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STEP > Cardio pharm > Flashcards

Cardio pharm Flashcards

1
Q

Essential hypertension tx

A

Thiazides, ACE inhib, ARBs, DHP CCBs

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2
Q

HTN w/ HF tx

A

Diuretics, ACE inhib, ARBs, B blockers IF COMPENSATED, aldosterone antagonists

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3
Q

CI to B blockers

A

Cardiogenic shock, decompensated HF

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4
Q

HTN w/ DM tx

A

ACE inhib or ARBs (protective against diabetic nephropathy), CCBs, thiazides, B blockers

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5
Q

HTN in pregnancy

A

Hydralazine, labetalol, methyldopa, nifedipine

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6
Q

CCB MOA

A

Block voltage dependent L-type Ca channels of cardiac/smooth muscle –> decrease contractility

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7
Q

CCBs that work on vasculature

A

amlodipine=nifedipine>diltiazem>verapamil

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8
Q

CCBs that work on heart

A

verapamil>diltiazem>amlodipine=nifedipine

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9
Q

Use of DHPs

A

HTN, angina, Raynaud

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10
Q

Nimodipine use

A

Subarachnoid hermorrhage (prevents cerebral vasospasm)

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11
Q

CCBs in hypertensive urgency/emergency

A

Nicardipine, clevidipine

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12
Q

Non-DHP use

A

HTN, angina, a fib/flutter

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13
Q

Adverse effects of Non DHPs

A

Cardiac depression, AV block, hyperprolactinemia, constipation, gingival hyperplasia

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14
Q

Adverse effects of DHPs

A

Peripheral edema, flushing dizziness

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15
Q

MOA of hydralazine

A

Increased cGMP–>smooth muscle relax–>vasodil of arterioles>veins –> afterload reduction

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16
Q

Clinical use of hydralazine

A

Severe/acute HTN, HF (w/ organic nitrate), can be used during pregnancy

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17
Q

Hydralazine pearl

A

Give w/ beta blocker to prevent reflex tachycardia

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18
Q

Hydralazine adverse effects

A

COmpensatory tach (CI in angina/CAD), fluid retention, headache, angina, lupus like syndrome

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19
Q

Nitroprusside MOA

A

Increases cGMP via direct release of NO

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20
Q

Nitroprusside use

A

Hypertensive emergency (is short acting)

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21
Q

Nitroprusside adverse effect

A

cyanide tox

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22
Q

Fenoldopam MOA

A

Dopamine D1r agonist –> coronary, peripheral, renal, splanchnic vasodil–> lower BP and increased natiuresis

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23
Q

Fendoldopam uses

A

Hypertensive emergency, post op anti HTN

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24
Q

Fenoldopam adverse events

A

Hypotension, tachycardia

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25
Q

Nitrates names

A

Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

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26
Q

Nitrate mechanism

A

Vasodilate by increased NO in vascular smooth muscle –> increased cGMP and smooth muscle relaxation (veins»arteries) –> reduced preload

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27
Q

Nitrate clinical use

A

Angina, acute coronary syndrome, pulm edema

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28
Q

Adverse effects of nitrates

A

Reflex tach (prevent w/ b blocker), hypotension, flushing, headache; CI in RV infarction!

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29
Q

Monday disease

A

Industrial exposure – tolerance during workweek, loss of tolerance over weekend –> tachycardia, dizziness, headache

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30
Q

Ranolazine MOA

A

Inhibits late phase of Na current – reduced diastolic wall tension and O2 consumption (no effect on HR or contractility)

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31
Q

Ranolazine use

A

Refractory angina

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32
Q

Ranolazine adverse efffects

A

Constipation, dizziness, headache, nausea, QT prolongation

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33
Q

Milrinone MOA

A

PDE-3 inhib –> increases cAMP in heart –> Ca influx –> increased inotropy and chronotropy
Increases cAMP in vascular smooth muscle –> inhib of MLCK–>vasodilation

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34
Q

Milrinone use

A

SHort term in acute decomp HF

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35
Q

Mirinone adverse effect

A

Arrhythmias, hypotension

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36
Q

Digoxin MOA

A

Directly inhibits Na/K ATPase–>downreg of Na/Ca exchanger –> increased Ca in cell –> positive inotropy
Also stims vagus nerve to decrease HR

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37
Q

Digoxin use

A

HF (increases contractility), a fib (decrease conduction at AV/SA node)

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38
Q

Dig adverse effects

A

Cholinergic – NVD, blurry yellow vision, arrhythmias, AV block
Hyperkalemia

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39
Q

Factors predisposing to dig tox

A

Renal failure (less excretion), hypokalemia (permissive for dig binding at K binding site on Na/K ATPase), drugs that displace dig from tissue binding sites, decreased clearance (verapamil, amiodarone, quinidine)

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40
Q

Antidote for dig tox

A

Slow normalization of hyperkalemia, cardiac pacer, anti-dig Fab, Mg2+

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41
Q

HMG CoA reductase inhibitors are..

A

Statins

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42
Q

Effect of HMG CoA reductase inhibitors on LDL, HDL, trig

A

LDL: VERY MUCH LOWERED
HDL: up
Trig: down

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43
Q

Statin MOA

A

Inhibits converstion of HMG-CoA to mevalonate (precursor to cholesterol) MORTALITY BENEFIT IN CAD

44
Q

Adverse effects of statins

A

Hepatotox (high LFTs)

Myopathy (esp w/ fibrates or niacin)

45
Q

Bile acid resin examples

A

Cholestyramine, colestipol, colesevelam

46
Q

Effects of bile acid resins on LDL, HDL trig

A

LDL: much lower
HDL: slightly up
Trig: slightly up

47
Q

MOA of bile acid resins

A

Prevents intestinal absoprtion of bile acids – liver must use cholestrol to make more

48
Q

Adverse effects of bile acid resins

A

GI upset, decreased absorption of other drugs/fat-sol vits

49
Q

Ezetimibe MOA

A

Prevents cholesterol absorption at brush border in SI

50
Q

Ezetimibe effect on LDL, HDL, and trig

A

LDL: much lower

51
Q

Adverse effects of ezetimibe

A

Rare – increased LFTs, diarrhea

52
Q

Fibrates examples

A

Gemfibrozil, bezafibrate, fenofibrate

53
Q

Effect of fibrates on LDL, HDL, trig

A

LDL: down
HDL: up
trig: VERY MUCH LOWERED

54
Q

Fibrates MOA

A

Upregulate LPL –>increased trig clearance; activates PPAR alpha to induce HDL synthesis

55
Q

Adverse effects of fibrates

A

Myopathy (more risk w/ statins), cholesterol gallstones

56
Q

Niacin effects on LDL, HDL, trig

A

LDL: much lower
HDL: much higher (best)
trig: down

57
Q

Niacin MOA

A

Inhibits lipolysis (hormone sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis

58
Q

Adverse effects of niacin

A

Red, flushed face (decreased by NSAIDs or long term), hyperglycemia, hyperuricemia

59
Q

PCSK9 inhibitor examples

A

Alirocumab, evolocumab

60
Q

PCSK9 effect on LDL, HDL, trig

A

LDL: VERY MUCH LOWER – used in familial hyper cholesterolemia
HDL: up
Trig: down

61
Q

MOA of PCSK9 inhibitors

A

Inactivates LDL receptor degradation –> more LDL removed from blood

62
Q

Adverse effects of PCSK9 inhibitors

A

myalgias, delirium, dementia, neurocognitive

63
Q

Class I antiarrhythmics

A

Na channel blockers, decrease slope of phase 0, state dependent

64
Q

Class IA AAR examples

A

Quinidine, Procainamide, Disopyramide

“the Queen Proclaims Diso’s PYRAMID”

65
Q

Class IA MOA

A

Increase AP duration, increase ERP, increase QT interval, some K channel blocking

66
Q

Class IA change in ekg

A

Mid lowered slope of phase 0, longer AP

67
Q

Class IA clinical use

A

Atrial and vent arrhythmias, esp reentrant and ectopic SVT and VT

68
Q

Class IA adverse effects

A

Cinchonism (headache, tinnitus w/ quinidine), reversible SLE like syndrome (w/ procainamide), HF (dispyramide)< thrombocytopenia, torsades bc longer QT

69
Q

Class IB examples

A 
Lidocaine Mexiletime (Phenytoin can fit)
"I'd Buy LIDdy's MEXIcan Tacos"
70
Q

Class IB MOA

A

Shorter AP duration, preferentially affect ischemic/depolarized Purkinje/vent tissue

71
Q

Class IB clinical use

A

Acute vent arrhythmias (esp post MI), dig induced AR

72
Q

Class IB adverse effects

A

CNS stim/depression, cardiovascular depression

73
Q

Class IC examples

A

Flecanide, Propafenone

“Can I have Fries Please?”

74
Q

Class IB effect on EKG

A

Slightly lowered slope of phase 0 (less than IA/C), shorter AP

75
Q

Class IC mechanism

A

Significantly prolongs ERP in AV node and accessory bypass tracts, no effect on ERP in purkinje/vent tissue; minimal AP effect

76
Q

Class IC clinical use

A

SVT (including a fib), last resort in refractory VT

77
Q

Class IC adverse effects

A

Proarrhythmic (esp post MI – CI!), CI in structural/ischemic heart disease

78
Q

Class IC effect on EKG

A

Greatest change in lower slope of phase 0, no AP change

79
Q

Class II examples

A

Metoprolol, propanolol, esmolol, atenolol, timolol, carvedilol

80
Q

Class II =

A

B blockers

81
Q

Class II MOA

A

Decreases SA/AV nodal activity by lowering cAMP and Ca current, suppresses abnormal pacemakers by lowering slope of phase 4
AV node more sensitive –> longer PR interval

82
Q

Esmolol is special because…

A

Short acting

83
Q

Class II clinical use

A

SVT, ventricular rate control for a fib/flutter

84
Q

Class II adverse effects

A

Impotence, exacerbation of COPD/asthma, cardiovascular effects (bradycardia, AV block, HF), CNS effects (sedation, sleep alterations), can mask signs of hypoglycemia

85
Q

Metoprolol special adverse effect

A

Dyslipidemia

86
Q

Propanolol special adverse effect

A

Exacerbation of vasospasm in prinzmetal angina

87
Q

Treatment for B blocker overdose

A

Saline, atropine, glucagon

88
Q

Class III AAR examples

A

Amiodarone, Ibutilide, Dofetilide, Sotalol

AIDS

89
Q

Class III MOA

A

K channel blockers – increase Ap duration, increase ERP, increase QT interval

90
Q

Class III clinical use

A

A fib/flutter, v tach (amiodarone, sotalol)

91
Q

Adverse effects of sotalol

A

Torsades, excessive b block

92
Q

Advese effects of Ibutilide

A

Torsades

93
Q

Adverse effects of amiodarone

A

Pulmonary fibrosis, hepatotox, hypo/hyperthyroidism (40% iodine by wt), hapten (corneal depositis, blue/grey skin deposits–>photodermatitis), neuro effects, constipation, cardiovascular effects (bradycardia, heart block, HF)

94
Q

Check before amiodarone…

A

PFTs, LFTs, TFTs

95
Q

Class IV AARs MOA

A

CCBs, decrease conduction velocity, increase ERP, increase PR interval

96
Q

Class IV examples

A

Verapamil, diltiazem

97
Q

Class IV clinical use

A

Prevent nodal arrhythmias (SVT), rate control in a fib

98
Q

Adverse effects of Class IV

A

Constipation, flushing, edema, cardiovascular (HF, AV clock, sinus node depression)

99
Q

Adenosine MOA

A

Increases K efflux –> hyperpolarize and lower Ca –> less AV node conduction

100
Q

Adenosine clinical use

A

DOC in diagnosing/terminating SVTs

101
Q

Adenosine time of action

A

15s

102
Q

Adenosine effects are blunted by

A

Caffeine, theophylline (adenosine receptor antagonists)

103
Q

Adenosine adverse effects

A

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

104
Q

Mg clinical use

A

Torsades and dig tox

105
Q

Ivabradine MOA

A

Selectively inhibits If (Na channels) prolonging slow depolarization phase (4) of nodes –> less SA node firing –> negative chronotropic w/o inotropic effect, reducing O2 reqs

106
Q

Ivabradine clinical use

A

Chronic stable angina if no ability to take B blockers, chronic HF w/ reduced EF

107
Q

Ivabradine adverse effects

A

Luminous phenomena/visual brightness, HTN, bradycardia

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