USMLE Cardio pharm

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USMLE Cardio pharm
2010-05-27 15:18:11
USMLE Cardio pharmacology step

Cardio pharm for USMLE Step 1 from FA 2010
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  1. Hydralazine: mechanism
    • increases cGMP to cause smooth muscle relaxation
    • vasodilates arterioles more than veins, reduces afterload
  2. Hyrdralazine: use
    • First line for HTN in pregnancy
    • CHF
    • Coadminister with beta blocker to prevent reflex tachycardia
  3. Hydralazine: toxicity
    • Compensatory tachycardia
    • Fluid retention, nausea, HA, angina
    • Lupus-like syndrome
  4. Minoxidil: mechanism and use
    • K channel opener, hyperpolarizes and relaxes vascular smooth muscle
    • For severe HTN
  5. Minoxidil: toxicity
    Hypertrichosis, pericardial effusion, reflex tachy, angina, salt retention
  6. CCBs: mechanism
    BLock voltage-dependent L-type calcium channels of cardiac and smooth uscle
  7. CCBs: order for vascular and heart action
    • Vascular: nifedipine > diltiazem > verapamil
    • Heart: verapamil > diltiazem > nefedipine
  8. CCBs: toxicity
    Catrdiac depression, AV block, edema, flushing, dizziness, constipation
  9. Nitroglycerin and isosorbide dinatrate: mechanism
    • Release NO in SM, causing increased cGMP and relaxation.
    • Dilate veins >> arteries. Decreases PRELOAD
  10. Nitroglycerin: toxicity
    • reflex tachycardia (sympathetic activation)
    • hypotension, flushing, HA
    • "Monday disease" in industrial exposure (loss of tolerance over the weekend)
  11. Drugs for malignant hypertension
    • Nitroprusside
    • Fenoldopam
    • Diazoxide
  12. Nitroprusside: MOA
    • short acting
    • increases cGMP by direct release of NO
    • releases CN (antidote co-administered)
  13. Fenoldopam: MOA
    Dopamine D1 receptor agonist causes relaxation of renal vascular smooth muscle
  14. Diazoxide: MOA
    • K+ channel opener hyperpolarizes and relaxes vascular SM.
    • Also reduces insulin release (hyperglycemia risk)
  15. Beta-blockers contraindicated in angina
    • Pindolol
    • Acebutolol
  16. Statins: MOA
    • HMG-CoA reductase inhibitors
    • Inhibit formation of mevalonate
    • LDL; also HDL up and TG down a little
  17. Niacin: MOA
    • Inhibits lipolysis in adipose tissue
    • Reduces hepatic VLDL secretion
    • Drops LDL and raises HDL
    • Can cause hyperglycemia and hyperuricemia
  18. Name the bile acid resins
    • cholestyramine
    • colestipol
    • colesevelam
  19. Ezetimibe: MOA
    • Cholesterol absorption blocker in small intestine brush border
    • Drops LDL only
  20. Fibrates: MOA and toxicity
    • Upregulate LPL to increase TG clearance
    • Best for TGs
    • Tox: mysotis, gallstones
  21. Effect of beta-1 receptors on the heart
    Gs - activate protein kinase A which phosphorylates L-type Ca channels and phospholamban, both of which increase intracellular Ca during contraction
  22. Digoxin: MOA
    • Inhibition of Na/K ATPase indirectly inhibits Na/Ca exchanger
    • (Less Na out means less Ca can leave the cell)
  23. Digoxin: use
    • For CHF to increase contractility
    • For a fib to decrease conduction at AV node and depress SA node
  24. Digoxin: toxicity
    • Cholinergic: nausea, vomiting, diarrhea, funny vision
    • ECG: increase PR interval, decrease QT, scooping T wave inversion, arrhythmia, hyperkalemia
    • RENAL excretion
    • Quinidine decreases digoxin clearance
  25. Class I antiarrhythmics: general
    • Na channel blockers
    • Slow or block conduction
    • Decrease slope of phase 4 depolarization and increase threshold
    • Hyperkalemia increases toxicity
  26. Class IA drugs and effect
    • Quinidine, procainamide, disopyramide
    • Increase AP duration
    • Increase effective refractory period
    • Increase QT interval
    • For atrial and ventricular arrhythmias
  27. Quinidine: toxicity
    • Cinchonism: headache, tinnitus, thrompocytopenia
    • Torsades
  28. Procainamide: toxicity
    drug-induced SLE
  29. Class IB drugs and effect
    • Lidocaine, mexiletine, tocainide (phenytoin)
    • Decrease AP duration
    • Preferentialy affect ischemic or depolarized Purkinje and vent tissue
    • Good post-MI
  30. Class IC drugs and effect
    • Flecainide, encainide, propafenone
    • NO AP duration effect
    • Prolong AV refractory period
    • For v-tachs progressing to VF
    • Last resort
  31. Class IC: toxicity
    Proarrhythmic, bad post-MI
  32. Shortest acting beta-blocker
  33. Class II antiarrhytmics (beta-blockers) general
    • decrease cAMP to decrease Ca current
    • Decrease slope of phase 4 to suppress abnormal pacemakers
    • AV node is sensitive so PR interval increases
    • For ventricular slowing
  34. Beta-blockers: toxicity
    • Impotence, asthma worsens, sedation
    • Bradycardia, AV block, CHF
    • Masks hypoglycemia
    • Metoprolol: dyslipidemia
    • Glucagon treats OD
  35. Class III antiarrhythmics (K+ channel blockers)
    • Sotalol
    • ibutilide
    • bretylium
    • dofetilide
    • amiodarone
  36. K channel blockers: MOA
    • Increase AP duration
    • Increase effective refractory period
    • Use when other antiarrhythmics fail (Increases QT interval)
  37. Sotalol class and toxicity
    • Class III (K channel)
    • Torsades, excessive beta block
  38. Ibutilide class and toxicity
    • K channel blocker
    • Torsades
  39. Bretylium class and toxicity
    • K channel blocker
    • New arrhythmia, hypotension
  40. Amiodarone: effects and toxicity
    • Class III (K) but has effects of all classes b/c it alters membrane
    • Pulmonary fibrosis, hepatotoxicty, thyroid, corneal deposits, blue/gray skin deposits, neuro effects, constipation, bradycardia/heart block/CHF
  41. Class IV (CCBs) antiarrhytmics: names and effect
    • Verapamil, diltiazem
    • Primarily affects AV node, decreasing conduction velocity
    • Increases effective refractory period and PR interval
    • Prevent nodal arrhythmias
  42. Mg as an antiarrhytmic
    Effective in torsades and digoxin toxicity
  43. K as an antiarrhytmic
    Depresses ectopic pacemakers in hypokalemia (digoxin toxicity)
  44. Adenosine as an antiarrhythmic
    • Causes K efflux causing hyperpolarization
    • Diagnose/abolish SVT
    • Effects are blocked by theophylline