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Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Torsades de pointes

A

magnesium sulfate

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2
Q

Atrial Fib

A

anticoagulation, rate control

possible cardioversion

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3
Q

Atrial Flutter

A

antiarrhythmic (Class IA, IC or III) to convert to sinus rhythm
rate control- beta blocker or CCB

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4
Q

Ventricular Fib

A

CPR & Defibrillation

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5
Q

Mobitz Type II- 2nd Degree Heart Block

A

pacemaker

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6
Q

3rd degree (complete) heart block

A

pacemaker

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7
Q

wolff-parkinson-white

A

antiarrythmic

RF ablation

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8
Q

patent ductus arteriosus (PDA)

A

close with Indomethacin (NSAID)

keep open with PG E1 & E2

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9
Q

tetrology of fallot

A

early primary surgical correction

squat to relieve cyanotic sx

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10
Q

Dilated Cardiomyopathy

A 
Na restriction
ACE-inhibitor
Diuretics
Digoxin
Heart transplant
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11
Q

Hypertrophic Cardiomyopathy

A

Beta-blocker

Calcium-Channel blocker (Verapamil)- non-dihydropyridine

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12
Q

Congestive Heart Failure

A 
ACE-Inhibitors
Beta-blockers (except if ACUTE DECOMPENSATED)
Angiotensin Receptor Antagonists
Spironolactone
(above = DECREASE MORTALITY)

Thiazide/ Loop diurectics
(DECREASE MORBIDITY ONLY)
Hydralazine w/ Nitrate tx improves Sx & mortality in select patients only

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13
Q

Temporal Arteritis (Giant Cell)

A

high-dose corticosteroids

prevent blindness via ophthalamtic artery

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14
Q

Takayasu’s Arteritis

A

corticosteroids

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15
Q

Polyarteritis Nodosa

A

corticosteroids

cyclophosphamide

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16
Q

Kawasaki Disease

A

IV Ig

Aspirin

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17
Q

Buerger’s Dz (Thromboangiitis obliterans)

A

smoking cessation

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18
Q

Microscopic polyangiitis

A

corticosteroids

cyclophosphamide

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19
Q

Wegener’s Granulomatosis

A

corticosteroids

cyclophosphamide

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20
Q

Churg-Strauss syndrome

A

corticosteroids

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21
Q

Essential HTN

A

ACET, ARB, CCB, diuretic

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22
Q

CHF

A

diuretic, ACEI/ARM, BB (only if COMPENSATED), K+ sparing diuretic (spironolactone)

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23
Q

DM

A

ACEI/ARB

CCB, Diuretic, BB, AB

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24
Q

Cardioselective Calcium channel blockers

A

verapamil > diltiazem

no use in CHF

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25
Q

Vascular smooth muscle-selective CCBs

A

amlodipine & nifedipine

okay to use in CHF

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26
Q

MOA of CCBs

A

block voltage-gated L-type Ca channels (cardiac & vascular sm muscle) = reduce contractility

  • nifedipine = similar to nitrates in antianginal effects
  • verapamil = similar to BB in antianginal effects
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27
Q

Clinical use of CCBs

A

HTN, angina- esp Prinzmetal’s, Raynaud’s phenomenon/Dz

Arrythmia (NOT nifedipine– causes tachycardia)

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28
Q

toxicity of CCBs

A

cardiac depression, AV block, peripheral edema, flushing, dizzy, constipation

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29
Q

Hydralazine MOA

A

increases cGMP which causes smooth muscle relaxation. vasodilates arterioles> veins (dec afterload)

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30
Q

clinical use hydralazine

A

severe HTN, CHF
1st line tx- pregnancy w/ HTN + methyldopa
coadmin w/ BB to prevent reflex tachy

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31
Q

toxicity of hydralazine

A

reflex tachycardia (contra in angina & CAD)
fluid retention, nausea, HA, angina
Lupus-like syndrome

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32
Q

Hypertensive Crisis/ malignant HTN tx

A

nitroprusside, nicardipine, clevidipine, labetalol, fendolopam

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33
Q

MOA nitroprusside

A

short acting

inc cGMP via direct release of NO.

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34
Q

toxicity of nitroprusside

A

cyanide toxicity (released when acts)

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35
Q

MOA fenoldopam

A

D1 receptor agonist causing coronary, peripheral, renal & splanchnic vasodilation
decreases BP & inc natriuresis (pee!)

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36
Q

Nitroglycerin/ Isosorbide dinitrate MOA

A

vasodilates by releasing NO in smooth muscle. causes inc cGMP and smooth muscle relaxation.
dilates veins > arteries (opposite of hydralazine)
dec preload

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37
Q

clinical use Nitroglycerine/ isosorbide dinitrate

A

angina

pulmonary edema

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38
Q

toxicity of Nitroglycerine/ isosorbide dinitrate

A

reflex tachycardia, hypotension
flushing headache
Monday Dz– tolerance during work week, loss of tolerance during weekend (tachycardia, dizzy, HA upon re-exposure)

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39
Q

contraindicated in angina

A

Pindolol
Acebutolol

partial beta-agonists

40
Q

Antianginal therapy: nitrates (alone)

A

Dec Preload via:
DEC: EDV, BP, ejection time & MVO2 (myocardial O2 consumption
INC: contracility & HR (reflex)

41
Q

Antianginal therapy: beta- blockers (alone)

A

Dec Afterload via:
DEC: BP, contractility, HR, MVO2 (myocardial O2 consumption)
INC: EDV, ejection time

42
Q

Antianginal therapy: Nitrates + Beta-blockers

A

Major effects:
Dec BP & HR = major dec MVO2 (myocardial O2 consumption)
Little to no effect on EDV, contractility, ejection time

43
Q

HMG-COA Reductase inhibitors

44
Q

MOA of HMG-CoA reductase inhibitors

A

inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)
Main effect: major dec LDL

45
Q

S/E of HMG-CoA reductase inhibitors

A

hepatotoxicity (inc LFTs)

rhabdomyolysis

46
Q

MOA Niacin (Vit B3)

A

dec hepatic HLDL secretion
inhibits lipolysis in adipose tissue
main effect: inc HDL (also dec LDL)

47
Q

S/E of niacin

A

red, flushed face (niacin flush– inhibited by ASA)
hyperglycemia (acanthosis nigricans)
hyperuricemia (exacerbates gout)

48
Q

Bile acid resins

A

cholestyramine
colestipol
colesevelam

49
Q

MOA bile acid resins

A

inhibit intestinal reabsorption of bile acids (forcing liver to use cholesterol to create bile acids)
main effect: dec LDL

50
Q

S/E of bile acid resins

A

tastes bad
GI upset (slimy feces)
fat-soluble vit deficiency (ADEK)
cholesterol gallstones

51
Q

cholesterol absorption blocker

52
Q

MOA ezetimibe

A

prevent cholesterol reabsorption at small intestine brush border

53
Q

S/E ezetimibe

A

diarrea

rare inc LFTs

54
Q

Fibrates

A

gemfibrozil
clofibrate
bezafibrate
fenofibrate

55
Q

MOA fibrates

A

upregulate lipoprotein lipase in periphery
increases triglyceride clearance
(main effect = major dec TGs)

56
Q

S/E fibrates

A

myositis
hepatotoxicity (inc LFTs)
cholesterol gall stones

57
Q

class of digoxin

A

cardiac glycoside

58
Q

MOA of digoxin

A

directly inhibits Na/K ATPase = indirectly inhibits Na/Ca exchanger
increases intracellular Ca = positive inotrophy
stimulates vagus = dec HR

59
Q

clinical use digoxin

A

CHF (inc contractility)

A-fib (dec conduction at AC node & depression of SA node)

60
Q

Toxicity of digoxin

A

Cholinergic: N/V/D, blurry yellow vision
ECG: inc PR, dec QT, ST scooping, T-wave inversion, AV block, arrythmia
Electrolytes: hyperkalemia (poor prognosis)

61
Q

Factors predisposing to digoxin toxicity

A 
renal failure (dec excretion)
hypokalemia (increases digoxin binding at K site on Na/K ATPsae)
quinidine (dec digoxin clearance = displaces digoxin from tissue binding site)
62
Q

Antidote to digoxin toxicity

A 
slowly normalize K+
Lidocaine
Anti-digoxin Fab fragments
Mg2+
cardiac pacer
63
Q

Class I Antiarrythmics

A

Na Channel Blockers
local anesthetics
slow/ block conduction (esp in depol cells)
decreases slope of phase ) depol & inc threshold for firing in abn pacemaker cells
state dependent (selectively depress tissue that is freq depol)

64
Q

Increased Toxicity of class I antiarrhythmics

A

qHyperkalemia

65
Q

Class IA drugs

A

Quinidine
Procainamide
Disopyramide

*the QUeen PROClaims Dis PYRAMID”

66
Q

MOA of Class IA Drugs

A

inc AP duration
inc effective refractory period (ERP)
inc QT interval

67
Q

Use of Class IA Drugs

A

BOTH atrial & ventricular arrhythmias

especially– reentrant & ectopic SVT & Ventricular Tachy

68
Q

Toxicity of class IA drugs

A

Generally– thrombocytopenia & Torsades de Pointes (d/t inc QT interval)
Quinidine– cinchonism (HA & tinnitus)
Procainamide– SLE syndrome (reversible)
Disopyramide– heart failure

69
Q

Class IB Drugs

A

Lidocaine
Mexiletine
Tocainide

“I’d Buy Lidy’s Mexi Tacos”
+/- phenytoin

70
Q

MOA of class IB

A

dec AP duration, preferentially affect ischemic or depol purkinje & ventricular tissue

71
Q

Use of Class IB

A

acute ventricular arrhythmias (esp post-MI)

Digitalis-induced arrhythmias

72
Q

toxicity of class IB

A

local anesthetic
CNS stimulation/ depression
CV depression

73
Q

Class IC drugs

A

Flecainide

Propafenone

74
Q

MOA class IC

A

no effect on AP duration

75
Q

Use of Class IC

A

ventricular tachycardias that progress to V-Fib
intractable SVT
last resort for refractory tachyarrhythmias
*pts w/o structural abns

76
Q

Toxicity of Class IC

A

pro-arrhythmic (esp post-MI = CONTRA)

prolongs refractory period in AV node

77
Q

Class II anti-arrythmics

A

Beta- blockers

metoprolol, propranolol, esmolol, atenolol, timolol

78
Q

MOA of class II

A

dec SA & AV nodal activity (dec cAMP & dec Ca currents)
suppress abn pacemakers by dec slow of phase 4
*AV node especially sensitive = inc PR interval
*esmolol = very short acting

79
Q

Clinical use of Class II

A

V-Tach, SVT

A-Fib & A-Flutter (slows ventricular rate)

80
Q

Toxicity of Class II

A

impotence, asthma exacerbation, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations)
may mask signs of hypoglycemia (use low-dose in DM, not 1st line tx)
*metoprolol = dyslipidemia
*Propranolol = exacerbate prinzemetals angia (+vasospasm)

81
Q

Tx Toxicity of Class II

82
Q

Class III anti-arrythmics

A

K+ Channel blockers

Amiodarone, Ibutilide, Dofetilide, Sotatol

83
Q

MOA of Class III

A

inc AP duration, inc ERP, inc QT interval

84
Q

Use of Class III

A

use with other anti-arrhythmics fail

85
Q

Toxicity of Class III

A

Sotalol = torsades de pointes, excessive beta-blockade
Ibutilide = torsades de pointes
amiodarone = pulmonary fibrosis*, hepatotoxicity, hypo/hyper-thyroidism (40% iodine wt), corneal deposits, skin deposits (blue/grey) = photodermatitis, neuro effects, constipation, CV effects (bradycardia, heart block, CHF)
*when using amiodarone = check PFTs, LFTs, TFTs

86
Q

What is special about amiodarone?

A

has class I, II, III, IV effects bc alters lipid membrane

87
Q

Class IV Antiarrhythmics

A

Ca-Channel Blockers

Verapamil, Diltiazem (cardio-selective)

88
Q

MOA of class IV

A

decrease conduction velocity, inc ERP, inc PR interval

89
Q

Use of Class IV

A

prevention of nodal arrhythmias (SVT)

90
Q

Toxicity of class IV

A

constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

91
Q

Non-class antiarrhythmics

A

Adenosine

Mg 2+

92
Q

MOA Adenosine

A

inc K+ efflux out of cells = hyperpolarizes the cell and decreases intracellular Ca
*very short acting (15sec)

93
Q

Use of adenosine

A

DOC = diagnosis/abolish SVT

94
Q

toxicity of adenosine

A

flushing, hypotension, chest pain

95
Q

drug interactions with adenosine

A

caffiene
theophylline
*block adenosine effects

96
Q

Use of Mg2+ as antiarrythmic

A

torsades de pointes

digoxin toxicity

Cardiovascular (8 decks)

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