FA Gastrointestinal Flashcards
H2 Blockers
Cimetidine, ranitidine, famotidine, nizatidine. H2 blockers before you “dine.”
H2 Blocker Mechanism
Reversible block of histamine H2 receptors → ↓ H+ secretion by parietal cells.
H2 Blocker Use
Peptic ulcer, gastritis, mild esophageal reflux
H2 Blocker Toxicity
Cimetidine is a potent inhibitor of cytochrome P-450 (multiple drug interactions); it also has antiandrogenic effects (prolactin release, gynecomastia, impotence, ↓ libido in males); can cross blood-brain barrier (confusion, dizziness, headaches) and placenta. Both cimetidine and ranitidine also ↓ renal excretion of creatinine. Other H2 blockers are relatively free of these effects.
Proton Pump Inhibitors
Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole
PPI Mechanism
Irreversibly inhibit H+/K+ ATPase in stomach parietal cells.
PPI Use
Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.
PPI Toxicity
Increased risk of C. difficile infection, pneumonia. Hip fractures, ↓ serum Mg2+ with long term use.
Bismuth, Sucralfate Mechanism
Bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucous layer.
Bismuth, Sucralfate Use
↑ ulcer healing, travelers’ diarrhea
Misoprostol Mechanism
A PGE1 analog. ↑ production and secretion of gastric mucous barrier, ↓ acid production.
Misoprostol Use
Prevention of NSAID-induced peptic ulcers (NSAIDs block PGE1 production); maintenance of a PDA. Also used to induce labor (ripens cervix).
Misoprostol Toxicity
Diarrhea. Contraindicated in women of childbearing potential (abortifacient).
Octreotide Mechanism
Long-acting somatostatin analog.
Octreotide Use
Acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors.