The role of an aggressive factor in peptic ulcer disease (pud)

Abstract

The stomach is the expanded part of the digestive tract between the esophagus and the small intestine. It acts as a reservoir and has chief function in enzymatic digestion. Several types of glands provide different types of secretions in the alimentary tract most of which act as lubricant and to protect the stomach mucosa from excoriation.
The pathophysiology of peptic ulcer disease (PUD) is often described as an imbalance between aggressive factors and mucosal protective mechanisms. Helicobacter pylori, a gram-negative organism that has been identified as a potential causative agent in the pathogenesis of peptic ulcer disease, which is diagnosed by invasive or non-invasive
methods. Three classes of drugs have been shown to have a direct effect on Helicobacter pylori: antibiotics, bismuth salts, and proton pump inhibitors. Because Helicobacter pylori is difficult to eradicate, most treatment regimes combine agents from two or even all three of these cases. In all of them, patients with active peptic disease should
also receive a total of 6 weeks of acid suppression with an H2-receptor antagonist. The discovery of Helicobacter pylori as a gastrointestinal pathogen has had a profound effect on current concepts of the pathogenesis and treatment of peptic ulcer disease.

Key words: peptic ulcer disease, Helicobacter pylori, H2-receptor antagonist, pathophysiology