Cario pharm

Card Set Information

Author:
Neda317
ID:
306000
Filename:
Cario pharm
Updated:
2015-08-03 20:55:54
Tags:
pharm
Folders:

Description:
304-310 cardio
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user Neda317 on FreezingBlue Flashcards. What would you like to do?


  1. tx Primary (essential)
    hypertension
    • Thiazide diuretics, ACE inhibitors, angiotensin
    • II receptor blockers (ARBs), dihydropyridine
    • Ca2+  channel blockers.
  2. Hypertension with
    heart failure
    • Diuretics,
    • ACE inhibitors/ARBs,
    • β blockers (compensated HF),
    • aldosterone antagonists
  3. what should be  used cautiously in
    decompensated HF, and CI in cardiogenic shock?
    β-blockers
  4. Hypertension with
    diabetes mellitus
    • ACE inhibitors/ARBs,
    • Ca2+  channel blockers,
    • thiazide diuretics,
    • β -blockers.
  5. ACE inhibitors/ARBs are protective against
    diabetic nephropathy
  6. Hypertension in
    pregnancy
    Hydralazine, labetalol, methyldopa, nifedipine
  7. Calcium channel
    blockers MOA
    • Block voltage-dependent L-type calcium channels of cardiac and smooth muscle => dec muscle
    • contractility.
  8. Calcium channel
    blockers 
    Vascular and heart
    •  Vascular smooth muscle—amlodipine =  nifedipine > diltiazem > verapamil.
    • Heart—verapamil > diltiazem > amlodipine =  nifedipine (v erapamil = v entricle).
  9. Calcium channel
    blockers use
    •  Dihydropyridines (except nimodipine): hypertension, angina (including Prinzmetal), Raynaud
    • phenomenon.
    • Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm).
    • Clevidipine: hypertensive urgency or emergency.
    • Non-dihydropyridines: hypertension, angina, atrial fibrillation/flutter.
  10. Dihydropyridines CCBs names
    Vascular smooth muscle—amlodipine =  nifedipine > diltiazem > verapamil.
  11. Non-dihydropyridines CCBs names
    Heart—verapamil > diltiazem > amlodipine =  nifedipine (v erapamil = v entricle).
  12. CCB toxicity
    • Cardiac depression, AV block (non-dihydropyridines), peripheral edema, flushing, dizziness,
    • hyperprolactinemia (verapamil), constipation, gingival hyperplasia
  13. which CCB gives hyperprolactinemia
    verapamil
  14. Hydralazine
    MOA
    • inc cGMP=> smooth muscle relaxation.
    • Vasodilates arterioles > veins; afterload reduction.
  15. Frequently coadministered with a β -blocker to prevent refl ex tachycardia
    Hydralazine
  16. Hydralazine use
    • Severe hypertension (particularly acute), HF (with organic nitrate). Safe to use during pregnancy.
    • Frequently coadministered with a β -blocker to prevent reflex tachycardia
  17. Hydralazine toxicity and CI
    • Compensatory tachycardia (contraindicated in angina/CAD),
    • fluid retention(sodium and fluid retention often given in combination w sympatholytics and diuretics.), headache, angina.
    • Lupus-like syndrome
  18. Hypertensive
    emergency
    Drugs include clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside
  19. Nitroprusside
    Short acting; inc cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide).
  20. Fenoldopam
    • Dopamine D1  receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation. dec BP,
    • dec natriuresis.
  21. Nitrates names
    • Nitroglycerin,
    • isosorbide dinitrate,
    • isosorbide mononitrate
  22. Nitrates MOA
    • Vasodilate by inc NO in vascular smooth muscle=> inc  in cGMP and smooth muscle relaxation.
    • Dilate veins >> arteries.
    • dec  preload.
  23. Nitrates use
    Angina, acute coronary syndrome, pulmonary edema
  24. Nitrates tox
    and what is Monday disease
    • Reflex tachycardia (treat with β -blockers), hypotension, flushing, headache, “Monday disease” in
    • industrial exposure: development of tolerance for the vasodilating action during the work week
    • and loss of tolerance over the weekend => tachycardia, dizziness, headache upon reexposure.
  25. HMG-CoA reductase
    inhibitors
    • lovastatin,
    • pravastatin,simvastatin,atorvastatin,
    • rosuvastatin
  26. HMG-CoA reductase
    inhibitors MOA 
    effect on LDL,HDL,TG
    • MOA:  Inhibit conversion of HMGCoA
    • to mevalonate, a
    • cholesterol precursor;
    • dec mortality in CAD patients
    • LDL ↧↧↧
    • HDL↥
    • TG ↧
  27. HMG-CoA reductase
    inhibitors
    SE
    • Hepatotoxicity (inc LFTs),
    • myopathy (esp. when used
    • with fibrates or niacin)
  28. Bile acid resins
    SE
    • GI upset, ↧ absorption of
    • other drugs and fat-soluble
    • vitamins
  29. cholestyramine,
    colestipol,
    colesevelam
    are family of
    Bile acid resins
  30. Bile acid resins
    MOA effect on LDL,HDL,TG
    • Prevent intestinal reabsorption of bile acids;
    • liver must use cholesterol to
    • make more
    • LDL ↧↧
    • HDL slightly ↥
    • TG slightly ↥
  31. Ezetimibe
    MOA effect on LDL,HDL,TG
  32. Prevent cholesterol absorption at small intestine brush border
    • LDL ↧
    • HDL -
    • TG -
  33. gemfibrozil,
    clofibrate,
    bezafibrate,
    fenofibrate
    Fibrates 
  34. Fibrates 
    MOA effect on LDL,HDL,TG
    • Upregulate LPL => inc TG clearance
    • Activates PPAR-α  to induce
    • HDL synthesis
    • LDL ↧
    • HDL↥
    • TG ↧↧↧
  35. Niacin (vitamin B3)
    MOA effect on LDL,HDL,TG
    Inhibits lipolysis (hormone sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis

    • LDL ↧↧
    • HDL↥↥
    • TG ↧
  36. Niacin (vitamin B3)
    SE
  37.  Red, flushed face, which is dec by NSAIDs or long-term use
    • Hyperglycemia
    • Hyperuricemia
  38. Fibrates
    SE
    Myopathy (inc risk with statins),

    cholesterol gallstones
  39. Cardiac glycosides
     Digoxin
  40.  Digoxin
    MOA
  41.  Direct inhibition of Na+ /K+  ATPase =>  indirect inhibition of Na+ /Ca2+  exchanger.
    inc [Ca2+ ]i =>  positive inotropy. Stimulates vagus nerve => dec HR.
  42. Digoxin
    use
    HF (inc  contractility); atrial fibrillation (dec  conduction at AV node and depression of SA node).
  43.  Factors predisposing to Digoxin toxicity 
  44.  renal failure (dec excretion), hypokalemia (permissive for digoxin binding at K+ -binding site on Na+ /K+  ATPase), verapamil, amiodarone, quinidine (dec digoxin clearance; displaces digoxin from tissue-binding sites).
  45. Antiarrhythmics— sodium channel
    blockers (class I)
    • Slow or block (dec ) conduction (especially in depolarized cells). dec slope of phase 0 depolarization.
    • Are state dependent (selectively depress tissue that is frequently depolarized [e.g.,tachycardia]).
  46. name 
    Class IA
    Procainamide, Disopyramide, Quinidine.

    “Ava Performed Dancing Quine”
  47. class 1A MOA
    • inc AP duration,  inc effective refractory period
    • (ERP) in ventricular action potential,  inc QT
    • interval.
  48. Class 1A
    use
    • Both atrial and ventricular arrhythmias,
    • especially re-entrant and ectopic SVT and VT.
  49. Class 1A
    tox with
    quinidine
    procainamide
    disopyramide
    • Cinchonism (headache, tinnitus with
    • quinidine), reversible SLE-like syndrome
    • (procainamide), heart failure (disopyramide),
    • thrombocytopenia, torsades de pointes due to
    • inc QT interval.
  50. Class 1B
    name
    • Lidocaine, MexileTine
    • "Like Mexican Taco"
  51. Class 1B
    MOA
    • dec AP duration. Preferentially affect ischemic or
    • depolarized Purkinje and ventricular tissue.
    • Phenytoin can also fall into the IB category.
  52. Class 1B
    use
    • Acute ventricular arrhythmias (especially post-
    • MI), digitalis-induced arrhythmias.

    IB  is Best post-MI.
  53. Class 1B
    tox
    • CNS stimulation/depression, cardiovascular
    • depression.
  54. Class 1C
    name
    Flecainide, Propafenone.

    “Can I have Fries, Please.”
  55. Class 1C
    MOA
    • Significantly prolongs ERP in AV node and
    • accessory bypass tracts. No effect on ERP in
    • Purkinje and ventricular tissue.
    • Minimal effect on AP duration.
  56. Class 1C
    use
    SVTs, including atrial fibrillation. Only as a last resort in refractory VT.
  57. Class 1C
    tox
    and CI
    • Proarrhythmic, especially post-MI
    • (contraindicated).

    • IC  is Contraindicated in
    • structural and ischemic heart disease.
  58. Class II
    name 
    type
    Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol.

    BB
  59. Class II
    MOA
    which one is very short acting
    • Decrease SA and AV nodal activity by dec cAMP,dec Ca2+  currents. Suppress abnormal pacemakers by dec slope of phase 4.
    • AV node particularly sensitive— inc PR interval. Esmolol very short acting.
  60. Class II
    use
    SVT, ventricular rate control for atrial fibrillation and atrial flutter.
  61. Class II treatment for toxicity
    Treat β -blocker overdose with saline, atropine, glucagon.
  62. Class II
    tox
    which one can cause dyslipidemia
    which one exacerbate vasospasm in Prinzmetal angina.
    • Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, HF),
    • CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.
    • Metoprolol can cause dyslipidemia. Propranolol can exacerbate vasospasm in Prinzmetal angina.
    • β -blockers cause unopposed α1 -agonism if given alone for pheochromocytoma or cocaine toxicity.
  63. Class III
    name
    type
    potassium channel blockers (class III)

    Amiodarone, Ibutilide, Dofetilide, Sotalol. "AIDS"
  64. Class III
    MOA
  65.  inc AP duration, inc ERP, inc QT interval.
  66. Class III
    use
    • Atrial fibrillation, atrial flutter; ventricular
    • tachycardia (amiodarone, sotalol).
  67. Class III
    tox
    Sotalol
    Ibutilide
    Amiodarone
    • Sotalol—torsades de pointes, excessive β
    •  blockade.
    • Ibutilide—torsades de pointes.
    • Amiodarone—pulmonary fibrosis,
    • hepatotoxicity, hypothyroidism/
    • hyperthyroidism (amiodarone is 40% iodine by
    • weight), acts as hapten (corneal deposits, blue/gray skin deposits resulting in photodermatitis),
    • neurologic effects, constipation, cardiovascular
    • effects (bradycardia, heart block, HF).
  68. using amiodarone need to check 
    • Remember to check PFTs, LFTs, and TFTs when
    • using amiodarone.
    • Amiodarone is lipophilic and has class I, II, III,
    • and IV effects
  69. Class IV
    name 
    type
    calcium channel blockers (class IV)

    Verapamil, diltiazem
  70. Class IV
    MOA
    dec conduction velocity, inc ERP, inc PR interval.
  71. Class IV
    use
    Prevention of nodal arrhythmias (e.g., SVT), rate control in atrial fibrillation.
  72. Class IV
    tox
    Constipation, flushing, edema, cardiovascular effects (HF, AV block, sinus node depression).
  73. Adenosine
    MOA
    Effects blunted by 
  74. inc K+ out of cells => hyperpolarizing the cell and  dec ICa. Drug of choice in diagnosing/abolishing
    supraventricular tachycardia. Very short acting (~ 15 sec). Effects blunted by theophylline and caffeine (both are adenosine receptor antagonists).
  75. Adenosine 
    Adverse effects
    include flushing, hypotension,chest pain, sense of impending doom, bronchospasm.
  76. Mg2+ Effective in
     Effective in torsades de pointes and digoxin toxicity.

What would you like to do?

Home > Flashcards > Print Preview