The gastrointestinal (GI) tract serves many important functions: digestive, excretory, endocrine, and exocrine. These functions are the targets of several important classes of drugs. Some of these drugs have been discussed previously. This chapter reviews their use in the GI system and discusses GI drugs that were not described in previous chapters.
High-Yield Terms to Learn
|Acid-peptic disease ||A group of disorders involving erosion or ulceration of the mucosal lining of the gastrointestinal tract; includes GERD, gastric and duodenal ulcers, nonulcer dyspepsia, and stress-related gastritis |
|Antiemetic ||A drug that reduces nausea and vomiting |
|Gastroesophageal reflux disease (GERD) ||Esophageal irritation or inflammation due to reflux of stomach acid; also known as heartburn |
|Gastroparesis ||Paralysis of the muscles of the stomach and possibly other parts of the gastrointestinal tract due to damage to gastrointestinal nerves or muscle; common in advanced diabetes and advanced Parkinson’s disease |
|Inflammatory bowel disease (IBD) ||Inflammatory disorder involving irritation and ulceration of the colon and rectum (ulcerative colitis) or the colon plus more proximal parts of the gastrointestinal tract (Crohn’s disease) |
|Irritable bowel syndrome (IBS) ||Disease of unknown origin characterized by episodes of abdominal discomfort and abnormal bowel function (diarrhea, constipation, or both) |
|Prokinetic ||A drug that promotes gastrointestinal motility |
|Proton pump ||The parietal cell H+/K+ ATPase that uses the energy of ATP to secrete protons into the stomach (Figure 59–1); final common target of drugs that suppress acid secretion |
A. Drugs Used in Acid-Peptic Diseases
Ulceration and erosion of the lining of the upper portion of the gastrointestinal tract are common problems that manifest as gastroesophageal reflux disease (GERD), gastric and duodenal peptic ulcers, and stress-related mucosal injury. Drugs used in acid-peptic disease reduce intragastric acidity by manipulating systems controlling acid secretion (Figure 59–1), promote mucosal defense or, in the case of peptic ulcers, eradicate the bacterium Helicobacter pylori, which is detectable in over 80% of patients with duodenal ulcers.
Schematic model of physiologic control of hydrogen ion (acid) secretion by the gastric parietal cells, which are stimulated by gastrin (acting on gastrin/CCK-B receptors), acetylcholine (ACh; M3 receptor), and histamine (H2 receptor). Acid is secreted across the parietal cell canalicular membrane by the H+/K+ ATPase proton pump into the gastric lumen. The gastrin that is secreted by antral G cells in response to intraluminal dietary peptides acts directly on parietal cells and also stimulates release of histamine from enterochromaffin-like (ECL) cells. The vagus nerve stimulates postganglionic neurons of the enteric nervous system to release ACh, which acts on parietal and ECL cells. In the antrum, release of gastrin-releasing peptide (GRP) from postganglionic neurons directly increases gastrin release, whereas release of ACh indirectly increases gastrin secretion by inhibiting release of somatostatin from antral D cells. The increase in intraluminal H+ concentration causes ...