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Cardiology Kaplan > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Dihydropyridine used in subarachnoid hemorrhage to prevent cerebral vasospasm

A

Nimodipine

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2
Q

Calcium channel blocker that can cause hyperprolactinemia

A

Verapamil

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3
Q

Secondary messenger elevated by hydralazine

A

cGMP

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4
Q

Type of vessel that is predominantly dilated by hydralazine

A

Arterioles

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5
Q

Antihypertensive that can cause cyanide toxicity

A

Nitroprusside

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6
Q

Type of vessel that is predominantly dilated by nitroprusside

A

Both venous and arterial dilator

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7
Q

Mechanism through which nitroprusside increases cGMP

A

Direct release of nitric oxide

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8
Q

Type of vessel that is predominantly dilated by nitrates (eg, nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)

A

Veins

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9
Q

Antihypertensives that develop tolerance

A

Nitrates

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10
Q

Nitrates are contraindicated in which type of infarction

A

Right ventricular infarction

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11
Q

Mechanism of action of ranolazine

A

Inhibits the late phase of sodium current (reducing calcium accumulation), thereby reducing diastolic wall tension (for coronary flow) and oxygen consumption

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12
Q

Drug used in drug resistant angina

A

Ranolazine

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13
Q

Mechanism of action of milrinone and inamrinone

A

Selective PDE-3 inhibitors

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14
Q

Mechanism of action of neprilysin inhibitors

A

Prevent degradation of ANP

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15
Q

Bile acid resins (eg, cholestyramine, colestipol, colesevelam) are contraindicated in patients with which type of hyperlipidemia

A

Hypertriglyceridemia

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16
Q

Hypolipidemic drug that inhibits NPC1L1, thereby preventing colesterol absorption

A

Ezetimibe

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17
Q

DOC for patients with hypertriglyceridemia

A

Fibrates (eg, gemfibrozil, bezafibrate, fenofibrate)

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18
Q

Mechanism of action of fibrates

A
  • Upregulate LPL to increase TG clearance

* Activate PPAR alpha to induce HDL synthesis

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19
Q

Adverse effects of fibrates

A
  • Myopathy (increased risk with statins)

* Cholesterol gallstones

20
Q

Mechanism of action of niacin

A
  • Inhibit hormone-sensitive lipase in adipose tissue

* Reduces hepatic VLDL synthesis

21
Q

Mechanism of action of PCSK9 inhibitors (eg, alirocumab, evolocumab)

A

Inactivation of LDL receptor degradation, increasing amount of LDL removed from bloodstream

22
Q

Hypolipidemic drugs that have neurocognitive effects

A

PCSK9 inhibitors

23
Q

How does cardiac glycosides decrease heart rate

A

Stimulation of the vagus nerve

24
Q

Clinical use of cardiac glycosides

A
  • HF (increase contractility)

* Atrial fibrillation (decreased conduction at AV node and depression of SA node)

25
Q

Factors that predispose to digoxin toxicity

A
  • Renal failure (decrease excretion)
  • Hypokalemia (permissive for digoxin binding at K binding site on Na/K ATPase)
  • Drugs that displace digoxin from tissue binding sites
  • Decreased clearance
26
Q

Mechanism of action of nesiritide

A

Recombinant form of human B type natriuretic peptide

27
Q

Type 1 antiarrhythmics depress which type of tissue

A

Tissue that is frequently depolarized

28
Q

Type of antiarrhythmics that block fast sodium channels on an open or activated state

A

Type 1A antiarrhythmics

29
Q

Effects of type 1 antiarrhythmics on action potential (AP) duration

A
  • Type 1A: increase AP
  • Type 1B: decrease AP
  • Type 1C: no effect
30
Q

Class of type 1 antiarrhythmics that preferntially affect ischemic or depolarized Purkinje and ventricular tissue

A

Type 1B

31
Q

Class of type 1 antiarrhythmics with the weakest binding to the channels

A

Type 1B

32
Q

Class of type 1 antiarrhythmic that prolongs effective refractory period (ERP) in AV node and accessory bypass tracts

A

Type 1C

33
Q

Class of type 1 antiarrhythmics with the strongest bindings to the channels

A

Type 1C

34
Q

Mechanism of action of beta blockers (as antiarrhythmics)

A
  • Decrease SA and AV nodal activity by decreasing cAMP and calcium currents
  • Suppress abnormal pacemakers by decreasing the slope of phase 4
  • Increase PR Interval (AV node is very sensitive)
35
Q

Mechanism of action of ivabradine

A

Selective inhibition of funny sodium channels

36
Q

Main contraindication of class 1A antiarrhythmics

A

Patients with prolonged QT interval

37
Q

Type of drugs used to diagnose Prinzmetal angina

A

Ergonovines

38
Q

Specific combination of drugs that show a survival benefit in African American patients with systolic heart failure

A

Hydralazine + isosorbide nitrate

39
Q

Mechanism through which fibrates exacerbate statin-associated myopathy

A

They impair statin clearance in the liver

40
Q

Intracellular event responsible for nitrates’ effects

A

Myosin light chain dephosphorylation by cGMP

  • Decreased intracellular calcium
  • Activation of myosin light chain phosphatase
41
Q

Vessels that are preferentially dilated by dihydropyridines

A

Precapillary vessels (arterioles)

42
Q

vessels that are preferentially dilated by renin-angiotensin system blockers (ACE inhibitors and ARBs)

A

Postcapillary vessels (venules)

43
Q

Class 1A antiarrhythmic that has antimuscarinic and alpha 1 blocking effects and thus, increases conduction through the AV node and shortens the PR interval

A

Quinidine

44
Q

Why is hydralazine contraindicated in patients with angina

A

Because it can potentiate it through reflex tachycardia

45
Q

Resistance to methicillin (in Staph) confers resistance to what other antibiotic

A

Cephalosporins, because the mechanism of methicillin resistance involves penicillin binding protein alterations (PBPs are also used by cephalosporins)

46
Q

Only statin that is not metabolized by P450 enzyme system

A

Pravastatin

47
Q

Sypmatholytic drug that is used for opiate withdrawal

A

Clonidine

Cardiology Kaplan (3 decks)

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