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Pharmacology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Amlodipine

A

Dihydropyridine calcium channel blocker
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reducing muscle contractility. Vascular smooth muscle > cardiac muscle.
Hypertension, angina (not Prinzmetal), Raynaud phenomenon
Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation.

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2
Q

Nimodipine

A 
Dihydropyridine calcium channel blocker
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reducing muscle contractility. 
Subarachnoid hemorrhage (prevents cerebral vasospasm)
Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation.
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3
Q

Nifedipine

A

Dihydropyridine calcium channel blocker
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reducing muscle contractility. Vascular smooth muscle > cardiac muscle.
Hypertension, angina (not Prinzmetal), Raynaud phenomenon
Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation.

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4
Q

Diltiazem

A

Non-dihydropyridine calcium channel blocker
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reducing muscle contractility. Cardiac muscle&raquo_space; vascular smooth muscle.
Hypertension, angina, atrial fibrillation/flutter.
Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation

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5
Q

Verapamil

A

Non-dihydropyridine calcium channel blocker
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reducing muscle contractility. Cardiac muscle&raquo_space; vascular smooth muscle.
Hypertension, angina, atrial fibrillation/flutter.
Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation

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6
Q

Hydralazine

A 
Increases cGMP, leading to smooth muscle relaxation, afterload reduction. Vasodilates arterioles > veins.
Severe hypertension, CHF. First-line therapy for hypertension in pregnancy (with methyldopa). Frequently co-administered with β-blocker to prevent reflex tachycardia.
Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina, lupus-like syndrome.
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7
Q

Nitroprusside

A

Increases cGMP via direct release of NO.
Hypertensive emergency.
Short acting. Can cause cyanide toxicity (releases cyanide)

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8
Q

Fenoldopam

A

Dopamine D1 receptor agonist. Coronary, peripheral, renal, and splanchnic vasodilation. Decreases blood pressure and increases natriuresis.
Hypertensive emergency.

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9
Q

Nitroglycerine

A

Vasodilates by increasing NO in vascular smooth muscle, leading to increased cGMP and smooth muscle relaxation. Dilates veins&raquo_space; arteries. Decreases preload.
Angina, acute coronary syndrome, pulmonary edema.
Reflex tachycardia (treat with β-blocker), hypotension, flushing, headache. “Monday disease” in industrial exposure - development of tolerance for vasodilating action during work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon re-exposure.

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10
Q

Isosorbide dinitrate

A

Vasodilates by increasing NO in vascular smooth muscle, leading to increased cGMP and smooth muscle relaxation. Dilates veins&raquo_space; arteries. Decreases preload.
Angina, acute coronary syndrome, pulmonary edema.
Reflex tachycardia (treat with β-blocker), hypotension, flushing, headache. “Monday disease” in industrial exposure - development of tolerance for vasodilating action during work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon re-exposure.

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11
Q

Lovastatin

A

HMG-CoA reductase inhibitor
Inhibits conversion of HMG-CoA to mevalonate, a cholesterol precursor.
Hepatotoxicity (increases LFTs), rhabdomyolysis (especially with concurrent use of fibrates and niacin)

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12
Q

Pravastatin

A

HMG-CoA reductase inhibitor
Inhibits conversion of HMG-CoA to mevalonate, a cholesterol precursor.
Hepatotoxicity (increases LFTs), rhabdomyolysis (especially with concurrent use of fibrates and niacin)

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13
Q

Simvastatin

A

HMG-CoA reductase inhibitor
Inhibits conversion of HMG-CoA to mevalonate, a cholesterol precursor.
Hepatotoxicity (increases LFTs), rhabdomyolysis (especially with concurrent use of fibrates and niacin)

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14
Q

Atorvastatin

A

HMG-CoA reductase inhibitor
Inhibits conversion of HMG-CoA to mevalonate, a cholesterol precursor.
Hepatotoxicity (increases LFTs), rhabdomyolysis (especially with concurrent use of fibrates and niacin)

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15
Q

Rosuvastatin

A

HMG-CoA reductase inhibitor
Inhibits conversion of HMG-CoA to mevalonate, a cholesterol precursor.
Hepatotoxicity (increases LFTs), rhabdomyolysis (especially with concurrent use of fibrates and niacin)

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16
Q

Niacin

A

Vitamin B3
Inhibits lipolysis in adipose tissue. Reduces hepatic VLDL synthesis.
Red, flushed face (decreased by aspirin or long-term use), hyperglycemia (acanthosis nigrans), hyperuricemia (gout)

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17
Q

Cholestyramine

A

Bile acid resin
Prevents intestinal reabsorption of bile acids. Liver must use cholesterol to make more.
Patients hate it (tastes bad, GI discomfort), decreases absorption of fat-soluble vitamins, cholesterol gallstones

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18
Q

Colestipol

A

Bile acid resin
Prevents intestinal reabsorption of bile acids. Liver must use cholesterol to make more.
Patients hate it (tastes bad, GI discomfort), decreases absorption of fat-soluble vitamins, cholesterol gallstones

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19
Q

Colesevelam

A

Bile acid resin
Prevents intestinal reabsorption of bile acids. Liver must use cholesterol to make more.
Patients hate it (tastes bad, GI discomfort), decreases absorption of fat-soluble vitamins, cholesterol gallstones

20
Q

Ezetimibe

A

Cholesterol absorption blocker
Prevents cholesterol absorption at small intestine brush border
Rare increases in LFTs, diarrhea

21
Q

Gemfibrozil

A

Fibrate
Upregulates LPL, leading to increased TG clearance. Activates PPAR-α to induce HDL synthesis.
Myositis (increased risk with concurrent statins), hepatotoxicity (increases LFTs), cholesterol gallstones (especially with concurrent bile acid resins).

22
Q

Clofibrate

A

Fibrate
Upregulates LPL, leading to increased TG clearance. Activates PPAR-α to induce HDL synthesis.
Myositis (increased risk with concurrent statins), hepatotoxicity (increases LFTs), cholesterol gallstones (especially with concurrent bile acid resins).

23
Q

Bezafibrate

A

Fibrate
Upregulates LPL, leading to increased TG clearance. Activates PPAR-α to induce HDL synthesis.
Myositis (increased risk with concurrent statins), hepatotoxicity (increases LFTs), cholesterol gallstones (especially with concurrent bile acid resins).

24
Q

Fenofibrate

A

Fibrate
Upregulates LPL, leading to increased TG clearance. Activates PPAR-α to induce HDL synthesis.
Myositis (increased risk with concurrent statins), hepatotoxicity (increases LFTs), cholesterol gallstones (especially with concurrent bile acid resins).

25
Q

Digoxin

A

Cardiac glycoside
Direct inhibition of Na/K ATPase, leading to indirect inhibition of Na/Ca exchanger/antiport, leading to increase inotropy. Stimulates vagus nerve, which decreases heart rate.
CHF (increases contractility), atrial fibrillation (decreases conduction at AV node and depression of SA node)
Nausea, vomiting, diarrhea, blurry yellow vision (cholinergic), increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block. Can lead to hyperkalemia (poor prognosis).
Predisposing factors to toxicity include renal failure, hypokalemia, verapamil, amiodarone, quinidine.
Antidote: Slowly normalize K, cardiac pacer, anti-digoxin Fab fragments, Mg.

26
Q

Quinidine

A

Na channel blocker. Class IA anti-arrhythmic
Increases AP duration, increases effective refractory period (ERP), increases QT interval.
Both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.
Cinchonism (headache, tinnitus), thrombocytopenia, torsades de points due to increased QT interval.

27
Q

Procainamide

A

Na channel blocker. Class IA anti-arrhythmic
Increases AP duration, increases effective refractory period (ERP), increases QT interval.
Both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.
Reversible SLE-like syndrome, thrombocytopenia, torsades de points due to increased QT interval.

28
Q

Disopyramide

A

Na channel blocker. Class IA anti-arrhythmic
Increases AP duration, increases effective refractory period (ERP), increases QT interval.
Both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.
Heart failure, thrombocytopenia, torsades de points due to increased QT interval.

29
Q

Lidocaine

A

Na channel blocker. Class IB anti-arrhythmic.
Decreases AP duration. Preferentially affects ischemic or depolarized Purkinje and ventricular tissue.
Acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias.
CNS stimulation/depression, cardiovascular depression.

30
Q

Mexiletine

A

Na channel blocker. Class IB anti-arrhythmic.
Decreases AP duration. Preferentially affects ischemic or depolarized Purkinje and ventricular tissue.
Acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias.
CNS stimulation/depression, cardiovascular depression.

31
Q

Phenytoin

A

Na channel blocker. Class IB anti-arrhythmic.
Decreases AP duration. Preferentially affects ischemic or depolarized Purkinje and ventricular tissue.
Acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias.
CNS stimulation/depression, cardiovascular depression.

32
Q

Flecainide

A

Na channel blocker. Class IC anti-arrhythmic.
Significantly prolongs refractory period in AV node. Minimal effect on AP duration.
SVTs, including atrial fibrillation. Only as a last resort in refractory VT.
Proarrhythmic, especially post-MI and in structural and ischemic heart disease (therefore contraindicated).

33
Q

Mexiletine

A

Na channel blocker. Class IC anti-arrhythmic.
Significantly prolongs refractory period in AV node. Minimal effect on AP duration.
SVTs, including atrial fibrillation. Only as a last resort in refractory VT.
Proarrhythmic, especially post-MI and in structural and ischemic heart disease (therefore contraindicated).

34
Q

Metoprolol

A

β-blocker. Class II anti-arrhythmic.
Decreases SA and AV nodal activity by decreasing cAMP, decreasing Ca currents. Suppress normal pacemakers by decreasing slope of phase 4. AV node is particularly sensitive (increases PR interval).
SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.
Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. Can cause dyslipidemia. Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor antagonist activity). Treat overdose with glucagon.

35
Q

Propanolol

A

β-blocker. Class II anti-arrhythmic.
Decreases SA and AV nodal activity by decreasing cAMP, decreasing Ca currents. Suppress normal pacemakers by decreasing slope of phase 4. AV node is particularly sensitive (increases PR interval).
SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.
Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. Can exacerbate vasospasm in Prinzmetal angina. Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor antagonist activity). Treat overdose with glucagon.

36
Q

Esmolol

A

β-blocker. Class II anti-arrhythmic. Very short acting.
Decreases SA and AV nodal activity by decreasing cAMP, decreasing Ca currents. Suppress normal pacemakers by decreasing slope of phase 4. AV node is particularly sensitive (increases PR interval).
SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.
Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor antagonist activity). Treat overdose with glucagon.

37
Q

Timolol

A

β-blocker. Class II anti-arrhythmic.
Decreases SA and AV nodal activity by decreasing cAMP, decreasing Ca currents. Suppress normal pacemakers by decreasing slope of phase 4. AV node is particularly sensitive (increases PR interval).
SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.
Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor antagonist activity). Treat overdose with glucagon.

38
Q

Carvedilol

A

β-blocker. Class II anti-arrhythmic.
Decreases SA and AV nodal activity by decreasing cAMP, decreasing Ca currents. Suppress normal pacemakers by decreasing slope of phase 4. AV node is particularly sensitive (increases PR interval).
SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.
Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor antagonist activity). Treat overdose with glucagon.

39
Q

Amiodarone

A

K channel blocker. Class III anti-arrhythmic. Has class I, II, III and IV effects and alters lipid membrane.
Increases AP duration, increases ERP. Used when other anti-arrhythmias fail. Increases QT interval.
Atrial fibrillation, atrial flutter, ventricular tachycardia.
Pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (40% iodine by weight), corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF).
Check LFTS, PFTs, and TFTs when using.

40
Q

Sotalol

A

K channel blocker. Class III anti-arrhythmic.
Increases AP duration, increases ERP. Used when other anti-arrhythmias fail. Increases QT interval.
Atrial fibrillation, atrial flutter, ventricular tachycardia.
Torsades de pointes, excessive β blockade

41
Q

Ibutilide

A

K channel blocker. Class III anti-arrhythmic.
Increases AP duration, increases ERP. Used when other anti-arrhythmias fail. Increases QT interval.
Atrial fibrillation, atrial flutter.
Torsades de pointes.

42
Q

Dofetilide

A

K channel blocker. Class III anti-arrhythmic.
Increases AP duration, increases ERP. Used when other anti-arrhythmias fail. Increases QT interval.
Atrial fibrillation, atrial flutter

43
Q

Verapamil

A

Ca channel blocker. Class IV anti-arrhythmic.
Decreases conduction velocity, increases ERP, increases PR interval.
Prevention of nodal arrhythmias (SVT), rate control in atrial fibrillation
Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

44
Q

Diltiazem

A

Ca channel blocker. Class IV anti-arrhythmic.
Decreases conduction velocity, increases ERP, increases PR interval.
Prevention of nodal arrhythmias (SVT), rate control in atrial fibrillation
Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

45
Q

Adenosine

A

Anti-arrhythmic
Increases K out of cells, leading to hyperpolarization of the cell and decreased ICa current. Drug of choice in diagnosing/abolishing supraventricular tachycardia. Very short acting (~15 seconds).
Flushing, hypotension, chest pain. Effects blocked by theophylline and caffeine.

46
Q

Magnesium

A

Anti-arrhythmic

Effective in torsades de pointes and digoxin toxicity.

Pharmacology (19 decks)

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