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40 Cards in this Set

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examples of H2 blockers
cimitidine
ranitidine
famotidine
nizatidine
(-tidine)
mechanism of H2 blockers
reversibly bind to H2 recetors, blocking H2 activation and decreased H+ release by parietal cells
toxicity of H2 blockers
cimitidine has the most: anti-androgenic effects, p450 interactions, crosses BBB (--> dizziness, confusion, HA), can cross placenta.
rantidine and cimetidine decrease renal excretion of creatinine
examples of PPI
omeprazole
lansoprazole
(-prazole)
MOA of PPI
irreversibly binds to H-K-ATPase pump in parietal cells
clinical use for H2 inhibitor
peptic ulcers
gastritis
mild GERD
clinical uses for PPI
peptic ulcers, gastritis, GERD, Zollinger-Ellison syndrome
MOA of bismuth
binds at the base of the ucler, giving physical protection
allows HCO3- secretion to re-establish pH gradient in mucus layer
clinical use of bismuth
ucler healing
traveller's diarrhea
MOA sucralfate
binds at base of ulcer, giving physical protection
allows HCO3- secretion to re-establish pH gradient in mucus layer
clinical use of sucralfate
increase ulcer healing
traveller's diarrhea
MOA of misoprostol
agonizes PGE1, increases production of mucous barrier
decreases acid production
what is the triple therapy against HP?
metronidazole
bismuth
amoxy (or tetracycline)
clinical uses for misoprostol
prevention of NSAID induced ulcers
maintain patent PDA
induce labor
toxicity of misoprostol
abortofacient
examples of muscarinic antagonists
pirenzepine
propantheline
MOA of muscarinic antagonists
blocks M1 receptors on ECL cells and M3 receptors on parietal cells (vagal stimulation goes ot M3)
blocking M1 receptor decreases H2 secretion and blocking M3 decreases H+ secretion
clinical uses for muscarinic antagonists
peptic ulcer
toxicity of muscarinic antagonist
tachycardia
dry mouth
difficulty focusing eyes
toxicity associated with Al(OH)3
constipation (minimum amt of feces)
muscle weakness
osteodystrophy
seizures
hypokalemia
toxicity associated with Mg(OH)2
diarrhea
hyporeflexia
hypotension
cardiac arrest
hypokalemia
toxicity associated with calcium carbonate
hypercalcemia
rebound acid increase
hypokalemia
MOA of infliximab
mAB against TNF-alpha
clinical uses of infliximab
Crohn's disease
RA
toxicity assicated with infliximab
respiratory infx
hypotension
fever
MOA sulfasalazine
combo of sulfapyridine and mesalamine (antibacterial and anti-inflammatory)
activated by colonic bacteria
clinical use of sulfasalazine
UC
CD
toxicity of sulfasalazine
malaise
nausea
sulfonamide toxicity
reversible oligospermia
MAO ondansetron
seratonin antagonist
antiemetic
clinical use for ondansetron
control vomiting post-op and in pts taking chemo
toxicity associated with ondansetron
HA
constipation
examples of pro-kinetic agents
cisapride
metoclopramide
MOA cisapride
increases ACh release at myenteric plexus
increases esophageal ton e
increases gastric and duo contractility
improves transit time
cisapride toxicity
NO LONGER USED b/c of interactions with erythromycin, ketoconazole, nefazodone, fluconazole
MOA metoclopramide
D2 recepotr antagonist
increses resting tone, contractility, LES tone, motolity
does not increase transit time through colon
which motility agent increases transit time through colon?
cisapride
clinical use of metoclopramide
diabetic and post-surggery gastroparesis
toxicity of metoclopramide
increased parkinsonian effects
restlessness
drowsiness
fatigue
depression
nausea
constipation
drug interactions with metoclopramide
digoxin
DM meds
when is metoclopramide contraindicated
pts with small bowel obstruction