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Step 1 Pharmacology > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What drugs are used to treat primary (essential) hypertension?

A

Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), and Calcium Channel Blockers

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2
Q

What drugs are used to treat Hypertension with CHF?

A

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

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3
Q

What drugs are used to treat Hypertension with Diabetes Mellitus?

A

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

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4
Q

Name the Calcium Channel Blockers.

A

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

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5
Q

What is the mechanism of Calcium Channel Blockers?

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 - What do you use Dihydropyridines (except nimodipine) for?

A

Hypertension, angina (including Prinzmetal), Raynaud phenomenon

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7
Q

Calcium Channel Blockers - What do you use Non-dihydropyridines for?

A

Hypertension, angina, atrial fibrillation/flutter

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8
Q

Calcium Channel Blockers - What do you use Nimodipine for?

A

Subarachnoid hemorrhage (prevents cerebral vasospasm)

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9
Q

What toxicity do Calcium Channel Blockers have?

A

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

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10
Q

What is the mechanism of Hydralazine?

A

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

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11
Q

What is the clinical use of Hydralazine?

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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12
Q

What toxicity does Hydralazine have?

A

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

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13
Q

What drugs are used for Hypertensive Emergency?

A

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

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14
Q

Hypertensive Emergency - What are the key features of Nitroprusside?

A

Short acting; ↑ cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide).

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15
Q

Hypertensive Emergency - What are the key features of Fenoldopam?

A

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

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16
Q

What is the mechanism of Nitroglycerin and Isosorbide dinitrate?

A

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

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17
Q

What is the clinical use of Nitroglycerin and Isosorbide dinitrate?

A

Angina, acute coronary syndrome, pulmonary edema

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18
Q

What is the toxicity of Nitroglycerin and Isosorbide dinitrate?

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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19
Q

What is the goal of Antianginal (Nitrates and β-blockers) therapy?

A

Reduction of myocardial O2 consumption (MVO2) by ↓ 1 or more of the determinants of MVO2: end-diastolic volume, blood pressure, heart rate, contractility.

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20
Q

Describe how Nitrates work in regards to Antianginal therapy.

A

Nitrates affect preload. ↓ End-diastolic volume ↓ Blood pressure ↑ Contractility ↑ Heart rate ↓ Ejection time ↓ MVO2

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21
Q

Describe how β-blockers work in regards to Antianginal therapy.

A

β-blockers affect afterload, ↑ End-diastolic volume ↓ Blood pressure ↓ Contractility ↓ Heart rate ↑ Ejection time ↓ MVO2

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22
Q

Describe how Nitrates and β-blockers work together in regards to Antianginal therapy.

A

No effect or ↓ End-diastolic volume ↓ Blood pressure Little/no effect - Contractility ↓ Heart rate Little/no effect - Ejection time ↓↓ MVO2

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23
Q

Name the HMG-CoA reductase inhibitors.

A

Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

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24
Q

What is the mechanism of action of HMG-CoA reductase inhibitors?

A

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

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25
Q

What are the side effects/problems of HMG-CoA reductase inhibitors?

A

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

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26
Q

What effect does HMG-CoA reductase have on LDL (bad cholesterol), HDL (good cholesterol), and triglycerides?

A

Effect on LDL (Bad Cholesterol): ↓↓↓

Effect on HDL (Good Cholesterol): ↑

Effect on Triglycerides: ↓

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27
Q

What is the mechanism of action of Niacin (vitamin B3)?

A

Inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis

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28
Q

What are the side effects/problems of Niacin (vitamin B3)?

A

Red, flushed face, which is ↓ by aspirin or longterm use

Hyperglycemia (acanthosis nigricans)

Hyperuricemia (exacerbates gout)

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29
Q

What effect does Niacin (vitamin B3) have on LDL (bad cholesterol), HDL (good cholesterol), and triglycerides?

A

Effect on LDL (Bad Cholesterol): ↓↓

Effect on HDL (Good Cholesterol): ↑↑

Effect on Triglycerides: ↓

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30
Q

What is the mechanism of action of Bile acid resins (cholestyramine, colestipol, colesevelam)?

A

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

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31
Q

What are the side effects/problems of Bile acid resins (cholestyramine, colestipol, and colesevelam)?

A

Patients hate it—tastes bad and causes GI discomfort, ↓ absorption of fat-soluble vitamins

Cholesterol gallstones

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32
Q

What effect do Bile acid resins have on LDL (bad cholesterol), HDL (good cholesterol), and triglycerides?

A

Effect on LDL (Bad Cholesterol): ↓↓

Effect on HDL (Good Cholesterol): Slightly ↑

Effect on Triglycerides: Slightly ↑

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33
Q

What is the mechanism of action of Cholesterol absorption blockers (ezetimibe)?

A

Prevent cholesterol absorption at small intestine brush border

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34
Q

What are the side effects/problems of Cholesterol absorption blockers (ezetimibe)?

A

Rare ↑ LFTs, diarrhea

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35
Q

What effect does Cholesterol absorption blockers (ezetimibe) have on LDL (bad cholesterol), HDL (good cholesterol), and triglycerides?

A

Effect on LDL (Bad Cholesterol): ↓↓

Effect on HDL (Good Cholesterol): -

Effect on Triglycerides: -

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36
Q

What is the mechanism of action of Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)?

A

Upregulate LPL → ↑ TG Clearance

Activates PPAR-α to induce HDL synthesis

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37
Q

What are the side effects/problems of Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)?

A

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

38
Q

What effect do Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate) have on LDL (bad cholesterol), HDL (good cholesterol), and triglycerides?

A

Effect on LDL (Bad Cholesterol): ↓

Effect on HDL (Good Cholesterol): ↑

Effect on Triglycerides: ↓↓↓

39
Q

What are some key features of Cardiac glycosides?

A

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

40
Q

What is the mechanism of Cardiac glycosides?

A

Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport

↑ [Ca2+]i → positive inotropy. Stimulates vagus nerve → ↓ HR

41
Q

What is the clinical use of Cardiac glycosides?

A

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

42
Q

What are the toxicities of Cardiac glycosides?

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).

43
Q

What is the antidote for Cardiac glycoside toxicity?

A

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

44
Q

Antiarrhythmics - What are the key features of Na+ channel blockers (class I)?

A

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.

45
Q

Antiarrhythmics - What are the Class IA drugs?

A

Quinidine, Procainamide, Disopyramide

46
Q

Antiarrhythmics - What is the mechanism of Class IA drugs?

A

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

47
Q

Antiarrhythmics - What is the clinical use of Class IA drugs?

A

Both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT

48
Q

Antiarrhythmics - What is the toxicity of class IA drugs?

A

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

49
Q

Antiarrhythmics - What are the Class IB drugs?

A

Lidocaine and Mexiletine

50
Q

Antiarrhythmics - What is the mechanism of Class IB drugs?

A

↓ AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.

Phenytoin can also fall into the IB category.

51
Q

Antiarrhythmics - What is the clinical use of Class IB drugs?

A

Acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias

52
Q

Antiarrhythmics - What is the toxicity of Class IB drugs?

A

CNS stimulation/depression, cardiovascular depression

53
Q

Antiarrhythmics - What are the Class IC drugs?

A

Flecainide and Propafenone

54
Q

Antiarrhythmics - What is the mechanism of Class IC drugs?

A

Significantly prolongs refractory period in AV node.

Minimal effect on AP duration.

55
Q

Antiarrhythmics - What is the clinical use of Class IC drugs?

A

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

56
Q

Antiarrhythmics - What is the toxicity of Class IC drugs?

A

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

57
Q

Antiarrhythmics - What are the β-blockers (class II)?

A

Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol

58
Q

Antiarrhythmics - What is the mechanism of β-blockers?

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.

59
Q

Antiarrhythmics - What is the clinical use of β-blockers?

A

SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

60
Q

Antiarrhythmics - What is the toxicity of β-blockers?

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.

61
Q

Antiarrhythmics - What are the K+ channel blockers (class III)?

A

Amiodarone, Ibutilide, Dofetilide, Sotalol

62
Q

Antiarrhythmics - What is the mechanism of K+ channel blockers?

A

↑ AP duration, ↑ ERP. Used when other antiarrhythmics fail. ↑ QT interval.

63
Q

Antiarrhythmics - What is the clinical use of K+ channel blockers?

A

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

64
Q

Antiarrhythmics - What is the toxicity of K+ channel blockers?

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.

65
Q

Antiarrhythmics - What are the Ca2+ channel blockers (class IV)?

A

Verapamil and diltiazem

66
Q

Antiarrhythmics - What is the mechanism of Ca2+ channel blockers?

A

↓ conduction velocity, ↑ ERP, ↑ PR interval

67
Q

Antiarrhythmics - What is the clinical use of Ca2+ channel blockers?

A

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

68
Q

Antiarrhythmics - What are the toxicities of Ca2+ channel blockers?

A

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

69
Q

Antiarrhythmics - What are the key features of Adenosine as an antiarrhythmic?

A

↑ K+ out of cells → hyperpolarizing the cell and ↓ ICa. Drug of choice in diagnosing/abolishing supraventricular tachycardia.

Very short acting (~ 15 sec). Adverse effects include flushing, hypotension, chest pain. Effects blocked by theophylline and caffeine.

70
Q

Antiarrhythmics - What are the key features of Mg2+as an antiarrhythmic?

A

Effective in torsades de pointes and digoxin toxicity

71
Q

What helps close PDA (patent)?

A

Indomethacin

72
Q

What keeps keeps PDA open?

A

Prostaglandins E1 and E2

73
Q

What drugs ↓ preload?

A

Venodilators (e.g., nitroglycerin), ACE inhibitors, and ARBs

74
Q

What drugs ↓ afterload?

A

Vasodilators (e.g., hydralazine), ACE inhibitors, and ARBs

75
Q

How does Digitalis ↑ contractility?

A

Blocks Na+/K+ pump → ↑ intracellular Na+ → ↓ Na+/Ca2+ exchanger activity → ↑ intracellular Ca2+

76
Q

What drugs affect Phase 4 of the pacemaker potential?

A

ACh/adenosine ↓ the rate of diastolic depolarization and ↓ HR, while catecholamines
↑ depolarization and ↑ HR.

77
Q

What drug treats Torsades de pointes?

A

Magnesium sulfate

78
Q

What drugs prolong the QT interval?

A

Some Risky Meds Can Prolong QT

Sotalol, Risperidone, Macrolides, Chloroquine, Protesase inhibitors (-navir), Quinidine (class Ia; also class III), Thiazides

79
Q

What drugs affect rate control in atrial flutter?

A

β-blocker or Ca++channel blocker

80
Q

What is the recombinant form of B-type (brain) natriuretic peptide used for treatment of heart failure?

A

Nesiritide

81
Q

What do you treat Variant angina (Prinzmetal) with?

A

Ca++ channel blockers, nitrates, and smoking cessation (if applicable)

82
Q

What is the treatment for Dilated cardiomyopathy?

A

Na+ restriction, ACE inhibitors, β-blockers, diuretics, digoxin, implantable cardioverter defibrillator (ICD), heart transplant

83
Q

What is the treatment for Hypertrophic cardiomyopathy?

A

Cessation of high-intensity athletics, use of β-blocker or non-dihydropyridine calcium channel blockers (e.g., verapamil). ICD if patient is high risk.

84
Q

What drugs are used to treat CHF?

A

ACE inhibitors, β-blockers (except in acute decompensated HF), angiotensin II receptor blockers, and spironolactone ↓ mortality. Thiazide or loop diuretics are used mainly for symptomatic relief. Hydralazine with nitrate therapy improves both symptoms and mortality in select patients.

85
Q

What do you treat Temporal (giant-cell) arteritis with?

A

High-dose corticosteroids prior to temporal artery biopsy to prevent vision loss

86
Q

What do you treat Takayasu arteritis with?

A

Corticosteroids

87
Q

What do you treat Polyarteritis nodosa with?

A

Corticosteroids and cyclophosphamide

88
Q

What do you treat Kawasaki disease with?

A

IV immunoglobulin and aspirin

89
Q

What do you treat Granulomatosis with polyangiitis (Wegener) with?

A

Cyclophosphamide and corticosteroids

90
Q

What do you treat Microscopic polyangiitis with?

A

Step 1 Pharmacology (18 decks)

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