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Step 1 - Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Primary HTA treatment

A
  1. Thiazide diuretics
  2. ACE inhibitors
  3. ARB
  4. Dihydropyridine Ca channel blockers
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2
Q

Hypertension with heart failure treatment

A
  1. Diuretics
  2. ACE inhibitors/ARB
  3. Beta blockers
  4. Aldosterone antagonists: espironolactone, eplerenone
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3
Q

Beta blockers in decompensated HF and cardiogenic shock

A

Dont use

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4
Q

Hypertension with DM treatment

A
  1. ACE inhibitors/ARBs
  2. Ca channel blockers
  3. Thiazide diuretics
  4. Beta blockers
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5
Q

Protective against DM nephropathy

A

ACE inhibitors/ARB

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6
Q

Hypertension in pregnancy treatment

A

Hydralazine
Labetalol
Methyldopa
Nifedipine

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7
Q

Dihydropyridines calcium channel blockers

A

Amlodipine
Clevidipine
Nifedipine
Nimodipine

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8
Q

Non dihydropyridines

A

Diltiazem

Verapamil

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9
Q

Mechanism of action of calcium channel blockers

A

Block voltage dependent L-type calcium channels of cardiac (non dihydropyridines) and smooth muscle (dihydropyridines)

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10
Q

Verapamil-diltiazem. Which of them has a stronger effect?

A

Verapamil on heart

Diltiazem on smooth muscle

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11
Q

Use of nimodipine

A

Subarachnoid hemorrhage: prevents cerebral vasospasm

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12
Q

Dihydropyridines use

A

Hypertension
Angina: including prinzmetal
Raynaud phenomenon

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13
Q

Non dihydropyridines use

A

Hypertension
Angina
Atrial fibrillation/flutter

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14
Q

Dihydropyridine side effects

A

peripheral edema
Flushing
Dizziness
Gingival hyperplasia

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15
Q

Non dihydropyridine side effects

A

Cardiac depression
AV block
Hyperprolactinemia
Constipation

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16
Q

Dihydropyridines used in hypertensive urgency or emergency

A

Nicardipine

Clevidipine

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17
Q

Drug that increases cGMP

A

Nitroprusside
Nitrates
Hydralazine

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18
Q

Hydralazine vasodilates

A

arterioles >veins: afterload reduction

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19
Q

Administered with a beta blocker to prevent reflex tachicardia

A

Hydralazine: arteriole vasodilation

Nitrates

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20
Q

Compensatory tachycardia is a common side effect

A

Hydralazine

Nitrates

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21
Q

Hydralazine is contraindicated in

A

Angina

Coronary artery disease: compensatory tachicardia

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22
Q

Hypertensive emergency tratment

A 
Clevidipine
Nicardipine
Fenoldopam
Labetalol
Nitroprusside
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23
Q

Treatment of severe and acute hypertension

A

Hydralazine

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24
Q

Can cause cyanide toxicity

A

Nitroprusside: releases cyanide

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25
Q

cGMP increase via direct release of NO

A

Nitroprusside

Nitrates

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26
Q

Dopamine D1 receptor antagonist used in hypertensive emergency and postoperatory antihypertensive

A

Fenoldopam

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27
Q

Nitrates

A

Nitroglycerin
Isosorbide dinitrate
Isosorbide mononitrate

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28
Q

Nitrates dilate

A

Veins>arteries: decrease preload

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29
Q

Monday disease

A

Nitrates
Development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend: tachycardia, dizziness, headache upon reexposure

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30
Q

Contraindicated in right ventricular infarction

A

Nitrates

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31
Q

Goal of antianginal therapy

A

Decrease myocardial O2 consumption by decreasing its determinants:

  • End diastolic volume (preload)
  • Blood pressure
  • Heart rate
  • Contractility
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32
Q

Mechanism of action of Ranolazine

A

Inhibits the late phase of sodium current thereby reducing dyastolic wall tension and O2 consumption

33
Q

Selective PDE-3 inhibitor

A

Milrinone

34
Q

Milrinone action

A

PDE-3 inhibition:
Cardiomyocites: +cAMP: + Ca influx:+inotropy and chronotropy
Smooth muscle: +cAMP: inhibits MLCK: general vasodilation

35
Q

Use of milrinone

A

Short term use in decompensated HF

36
Q

Lipid-lowering agents

A
  1. HMG-CoA reductase inhibitors
  2. Bile acid resins
  3. Ezetimibe
  4. Fibrates
  5. Niacin (B3)
  6. PCSK9
37
Q

Statins mechanism of action

A

Inhibit HMG-CoA reductase: inhibits conversion of HMG-CoA to mevalonate a cholesterol precursor

38
Q

Adverse effect of statins

A

Hepatotoxicity

Myopathy

39
Q

Myopathy as an adverse effect of lipid lowering treatment is particularly dangerous when

A

Combining statins with fibrates or niacin

40
Q

Mechanism of action of bile acid resins

A

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

41
Q

Bile acid resins: drugs

A

Cholestyramine
Clestipol
Colesevelam

42
Q

Problem associated to bile acid resins

A

Malabsorption of fat soluble vitamins: ADEK

43
Q

Ezetimibe mechanism of action

A

Prevent cholesterol absorption at small intestine brush border

44
Q

Most effective decreasing triglycerides

A

Fibrates

45
Q

Activates PPAR alpha

A

Fibrates

46
Q

Fibrates mechanism of action

A
  1. Upregulate LPL: TGL clearance

2. Activates PPAR alpha to induce HDL synthesis

47
Q

Niacin lipid lowering mechanism of action

A

Inhibits lipolysis: hormone sensitive lipase in adipose tissue
Reduces hepatic VLDL synthesis

48
Q

PCSK9 inhibitors mechanism of action

A

Inactivation of LDL receptor degradation: increases amount of LDL receptors increasing amount o LDL removed from bloodstream

49
Q

PCSK9 inhibitors

A

Alirocumab

Evolocumab

50
Q

Cardiac glycosides

A

Digoxin

51
Q

Direct inihbition of Na/k ATPase: indirect inhibition of Na/Ca exchanger

A

Digoxin

52
Q

Clinical use of digoxin

A
  1. Heart failure: increases contractility (inotropic +)

2. Atrial fibrillation: decreases conduction at AV node and depression of SA node)

53
Q

Can lead to hyperkalemia

A

Digoxin: inhibits Na/k ATPase

54
Q

Decreases digoxin clearance

A

Verapamil
Amiodarone
Quinidine

55
Q

Antidote for digoxin

A

Normalize K
Cariac pacer
Anti digoxin Fab fragments
Mg2+

56
Q

Antiarrhytmics types

A

Class I: Na channel blockers
Class II: beta blockers
Class III: Potassium channel blockers
Class IV: Calcium channel blockers

57
Q

Class IA antiarrhytmics

A

The Queen Proclaims Dis Pyramid
Quinidine
Procainamide
Disopyramide

58
Q

Class IB antiarrythmics

A

Liddy’s Mexican Tacos
Lidocaine
Mexiletine

59
Q

Decrease slope of phase 0 depolarization

A

Antiarrythmics class I: sodium channel blockers

60
Q

Antiarrythmics class I: sodium channel blockers that increase AP duration

A

Antiarrythmics class IA

61
Q

Antiarrythmics class I: sodium channel blockers that decrease AP duration

A

Antiarrythmics class IB

62
Q

Antiarrythmics class I: sodium channel blockers that have no effect in Effective refractory period

A

Antiarrythmics class IC

63
Q

Class IC antiarryhtmics

A

Fries Please
Flecainamide
Propafenone

64
Q

Best antiarrhythmic post MI

A

Class IB

65
Q

Class IC antiarryhtmics are contraindicated in

A

Structural and ischemic heart disease

DONT use post MI

66
Q

Very short acting beta blocker

A

Esmolol

67
Q

Exacerbates vasospasm in Prinzimetal angina

A

Propranolol–>Prinzimetal

68
Q

Class III antiarryhtmics

A

AIDS:

  • Amiodarone
  • Ibutilide
  • Dofetilide
  • Sotalol
69
Q

Mechanism of action of Class III antiarryhtmics

A

Increase action potential duration: markedly prolonged repolarization: increase ERP and QT interval

70
Q

Use of Class III antiarryhtmics

A
  1. Atrial fibrillation
  2. Atrial flutter
  3. Ventricular tachycardia: sotalol, amiodarone
71
Q

State dependent antiarrhythmics

A

Sodium channel blockers (class I)

72
Q

Amiodarone toxicity

A
  1. Pulmonary fibrosis
  2. Hepatotoxicity
  3. Hypo/hyperthiroidism: 40% iodine
  4. Corneal deposit, photodermatitis
    PFT, LFT, TFT
73
Q

Class IV antiarryhtmics

A

Calcium channel blockers: verapamil, diltiazem

74
Q

Rate control in atrial fibrillation

A

Class IV antiarryhtmics: verapamil, diltiazem

75
Q

Adenosine as an antiarrhythmic

A

K out of cells: hyperpolarizing the cell

Decrease Ica: decreases AV node conduction

76
Q

Adenosine effects are blunted by

A

Theophylline
Caffeine
Adenosine receptor antagonists

77
Q

Effective in torsades de pointes and digoxin toxicity

A

Magnesium

78
Q

Selective inhibition of funny sodium channels If

A

Ivabradine

79
Q

Use in chronic stable angina in patients who cannot take beta blockers

A

Ivabradine

Step 1 - Cardiovascular (5 decks)

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