Peptic Ulcers
Occurring as circumscribed lesions in the mucosal membrane, peptic ulcers can develop in the lower esophagus, stomach, duodenum, or jejunum. The major forms are duodenal ulcer and gastric ulcer; both are chronic conditions resulting from contact of the mucosa with gastric juice (especially hydrochloric acid and pepsin).
Duodenal ulcers, which account for about 80% of peptic ulcers, affect the proximal part of the small intestine. These ulcers follow a chronic course characterized by remissions and exacerbations; 5% to 10% of patients develop complications that necessitate surgery. They occur most commonly in males between ages 20 and 50.
Gastric ulcers, which affect the stomach mucosa, are most common in middle-aged and elderly males, especially among the poor and undernourished, and in long-term users of aspirin or alcohol.
Causes
In duodenal ulcers, there’s increased acid production. Recent findings indicate that a bacterial infection with Helicobacter pylori is a leading factor of peptic ulcer disease. Two other leading causes of peptic ulcer include the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and pathologic hypersecretory states such as Zollinger-Ellison syndrome. (See Peptic ulcers: Causes and risk factors.)
Complications
Erosion of the mucosa can cause GI hemorrhage, which can progress to hypovolemic shock. Pyloric obstruction from recurring scarring may cause the stomach to distend with food and fluid and result in abdominal or intestinal infarction, perforation, and hemorrhage.
Penetration (the ulcer crater extends beyond the duodenal walls into attached structures, such as the pancreas, biliary tract, liver, or gastrohepatic omentum) occurs fairly frequently in duodenal ulcer.
Assessment
Typically, the patient describes periods of exacerbation and remission of his symptoms, with remissions lasting longer than exacerbations. The patient’s history may reveal possible causes or predisposing factors, such as smoking, use of aspirin or other medications, or associated disorders.
Peptic ulcers: Causes and risk factors
Research has identified several causes of peptic ulcers as well as various factors that predispose some individuals to the formation of these ulcers.
Causes
Bacterial infection. A leading cause of peptic ulcers, Helicobacter pylori releases a toxin that promotes mucosal inflammation and ulceration. In a peptic ulcer due to H. pylori, acid functions as a contributor—increasing the inflammation and erosion triggered by the bacteria—rather than the dominant cause.
Drug therapy. Salicylates and other nonsteroidal anti-inflammatory drugs (NSAIDs), reserpine, or caffeine may erode the mucosal lining. NSAIDs may cause a gastric ulcer by inhibiting prostaglandins (the fatty acids that mediate and suppress ulceration)—particularly the E-series prostaglandins. These substances, present in large quantities in the gastric mucosa, inhibit injury by stimulating secretion of gastric mucus and gastric and duodenal mucosal bicarbonate (a neutralizing agent). Prostaglandins also promote gastric mucosal blood flow, maintain the integrity of the gastric mucosal barrier, and help renew the epithelium after a mucosal injury. Glucocorticoids also predispose the patient to ulcer formation. These drugs inhibit prostaglandin synthesis, increase gastric acid and pepsin secretion, reduce gastric mucosal blood flow, and decrease cytoprotective mucous production. Because these drugs also decrease gastric pain, they can mask signs of ulcer development until hemorrhage or perforation occurs.
Certain illnesses. Pancreatitis, hepatic disease, Crohn’s disease, preexisting gastritis, and pathologic hypersecretory states, such as Zollinger-Ellison syndrome, are associated with ulcer development. In Zollinger-Ellison syndrome, for example, gastrinomas (commonly found in the pancreas) stimulate gastric acid secretion. This large volume of acid eventually erodes the gastric mucosa and contributes to ulcer formation.
Risk factors
Blood type. For unknown reasons, gastric ulcers commonly strike people with type A blood. Duodenal ulcers tend to afflict people with type O blood, perhaps because these people don’t secrete blood group antigens (mucopolysaccharides, which may serve to protect the mucosa) in their saliva and other body fluids.
Genetic factors. Duodenal ulcers are about three times more common in first-degree relatives of duodenal ulcer patients than in the general population.
Exposure to irritants. Like certain other drugs, alcohol inhibits prostaglandin secretion, triggering a mechanism much like the one caused by NSAIDs. Cigarette smoking also appears to encourage ulcer formation by inhibiting pancreatic secretion of bicarbonate. It may also accelerate the emptying of gastric acid into the duodenum and promote mucosal breakdown.
Trauma. Critical illness, shock, or severe tissue injury from extensive burns or from intracranial surgery may lead to a stress ulcer.
Psychogenic factors.
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