Porth's Essentials of Pathophysiology, 4e

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Gastrointestinal and Hepatobiliary Function

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Zollinger-Ellison Syndrome Zollinger-Ellison syndrome is a rare condition caused by gastrin-secreting tumors (gastrinomas) that are most commonly found in the small intestine or pancreas. 7 In persons with this disorder, gastric acid secretion reaches such levels that ulceration becomes inevitable. The increased gastric secretions cause symptoms related to peptic ulcer. Diarrhea may result from hypersecretion of acid or from the activation of intestinal lipase and impaired fat digestion that occurs with a decrease in intestinal pH. Most gastrinomas are solitary or multi- focal nodules that are potentially resectable. Over two thirds of gastrinomas are malignant and one third have metastasized at the time of diagnosis. 8 Stress Ulcers A stress ulcer, sometimes called a Curling ulcer, refers to gastrointestinal ulcerations that develop in relation to major physiologic stress. 7,22,23 Persons at high risk for development of stress ulcers include those with large– surface-area burns, trauma, sepsis, acute respiratory distress syndrome, severe liver failure, and major surgi- cal procedures. These lesions occur most often in the fundus of the stomach and proximal duodenum and are thought to result from ischemia, tissue acidosis, and bile salts entering the stomach in critically ill persons with decreased gastrointestinal tract motility. Another form of stress ulcer, called Cushing ulcer, consists of gastric, duodenal, and esophageal ulcers arising in persons with intracranial injury, operations, or tumors. They are thought to be caused by hypersecretion of gastric acid resulting from stimulation of vagal nuclei by increased intracranial pressure. Persons admitted to hospital intensive care units are at particular risk for development of stress ulcers. They usually manifest with painless upper gastrointes- tinal tract bleeding. H 2 -receptor antagonists and proton pump inhibitors are often used in the prevention and treatment of stress ulcers. Cancer of the Stomach Although the incidence of cancer of the stomach has declined over the past 50 years in the United States, it continues to remain a leading cause of cancer deaths worldwide. 6 It is more common in lower socioeconomic groups and exhibits a male-to-female ratio of about 2:1. Among the factors that increase the risk of gastric cancer are genetic predisposition, carcinogenic factors in the diet (e.g., N -nitroso compounds and benzo[ α ]pyrene found in smoked and preserved foods), autoimmune gastritis, and gastric adenomas or polyps. The incidence of stomach cancer in the United States has decreased fourfold since 1930, presumably because of improved storage of food with decreased consumption of smoked and preserved foods. 6,7 Chronic infection with H. pylori appears to serve as a co-factor in some types of gastric carcinomas. However, the vast majority of people with H. pylori infection do not develop gastric cancer, and not all H. pylori infections increase the risk of gastric

an artery or vein. It occurs in up to 20% of persons with peptic ulcer. 7 Evidence of bleeding may consist of hematemesis or melena. Bleeding may be sudden, severe, and without warning, or it may be insidious, producing only occult blood in the stool. Up to 20% of persons with bleeding ulcers have no antecedent symptoms of pain; this is particularly true in persons using NSAIDs. Acute hemorrhage is evidenced by the sudden onset of weakness; dizziness; thirst; cold, moist skin; the desire to defecate; and the passage of loose, tarry, or even red stools and coffee-ground emesis. Signs of circulatory shock develop depending on the amount of blood lost. Perforation occurs when an ulcer erodes through all the layers of the stomach or duodenum wall. Perforation develops in approximately 5% of persons with peptic ulcers, usually from ulcers on the anterior wall of the stomach or duodenum. 7 With perforation, gastrointesti- nal contents enter the peritoneum and cause peritonitis. Radiation of the pain into the back, severe night dis- tress, and inadequate pain relief from eating foods or taking antacids in persons with a long history of peptic ulcer may signify perforation. Penetration is a process similar to perforation, but with penetration the ulcer crater erodes into adjacent organs, including the small bowel, pancreas, liver, or biliary tree. 20 Typically, it has a subtle presentation marked by a gradual increase in severity and frequency of pain. Gastric outlet obstruction is caused by edema, spasm, or contraction of scar tissue and interference with the free passage of gastric contents through the pylorus or adja- cent areas. The presentation of an obstruction is typically insidious, with symptoms of early satiety, feeling of epi- gastric fullness and heaviness after meals, gastroesopha- geal reflux, weight loss, and abdominal pain. With severe obstruction, there is vomiting of undigested food. Diagnosis and Treatment. Diagnostic procedures for peptic ulcer include history taking, laboratory tests, radiologic imaging, and endoscopic examination. The history should include careful attention to aspirin and NSAID use. Peptic ulcer should be differentiated from other causes of epigastric pain. Laboratory findings of hypochromic anemia and occult blood in the stools indicate bleeding. Endoscopy (i.e., gastroscopy and duodenoscopy) can be used to visualize the ulcer area and obtain biopsy specimens to test for H. pylori and exclude malignant disease. X-ray studies with a contrast medium such as barium are used to detect the presence of an ulcer crater and to exclude gastric carcinoma. The treatment of peptic ulcer has changed dramati- cally over the past several decades and now aims to eradicate the cause and promote a permanent cure for the disease. Pharmacologic treatment focuses on eradi- cating H. pylori, relieving ulcer symptoms, and heal- ing the ulcer crater. Aspirin and NSAID use should be avoided when possible. With current therapies aimed at neutralization of gastric acid, inhibition of gastric acid (H 2 antagonists and proton pump inhibitors), and pro- motion of mucosal protection, most ulcers heal within a matter of weeks. When surgery is needed, it usually is performed using minimally invasive methods.