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  1. which phase is pleateu phase?
    phase 2 is plea2 phase
  2. where are fast respond fibres and slow response fibres  present?
    cardiac muscels and specialised cells (SA node and AV node)
  3. which ion channel is absent in slow response fibres?
  4. what are the types of sodium channels? what are the gates in sodium channels?
    resting or ready state, open or active state , inactive or refractory state  

    gates are M(activating) and h( inactivating)
  5. which phase of action potential does b-blocker act?
    phase 4, decreases the slope of phase 4 
  6. why are b blockers preferred in SVT?
    because they decrease the autonimic  activity of SA and AV node
  7. name antiarrythmic b blockers /
    • propranolol- non selective 
    • acebutolol and esmolol - selective  
  8. what is the action of potassium channel blockers in AP?
    it slows phase 3 , increase the action potential duration and effective refractory period . 
  9. what are smurfs ?
    smurfs are blue faced  fictional creatures. 
  10. what happens when u stain raw potato with betadine and why?
    it stains potato to purple because the iodine stains carbohydrate to purple, its the same side effect of bluish discoloration side effect of amiodarone that contains iodine. 
  11. which phase does the potassium channel blocker act ?
    phase 3
  12. which is the drug that mimics all group of drugs ?
  13. what is the major side effect of aniodarone to cause its limitation to use though it mimics all groups of drugs ?
    half life more than 80 days because if has the high tissue  protein binding capacity. because of iodination of proteins. once iodinated it gets stuck to the tissues and cause damage to the tissues eg  lungs(pulmonary fibrosis)  skin(smurf skin) cornea liver thyroid etc
  14. name another K channel blocker ?
    sotalol, also a b blocker
  15. where is the target of calcium channel blocker ?
    SA and AV node - because calcium channel is the prominent ion channel in action potential of slow response fibres treatment of SVT
  16. what are the examples of CCB anti arrythmics ?
    diltiazem and verapamil they are cardio selective
  17. what is the half life of adenosine { Osine means sugar and sugar are water soluble} ?
    less than 10 seconds ( as it is a neurotransmitter )
  18. what is the most useful use of adenosine/
    PSVT, it is the drug of choice 
  19. what antagonises adenosine ?
    methylxanthines (theophylline and caffeine ), adenosine causes severe bronchospasm , methylxanthines causes bronchodilatation , and increased AV nodal activity .
  20. what is the mechanism of action of magnesium as anti arrythmic ?
    competes with calcium so blocks calcium effect 
  21. what are the drugs causing torsades ?
    • potassium channel blockers 
    • TCA
    • anti psychotics
    • anti muscarines 
    • (torsades means to keep the cells in depolarised state )
  22. what is the MOA of 1A 1B and 1C drugs ?
    • 1A act on activated fast sodium channels
    • !B act on inactivated sodium channels  (slow conduction of ischaemic cells ) and blocks slow sodium window channels and thus decreases the action potential duration and prolonging the recovery phase in ischaemic cells
    • 1C blocks all sodium channels  
  23. name class 1 anti arrythmic drugs ?
    • 1A  quinidine , procainamide
    • 1B lidocaine ,
  24. what is the additional  MOA of quinidine ?
    • anti muscarinic 
    • alpha blockage
  25. why is the drug interaction between quinidine and digoxin so important?
    because quinidine always cause initial digitalisation as it may precipitate tachycardia
  26. name the drugs causing SLE?
    • procainamide 
    • hydralazine
    • Isoniazide
  27. which is the least cardiotoxic anti arrythmic?
    lidocaine , though  we are worried about its side effect when  used as local anaesthecic, it has more cns toxicity 
  28. what are the oral analogues of lidocaine ?
    mexiletine and tocainide 
  29. which anti arrythmic we use when all have failed and try at last ?
    1C drugs flecainide , blocks all sodium channels 
  30. what is the difference between the drugs that decrease the blood pressure by decreasing SANS and without decreasing SANS ?
    by decreasing SANS - no reflex tachycardia . orthostatic HTN , increased PANS activity , no such effect in other group
  31. what are the group of drugs that act on sympathetic activity?
    alpha 2 agonist .  drugs acting on storage vesicles , alpha 1 blocker and beta blocker
  32. give exammples of alpha 2 agonists ?
    methyl dopa and clonidine 
  33. which drug is used in opiate withdrawl ?
  34. what kind of drugs can be used in pregnancy in relation to protein binding ?
    high protein binding drugs but high plasma protein binding dugs  drugs can always behave as a hapten and can act as foreign body
  35. why is coombs test positive in methyldopa used in pregnancy ?
    because it has high plasma protein binding and behaves as hapten and thus induce immune response 
  36. how do TCA interact with antihypertensives alpha 2 agonists  ?
    decrease the anti hypertensive action 
  37. what are the drugs acting on storage vesicles ?
    reserpine that destroy storage (reserve ) vesicles of NE, dopamine and setotonin 
  38. what is the major side effect of reserpine?
    depression due to  decreased effect of NE, dopamine and serotonin 
  39. name selective alpha 1 blockers 
    prazocine terazocine 
  40. what is the only  drug altering sympathetic activity that causes reflex tachycardia ?
    alpha 1 blockers 
  41. what is the effect of alpha 1 blocker and beta blocker in lipid profile ?
    alpha 1 decrease . beta blocker increase lipid 
  42. what is the major contraindications of BB?
    asthma . vasospastic diseases . diabetes ( mask the hypoglycemic effects )
  43. what are the drugs that act on nitric oxide ?
    hydralazine and nitropruside 
  44. what  is the difference in MOA between hydralazine and nitropruside though they both act by NO?
    hydralazine act by dilating arterioles but nitropruside act by dilating arterioles and veins 
  45. what is the drug of choice for hypertensive emergencies and why ?
    nitropruside because it  dilates both arterioles and veins
  46. why are nitroprusside coadministered with nitrites and thiosulphates ?
    prusside component  of nitropruside causes cyanide toxicity , nitrites increases the release of meth hemoglobin which releases more oxygen to the tissue and  cyanide has more binding sites to meth hemoglobin thus it acts as the carrier for cyanide , thus cyanide will not block the electron transport chain, thiosulphate grabs cyanide as thiocyanate 
  47. what are the drugs  that open ATP dependent potassium channel ? what is the major side effect ? 
    minoxidil and diazoxide (major side effect is  drug induced DM- 
  48. name the drug for topical treatment of baldness ?
  49. name drug for insulinoma?
  50. name 2 drugs causing gingival hyperplasia ?
    • phenytoin and -dipines (amlodipine), a simple dental surgery may cause infection and cause septicemia and bacteraial endocarditis in such patients) = such patients such visit dentists 
  51. which drug blocks renin ?
  52. name two functions of ACE  ?
    convery angiotensin 1 to 11 
     inactivate bradykinin  (ACEI prevent bradykinin degradation )
  53. if u have to stop ACEI due to cough , which group of antihypertensives u use ?
  54. name absolute contraindication for ACEI and ARBS?
    bilateral renal artery stenosis 
  55. drug of choice for heart falure and diabetes ?
    ACEI and ARBs
  56. DOC for post MI?
  57. DOC for BPH?
    alpha blocker
  58. DOC for dyslipidemias ?
    alpha blockers , CCB, ACEI ARBs (BB and thiazides are never used)
  59. which is the most powerful vasoconstrictor known to date ?
    endothelin , more powerful than angiotensin 2 
  60. name the drugs used in pulmonary HTN and their MOA?
    • bosentan - endothelin receptor antagonist 
    • epoprostenol  - prostacyclin analogue
    • sidenafil - phosphodiesterase 5 inhibitor
Card Set:
2012-07-15 11:30:33

usmle pharmacology
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