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FIRST AID > Cardiology Pharm > Flashcards

Cardiology Pharm Flashcards

1
Q

What are common therapies for essential hypertension?

A

diruetics
ACE inhibitors
ARBs
calcium channel blockers

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2
Q

What are common therapies for CHF?

A

diuretics
ACEs/ARBs
B blockers (compensated CHF)
K+ sparing diruetics

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3
Q

When must B blockers be used with caution?

A

decompensated CHF

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4
Q

What is a B blocker contraindicated?

A

cardiogenic shock

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5
Q

What are common therapies for HTN associated with diabetes mellitus?

A 
ACEs
ARBs
Calcium channel blockers
B blockers
a blockers
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6
Q

What makes ACE inhibitors an especially good choice for treating diabetes mellitus associated HTN?

A

they are protective against diabetic nephropathy

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7
Q

What are the calcium channel blockers’ names?

A

nifedipine, verapamil, diltiazem, amlodipine

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8
Q

What is the mechanism of the calcium channel blockers?

A

block voltage dependent L type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility

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9
Q

Which calcium channel blockers work better on vascular smooth muscle?

A

amlodipine & nifedipine

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10
Q

Which calcium channel blockers work better on heart muscle?

A

verapamil>diltiazem

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11
Q

What are the calcium channel blockers used for?

A

hypertension, angina, arrhythmias (not nifedipine), prinzmetal’s angina, raynaud’s

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12
Q

What occurs with calcium channel blocker toxicity?

A

cardiac depression, AV block, CHF, sinus node depression, peripheral edema, flushing, dizziness and constipation

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13
Q

What is the mechanism of hydralazine?

A

increases cGMP leading to smooth muscle relaxation

vasodilates arterioles>veins; afterload reduction

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14
Q

What is hydralazine used for?

A

severe HTN, CHF
first line for HTN in pregnancy w/methydopa
frequently coadministered with a B blocker to prevent reflex tachycardia

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15
Q

What occurs with hydralazine toxicity?

A

compensatory tachycardia (contraindicated in angina/CAD)
fluid retention, nausea, headache, angina
lupus like syndrome

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16
Q

What drugs are commonly used to treat malignant hypertension?

A

nitroprusside, nicardipine, clevidipine, labetalol and fenoldopam

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17
Q

What is the mechanism of nitroprusside action?

A

increases cGMP via direct release of NO

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18
Q

How long does nitroprusside work?

A

short acting

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19
Q

What is a side effect of nitroprusside?

A

cyanide toxicity (releases cyanide)

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20
Q

What is the mechanism of fenoldopam action? It’s effects?

A

dopamine D1 receptor agonist, leads to coronary, renal and splanchnic vasodilation
decreased BP, increases natriuresis

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21
Q

How do nitroglycerine & isosorbide dinitrate work?

A

vasodilate by releasing nitroc oxide in smooth muscle, causig increase in cGMP and smooth muscle relaxation
dilates veins&raquo_space; arteries,
decreased preload

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22
Q

What is nitroglyercine/isosorbide dinitrate used for?

A

angina

pulmonary edema

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23
Q

What happens with nitroglycerin/isosorbide dinitrate toxicity?

A

reflex tachycardia, hypotension, flushing, headache,

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24
Q

What is “Monday disease”?

A

nitroglycerin/isosorbide dinitrate toxicity in industrial exposure
development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend
results in tachycardia, dizziness and headache upon reexposure

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25
Q

What factors does antianginal therapy seek to decrease?

A

reduction of myocardial O2 consumption (MVO2) by decreasing 1 or more of the determinants of MVO2

  • end diastolic volume
  • blood pressure
  • heart rate
  • contractility
  • ejection time
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26
Q

What drug group does nifedipine act similarly to? (angina)

A

nitrates

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27
Q

What drug group does verapamil act similarly to? (angina)

A

B blockers

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28
Q

What drugs are contraindicated in angina?

A

pindolol and acebutolol (partial B agonists)

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29
Q

How do nitrates affect the CV system?

A 
decrease EDV
decrease BP
increase contractility (reflex response)
increase HR (reflex response)
decrease ejection time
decrease MVO2
(affect preload)
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30
Q

How do B blockers affect the CV system?

A 
(affect afterload)
increase EDV
decrease BP
decrease contractility
decrease HR
increase ejection time
decrease MVO2
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31
Q

How do nitrates and B blockers affect the CV system when used in combination?

A 
no effect/decrease EDV
decrease BP
little/no effect contractility
decrease HR
little/no effect ejection time
LARGE decrease MVO2
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32
Q

What are the HMG CoA reducates inhibitors?

A

lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

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33
Q

What is the mehcanism of action of hte statins?

A

inhibit conversion of HMG CoA to mevalonate, a cholesterol precursor

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34
Q

What are the side effects of statins?

A

hepatotoxicity (increased LFTs)

rhabdomyolysis

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35
Q

What effects do statins have on the different types of cholesterol?

A

largest decreased LDL
increase HDL
decrease TGs

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36
Q

What is the mechanism of action of niacin (vitamin b3)

A

inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation

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37
Q

What are the side effects of niacin?

A

red, flushed face, which is decreased by aspirin or long term use
hyperglycemia (acanthosis nigricans)
hyperuricemia (exacerbates gout)

38
Q

What effects does niacin have on the different types of cholesterol?

A

large decrease LDL
largest increase HDL
decrease TGs

39
Q

What is the mechansim of action of bile acid resins?

A

prevent intestinal reabsoption of bile acids; liver must use cholesterol to make more

40
Q

What are the names of the bile acid resins?

A

cholestyramine, colestipol, colesevelam

41
Q

What are the side effects of bile acid resins?

A

patients hate it-taste bad and causes GI discomfort
decreased absorption of fat soluble vitamines
cholesterol gallstones

42
Q

What effects do bile acid resins have on the different types of cholesterol?

A

large decrease LDL
slight increase HDL
slight increase TGs

43
Q

What is the name of the cholesterol absorption blocker?

A

ezetimibe

44
Q

What is the mechanism of action of ezetimibe?

A

prevents cholesterol reabsorption at the small intestine brush border

45
Q

What are the side effects of ezetimibe?

A

rare
increased LFTs
diarrhea

46
Q

What are the effects of ezetimibe on the different kinds of cholesterol?

A

large decreased LDL only

47
Q

What are the names of the fibrates?

A

gemfibrozil
clofibrate
bezafibrate
fenofibrate

48
Q

What is the mechanisim of action of the fibrates?

A

upregulate LPL, leading to increased TG clearance

49
Q

What are the side effects of fibrates?

A

myositis
hepatotoxicity (increased LFTs)
cholesterol
gallstones

50
Q

What are the effects of fibrates on the different kinds of cholesterol?

A

decrease LDL
increase HDL
largest decrease TGs

51
Q

What is the name of the cardiac glycoside?

A

digoxin

52
Q

What is the mechanism of digoxin?

A

direct inhibition of Na+/K+/ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport
increased [Ca2+] leads to positive inotropy
stimulates vagus nerve leading to decreased HR

53
Q

What is digoxin used for?

A

CHF (increase contractility)

AFib (decrease conduction at AV node and depression of SA node)

54
Q

What are the effects of cardiac glycoside toxicity?

A

cholinergic-N/V, diarrhea, blurry yellow vision
EKG-increase PR, decrease QT, ST scooping, T-wave inversion, arrhythmia, AV block
can lead to hyperkalemia (poor prog indicator)

55
Q

What factors predispose someone to cardiac glycoside toxicity?

A

renal failure (decreased excretion)
hypokalemi (permissive for digoxin binding at K+ binding site on Na+/K+/ ATPase)
quinidine (decreased digoxin clearance; displaces digoxin from tissue binding sites)

56
Q

What is the antidote for cardiac glycoside (digoxin) toxicity?

A 
slowly normalize K+
lidocain
cardiac pacer
anti-digoxin Fab fragments
Mg2+
57
Q

What are the class 1A antiarrhythmics?

A

Quinidine
Procainamide
Disopyramide

58
Q

What are the class 1B antiarrhythmics?

A

Lidocaine
Mexiletine
Tocainide

59
Q

What are the class 1C antiarrhythmics?

A

Flecainide

propafenone

60
Q

What are the class 2 antiarrhythmics?

A

B blockers

-metoprolol, propranolol, esmolol, atenolol, timolol

61
Q

What are the class 3 antiarrhythmics?

A

amiodarone
ibutilide
dofetilide
sotalol

62
Q

What are the class 4 antiarrhythmics?

A

Calcium channel blockers

-verapamil, diltiazem

63
Q

What are 2 antiarrhythmics that don’t fall into the 4 main classes?

A

adenosine

Mg2+

64
Q

How do class 1A antiarrhythmics work?

A

increase AP duration, increase effective refractory period, increase QT interval
affect both atrial and ventricular arrhythmias, esp reentrant and ectopic SVT and VT

65
Q

What occurs in class 1A toxicity?

A

quinidine: (cinchonism-headache, tinnitus)
procainamide: (reversible SLE-like syndrome)
disopyramide: (heart failure);
thrombocytopenia, torsades de pointes

66
Q

How do class 1B antiarrhythmics work?

A

decrease AP duration

affect ischemic or depolarized purkinje and ventricular tissue preferentially

67
Q

When are class 1B antiarrhythmics useful?

A

in acute ventricular arrhythmias (esp post MI) and in digitalis-induced arrhythmias
(1B is Best post-MI)

68
Q

What occurs in class 1B toxicity?

A

local anesthetic
CNS stim/depression
cardiovascular depression

69
Q

How do class 1C antiarrhythmics work?

A

no effect on AP duration

70
Q

When are class 1C antiarrhythmics useful?

A

useful in ventricular tachycardias that progress to VF and in intractable SVT
used only as a last resort in refractory tachyarrhythmias
for patients withOUT structural abnormalities

71
Q

What occurs with class 1C antiarrhythmic toxicity?

A

proarrythmic, especially post-MI

significantly prolongs refractory period in AV node

72
Q

When are class 1C drugs counterindicated?

A

Post-MI and structural heart disease

73
Q

What is the mechanism of action of the class 2 antiarrythmics?

A

Bblockers
decrease SA and AV nodal activity by decreasing cAMP and Ca2+ currents
suppress abnormal pacemakers by decreasing the slope of phase 4
AV node particularly sensitive (leads to increased PR interval)

74
Q

Which B blocker is very short acting?

A

esmolol

75
Q

What are class 2 antiarrhythmics used for?

A

VT, SVT, slowing ventricular rate during AFib and Aflutter

76
Q

What occurs with class 2 antiarrhythmic (B blocker) toxicity?

A 
impotence
exacerbation of asthma
CV effects (bradycardia, AV block, CHF)
CNS effects (sedation, sleep alterations)
may mask the signs of hypoglycemia
77
Q

Which beta blocker can cause dyslipidemia?

A

metoprolol

78
Q

Which B blocker can exacerbate vasospasm in Prinzmetal’s angina?

A

propranolol

79
Q

What can you treat B blocker overdose with?

A

glucagon

80
Q

How do the class 3 antiarrhythics work?

A

increase AP duration
increase ERP
used when other antiarrhythmics fail
increase QT interval

81
Q

What is the toxicty of Sotalol?

A

torsade de pointes, excessive B block

82
Q

What is the toxicity of ibutilide?

A

torsades de pointes

83
Q

What is the toxicity of amiodarone?

A 
pulmonary fibrosis
hepatotoxicity
hypo/hyper-thyroidism
corneal deposits
skin deposits results in in photdermatits (blue/grey)
neuro effects
constipation
cardiovascular effects (bradycardia, heart block, CHF)

*remember to check PFTs, LFTs, and TFTs when using amiodarone

84
Q

Why does amiodarone have all the side effects of class I, II, III, and IV effects?

A

it alters the lipid membrane

85
Q

When are Ca2+ channel blockers used as antiarrythmics?

A

prevention of nodal arrhythmias (SVT)

86
Q

How does adenosine work?

A

increases K+ out of cell, leads to hyperpolarizine of the cell + decreases ICa

87
Q

When is adenosine the drug of choice?

A

diagnosing/abolishing SVT

88
Q

How long does adenosine have an effect?

A

15s

89
Q

What are the effects of adensoine toxicity?

A

flushing, hypotension, chest pain

90
Q

What drugs can block the effects of adenosine?

A

theophylline and caffiene

91
Q

When is Mg2+ used?

A

torsades de pointes

digoxin toxicity

FIRST AID (8 decks)

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