GU Pharm

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  1. a prodrug metabolized to its active form by CYP 2C19
    Clopidigril (plavix)
  2. Do not administer ________ with drugs that inhibit 2C19.
    Clopidigrel (plavix)
  3. Drugs that work in distal tubule to ↑ Na excretion 5-10%
    • Thiazides
    • Metolazone
    • K+ sparing aldosterone antagonists
  4. How do diuretics work?
    decrease renal Na+ reabsorption, which reduces water reapsorption
  5. _________  diuretics are used to alleviate congestive symptoms.
  6. ________ diuretics inhibit reabsorption of Ca++ and Mg+ back into systemic circulation.
  7. ________ diuretics can mimic a sulfa allergy.
  8. Electrolyte-related AE of loop diuretics.
    • Hypocalcemia
    • Hypomagnesemia
    • Hypokalemia (increase K+ excretion)
  9. _______ diuretics can have dose-related ototoxicity.
  10. Loop or thiazide diuretics better for HF? for HTN?
    • HF: Loop
    • HTN: Thiazide
  11. _________ are ineffecive as monotherapy if GFR less than 30.
  12. ________  sometimes coadministered with loop diuretics if reduced GFR.
  13. Avoid _______ in patients with elevated Scr (>2-2.5)
    loop diuretics
  14. Competitive antagonism of Na+-Cl- cotransporter .
    Thiazide diuretics
  15. Thiazide diuretics result in decrease in _______ and have a direct _______ effect.
    • intravascular volume
    • vasodilatory
  16. AE of thiazides.
    • hypokalemia
    • hyperuricemia
    • hyperglycemia
    • dehydration
  17. Cause  Na+ channel blockade; increase reabsorption of potassium into plasma from renal tubules.
    Potassium-sparing Diuretics
  18. AE of Potassium-sparing Diuretics.
  19. Potassium-sparing diuretics are mostly used in  combo with __________. Why?
    • HCTZ/TMT (Maxide)
    • If used alone, can cause hyperkalemia
  20. Decreases K+/Na+ exchange in distal tubule and collecting duct of nephron
    Aldosterone Antagonist
  21. Diuretic that inhibits both androgen and mineralocorticoid receptors
    Spironolactone (Aldactone)
  22. Diuretic that is more selective for mineralocorticoid receptors = Less AE.
    Eplerenone (Inspra)
  23. When would you NOT use a BB?
    acute decompensated HF
  24. Attenuation of cytotoxic and signaling effects of circulating catecholamines, which induce sympathetic tone, increase HR, and can increase pathogenesis of HF.
  25. ________ can be beneficial for and may help prevent acute coronary syndrome.
  26. Pts without s/s may not realize benefit of ACEI and BB b/c they are not necessarily used for symptomatic relief, they are used for mortality & survival benefits.
    ACEI & BB
  27. _______ agonize β receptors to increase contractility
  28. β-Blockers cause antagonism of _________.
  29. How do β-Blockers decrease C.O.?
    by decreasing heart rate and contractility, which decreases BP (catecholamine antagonism)
  30. What happens with PVR initially with BB?
    body compensates for decrease in BP by increasing PVR
  31. What happens in the long run with BB and PVR?
    they decrease PVR by inhibiting β-receptors in kidney, which decreases renin (decreases BP by decreasing vasoconstriction & Na+ & water retention)
  32. _________ produce resting bradycardia and therefore reduce exercise-induced tachycardia.
  33. Can cause AV block; risk is increased when used with Digoxin.
  34. Can mask s/s of hypoglycemia.
  35. Detrimentally affects lipid profile (can cause hyperlipidemia!).
  36. B-2 receptors cause bronchoconstriction, so pts with asthma should NOT be on a __________.
    non-selective BB
  37. Why should a pt avoid sudden w/d of BB?
    body compensates by upregulating beta receptors, so when you abruptly stop, you have more beta receptors available for catecholamine action → rebound HTN, tachycardia
  38. Antagonizes catecholamines at β1 and β2 receptors, inhibition of sympathetically induced renin secretion
    Non-selective β-Blockers
  39. Why are non-selective β-Blockers contraindicated in pts with asthma?
    they block B-2 receptors and cause bronchoconstriction
  40. Two types of selective β-Blockers.
    • Metoprolol
    • Atenolol
  41. Metoprolol is hepatically metabolized by _________.
  42. Selective β-Blocker that has dose-dependent cardioselectivity.
  43. Selective β-Blocker that is less lipid-soluble and more water-soluble.
  44. Why does it matter that atenolol is more water-soluble than metoprolol?
    it is less metabolized, and will be even more slowly metabolized in pts with renal dysfunction
  45. Acebutolol, carteolol, penbutolol, pindolol
    Partial β-Blockers (mixed agonist-antagonist)
  46. Benefit to Partial β-Blockers over β-Blockers.
    Less resting bradycardia (act as agonist when sympathetic tone is low)
  47. Labetalol and Carvedilol
    Mixed α1/β1/2 Blockers
  48. Precaution: “first dose effect” – postural hypotension, body will eventually compensate, but can titrate slowly over time or give at bedtime
    α1- Blockers
  49. What do you need to give with α1- Blockers? Why?
    • diuretic
    • w/o it, there will be Na+ & H2O retention
  50. Inhibit peripheral vasomotor tone, reducing vasoconstriction and decreasing SVR, which decreases BP
    α1- Blockers
  51. What are α1- Blockers used to treat?
  52. How are α1- Blockers metabolized?
    hepatic ally, non-CYP
  53. Reduce sympathetic outflow from vasopressor centers in the brain stem, so work in CNS
    Centrally Acting Agents (alpha-2 agonists)
  54. Reverses vasoconstriction and volume retention that is caused by renin-angiotensin-aldosterone system activation
    ACE Inhibitors
  55. What happens with abrupt w/d of Clonidine?
    Rebound hypertension (downregulates alpha-2 receptors, once drug is removed, there is less feedback inhibition)
  56. What happens when TCA's are administered with Clonidine?
    effect of Clonidine is blocked (b/c TCA’s inhibit reuptake of NE & will increase action of catecholamines further)
  57. How is Clonidine metabolized?
    50/50 hepatic metabolism and renal excretion
  58. Block ACE conversion of angiotensin I to angiotensin II; *also block inactivation of bradykinin
    ACE Inhibitors
  59. __________ are beneficial for diabetics with proteinuria.
  60. Elicits maximal response; Stabilizes DR*
    Full agonist
  61. Stabilizes DR and DR*
    Partial or mixed agonist-antagonist
  62. Stabilizes DR in the case of R*
    Inverse - inactivates free active receptors
  63. Stabilization of DR; Prevention of DR*
  64. reversible binding, active site
    Competitive antagonist
  65. irreversible active site or allosteric site
    Noncompetitive antagonist
  66. MOA: Na channel blockade in collecting duct, increased K reabsorption
    • K sparing:
    • Triamterene, amiloride
  67. MOA: inhibit Na-K-CL cotransporter in loop of Henle
    • Loop diuretics:
    • Furosemide, bumetanide, torsemide
  68. MOA: competitive antagonism of Na-Cl transporter in distal tubule
  69. MOA: competitive antagonist at aldosterone receptor; inhibits mineralcorticoid receptors
    • Aldosterone antagonist:
    • Spironolactone, eplerenone
  70. Less effective if CrCl <30 (diuretic)
  71. Diuretic that alleviates congestive sxs of HF
  72. AE: dose related ototoxicity, ↓ Mg, ↓ Ca, “sulfa” allergy
  73. What drug would be a good choice for someone with HTN and BPH?
    Prazosin α1 blocker
  74. AEs if Dihydropyridines.
    • peripheral edema,
    • dizziness,
    • headache,
    • flushing,
    • reflex tachycardia,
    • constipation
  75. AE of Procainamide.
    • SLE,
    • neutropenia,
    • anemia
Card Set
GU Pharm
pharm mod 7
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