Ulcers, Peptic (Gastric, Duodenal)

Peptic ulcer– A circumscribed excavation of the gastric or duodenal mucosal wall that penetrates the muscularis mucosae and exposes it to acid and pepsin.

Causes and Incidence

The precise etiologic mechanisms of peptic ulcer formation are unclear. However, recent research points to infection by Helicobacter pylori bacteria as the major factor in ulcer formation. Other factors that have been implicated include use of certain drugs (e.g., aspirin and other nonsteroidal antiinflammatory agents ([NSAIDs]); use of alcohol, cigarettes, and caffeine; and a familial history of ulcers. Those at risk of a duodenal ulcer have increased acid production and type O blood. Risk factors for a gastric ulcer include type A blood and underlying disease processes such as pancreatitis, gastritis, and hepatic disorders. About 80%of all peptic ulcers are duodenal in origin, and the remain-ing 20% are gastric. Gastric ulcers strike men and women equally, with the peak incidence occurring between ages 55 and 65. There are 40,000 to 80,000 cases reported annually in the United States. Duodenal ulcers occur in men two to three times as often as in women, and the incidence increases with age. The annual incidence is 200,000 to 300,000, but it has been steadily decreasing since the 1950s.

Disease Process

The pathology is unclear, but it is hypothesized that H. pylori or other factors may upset the balance between ulcer-promoting factors, such as secretion of acid and pepsin and factors that serve as protectors of the mucosal lining, such as mucus production and replacement of damaged mucosal cells. This sets up an inflammatory process, with resultant ulceration, thrombosis, fibrosis, and scarring of the muscularis mucosae layer of the stomach or duodenum.

Symptoms

Manifestations vary with location, and ulcers are often asymptomatic or associated with vague symptoms. Only about 50% of individuals have a characteristic pattern of symptoms. The characteristic pain is described as burning, gnawing, or aching and is located in a well-circumscribed epigastric area. In duodenal ulcers the pain usually appears midmorning, is relieved by food, and then reappears 2 to 3 hours after eating. It also wakens the individual 2 to 3 hours after falling asleep. It occurs daily for 1 week or longer and may then disappear without treatment. With a gastric ulcer the pain usually occurs after eating food, is located in the left midgastric area, and often radiates to the back. Epigastric pain occurs with an empty stomach. Pain in both instances is typically relieved by antacids or milk.

Potential Complications

Complications include hemorrhage and perforation of the stomach or duodenum, with resulting peritonitis and obstruction of the pylorus or gastric outlet.

Diagnostic Tests

Endoscopy/biopsy
To establish presence of ulcer and determine whether malignancy is present

Upper gastrointestinal series
May reveal ulcers overlooked on endoscopy

Gastric analysis
Increased output with duodenal ulcer; decreased or normal output with gastric ulcer

Carbon 13 urea breath test
Low levels of 13C in exhaled breath indicative of H. pylori infection

Treatments

Surgery
Gastrectomy, gastroduodenostomy, gastrojejunostomy to remove gastrin-producing portion of stomach in intractable cases with complications; fundic vagotomy with chronic duodenal ulcer disease.

Drugs
Histamine receptor antagonists to block gastric acid output; antacids to reduce pain; cytoprotectives (Sucralfate) to form a protective coating in the base of the ulcer; bismuth preparations in combination with antiinfective drugs for H. pylori (not yet approved in the United States); omeprazole is a proton pump inhibitor in clinical trials in the United States; prostaglandins are in clinical trials for treatment associated with NSAID use.

General
Avoidance of alcohol and tobacco products; avoidance of pepper, coffee (caffeinated and decaffeinated), and foods that cause epigastric distress; avoidance of NSAIDs.