Pharmacology Flashcards

(47 cards)

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
Factors that predispose to digoxin toxicity
* 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
Mechanism of action of nesiritide
Recombinant form of human B type natriuretic peptide
27
Type 1 antiarrhythmics depress which type of tissue
Tissue that is frequently depolarized
28
Type of antiarrhythmics that block fast sodium channels on an open or activated state
Type 1A antiarrhythmics
29
Effects of type 1 antiarrhythmics on action potential (AP) duration
* Type 1A: increase AP * Type 1B: decrease AP * Type 1C: no effect
30
Class of type 1 antiarrhythmics that preferntially affect ischemic or depolarized Purkinje and ventricular tissue
Type 1B
31
Class of type 1 antiarrhythmics with the weakest binding to the channels
Type 1B
32
Class of type 1 antiarrhythmic that prolongs effective refractory period (ERP) in AV node and accessory bypass tracts
Type 1C
33
Class of type 1 antiarrhythmics with the strongest bindings to the channels
Type 1C
34
Mechanism of action of beta blockers (as antiarrhythmics)
* 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
Mechanism of action of ivabradine
Selective inhibition of funny sodium channels
36
Main contraindication of class 1A antiarrhythmics
Patients with prolonged QT interval
37
Type of drugs used to diagnose Prinzmetal angina
Ergonovines
38
Specific combination of drugs that show a survival benefit in African American patients with systolic heart failure
Hydralazine + isosorbide nitrate
39
Mechanism through which fibrates exacerbate statin-associated myopathy
They impair statin clearance in the liver
40
Intracellular event responsible for nitrates' effects
Myosin light chain dephosphorylation by cGMP * Decreased intracellular calcium * Activation of myosin light chain phosphatase
41
Vessels that are preferentially dilated by dihydropyridines
Precapillary vessels (arterioles)
42
vessels that are preferentially dilated by renin-angiotensin system blockers (ACE inhibitors and ARBs)
Postcapillary vessels (venules)
43
Class 1A antiarrhythmic that has antimuscarinic and alpha 1 blocking effects and thus, increases conduction through the AV node and shortens the PR interval
Quinidine
44
Why is hydralazine contraindicated in patients with angina
Because it can potentiate it through reflex tachycardia
45
Resistance to methicillin (in Staph) confers resistance to what other antibiotic
Cephalosporins, because the mechanism of methicillin resistance involves penicillin binding protein alterations (PBPs are also used by cephalosporins)
46
Only statin that is not metabolized by P450 enzyme system
Pravastatin
47
Sypmatholytic drug that is used for opiate withdrawal
Clonidine