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
Increase digoxin toxicity via:
Hypokalemia, renal failure, verapamil, amiodarone, quinidine (decrease clearance + displaces from tissue)
26
Digoxin antedote
fix K+, Mg, anti-digoxin Fab, pacer
27
Class I AA MOA
block Na+ channels slowing conduction, especially in depolarized muscle cells
28
Class IA names
Disopyramide, Quinidine, Procainamine
29
Class 1B names
Lidocaine, Tocainide, Mexiletine
30
Class 1C names
Flecainide, Propafenone, Moricizine
31
Class 1A AE
Cinchonism (quinidine - HA, tinnitus), SLE-like (procainamide), heart failure (disopyramide), thrombocytopenia, torsades
32
Post MI acute ventricular arrhythmia rx (class)
Class 1B
33
Class 1C AE
pro-arrythmic (especially post-MI)
34
Class 1 affinities for phase 0 inhibition
A = intermediate, B = weak, C = strongest
35
Class 1 alterations in QT (AP duration)
A = increase, B = decrease, C = N/A
36
Class II: group and specific AEs
beta blockers. Metoprolol = dyslipidemia. Propanolol = prizmetal exacerbation
37
Phase of AP altered by Class II
Phase 4 (Ca channels of nodal tissue)
38
Class III: names and function
K+ blockers, increasing AP, ERP, QT. | Amiodarone, Ibutilide, Dofetilide, Sotalol.
39
Sotalol AE
Torsades, excessive beta blockade (K+ and Na+ blocker)
40
Ibutilide AE
Torsades
41
Amiodarone AE
*NO torsades! PULMONARY FIBROSIS, hepatotoxicity, hypo/hyper-thyroidism and blue-grey skin in sun (via iodine content), neurological, constipation. Check LFTs, TFTs, PFTs
42
Class IV names
CCBs verapamil and diltiazem
43
Class IV mechanism
Decrease conduction velocity. Increase ERP and PR
44
Class IV
constipation (verapamil), flushing, edema
45
Adenosine use in cardio
Diagnosing/abolishing SVTs (including paroxysmal SVTs)
46
Blunting adenosine via:
theophylline and caffeine
47
Adenosine AE
Flushing, hypotension, sense of impending doom, bronchospasm, chest pain
48
Mg++ in cardio treats
Torsades, digoxin toxicity (because it antagonizes Ca)
49
drugs causing kyperkalemia:
ACE-I. ARB. K+ sparing diuretics. Digoxin. Non-selective beta antag (b2 causes intracellular uptake). NSAIDs (block PG, decrease renin + aldost.)