GI Drugs Flashcards
Name the H2 blockers
“-tidine”
cimetidine, ranitidine, famotidine, nizatidine
Mechanism of H2 blockers
reversible block of the histamine H2 receptors –> decrease H+ secretion by parietal cells
Use of H2 blockers
peptic ulcer, gastritis, mild GERD
Toxicity of cimetidine specifically
inhibits cytochrome p450 (multiple drug interactions) antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males) can cross BBB (cause confusion, dizziness, headaches) and can cross placenta
Toxicity of cimetidine and ranitidine
decrease renal excretion of creatinine
Name the proton pump inhibitors
“-prazole”
omeprazole, lansoprazole, esmeprazole, pantoprazole, dexlansoprazole
Mech of PPIs
irreversibly inhibit H+/K+ ATPase in stomach parietal cells
Use of PPIs
peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome
Toxicity of PPIs
increased risk of C. difficile infection, pneumonia
decreased serum Mg2+ with long-term use
Mechanism of bismuth and sucralfate
bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucous layer
Use of bismuth and sucralfate
increase ulcer healing, travelers diarrhea
Mechanism of misoprostol
a PGE1 analog
increases production and secretion of gastric mucous barrier, decreases acid production
Use of misoprostol
prevention of NSAID-induced peptic ulcers (NSAIDs block PGE1 production); maintenance of a PDA
also off label for induction of labor (ripens cervix)
Toxicity of misoprostol
diarrhea
contraindicated in women of childbearing potential (abortifactant)
Mechanism of octreotide
long-acting somatostatin analog; inhibits actions of many splanchnic vasodilatory hormones
Use of octreotide
acute variceal bleeds, acromegaly, VIPoma, carcinoid tumor