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30 Cards in this Set
- Front
- Back
- 3rd side (hint)
4 H2 blockers
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cimetidine, ranitidine, famotidine, nizatidine
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MOA of H2 blockers
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reversibly block H2 receptors which causes decreased H+ secretion by gastric parietal cells
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cimetidine toxicities
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P450 inhibitor; antiandrogenic; crosses BBB (confusion, HAs, dizziness) and placenta
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None
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2 proton pump inhibitors
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omeprazole, lansoprazole
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MOA of PPIs
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irreversibly bind H+/K+ ATPase in gastric parietal cells
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MOA of bismuth, sucralfate
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bind to ulcer base and provide physical protection, allow bicarb secretion to reestablish pH gradient in mucous layer
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triple tx of H. pylori?
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metronidazole + bismuth + amoxicilin/tetracycline
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MOA of misoprostol
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PGE1 analog, that increases production and secretion of gastric mucous barrier and decreases acid production
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toxicity/contraindications for misoprostol
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(PGE1 analog) diarrhea, not for women of childbearing potential
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which 2 muscarinic antagonists used for treatment of peptic ulcer?
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pirenzepine, propantheline
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toxicities of pirenzepine and propantheline?
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tachycardia, dry mouth, difficulty focusing eyes
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overuse of aluminum hydroxide can cause what problems?
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(antacid) constipation, hypophosphatemia, proximal mm weakness, osteodystrophy, seizures
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overuse of magnesium hydroxide can cause what problems?
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(antacid) diarrhea, hyporeflexia, hypotension, cardiac arrest
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overuse of calcium carbonate can cause what problems?
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(antacid)hypercalcemia, rebound acid increase
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MOA of infliximab
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monoclonal TNF-alpha ab
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clinical use of infliximab
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Crohn's dz, rheumatoid arthritis
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infliximab toxicity
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respiratory infection, fever, hypotension
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MOA sulfasalazine
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combo antibacterial (sulfapyridine) and anti-inflammatory (mesalamine); activated by colonic bacteria
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clinical use of sulfasalazine
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UC, Crohn's disease
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toxicity of sulfasalazine (5)
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malaise, nausea, sulfonamide toxicity, reversible oligospermia
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MOA of ondansetron
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5-HT3 antagonist (powerful central acting anti emetic)
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clinical use of ondansetron
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antiemetic; to control vomiting post-op and in pts undergoing chemotherapy
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toxicity of ondansetron
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headache, constipation
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MOA of cisapride
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acts thru serotoni R to increase Ach release at myenteric plexus; increases esophageal tone; increases gastric and duodenal contracitlity and improves transit time (prokinetic)
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Clinical use of cisapride
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prokinetic (on GIT) but no longer used because of serious interactions with erythromycin, ketoconazole, nefazodone, fluconazole (-->torsades de pointes!)
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MOA of metoclopramide
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D2 R antagonist; increases resting tone, contractility, LES tone, motility but does not increase transit time thru colon. (pro-kinetic)
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clinical use of metoclopramide
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diabetic and post-surgery gastroparesis
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toxicity of metoclopramide
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(D2 R antag). Increased Parkinsonian effects; restlessness, drowsiness, fatigue, depression, nausea, constipation.
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drug interactions of metoclopramide
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digoxin and diabetic agents
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contraindications for metoclopramide?
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(D2 R antag) pts with small bowel obstruction
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