GI drugs MOA, ADE, and interactions Flashcards
Antacids MOA
composed of a metal ion + base that work by neutralizing (buffering) hydrochloric acid (HCl) and forming a salt and water
Histamine2-Receptor Antagonists (H2RA) MOA
reversibly compete with histamine at the H2 receptor sites in the parietal cell of the stomach to inhibit acid secretion
Proton Pump Inhibitors (PPIs) MOA
irreversibly inhibit the K+-H+-ATPase (proton pump) which inhibits the final step in the secretion of hydrogen ions into the gastric lumen
Synthetic Prostaglandin MOA
natural prostaglandins produced by gastric mucosa act to inhibit acid secretion and to protect deep mucosa against injury (cytoprotective); production of these prostaglandins blocked by NSAIDs
Sucralfate (Carafate®)
Large aluminum salt (aluminum sucrose sulfate) forms a protective barrier at the ulcer site by binding to necrotic ulcer tissue; May also stimulate endogenous prostaglandin synthesis and adsorb bile salts
Prokinetic Agents
Increase lower esophageal sphincter (LES) tone; Promote gastric emptying
Metoclopramide (Reglan®)
Central dopamine [and serotonin (5-HT3) antagonist]; also increases response of GI tissue to acetylcholine resulting in enhanced motility and gastric emptying
Erythromycin
Motilin agonist
Domperidone
Dopamine antagonist that acts peripherally (limits extrapyramidal symptoms)
Calcium ADE
Constipation
Aluminum ADE
Constipation
Magnesium ADE
Diarrhea
Sodium ADE
Fluid retention
Cimetidine ADE
Hematologic abnormalities, confusion, delusions, gynecomastia, increased etoh levels
Ranitidine ADE
Hematologic abnormalities, confusion, delusions, increased etoh levels