Pharmacology Flashcards

(79 cards)

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
cGMP increase via direct release of NO
Nitroprusside | Nitrates
26
Dopamine D1 receptor antagonist used in hypertensive emergency and postoperatory antihypertensive
Fenoldopam
27
Nitrates
Nitroglycerin Isosorbide dinitrate Isosorbide mononitrate
28
Nitrates dilate
Veins>arteries: decrease preload
29
Monday disease
Nitrates Development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend: tachycardia, dizziness, headache upon reexposure
30
Contraindicated in right ventricular infarction
Nitrates
31
Goal of antianginal therapy
Decrease myocardial O2 consumption by decreasing its determinants: - End diastolic volume (preload) - Blood pressure - Heart rate - Contractility
32
Mechanism of action of Ranolazine
Inhibits the late phase of sodium current thereby reducing dyastolic wall tension and O2 consumption
33
Selective PDE-3 inhibitor
Milrinone
34
Milrinone action
PDE-3 inhibition: Cardiomyocites: +cAMP: + Ca influx:+inotropy and chronotropy Smooth muscle: +cAMP: inhibits MLCK: general vasodilation
35
Use of milrinone
Short term use in decompensated HF
36
Lipid-lowering agents
1. HMG-CoA reductase inhibitors 2. Bile acid resins 3. Ezetimibe 4. Fibrates 5. Niacin (B3) 6. PCSK9
37
Statins mechanism of action
Inhibit HMG-CoA reductase: inhibits conversion of HMG-CoA to mevalonate a cholesterol precursor
38
Adverse effect of statins
Hepatotoxicity | Myopathy
39
Myopathy as an adverse effect of lipid lowering treatment is particularly dangerous when
Combining statins with fibrates or niacin
40
Mechanism of action of bile acid resins
Prevent intestinal reabsorption of bile acids: liver must use cholesterol to make more
41
Bile acid resins: drugs
Cholestyramine Clestipol Colesevelam
42
Problem associated to bile acid resins
Malabsorption of fat soluble vitamins: ADEK
43
Ezetimibe mechanism of action
Prevent cholesterol absorption at small intestine brush border
44
Most effective decreasing triglycerides
Fibrates
45
Activates PPAR alpha
Fibrates
46
Fibrates mechanism of action
1. Upregulate LPL: TGL clearance | 2. Activates PPAR alpha to induce HDL synthesis
47
Niacin lipid lowering mechanism of action
Inhibits lipolysis: hormone sensitive lipase in adipose tissue Reduces hepatic VLDL synthesis
48
PCSK9 inhibitors mechanism of action
Inactivation of LDL receptor degradation: increases amount of LDL receptors increasing amount o LDL removed from bloodstream
49
PCSK9 inhibitors
Alirocumab | Evolocumab
50
Cardiac glycosides
Digoxin
51
Direct inihbition of Na/k ATPase: indirect inhibition of Na/Ca exchanger
Digoxin
52
Clinical use of digoxin
1. Heart failure: increases contractility (inotropic +) | 2. Atrial fibrillation: decreases conduction at AV node and depression of SA node)
53
Can lead to hyperkalemia
Digoxin: inhibits Na/k ATPase
54
Decreases digoxin clearance
Verapamil Amiodarone Quinidine
55
Antidote for digoxin
Normalize K Cariac pacer Anti digoxin Fab fragments Mg2+
56
Antiarrhytmics types
Class I: Na channel blockers Class II: beta blockers Class III: Potassium channel blockers Class IV: Calcium channel blockers
57
Class IA antiarrhytmics
The Queen Proclaims Dis Pyramid Quinidine Procainamide Disopyramide
58
Class IB antiarrythmics
Liddy's Mexican Tacos Lidocaine Mexiletine
59
Decrease slope of phase 0 depolarization
Antiarrythmics class I: sodium channel blockers
60
Antiarrythmics class I: sodium channel blockers that increase AP duration
Antiarrythmics class IA
61
Antiarrythmics class I: sodium channel blockers that decrease AP duration
Antiarrythmics class IB
62
Antiarrythmics class I: sodium channel blockers that have no effect in Effective refractory period
Antiarrythmics class IC
63
Class IC antiarryhtmics
Fries Please Flecainamide Propafenone
64
Best antiarrhythmic post MI
Class IB
65
Class IC antiarryhtmics are contraindicated in
Structural and ischemic heart disease | DONT use post MI
66
Very short acting beta blocker
Esmolol
67
Exacerbates vasospasm in Prinzimetal angina
Propranolol-->Prinzimetal
68
Class III antiarryhtmics
AIDS: - Amiodarone - Ibutilide - Dofetilide - Sotalol
69
Mechanism of action of Class III antiarryhtmics
Increase action potential duration: markedly prolonged repolarization: increase ERP and QT interval
70
Use of Class III antiarryhtmics
1. Atrial fibrillation 2. Atrial flutter 3. Ventricular tachycardia: sotalol, amiodarone
71
State dependent antiarrhythmics
Sodium channel blockers (class I)
72
Amiodarone toxicity
1. Pulmonary fibrosis 2. Hepatotoxicity 3. Hypo/hyperthiroidism: 40% iodine 4. Corneal deposit, photodermatitis PFT, LFT, TFT
73
Class IV antiarryhtmics
Calcium channel blockers: verapamil, diltiazem
74
Rate control in atrial fibrillation
Class IV antiarryhtmics: verapamil, diltiazem
75
Adenosine as an antiarrhythmic
K out of cells: hyperpolarizing the cell | Decrease Ica: decreases AV node conduction
76
Adenosine effects are blunted by
Theophylline Caffeine Adenosine receptor antagonists
77
Effective in torsades de pointes and digoxin toxicity
Magnesium
78
Selective inhibition of funny sodium channels If
Ivabradine
79
Use in chronic stable angina in patients who cannot take beta blockers
Ivabradine