Abstract

The primary aim in antiulcer therapy is either prevention of acid secretion from the gastric parietal cells or neutralization of the acid before it comes into contact with the ulcerated areas of the gastrointestinal tract. Long established therapy of duodenal ulcers, included diet, antacids, and anticholinergics. Of these, only antacids have been shown conclusively to be effective. The antacids can produce healing, but only when given in large and frequent doses. Antacids include aluminum hydroxide gel, precipitated calcium carbonate, magnesia and alumina suspension, magnesium oxide, magnesium trisilicate, magaldrate, and sodium bicarbonate.

The therapy for duodenal ulcers changed drastically upon the introduction of cimetidine (an H₂ blocker) in the United States in 1977. Omeprazole is a potent antisecretory agent and is used only for acute therapy of ulcerative disease and esophagitis.

Drugs acting by mechanisms not related to inhibition of gastric acid secretion have been introduced into therapy in the United States. Use of sucralfate and misoprostil therapy also has been changed by the acceptance that Helicobacter pylori, an organism able to withstand the acid media of the stomach, is associated with gastritis and ulcerative disease.

Laxatives facilitate the passage and elimination of feces. Laxatives have traditionally been classified as bulking agents: contact, stimulant; saline, osmotic; and emollients, lubricant.

Commonly used antidiarrheals work by one of two mechanisms: effects on net intestinal secretion, or a decrease in intestinal propulsive motility.

Antiemetics may act at a variety of physiological locations, eg, blockade of dopamine and effects at the chemoreceptor trigger zone, vestibular apparatus, or serotonin (5-HT₃) receptors. Gastric prokinetics are a new class of agent that can augment gastric emptying.