximal duodenum and stomach and less occur in the distal duodenum, lower esophagus, jejunum, and ectopic gastric mucosa. The pathogenesis of peptic ulcer the binding to H2 receptor in paracrine fashion in parietal cells was activates by the release of histamine from HCL. In antral G cells primarily occur gastrin. The activation of central neural, chemical composition and local distension of gastric content having a gastrin release by their regulation. The influence of gastrin and vegal stimulation the histamine release from a mast cell and paracrine-ECL cells. Expend the level of intracellular Ca2+ through cyclic AMP, Ach/gastrin via histamine that causes acid secretion. H+/K+ ATPase stimulates the last step in acid secretion. which is also termed as a gastric proton pump. cAMP or Ca2+ ion-dependent pathways activation or H+/K+ ATPase activation from parietal cells the pathophysiology of peptic ulcer. ulcer disease are a disproportion between pepsin and acid and mucosa digestion inactivity of digestive. The three viable etiology group of peptic ulcer. 1) In Zollinger-Ellison Syndrome was occur the enormous hypersecreation of acid peptic. 2) by occurring nonsteroidal anti-inflammatory drugs (NSAIDs). 3) By the helicobacter pylori infections associate the ulcer. Modern technique which is used in treatment of peptic ulcer is Antacids, Pyroloplasty and SPV, Histamine H2 receptors, Pirenzepin, Proton pump inhibitors, H. Pylori infection more recent advancement are needed for peptic ulcer.