About Peptic Disorder Posted on 28/2/2008
Peptic disorder is also known as stomach disease. Most commonly seen disease includes peptic ulcer, gastritis and gastroperesis.
Peptic ulcer is a non-malignant ulcer of the stomach (called gastric ulcer) or duodenum (called duodenal ulcer). Peptic ulcers occur only in those areas of the digestive system that come in contact with digestive juices secreted by the stomach. Gastrointestinal bleeding is one of the most serious complications of ulcers.
Encyclopedia
SPECIFIC ACID – PEPTIC DISORDERS AND THERAPEUTIC STRATEGIES
Peptic Ulcer Disease
The pathophysiology of peptic ulcer disease is best viewed as an imbalance between mucosal defense factors (bicarbonate, mucin, prostaglandin, nitric oxide, and other peptides and growth factors) and injurious factors (acid and pepsin). H.pylori and exogenous agent such as nonsteroidal anti-inflammatory drugs (NSAIDs) interact in complex ways to cause an ulcer. Up to 60% of peptic ulcers are associated with H.pylori infection of the stomach. This infection may lead to impaired production of somatostatin by D cells of the pancreas, and in time, decreased inhibition of gastrin production, resulting in increased acid production and reduced duodenal bicarbonate production.
H.pylori has been associated with gastritis and the subsequent development of gastric and duodenal ulcers, gastric adenocarcinoma, and gastric B- cell lymphoma. Because of the critical role of H.pylori in the pathogenesis of peptic ulcers, to eradicate this infection is standard care in patients with gastric and duodenal ulcers. Provided that patients are not taking NSAIDs, this strategy almost completely eliminates the risk of ulcer recurrence. NSAIDs also are very frequently associated with peptic ulcers (in up to 60% of patients, particularly those with complications such as bleeding). The effects of these drugs are mediated systemically; the critical element is suppression of the constitutive form of cyclooxygenase-1 (COX-1) in the mucosa and decreased production of cytoprotective prostaglandins PGE2 and PGI2. More »