A Pharm- summer 1- cardiac

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Anonymous
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223315
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A Pharm- summer 1- cardiac
Updated:
2013-06-10 22:57:05
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aa emory pharm
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cardiac drugs
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  1. Inotropes:  Improve
    ____________, treating _____ prob.
    • CONTRACTILITY
    • PUMP
  2. Vasopressors: Increase ________, and ________ and treat ____ problem
    • VASCULAR tone
    • SVR
    • treat PIPE problem
  3. Relaxation of cardiac myocytes occurs when _____ ____ channels close.
    Slow Ca2+
  4. INOtropy:  ________ of intracellular Ca2+ and ________.  (IQT)
    • QUANTITY
    • Max Tension developed
  5. CHRONOtropy: _____ of Ca2+ delivery. 
    Rate of __________. (CRC^2)
    • RATE
    • Contraction
  6. LUSItropy:  _________ of
    intracellular Ca2+.  _______ of __________.  (LRR)
    • REMOVAL
    • Rate of Relaxation
  7. An increase in cAMP in heart cell will increase ______ release.  What are two drugs that use this pathway?
    • Ca2+
    • Milrinone
    • B-agonists
  8. β- Agonists mechanism of action? Main method?
    • stimulate adenylate cyclase, ^ cAMP.
    • catecholamine
  9. B1 increases what?
    • Inotropy
    • Chronotropy
  10. B2 increases what?
    • Inotropy
    • Smooth muscle vasodilation (pulm)
  11. A1 causes what effect?
    vasoconstriction
  12. Epi has _____ fx on B1, B2, a1.  side fx include:
    • equal
    • arrhythmias
  13. What two drugs have higher a than B fx?
    dopamine, norepi
  14. Norepi side fx:
    intense SVR increase can cause CO drop
  15. Dobutamine side fx:
    Tachycardia
  16. Isoproteronol is a _____ __ _______.  side fx include what three things?
    • Pure B agonist.
    • Significant TACHY, ARRHYTMIA, drop SVR.
  17. Phosphodiesterase Inhibitors mechanism of action:
    prevent cAMP breakdown.
  18. PDE’s breakdown cyclic nucleotides (____, ____) and are ________ __________ that ACTIVATE PROTEIN KINASES and OPEN ___ ________.
    • camp, cgmp
    • second messengers
    • PROTEIN KINASES
    • ION CHANNELS
  19. PDE3 A receptors found where?
    CARDIOVASCULAR SYSTEM and PLATELETS
  20. PDE3 B receptors found where? activated by?
    • Adipose/liver
    • insulin
  21. PDE3 INHIBITORS: What two areas are effected by these drugs?
    • Cardiac myocytes: ^ cAMP = ^ Ca2+, increase contractility
    • Vascular tissue: ^ cyclic nucleotides, smooth muscle relaxation, Decrease PA pressure and SVR

                                                            “INODILATOR”
  22. what are 3 PDE-I drugs?
    • Amrinone
    • Milrinone
    • Enoximone
  23. How is Enoximone excreted?
    Hepatic
  24. Why is NOREPI 1st line of support?  What can be added is systolic function is poor?
    • some + inotropy, maintain perfusion pressure
    • Epi, dobutamine, PDE-I
  25. T or F, second messenger in a receptors of vasculature is cAMP?  Do they cause Ca2+ release?
    • F
    • Yes
  26. What are the non-catecholamine sympathomimetics? (3) PME
    • Phenylephrine- pure direct a agonist
    • Methoxamine- direct direct a agonist
    • Ephedrine- indirect
  27. What are the 2 pure direct a agonists?
    • Phenylephrine
    • Methoxamine
  28. how does Ephedrine work?
    causes Norepi release from neurons
  29. T or F, Ephedrine has some B2 activation?  Is it direct?  What prolongs ephedrine?  How much is excreted unchanged from the kidney?  Does it affect uterine vasc resistance?
    • T
    • Yes
    • MAOI's
    • 40%
    • NO
  30. Vasopressin:   a ___-______________ vasopressor.  No __ receptors involved, vasoconstriction due to ___ receptors.  Second messenger system is utilized, and Ca2+ release causes vasoconstriction- T or F?
    • non-sympathomimetic
    • a
    • V1
    • T
  31. Where are the following receptors located?
    V2
    V3
    • kidneys
    • pituitary
  32. AVP main role is not ___ _____ _____.  levels increase by 2-3X with _____.  Levels decrease following ___
    • vasc tone reg
    • sepsis
    • CPB
  33. Vasopressin side effects and what causes them:
    • Intense vasoconstriction = Myocardial ischemia, decreased CO, mesenteric ischemia
    • less effect on pulmonary vasculature
  34. why can Vasopresson be beneficial with pulmonary HTN?
    Less of an effect on pulmonary vasculature
  35. Conventional Inotropes are ______ __________.
    “Calcium Mobilizers”
  36. “Calcium Sensitizers”  work at the interaction
    of_______/____ or response to ____ binding.
    • troponin/Ca2+
    • Ca2+
  37. Why the fact that calcium sensitizers don't increase calcium possibly a benefit?
    • Less arrythmogenic
    • Do not increase O2 consumption
  38. Calcium Sensitizers are _________ with other agents.
    synergistic
  39. What are the Calcium Sensitizer drugs? (3)
    • Pimobendan
    • Levosimendan
  40. What is Methylene Blue mechanism? what are side fx of high doses?
    • Block GC activation by NO, leading to LESS vasodilation.
    • High doses = hyperbilirubinemia/ hemolytic anemia
  41. What causes a higher change in VO2?  Milrinone or Levosimendan?
    Milrinone

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