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Pharmacology > FA Cardiovascular > Flashcards

FA Cardiovascular Flashcards

1
Q

Primary (Essential) Hypertension Therapy

A

Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers.

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2
Q

Hypertension with

CHF Therapy

A

Diuretics, ACE inhibitors/ARBs, β-blockers (compensated CHF), aldosterone antagonists.
β-blockers must be used cautiously in decompensated CHF and are contraindicated in cardiogenic shock.

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3
Q

Hypertension with

Diabetes Mellitus

A

ACE inhibitors/ARBs. Calcium channel blockers, diuretics, β-blockers, α-blockers.
ACE inhibitors/ARBs are protective against diabetic nephropathy.

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4
Q

Calcium Channel Blockers

A

Amlodipine, nimodipine, nifedipine (dihydropyridine); diltiazem, verapamil (non-dihydropyridine).

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5
Q

Calcium Channel Blockers Mechanism

A

Block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reduce muscle contractility.
Vascular smooth muscle—amlodipine = nifedipine > diltiazem > verapamil.
Heart—verapamil > diltiazem > amlodipine = nifedipine (verapamil = ventricle).

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6
Q

Calcium Channel Blockers Use

A

Dihydropyridine (except nimodipine): hypertension, angina (including Prinzmetal), Raynaud phenomenon.
Non-dihydropyridine: hypertension, angina, atrial fibrillation/flutter.
Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm).

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7
Q

Calcium Channel Blockers Toxicity

A

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

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8
Q

Hydralazine Mechanism

A

↑ cGMP Ž smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction.

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9
Q

Hydralazine Use

A

Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with methyldopa. Frequently coadministered with a β-blocker to prevent reflex tachycardia.

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10
Q

Hydralazine Toxicity

A

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

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11
Q

Hypertensive Emergency

A

Commonly used drugs include nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.

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12
Q

Nitroprusside Mechanism

A

Short acting; ↑ cGMP via direct release of NO.

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13
Q

Nitroprusside Use

A

Hypertensive emergency

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14
Q

Nitroprusside Toxicity

A

Can cause cyanide toxicity (releases cyanide).

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15
Q

Fenoldopam Mechanism

A

Dopamine D1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation. ↓ BP and ↑ natriuresis.

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16
Q

Fenoldopam Use

A

Hypertensive emergency

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17
Q

Nitroglycerin, Isosorbide Dinitrate Mechanism

A

Vasodilate by ↑ NO in vascular smooth muscle → ↑ in cGMP and smooth muscle relaxation. Dilate veins&raquo_space; arteries. ↓ preload.

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18
Q

Nitroglycerin, Isosorbide Dinitrate Use

A

Angina, acute coronary syndrome, pulmonary edema.

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19
Q

Nitroglycerin, Isosorbide Dinitrate Toxicity

A

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 results in tachycardia, dizziness, and headache upon reexposure.

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20
Q

Lipid Lowering Agents

A

HMG-CoA Reductase Inhibitors (lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin), Niacin (vitamin B3), Bile Acid Resins (cholestyramine, colestipol, colesevelam), Cholesterol Absorption Blockers (ezetimibe), Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

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21
Q

HMG-CoA Reductase Inhibitor Mechanism

A

Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor.
↓↓↓ LDL, ↑ HDL, ↓ triglycerides

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22
Q

HMG-CoA Reductase Inhibitor Toxicity

A

Hepatotoxicity ( LFTs),
rhabdomyolysis (esp.
when used with fibrates
and niacin)

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23
Q

Niacin (Vitamin B3) Mechanism

A

Inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis.
↓↓ LDL, ↑↑ HDL, ↓ triglycerides

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24
Q

Niacin (Vitamin B3) Toxicity

A

Red, flushed face, which is ↓ by aspirin or longterm use.
Hyperglycemia (acanthosis nigricans).
Hyperuricemia (exacerbates gout).

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25
Q

Bile Acid Resin Mechanism

A

Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more.
↓↓ LDL, slighlty ↑ HDL, slightly ↑ triglycerides

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26
Q

Bile Acid Resin Toxicity

A

Patients hate it—tastes bad and causes G discomfort, ↓ absorption of fat-soluble vitamins. Cholesterol gallstones.

27
Q

Ezetimibe Mechanism

A

Prevent cholesterol absorption at small intestine brush border.
↓↓ LDL, no effect on HDL, no effect on triglycerides

28
Q

Ezetimibe Toxicity

A

Rare ↑ LFTs, diarrhea.

29
Q

Fibrate Mechanism

A

Upregulate LPLŽ → ↑ TG clearance.
Activates PPAR-α to induce HDL synthesis.
↓ LDL, ↑ HDL, ↓↓↓ triglycerides

30
Q

Fibrate Toxicity

A

Myositis (↑ risk with concurrent statins), hepatotoxicity (↑ LFTs), cholesterol gallstones (esp. with concurrent bile acid resins)

31
Q

Cardiac Glycosides

A

Digoxin—75% bioavailability, 20–40% protein bound, t1/2 = 40 hours, urinary excretion.

32
Q

Digoxin Mechanism

A

Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport.Ž ↑ [Ca2+]iŽ → positive inotropy. Stimulates vagus nerveŽ → ↓ HR.

33
Q

Digoxin Use

A

CHF (↑ contractility); atrial fibrillation (↓ conduction at AV node and depression of SA node).

34
Q

Digoxin Toxicity

A

Cholinergic—nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh).
ECG— ↑ PR, ↓ QT, ST scooping, T-wave inversion, arrhythmia, AV block.
Can lead to hyperkalemia, which indicates poor prognosis.
Factors predisposing to toxicity—renal failure (↓ excretion), hypokalemia (permissive for digoxin binding at K+-binding site on Na+/K+ ATPase), verapamil, amiodarone, quinidine (↓ digoxin clearance; displaces digoxin from tissue-binding sites).

35
Q

Digoxin Antidote

A

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

36
Q

Class I Antiarrhythmic Mechanism

A 
Na+ channel blockers.
Slow or block (↓) conduction (especially in depolarized cells). ↓ slope of phase 0 depolarization and ↑ threshold for firing in abnormal pacemaker cells. Are state dependent (selectively depress tissue that is frequently depolarized [e.g., tachycardia]). Hyperkalemia causes ↑ toxicity for all class I drugs.
37
Q

Class IA Antiarrhythmics

A

Quinidine, Procainamide, Disopyramide.

38
Q

Class IA Antiarrhythmic Mechanism

A

↑ AP duration, ↑ effective refractory period (ERP), ↑ QT interval.

39
Q

Class IA Antiarrhythmic Use

A

Both atrial and ventricular arrhythmias,

especially re-entrant and ectopic SVT and VT.

40
Q

Class IA Antiarrhythmic Toxicity

A

Cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades de pointes due to ↑ QT interval.

41
Q

Class IB Antiarrhythmics

A

Lidocaine, Mexiletine.

42
Q

Class IB Antiarrhythmic Mechanism

A

↓ AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Phenytoin can also fall into the IB category.

43
Q

Class IB Antiarrhythmic Use

A

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

44
Q

Class IB Antiarrhythmic Toxicity

A

CNS stimulation/depression, cardiovascular

depression.

45
Q

Class IC Antiarrhythmic Mechanism

A

Significantly prolongs refractory period in AV node.

Minimal effect on AP duration.

46
Q

Class IC Antiarrhythmics

A

Flecainamide, Propafenone

47
Q

Class IC Antiarrhythmic Use

A

SVTs, including atrial fibrillation. Only as a last resort in refractory VT.

48
Q

Class IC Antiarrhythmic Toxicity

A

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

49
Q

Class II Antiarrhythmics

A

β-blockers (metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol)

50
Q

β-blocker Mechanism

A

Decrease SA and AV nodal activity by ↓ cAMP, ↓ Ca2+ currents. Suppress abnormal pacemakers by ↓ slope of phase 4.
AV node particularly sensitive—↑ PR interval. Esmolol very short acting.

51
Q

β-blocker Use

A

SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.

52
Q

β-blocker Toxicity

A

Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.
Metoprolol can cause dyslipidemia. Propranolol can exacerbate vasospasm in Prinzmetal angina. Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor agonist activity). Treat overdose with glucagon.

53
Q

Class III Antiarrhythmics

A

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

54
Q

Class III Antiarrhythmic Mechanism

A

↑ AP duration, ↑ ERP. Used when other

antiarrhythmics fail. ↑ QT interval.

55
Q

Class III Antiarrhythmic Use

A

Atrial fibrillation, atrial flutter; ventricular tachycardia (amiodarone, sotalol).

56
Q

Class III Antiarrhythmic Toxicity

A 
Sotalol—torsades de pointes, excessive β blockade.
Ibutilide—torsades de pointes.
Amiodarone—pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF).
Remember to check PFTs, LFTs, and TFTs when using amiodarone.
Amiodarone has class I, II, III, and IV effects and alters the lipid membrane.
57
Q

Class IV Antiarrhythmics

A

Ca2+ Channel Blockers: Verapamil, diltiazem.

58
Q

Verapamil, Diltiazem Mechanism

A

↓ conduction velocity, ↑ ERP, ↑ PR interval.

59
Q

Verapamil, Diltiazem Use

A

Prevention of nodal arrhythmias (e.g., SVT), rate control in atrial fibrillation.

60
Q

Verapamil, Diltiazem Toxicity

A

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

61
Q

Adenosine Mechanism

A

↑ K+ out of cells → hyperpolarizing the cell and ↓ ICa

62
Q

Adenosine Use

A

Drug of choice in diagnosing/abolishing supraventricular tachycardia. Very short acting (~15 sec).

63
Q

Adenosine Toxicity

A

Adverse effects include flushing, hypotension, chest pain. Effects blocked by theophylline and caffeine.

64
Q

Mg2+ Use

A

Effective in torsades de pointes and digoxin toxicity.

Pharmacology (14 decks)

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