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