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10 Cards in this Set
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H2 blockers: Cimetidine, ranitidine, famotidine, nizatidine.
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Mechanism: Reversible block of histamine H2 receptors --> decrease H+ secretion by parietal cells.
Take H2 blockers before you DINE. Think "table for 2" to remember H2. Clinical Use: Peptic ulcer, gastritis, mild esophageal reflux. Toxicity: - Cimetidine is a potent inhibitor of P-450 - antiandrogenic effects (prolactin - release, gynecomastia, impotence, decreased libido in males); - can cross BBB (confusion, dizziness, headaches) and placenta. - both cimetidine and ranitidine decrease renal excretion of creatinine (illusion of renal failure). other H2 blockers are relatively free of these effects. |
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Proton Pump inhibitors: Omeprazole, lansoprazole.
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Mechanism: irreversibly inhibit H+/K+-ATPase in stomach parietal cells.
Clinical use: Peptic ucler, gastritis, esophageal reflux, Zollinger-Ellison syndrome. |
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Bismuth, sucralfate
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Mechanism: Bind to ulcer base, providing physical protection, and all HCO3- secretion to reestablish pH gradient in the mucous layer.
Clinical use: increase ulcer healing, traveler's diarrhea. Triple therapy of H pylori: Metronidazole, Amoxicillin (or Tetracycline), Bismuth Can also use PPI |
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Misoprostol
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Mechanism: A PGE1 analog. increase production and secretion of gastric mucous barrier, decrease acid production.
Clinical use: - Prevention of NSAID-induced peptic ulcers - maintenance of a patent ductus arteriosus. - used to induce labor (analogous to PGE2). Toxicity: Diarrhea. Contraindicated in women of childbearing potential (abortifacient). |
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Muscarinie antagonists: Pirenzepine, propantheline.
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Mechanism: Block M1 receptors on ECL cells (decrease histamine secretion) and M3 receptors on parietal cells (decrease H+ secretion).
Clinical use: peptic ulcer (rarely used). Toxicity: Tachycardia, dry mouth, difficulty focusing eyes. |
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Antacid Use
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Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
Overuse can cause the following problems. 1. Aluminum hydroxide - constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures Aluminimum amount of feces . 2. Magnesium hydroxide - diarrhea, hyporeflexia, hypotension, cardiac arrest. Mg= Must go to the bathroom. 3. Calcium carbonate - hypercalcemia, rebound acid increase Can chelate and decrease effectiveness of other drugs (e.g. tetracycline). All can cause hypokalemia. |
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Infliximab
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Mechanism: A monoclonal antibody to TNF, proinflammatory cytokine.
"INFLIXimab INFLIX pain on TNF" Clinical use: Crohn's disease, rheumatoid arthritis. Toxicity: Respiratory infection (including reactivation of latent TB), fever, hypotension. |
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Sulfasalazine
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Mechanism: a combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory). Activated by colonic bacteria.
Clinical Use: Ulcerative colitis, Crohn's disease. Toxicity: Malaise, nausea, sulfonamide toxicity, reversible oligospermia. |
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Ondasetron
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Mechanism: 5-HT3 antagonist. Powerful central-acting antiemetic.
Clinical use: control vomiting postoperatively and in patients undergoing cancer chemotherapy. Toxicity: Headache, constipation. "You will not vomit with ONDASetron, so you can go ON DANCing." |
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Metoclopramide
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Mechanism: D2 receptor antagonist. Increase resting tone, contractility, LES tone, motility. Does not influence colon transport time.
Clinical use: Diabetic and post-surgery gastroparesis. Toxicity: increases parkinsonian effects. Restlessness, drowsiness, fatigue, depression, nausea, diarrhea. Drug interaction with digoxin and diabetic agents. Contraindicated in patients with small bowel obstruction. |
