* Peptic Ulcer is a break in the gastric or duodenal mucosa that arises when the normal mucosal defensive factors are impaired or are overwhelmed by aggressive luminal factors such as acid and pepsin. * Ulcers extend through the musvularis mucosae and are usually over 5 mm in diameter. * In the United States, there are about 500,000 new cases per year of peptic ulcer and 4 million ulcer recurrences; the lifetime prevalence of ulcers in the adult population is approximately 10%. * Ulcers occur five times more commonly in the duodenum, where over 95% are in the bulb or pyloric channel. In the stomach, benign ulcers are located most commonly in the antrum (60%) and at the junction of the antrum and body on the lesser curvature (25%). * Ulcers occur slightly more commonly in men than in women. Although ulcers can occur in any age group, duodenal ulcers most commonly occur in patients between the ages of 30 and 55 years, whereas gastric ulcers are more common in smokers and in patients taking NSAIDs on a chronic basis. * Alcohol, dietary factors, and stress do not appear to cause ulcer disease. * The incidence of duodenal ulcer disease has been declining dramatically for the last 30 years, but the incidence of gastric ulcers appears to be increasing as a result of the widespread use of NSAIDs and low-dose aspirin. Reason for the Development/ Occcurence of the Disease
Three major causes of peptic ulcer disease are now reorganized: NSAIDs, chronic H pylori infection, and acid hypersecretory staes such as Zollinger-Ellison syndrome. Evidence of H pylori infection or NSAID ingestion should be sought in all patients with peptic ulcer. Uncommon causes of ulcer disease include CMV (especially in transplant recipients), systemic mastocytosis, Crohn’s disease, lymphoma, and medications (eg, alendronate). Up to 10% of ulcers are idiophatic. A. H pylori-Associated Ulcers
* H pylori appears to be a necessary cofactor for the majority of duodenal and gastric ulcers not associated with NSAIDs. It is estimated that one in six infected patients will develop ulcer disease. * The prevalence of H pylori infection in duodenal ulcer patients have infection predominantly in the gastric antrum, which is associated with increased gastric acid secretion and decreased duodenal mucosal bicarbonate secretion. * It is hypothesized that increased acid exposure can give rise to small islands of gastric metaplasia in the doudenal bulb. * Colonization of these islands by H pylori may lead to duodenitis or duodenal ulcer. The association with gastric ulcer is lower, but H pylori is found in the majority of patients in whom NSAIDs cannot be implicated. H pylori-associated gastric ulcers tend to form at the junction of the gastricbody and antrum--the site of transition from oxyntuc to pyloric epithelium. * Most H pylori-infected gastric ulcer patients have infection that predominates in the gastric body and is associated with decreased acid secretion. * It is hypothesized that chronic inflammation overwhelms the gastric mucosal defense mechanisms.
B. NSAID-induced Ulcers
* There is a 10-20% prevalence of gastric ulcers and a 2-5% prevalence of duodenal ulcers in long-term NSAID users. * The relative risk of gastric ulcers is increased 40-fold, but the risk of duodenal ulcers is only slightly increased. Users of NSAIDs are at least three times more likely than nonusers to suffer serious gastrointestinal complications from these ulcers such as bleeding, perforation, or death. It is noteworthy that gastric ulcers and duodenal ulcers cause about the same number of complications. * Approximately 1-2% of long-term NSAID users will have a major complication within 1 year. The risk of NSAID complications is greater within the first 3 months of therapy and in patients who are older, patients who take higher doses of NSAIDs, as well as patients with a prior history of...