Gastrointestinal Pharmacology Flashcards
name the H2 blockers
-dine
Cimetidine
ranitidine
famotidine
nizatidine
“Take H2 blockers before you dine. Think ‘table for 2’ to remember H2.”
H2 blockers–mechanism
reversible block of histamine H2 receptors –> decrease H+ secretion by parietal cells
H2 blockers–use
peptic ulcer
gastritis
mild esophageal reflux
cimetidine–toxicity
(H2 blocker)
potent inhibitor of cytochrome P-450
antiandrogenic effects–prolactin release, gynecomastia, impotence, dec libido in males
can cross blood brain barrier–confusion, dizziness, headaches
can cross placenta
cimetidine and ranitidine–toxicity
(H2 blockers)
dec renal excretion of creatinine
name the proton pump inhibitors
omeprazole
lansoprazole
esomeprazole
pantoprazole
dexlansoprazole
proton pump inhibitors–mechanism
irreversibly inhibit H+/K+ ATPase in stomach parietal cells
proton pump inhibitors–use
peptic ulcer
gastritis
esophageal reflux
Zollinger-Ellison syndrome
proton pump inhibitors–toxicity
inc risk of C. difficile infection, pneumonia
decrease serum Mg2+ with long term use
how does antacid usage affect other drugs?
affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
name 3 types of antacids
aluminum hydroxide
calcium carbonate
magnesium hydroxide
what can all antacids cause?
hypokalemia
aluminum hydroxide–toxicity
contipation
hypophosphatemia
proximal muscle weakness
osteodystrophy
seizures
“Aluminimum amount of feces”
calcium carbonate–toxicity
hypercalcemia–milk alkali syndrome
rebound acid increases
can chelate and decrease effectiveness of other drugs (ie. tetracycline)
magnesium hydroxide–toxicity
diarrhea
hyporeflexia
hypotension
cardiac arrest
“Mg2+ = Must go to the bathroom”
bismuth, sucralfate–mechanism
bind to ulcer base which protects it and allows HCO3- secretion to reestablish pH gradient in the mucous layer
bismuth, sucralfate–use
inc ulcer healing
travelers’ diarrhea
misoprostol–mechanism
a PGE1 analog
inc production and secretion of gastric mucous barrier
dec acid production
misoprostol–use
prevention of NSAID induced peptic ulcers (NSAIDs block PGE1 production)
maintenance of a patent ductus arteriosis
also used off label for induction of labor–ripens cervix