Cardiac Flashcards

(69 cards)

1
Q

Use for Primary HTN

A

thiazides
Ace inhibitors
Angiotensin receptor blockers

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2
Q

HTN with HF

A

diuretic, ace inhibitor, and arb (only use beta blockers in compensated HF)

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3
Q

HTN with DM

A

ace inhibitors and angiotensin receptor blockers

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4
Q

HTN in pregnancy

A

hydrazine, nifedipine, methyldopa, labetalol

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5
Q

Dihydropyridine calcium channel blockers work on?

A

vascular smooth muscle

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6
Q

Amlodipine, clevidipine, nifedipine, nimodipine

A

dihydropyridine calcium channel blockers

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7
Q

nondihydropyridine calcium channel blockers

A

work on the heart

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8
Q

dilitazem, verapamil

A

nondihydropyridine calcium channel blockers

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9
Q

-“dipine”=

A

Dihydropyridine calcium channel blockers

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10
Q

MOA of calcium channel blockers

A

block voltage gated L type calcium channels of cardiac and smooth muscle

(Class 4 will decrease conduction velocity and increase EP and increase PR interval)

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11
Q

Use all Dihydropyridines except nimodipine for:

A

HTN, angina, raynaud phenomenon

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12
Q

nimodipine used for

A

subarachnoid hemorrhage

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13
Q

nondihydropyridines used for

A

HTN, angina, a fib/flutter, and to prevent SVT

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14
Q

SE of dihydropyridines

A

cardiac depolarization, av block, hyperprolactinemia, constipation

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15
Q

SE of nondihydropyridines

A

peripheral edema, flushing, dizziness, gingival hyperplasia

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16
Q

Hydralazine works by:

A

increased cGMP; which works to vasodilator arterioles > veins ; decreases afterload

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17
Q

Hydralazine is used for HF when given with?

A

nitrate

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18
Q

Hydralazine avoids reflex tachycardia with?

A

beta blockers

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19
Q

SE: of hydralazine

A

SLE like symptoms, increase HR, and fluid retention

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20
Q

1 drug for HTN emergency =

A

nitroprusside

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21
Q

NItroprusside works by:

A

increase cGMP–> by releasing NO and can cause Cyanide toxicity

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22
Q

Nitrates examples:

A

nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

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23
Q

MOA of nitrates:

A

dilate veins> arterioles; which decreases preload

**Will also see a decrease in EDV, BP, ejection time, and MVO2

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24
Q

Nitrates work on EDV and BP by:

A

decreases MVO2

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25
Beta blockers work on contractility and BP by:
MVO2
26
Inhibits late phase of sodium current --> decreases diastolic wall tension and oxygen consumption
ranolazine
27
use for angina due to other therapies; that doesn't affect the HR or contractility?
ranolazine
28
Inhibit NA/K ATPase; which indirectly inhibits the Na/Ca exchanger which increases calcium
digoxin
29
increases calcium means increasing contractility; also + ionotrophy ; which stimulates vagus nerve and decreases the HR
digoxin
30
digoxin SE:
blurry yellow vision
31
HMG COA reductase inhibitors MOA:
prevent mevalonate synthesis
32
Which lipid lowering agents decrease LDL?
HMG COA reductase inhibitors; bile acid resins, ezetimibe
33
Which lipid lowering agents increase HDL?
niacin
34
Which lipid lowering agents decrease triglycerides?
fibrates, omega 3 FA
35
Which lipid lowering agent increases LFTs?
ezetimibe
36
Statins cause increased or decreased mortality in CAD patients?
decreased
37
SE of statins:
statin induced myopathy ; esp with vibrates or niacin
38
examples of bile acid resins:
cholestyramine, colestipol, colesevelam
39
Bile acid resins MOA:
prevent intestinal reabsorption of bile acids
40
SE of bile acid resins
decrease absorption of other drugs and fat soluble vitamins *** cholestyramine can bind C. difficle
41
MOA: prevent cholesterol absorption at the small intestine brush border
ezetimibe
42
can be used when a patient cannot handle statins?
ezetimibe
43
MOA of fibrates:
upregulate LPL which increase TG clearance; use PPAR gamma to decrease hepatic LDL and increase LPL activity which will ultimately decrease TG and increase HDL
44
Fibrates SE:
myopathy and cholesterol gallstones
45
Inhibit lipolysis in adipose tissue:
Niacin
46
SE of Niacin:
red flushed, face * can be decreased with NSAIDS
47
Class 3 K+ channel blockers drugs:
amiodarone, ibutilide, dofetilide, sotalol (AIDS)
48
Increase AP, increase ERP Increase QT interval
Class 3 K+ channel blockers drugs:
49
Use for A-fib/flutter, V-tach
Class 3 K+ channel blockers drugs: For Vtach ( use amiodarone or sotalol)
50
Sotalol has more risk of _________ and amiodarone has a less risk of _________.
Torsades
51
You must check what with amiodarone?
PFTS, LFTS, TFTS
52
Adenosine MOA:
increases K+ out of cells which hyper-polarizes and then decreases intercellular calcium
53
Adenosine indications:
diagnose and terminate SVT ** effect is blunted by theophylline and caffeine
54
Magnesium use:
torsades and digoxin toxicity
55
Class 2 Anti arrhythmic: Beta blockers
metoprolol, propanolol, esmolou, atenolol, timolol, carvedilol
56
decrease SA / AV node activity by decreases cAMP and decreasing calcium current which also decreases slope of phase 4
Class 2 Anti arrhythmic: Beta blockers
57
SE of Class 2 Anti arrhythmic: Beta blockers
impotence, COPD exacerbation, can masks signs of hypoglycemia **** beta blockers can cause unopposed alpha 1 agonism if given alone for pheochromocytoma or cocaine toxicity
58
Class 1 (Sodium channel blockers) action of what phase?
Phase 0; by decreasing slope
59
Class 1A: drugs?
quinidine, procainamide, disopyramide
60
Class 1B: drugs?
lidocaine and mexiletine
61
Class 1C: drugs?
flecainide, propafenone
62
Class 1A MOA:
prolong the AP, prolong the QT (causes torsades de pointes) , increases effective refractory period
63
Class 1A SE:
reversible SLE like symptoms ( esp. procainamide) , cinchonism ( esp. quinidine) and heart failure (disopyramide)
64
Class 1A used for?
atrial and ventricular arrhythmias
65
Class 1B MOA
decerase AP duration
66
Class 1B used for?
best for: ventricular arrhythmias that are post MI
67
Class 1C MOA
prolong ERP in AV node and accessory bypass tracts
68
Class 1C used for?
use for SVTS ; CONTRAINDICATED POST MI ;
69
Mneumonic for Class 1 anti-arrhythmics (Sodium) channel blockers
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