CARDIO - drugs Flashcards

1
Q

Primary HTN rx

A

ACEI, ARB, Thiazide, CCB

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2
Q

HTN with HF rx

A

ACEI, ARB, Diuretics, aldosterone antagonists, b-blockers

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3
Q

HTN with DM

A

ACEI, ARB, Thiazide, CCB, b-blocker

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4
Q

HTN in pregnancy

A

Hydralazine, methyldopa, labetalol, nifedipine

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5
Q

methyldopa AE

A

HTN pregnancy
a2 agonist
SLE-like
Coombs +

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6
Q

hydralazine AE

A

SLE-like

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7
Q

CCB’s block:

A

L-type VG Ca channels of cardiac and smooth muscle

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8
Q

general CCB dihydropyridine use

A

HTN, angina (including prizmetal), raynaud

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9
Q

CCB for SAH

A

Nimodipine (cerebral selectivity)

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10
Q

CCB for hypertensive urgency/emergency

A

Clevidipine and nicardipine

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11
Q

General non-dihydropyridine CCB use

A

HTN, angina, atrial fib/flutter

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12
Q

Verapamil AE

A

hyperprolactinemia

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13
Q

General CCB AE

A

constipation, gingival hyperplasia

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14
Q

hydralazine MOA

A

increases cGMP causing vasodilation of arteries > veins. Can cause reflex tachycardia so can give with b-blocker, also avoid in angina/CAD

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15
Q

Hydralazine use

A

acute/severe HTN, HTN pregnancy, HTN HF

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16
Q

HTN emergencies

A

Clevidipine, nicardipine, labetalol, fenoldopam, nitroprusside

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17
Q

CCB for pregnancy

A

Nifedipine

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18
Q

Nitroprusside MOA and AE

A

MOA = release of NO causing increased cGMP.

AE = cyanide poisoning

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19
Q

Fenoldopam

A

D1 agonist - vasodilation of coronaries, renal, peripheral, splanchnic - keep up naturesis

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20
Q

nitrates MOA

A

Release NO causing cGMP, veins > arteries, decreases preload

21
Q

nitrates AE

A

Hypotension, reflex tachycardia, headache, flushing

22
Q

Digoxin MOA (2)

A

Direct block Na//K; indirect block Na//Ca; so increased contractility.

Stimulates vagus to decrease HR.

23
Q

Digoxin use

A

HF for contractility

A fib for slowed AV and depressed SA

24
Q

Digoxin toxicity

A

Cholinergic: blurry yellow vision, arrhythmia, AV block.

Hyperkalemia.

25
Q

Increase digoxin toxicity via:

A

Hypokalemia, renal failure, verapamil, amiodarone, quinidine (decrease clearance + displaces from tissue)

26
Q

Digoxin antedote

A

fix K+, Mg, anti-digoxin Fab, pacer

27
Q

Class I AA MOA

A

block Na+ channels slowing conduction, especially in depolarized muscle cells

28
Q

Class IA names

A

Disopyramide, Quinidine, Procainamine

29
Q

Class 1B names

A

Lidocaine, Tocainide, Mexiletine

30
Q

Class 1C names

A

Flecainide, Propafenone, Moricizine

31
Q

Class 1A AE

A

Cinchonism (quinidine - HA, tinnitus), SLE-like (procainamide), heart failure (disopyramide), thrombocytopenia, torsades

32
Q

Post MI acute ventricular arrhythmia rx (class)

A

Class 1B

33
Q

Class 1C AE

A

pro-arrythmic (especially post-MI)

34
Q

Class 1 affinities for phase 0 inhibition

A

A = intermediate, B = weak, C = strongest

35
Q

Class 1 alterations in QT (AP duration)

A

A = increase, B = decrease, C = N/A

36
Q

Class II: group and specific AEs

A

beta blockers. Metoprolol = dyslipidemia. Propanolol = prizmetal exacerbation

37
Q

Phase of AP altered by Class II

A

Phase 4 (Ca channels of nodal tissue)

38
Q

Class III: names and function

A

K+ blockers, increasing AP, ERP, QT.

Amiodarone, Ibutilide, Dofetilide, Sotalol.

39
Q

Sotalol AE

A

Torsades, excessive beta blockade (K+ and Na+ blocker)

40
Q

Ibutilide AE

A

Torsades

41
Q

Amiodarone AE

A

*NO torsades!
PULMONARY FIBROSIS, hepatotoxicity, hypo/hyper-thyroidism and blue-grey skin in sun (via iodine content), neurological, constipation.
Check LFTs, TFTs, PFTs

42
Q

Class IV names

A

CCBs verapamil and diltiazem

43
Q

Class IV mechanism

A

Decrease conduction velocity. Increase ERP and PR

44
Q

Class IV

A

constipation (verapamil), flushing, edema

45
Q

Adenosine use in cardio

A

Diagnosing/abolishing SVTs (including paroxysmal SVTs)

46
Q

Blunting adenosine via:

A

theophylline and caffeine

47
Q

Adenosine AE

A

Flushing, hypotension, sense of impending doom, bronchospasm, chest pain

48
Q

Mg++ in cardio treats

A

Torsades, digoxin toxicity (because it antagonizes Ca)

49
Q

drugs causing kyperkalemia:

A

ACE-I.
ARB.
K+ sparing diuretics.
Digoxin.
Non-selective beta antag (b2 causes intracellular uptake).
NSAIDs (block PG, decrease renin + aldost.)