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Pharmacology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Amlodipine (MOA)

A

Voltage-dependent L-type calcium channel blocker of cardiac and smooth muscle -> reducing muscle contraction
Vasodilation of vascular smooth muscle

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2
Q

Amlodipine (CU)

A

HTN, angina, Raynaud

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3
Q

Amlodipine (T)

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactenemia and constipation

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4
Q

Nimodipine (MOA)

A

Voltage-dependent L-type calcium channel blocker of cardiac and smooth muscle -> reducing muscle contraction
Vasodilation of vascular smooth muscle
(-) inotrope for heart muscle

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5
Q

Nimodipine (CU)

A

Subarachnoid hemorrhage (prevents cerebral vasospasm)

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6
Q

Nimodipine (T)

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactenemia and constipation

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7
Q

Nifidipine (MOA)

A

Voltage-dependent L-type calcium channel blocker of cardiac and smooth muscle -> reducing muscle contraction
Vasodilation of vascular smooth muscle

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8
Q

Nifidipine (CU)

A

HTN, angina, Raynaud

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9
Q

Nifidipine (T)

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactenemia and constipation

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10
Q

Diltiazem (MOA)

A

Voltage-dependent L-type calcium channel blocker of cardiac and smooth muscle -> reducing muscle contraction
Vasodilation of vascular smooth muscle
(-) inotrope
Class IV antiarrhythmics - decreased conduction velocity, increased effective refractory period, increased PR interval

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11
Q

Diltiazem (CU)

A

HTN, angina, A Fib/flutter, SVT

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12
Q

Diltiazem (T)

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactenemia and constipation

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13
Q

Verapamil (MOA)

A

Voltage-dependent L-type calcium channel blocker of cardiac and smooth muscle -> reducing muscle contraction
Vasodilation of vascular smooth muscle
(-) inotrope
Class IV antiarrhythmics - decreased conduction velocity, increased effective refractory period, increased PR interval

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14
Q

Verapamil (CU)

A

HTN, angina, A Fib/flutter, SVT

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15
Q

Verapamil (T)

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactenemia and constipation

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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

Hydralazine (CU)

A

Severe HTN, CHF. 1st line for HTN in pregnancy w/ methyldopa. Frequently coadministered with a B-blocker to prevent reflex tachycardia

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18
Q

Hydralazine (T)

A

Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, HA, angina. LUPUS LIKE SYNDROME

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19
Q

Nitroprusside (MOA)

A

Short acting; increases cGMP via direct release of NO.

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20
Q

Nitroprusside (CU)

A

HTN emergency

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21
Q

Nitroprusside (T)

A

Cyanide toxicity

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22
Q

Fenoldopam (MOA)

A

Dopamine D1 receptor agonist -> coronary, peripheral, renal and splanchnic vasodilation. Decrease BP and increase natriuresis

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23
Q

Fenoldopam (CU)

A

Severe HTN

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24
Q

Nitroglycerine (MOA)

A

Vasodilate by increasing NO in vascular smooth muscle -> increase in cGMP and smooth muscle relaxation. Dilate veins&raquo_space; arteries. Decreases preload

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25
Q

Nitroglycerine (CU)

A

Angina, acute coronary syndrome, pulmonary edema

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26
Q

Nitroglycerine (T)

A

reflex tach, flushing, HA. “Monday ds” in industrial exposure

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27
Q

Digoxin (MOA)

A

Direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger. (+) inotrope. Stimulates verges nerve -> decreases HR

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28
Q

Digoxin (CU)

A

CHF, A fib(decreased conduction at AV node and depression of SA node

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29
Q

Digoxin (T)

A

Blurry yellow vision. ECG: increased PR. decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block.

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30
Q

Quinidine (MOA)

A

Class 1A (Na channel blockers) increased AP duration, increases effective refractory period , increases QT interval

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31
Q

Quinidine (CU)

A

Atrial and ventricular arrhythmia re-entrant and ectopic SVT and VT

32
Q

Quinidine (T)

A

Cinchonism, reversible SLE-like symptoms, heart failure, thrombocytopenia, Torsades de point due to increase in QT

33
Q

Procainamide (MOA)

A

Class 1A (Na channel blockers) increased AP duration, increases effective refractory period , increases QT interval

34
Q

Procainamide (CU)

A

Atrial and ventricular arrhythmia re-entrant and ectopic SVT and VT

35
Q

Procainamide (T)

A

Cinchonism, reversible SLE-like symptoms, heart failure, thrombocytopenia, Torsades de point due to increase in QT

36
Q

Disopyramide (MOA)

A

Class 1A (Na channel blockers) increased AP duration, increases effective refractory period , increases QT interval

37
Q

Disopyramide (CU)

A

Atrial and ventricular arrhythmia re-entrant and ectopic SVT and VT

38
Q

Disopyramide (T)

A

Cinchonism, reversible SLE-like symptoms, heart failure, thrombocytopenia, Torsades de point due to increase in QT

39
Q

Lidocaine (MOA)

A

Class 1B (Na channel blockers) decreases AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.

40
Q

Lidocaine (CU)

A

Acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias. IB is best post-MI

41
Q

Lidocaine (T)

A

CNS stimulation/depression, CV depression

42
Q

Flecainide (MOA)

A

Class IC (Na channel blockers) significantly prolongs refractory period in AV node. Minimal effect on AP duration.

43
Q

Flecainide (CU)

A

SVTs, including A Fib. Only as a last resort in refractory VT

44
Q

Flecainide (T)

A

Proarrhythmic, especially post-MI (contraindicated). IC is Contraindicated in structural and ischemic heart ds.

45
Q

Propafenone (MOA)

A

Class IC (Na channel blockers) significantly prolongs refractory period in AV node. Minimal effect on AP duration.

46
Q

Propafenone (CU)

A

SVTs, including A Fib. Only as a last resort in refractory VT

47
Q

Propafenone (T)

A

Proarrhythmic, especially post-MI (contraindicated). IC is Contraindicated in structural and ischemic heart ds.

48
Q

Class I Antiarrhythmics

A

Slow or block conduction of Na channels. Decrease slop of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells. State dependent (selectively depress tissue that is frequently depolarized (tachy). Hyperkalemia causes increased toxicity for all class I drugs.

49
Q

Class II Antiarrhythmics

A

B-blockers

50
Q

Metoprolol, Propranolol, Esmolol, Timolol, Carvedilol (MOA)

A

Class II (B-blockers) Decrease SA and AV nodal activity by decreasing cAMP, decreasing Ca currents. Suppress abnormal pacemakers by decreasing love of phase 4. AV node particularly sensitive - increased PR interval.

51
Q

Metoprolol, Propranolol, Esmolol, Timolol, Carvedilol (CU)

A

SVT, slowing ventricular rate during A Fib/flutter

52
Q

Metoprolol, Propranolol, Esmolol, Timolol, Carvedilol (T)

A

Impotence, exacerbation of COPD and asthma, CV effects, CNS effects. Metoprolol-> Dyslipidemia. Propranolol-> can exacerbate vasospasm in Prinzmental angina.

53
Q

Class III Antiarrthythmics

A

K+ channel blockers

54
Q

Amiodarone (MOA)

A

Increase AP duration, Increase effective refractory period. Used when other antiarrthythmics fail. Increase QT interval.

55
Q

Amiodarone (CU)

A

A Fib/flutter. V tach.

56
Q

Amiodarone (T)

A

Pulmonary fibraosis, hepatotoxicity, hypo/hyperthyroidism, corneal deposits, skin deposits-> photodermatitis, near effects, constipation, CV effects (brady, CHF, heart block)

57
Q

Ibutilide (MOA)

A

Increase AP duration, Increase effective refractory period. Used when other antiarrthythmics fail. Increase QT interval.

58
Q

Ibutilide (CU)

A

A Fib/flutter.

59
Q

Ibutilide (T)

A

Torsades de pointes

60
Q

Dofetilide (MOA)

A

Increase AP duration, Increase effective refractory period. Used when other antiarrthythmics fail. Increase QT interval.

61
Q

Dofetilide (CU)

A

A Fib/flutter.

62
Q

Sotalol (MOA)

A

Increase AP duration, Increase effective refractory period. Used when other antiarrthythmics fail. Increase QT interval.

63
Q

Sotalol (CU)

A

A Fib/flutter. V tach.

64
Q

Sotalol (T)

A

Torsades de pointes, excessive B blockade

65
Q

Adenosine (MOA)

A

Increases K current out of cell -> hyper depolarizing the cell and decreasing funny Ca current.

66
Q

Adenosine (CU)

A

Drug of choice for diagnosing and treating SVT. Very short acting.

67
Q

Magnesium (CU)

A

Effective in torsades de points and digoxin toxicity

68
Q

Statins (T)

A

Hepatotoxicity (increase LFTs), rhabdomylosis (especially when used with fibrates and niacin)

69
Q

Niacin (MOA)

A

Vitamin B3, reduces hepatic VLDL synthesis; inhibits lipolysis in adipose tisse. decreases LDL AND increases HDL.

70
Q

Niacin (T)

A

Red, flushed face, decreased by aspirin or long term use. Hyperglycemia (acanthuses nigricans). Hyperuricemia (exacerbates gout)

71
Q

Cholestyramine, Colestipol, colesevelam (MOA)

A

Bile acid resins.

72
Q

Cholestyramine, Colestipol, colesevelam (T)

A

Pts hate it- tastes bad and causes GI discomfort, decreases absorption of fat soluble vitamins. Cholesterol gallstones.

73
Q

Ezetimibe (MOA)

A

Prevent cholesterol absorption at small intestine brush border

74
Q

Fibrates (MOA)

A

Upregulate lipoprotein lipase -> increased TG clearance. Activates PPAR-alpha to induce HDL synthesis. Greatest effect on decreasing triglycerides.

75
Q

Fibrates (T)

A

Myositis (increased risk with concurrent statins). Hepatotoxicity (Increases LFT), cholesterol gallstones (esp with concurrent bile acid resins)

Pharmacology (10 decks)

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