Pharmacology Antiarrhythmics 4

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kyleannkelsey
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249695
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Pharmacology Antiarrhythmics 4
Updated:
2013-11-29 19:59:18
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Pharmacology Antiarrhythmics
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Pharmacology,Antiarrhythmics,4
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Pharmacology Antiarrhythmics 4
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  1. What is the major toxicity of ibutilide and at what rate does it occur?
    Torsades de pointes at ~6%
  2. How is Ibutilide administered?
    Rapid infusion (1mg/10 minutes)
  3. What is Ibutilide given for?
    Immediate conversion of atrial fibrillation or flutter to sinus rhythm
  4. What is the MOA of Ibutilide?
    I(Kr) blocker that also activates an inward Na current
  5. What is the MOA o Dofetilide?
    Pure class III, I(Kr) selective inhibitor that prolongs the QT interval
  6. What is the incidence of torsades with Dofetilide?
    1-3%
  7. How is Dofetilide administered?
    In a hospital with72 hours of monitoring (due to risk of torsades)
  8. What is Dofetilide used for?
    Maintenance of sinus rhythm in patients with atrial fibrillation
  9. What is the risk of torsades de pointes with Quinadine?
    2-8%
  10. What is the risk of torsades de pointes with Procainamide?
    2-3%
  11. What is the risk of torsades de pointes with Disopyramide?
    2-3%
  12. What is the risk of torsades de pointes with d,l-Sotalol?
    1-5%
  13. What is the risk of torsades de pointes with d-Sotalol?
    1-2%
  14. What is the risk of torsades de pointes with Ibutilide?
    6%
  15. What is the risk of torsades de pointes with Dofetilide?
    1-3%
  16. What is the risk of torsades de pointes with Amiodarone?
    <1%
  17. What effects do CCBs like Verapamil and Diltiazem have on the heart?
    Reduce automaticity, Increase RP, Decrease Velocity of AV node, Inhibit contractility
  18. What effect do CCBs like Verapamil and Diltiazem have on the blood vessels?
    Vasodilators
  19. What is the MOA for CCBs like Verapamil and Diltiazem?
    Block slow inward Ca current
  20. What are the adverse effect sof CCBs, like Verapamil and Diltiazem?
    Flushing, Reduced contraction, AV node conduction effects, constipation
  21. What type of arrhythmias are CCBs used for?
    Supraventricular arrhythmias
  22. What are the Antiarrhythmic Na channel blockers?
    Lidocaine, Phenytoin, Mexiletine, Procainamide, quinidine and “amiodarone”
  23. What are the K channel blocking antiarrhythmics?
    Dofetilide, ibutilide, amiodarone, sotalol, quinidine, procainamide
  24. What are the Ca channel blocker antiarrhythmics?
    Verapamil, Amiodarone and Diltiazem
  25. What are the B blocker antiarrhythmics?
    Propranolol, esmolol, sotalol and amiodarone
  26. What types of Arrhythmias can be treated by Ranolazone?
    AF and Ventricular tachyarrhythmia
  27. How does Ranzoline prevent arrhythmias?
    Blocks Na channel late phase influx, blocks I(Kr) at therapeutic concentration
  28. How many adenosine receptor types are there and what are they?
    4, A(1), A(2A), A(2B), A(3)
  29. What type of receptors are the adenosine receptor?
    G protein coupled
  30. What are competitive antagonists for the Adenosine receptors?
    Methylxanthines, such as caffeine and theophylline
  31. What is a normal plasma level of Adenosine?
    300 nM (can reach mM conc.)
  32. Which cells release Adenosine?
    Most cells
  33. What is the trade name for Adenosine?
    Adenocard
  34. Which Adenosine receptors are stimulatory?
    A(2A) and A(2B)
  35. Which adenosine receptors are inhibitory?
    A1 and A3
  36. What is the MOA of adenosine in the treatment of arrhythmias?
    Stimulates A1 adenosine receptors on the heart, ↑K conductance, inhibits opening of Ca channels, ↓ NOR release, ↓ automaticity and AV nodal conduction
  37. What are the adverse effects of Adenosine?
    Flushing, Asthma, chest pain, dyspnea, SA nodal arrest, AV nodal block

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