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Pharmacology > Cardio Pharm > Flashcards

Cardio Pharm Flashcards

1
Q

Primary (essential) HTN - treatment (4)

A

Diuretics, ACE inhibitors, ARBs, Ca2+ channel blockers

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2
Q

HTN with CHF - treatment (5)

A

Diuretics, ACE inhibitors, ARBs, B-blockers (compensated CHF, use cautiously in decompensated and contraindicated in cardiogenic shock), aldosterone antagonists

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3
Q

HTN with Diabetes Mellitus - treatment (6)

A

ACE inhibitors/ARBs (protective against diabetic nephropathy), Ca2+ channel blockers, diuretics, beta-blockers, alpha-blockers

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4
Q

MOA of calcium channel blockers

A

Block voltage-dependent L-type calcium channels of cardiac & smooth muscle –> decreased contractility

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5
Q

Which Ca2+ channel blockers work on the vascular smooth muscle?

A

amlodipine = nifedipine > diltiazem > verapamil

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6
Q

Which Ca2+ channel blockers work on the heart?

A

verapamil > diltiazem > amlodipine = nifedipine (verapimil = ventricle)

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7
Q

Clinical uses of amlodipine and nifedipine

A

HTN, angina (incl. Prinzmetal), Raynaud’s

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8
Q

Clinical uses of non-dihydropyridines

A

HTN, angina, a-fib/a-flutter

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9
Q

Clinical use of nimodipine

A

Subarachnoid hemorrhage (prevents cerebral vasospasm)

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10
Q

Toxicity of calcium channel blockers

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation

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11
Q

Amlodipine

A

Dihydropyridine Ca2+ channel blocker

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12
Q

Nimodipine

A

Dihydropyridine Ca2+ channel blocker

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13
Q

Nifedipine

A

Dihydropyridine Ca2+ channel blocker

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14
Q

Diltiazem

A

Non-dihydropyridine Ca2+ channel blocker

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15
Q

Verapamil

A

Non-dihydropyridine Ca2+ channel blocker

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16
Q

Hydralazine - MOA

A

Increase cGMP –> smooth muscle relaxation; vasodilates arterioles > veins; afterload reduction

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17
Q

Clinical uses of hydralazine

A

Severe HTN, CHF. 1st line for HTN in pregnancy (w/ methyldopa); frequently coadministered w/ B-blocker to prevent reflex tachycardia

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18
Q

Toxicity of hydralazine

A

Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina. Lupus-like syndrome

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19
Q

Drugs used for hypertensive emergency

A

Nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam

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20
Q

Nitroprusside - MOA, toxicity

A

Short acting
Increase cGMP via direct release of NO
Releases cyanide (toxic)

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21
Q

Fenoldopam - MOA

A

Dopamine D1 receptor agonist – coronary, peripheral, renal, & splanchnic vasodilation. Decrease BP & increased natriuresis

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22
Q

Nitroglycerin, isosorbide dinitrate - MOA

A

Vasodilate via increase NO in vascular smooth muscles –> increased cGMP & smooth muscle relaxation (veins&raquo_space; arteries)
Decreases preload

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23
Q

Clinical use of nitroglycerin and isosorbide dinitrate

A

Angina, acute coronary syndrome, pulm edema

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24
Q

Nitroglycerine and isosorbide dinitrate toxicity

A

Reflex tachycardia (tx: B-blockers); hypotension, flushing, headache, “Monday disease”

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25
Q

What is Monday disease?

A

In industrial exposure, youdevelop tolerance for the vasodilating action during the work week and loss of tolerance over the weekend –> tachycardia, dizziness, and headache upon reexposure to nitrates

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26
Q

MOA of HMG - CoA reductase inhibitors

A

Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor

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27
Q

Side effects of statins

A

Hepatotoxicity (LFTs)
Rhabdomyolysis (esp. when used w/ fibrates & niacin)

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28
Q

Effects of statins on LDL, HDL, and TGs

A

Large decrease in LDL, slight increase in HDL, small decrease in TGs

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29
Q

Effects of niacin on LDL, HDL, and TGs

A

Decrease in LDL, increase in HDL, small decrease in TGs

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30
Q

Effects of bile acid resins on LDL, HDL, and TGs

A

Decrease in HDL, slightly increased HDL, slightly increased TGs

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31
Q

Effects of ezetimibe on LDL, HDL, and TGs

A

Decreased LDL (no effect on HDL or TG)

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32
Q

Effects of fibrates on LDL, HDL, and TGs

A

Small decrease in LDL, small increase in HDL, large decrease in TGs

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33
Q

MOA of niacin

A

Inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis

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34
Q

Side effects of niacin

A

Red flushed face which is decreased with aspirin or long term use
Hyperglycemia (acanthosis nigricans)
Hyperuricemia (exacerbates gout)

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35
Q

What are the bile acid resins?

A

Cholestyramine, colestipol, colesevelam

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36
Q

MOA of bile acid resins

A

Prevent intestinal reabsorption of bile acids – liver must use cholesterol to make more

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37
Q

Side effects of bile acid resins

A

Tastes bad, GI discomfort, decreased absorption of fat soluble vitamins, cholesterol gallstones

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38
Q

What is the cholesterol absorption blocker?

A

Ezetimibe

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39
Q

MOA of ezetimibe

A

Prevents cholesterol absorption at small intesting brush border

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40
Q

Side effects of ezetimibe

A

Rare increase in LFTs, diarrhea

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41
Q

MOA of fibrates

A

Upregulates LPL –> TG clearance
Activates PPAR-a to induce HDL synthesis

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42
Q

side effects of fibrates

A

Myositis (increased risk w/ concurrent statins)
Hepatotoxicity
Cholesterol gallstones (esp. w/ concurrent bile acid resins)

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43
Q

What is the most common cardiac glycoside?

A

Digoxin

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44
Q

MOA of digoxin

A

Direct inhibition of Na/K ATPase –> indirect inhib of Na/Ca exchanger/antiporter –> inceased intracellular Ca2+ –> positive inotropy; stimulates vagus nerve –> decr. HR

45
Q

Clinical use of digoxin

A

CHF (incr. contractility); A-fib (decr. conduction at AV node & depression of SA node)

46
Q

Toxicity of digoxin

A

Cholinergic: N/V, diarrhea, blurry yellow vision
ECG: incr. PR, decr. QT, ST scooping, T-wave inversion, arrhythmia, AV block
Can lead to hyperkalemia = poor prognosis

47
Q

What are factors predisposing to digoxin toxicity?

A

Renal failure (decr. excretion), hypokalemia (permits digoxin binding at K+ binding site on Na/K ATPase

48
Q

What other drugs can increase digoxin toxicity? (3)

A

Verapimil, amiodarone, quinidine (decr. digoxin clearance; displaces digoxin from tissue-binding sites)

49
Q

Antidote to digoxin

A

Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+

50
Q

Quinidine

A

Class 1A antiarrhythmic - Na+ channel blocker

51
Q

Procainamide

A

Class 1A antiarrhythmic - Na+ channel blocker

52
Q

Disopyramide

A

Class 1A antiarrhythmic - Na+ channel blocker

53
Q

Lidocaine

A

Class 1B antiarrhythmic - Na+ channel blocker

54
Q

Mexiletine

A

Class 1B antiarrhythmic - Na+ channel blocker

55
Q

Flecainide

A

Class 1C antiarrhythmic - Na+ channel blocker

56
Q

Propafenone

A

Class 1C antiarrhythmic - Na+ channel blocker

57
Q

Metoprolol

A

Class 2 antiarrhythmic - B-blocker

58
Q

Propranolol

A

Class 2 antiarrhythmic - B-blocker

59
Q

Esmolol

A

Class 2 antiarrhythmic - B-blocker

60
Q

Atenolol

A

Class 2 antiarrhythmic - B-blocker

61
Q

Timolol

A

Class 2 antiarrhythmic - B-blocker

62
Q

Carvedilol

A

Class 2 antiarrhythmic - B-blocker

63
Q

Amiodarone

A

Class 3 antiarrhythmic - K+ channel blocker

64
Q

Ibutilide

A

Class 3 antiarrhythmic - K+ channel blocker

65
Q

Dofetilide

A

Class 3 antiarrhythmic - K+ channel blocker

66
Q

Sotalol

A

Class 3 antiarrhythmic - K+ channel blocker

67
Q

Verapamil

A

Class 4 antiarrhythmic - Ca2+ channel blocker

68
Q

Diltiazem

A

Class 4 antiarrhythmic - Ca2+ channel blocker

69
Q

Class 1A antiarrhythmics - names & type of blocker

A

Quinidine, Procainamide, Disopyramide (Queen Proclaim’s Disco)
Na+ channel blockers

70
Q

Class 1B antiarrhythmics - names & type of blocker

A

Lidocaine, Mexiletine, sometimes phenytoin
Na+ channel blockers

71
Q

Class 1C antiarrhythmics - names & type of blocker

A

Flecainide, Propafenone
Na+ channel blockers

72
Q

Class 2 antiarrhythmics - names & type of blocker

A

Metoprolol, Propanolol, Esmolol, Atenolol, Timolol, Carvedilol
B-blockers

73
Q

Class 3 antiarrhythmics - names & type of blocker

A

Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)
K+ channel blockers

74
Q

Class 4 antiarrhythmics - names & type of blocker

A

Verapimil, Diltiazem
Ca2+ channel blockers

75
Q

Na+ channel blockers (class I) overall mechanism

A

Slow or block conduction (esp. in depolarized cells). Decr. slope of phase 0 depolarization and incr. threshold for firing in abnormal pacemaker cells; state-dependent (selectively depress tissue that is frequently depolarized)

76
Q

What causes increased toxicity for ALL class I drugs?

A

Hyperkalemia

77
Q

Class 1A antiarrhythmics - mechanism

A

Incr. AP duration
Incr. ERP
Incr. QT

78
Q

Clinical use of class 1A antiarrhythmics

A

Atrial & ventricular arrhythmias, esp. re-entrant and ectopic SVT & VT

79
Q

General toxicity of class 1A antiarrhythmics

A

Thrombocytopenia, torsades de pointes (incr. QT)

80
Q

Specific toxicity of quinidine

A

Cinchonism - headache, tinnitus

81
Q

Specific toxicity of procainamide

A

Reversible SLE-like syndrome

82
Q

Specific toxicity of disopyramide

A

Heart failure

83
Q

Class 1B antiarrhythmics - mechanism

A

Decr. AP duration - preferentially affects ischemic or depolarized Purkinje & ventricular tissue

84
Q

Clinical use of class 1B antiarrhythmics

A

Acute ventricular arrhythmias (esp. post-MI)
Digitalis-induced arrhythmias

85
Q

Toxicity of class 1B antiarrhythmics

A

CNS stimulation/depression, cardiovascular depression

86
Q

Class 1C antiarrhythmics - mechanism

A

Prolongs refractory period in AV node; minimal effect on AP duration

87
Q

Clinical use of class 1C antiarrhythmics

A

SVTs, including A-fib; only as last resort in refractory VT

88
Q

Toxicity of class 1C antiarrhythmics

A

Proarrhythmic, esp. post MI (contraindicated in structural & ischemic heart disease)

89
Q

B-blockers (class II) - mechanism

A

Decrease SA & AV nodal activity by decr. cAMP & Ca2+ currents; suppress abnormal pacemakers by decr. slope of phase 4; incr. PR interval

90
Q

Clinical use of B-blockers

A

SVT, slowing ventricular rate during A-fib & A-flutter

91
Q

General toxicity of B-blockers

A

Impotence, COPT/asthma exacerbation, CV effects (bradycardiam AV block, CHF), CNS effects (sedation, sleep alterations); may mask hypoglycemia

92
Q

Specific toxicity of metoprolol

A

Dyslipidemia

93
Q

Specific toxicity of propanolol

A

Exacerbate vasospasm in Prinzmetal angina

94
Q

B-blockers are contraindicated in what patients?

A

Cocaine users (risk of unopposed a-adrenergic receptor agonist activity)

95
Q

Treatment for B-blocker O/D?

A

Glucagon

96
Q

K+ channel blockers (class III) - mechanism

A

Incr. AP duration; incr ERP; incr. QT
Used when other antiarrhythmics fail

97
Q

Clinical use of K+ channel blockers

A

A-fib, A-flutter, V-tach (amiodarone, sotalol)

98
Q

Specific toxicity of sotalol

A

Torsades de pointes, excessive B-blockade

99
Q

Specific toxicity of ibutilide

A

Torsades de pointes

100
Q

Specific toxicity of amiodarone

A

Pulm fibrosis, hepatotoxicity, hypo or hyperthyroidism, corneal deposits, blue/gray skin deposits –> photodermatitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF)

101
Q

What must you check when using amiodarone?

A

PFTs, LFTs, & TFTs

102
Q

Ca2+ channel blockers (class IV) - mechanism

A

Decr. conduction velocity; incr. ERP; incr. PR

103
Q

Clinical use of Ca2+ channel blockers

A

Prevention of nodal arrhythmias (SVT), rate control in A-fib

104
Q

Toxicity of Ca2+ channel blockers

A

Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

105
Q

MOA of adenosime

A

Incr. K+ efflux –> hyperpolarizes cell & decr. Ca current.

106
Q

Clinical use of adenosine

A

Drug of choice in diagnosing/abolishing SVT; very short-acting

107
Q

Toxicity of adenosine

A

Flushing, hypotension, chest pain

108
Q

Effects of adenosine are blocked by what?

A

Theophylline, caffeine

109
Q

Clinical use of Mg2+

A

Torsades de pointes; digoxin toxicity

Pharmacology (4 decks)

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