A Review on Overview of Peptic Ulcer

A Review on Overview of Peptic Ulcer

Author Name : Dr. Akanksha Jagwani, Assistant Prof. Anjali Chourasiya, Dr. Pradeep Pal, Sakshi Aole, Assistant Prof. Safiya Bee, Dr. Ajay Sharma

INTRODUCTION

Peptic ulcer embraces both gastric and duodenal ulcers and has been a major threat to the world's population over the past two centuries, with a high morbidity and substantial mortality. Discovery of gastric mucosa infection with Helicobacter pylori (H. pylori) and its association with chronic antral gastritis and peptic ulcer revolutionized the treatment of ulcer illness. H. pylori are causally related to a majority of cases of both duodenal and gastric ulcer, in the west and developing countries. Despite extensive scientific advancements, this disease remains an important clinical setback, largely because of H. pylori infection and widespread use of non-steroidal anti-inflammatory drugs (NSAIDS). Management of peptic ulcer disease generally involves the practice of H2 receptor antagonists, use of proton pump inhibitors, antacids and different H. pylori eradication regimens. Peptic ulcer disease is a group of disorders characterized by the presence of ulcers in any portion of gastrointestinal tract (GIT) exposed to acid in sufficient concentration and duration. Although these ulcerations most commonly occur in the stomach (gastric ulcer), or small intestine (duodenal ulcer), this disease  also includes Barrett ulcer of the esophagus (Barrett's esophagus or Barrett's metaplasia) and other upper GI ulcers (Ainsworth et al., 1994). An ulcer is a crater like lesion in a membrane; ulcers that develop in areas of the GIT exposed to acidic gastric juice are called peptic ulcers (Ansel et al., 2000). Word 'peptic derives from the Greek term 'peptikos,' meaning related to digestion. Peptic ulcer is due to exposure of stomach  and duodenum to pepsin and gastric acid. Imbalance occurs between aggressive factors like acid, pepsin, H. pylori and defensive factors such as gastric mucus, bicarbonate ions, and prostaglandins along with innate resistance of mucosal cells (Allen et al., 1988). Gastro-duodenal mucosa utilizes several defence mechanisms against the aggressive factors such as hydrochloric acid and pepsin. Danish physiologist Schierbeck in 1892 reported that food ingestion caused an increase in canine gastric CO2. However, few years later, Pavlov investigated about the protective role of gastric alkaline mucus. It is well established that gastric and duodenal epithelial cells in mammals actively secrete bicarbonate into the lumen (Chawla et al., 2003). This secretion interacting with the surface mucus gel layer comprises first line of mucosal defence. Proximal duodenal mucosal bicarbonate secretion capacity in man is about five times the gastric bicarbonate secretion (Erni et al., 1987). Mucus is secreted by mucus secreting cells that are available abundantly in the neck region of gastric glands. Mucin forms a protective layer on the gastric epithelium. It retains bicarbonate and has alkaline pH. Thus, it protects the stomach from acid peptic digestion, as it buffers hydrochloric acid. Mucus secretion is also stimulated by increased blood flow to the stomach. Activation of prostaglandin receptors also inhibits gastric acid secretion. Mucosal prostaglandins are known to afford cyto protection by various mechanisms. Natural aggressors secreted into the gastric lumen are acid and pepsin. Various studies reveal that the Gastro duodenal mucosal barrier is damaged by pepsin under conditions in which it is resistant to acid alone. Pepsin has mucolytic activity and progressively digests the adherent mucus layer at its luminal surface (Hiesse et al., 1985).