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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
What factors does antianginal therapy seek to decrease?
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
26
What drug group does nifedipine act similarly to? (angina)
nitrates
27
What drug group does verapamil act similarly to? (angina)
B blockers
28
What drugs are contraindicated in angina?
pindolol and acebutolol (partial B agonists)
29
How do nitrates affect the CV system?
``` decrease EDV decrease BP increase contractility (reflex response) increase HR (reflex response) decrease ejection time decrease MVO2 (affect preload) ```
30
How do B blockers affect the CV system?
``` (affect afterload) increase EDV decrease BP decrease contractility decrease HR increase ejection time decrease MVO2 ```
31
How do nitrates and B blockers affect the CV system when used in combination?
``` no effect/decrease EDV decrease BP little/no effect contractility decrease HR little/no effect ejection time LARGE decrease MVO2 ```
32
What are the HMG CoA reducates inhibitors?
lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin
33
What is the mehcanism of action of hte statins?
inhibit conversion of HMG CoA to mevalonate, a cholesterol precursor
34
What are the side effects of statins?
hepatotoxicity (increased LFTs) | rhabdomyolysis
35
What effects do statins have on the different types of cholesterol?
largest decreased LDL increase HDL decrease TGs
36
What is the mechanism of action of niacin (vitamin b3)
inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation
37
What are the side effects of niacin?
red, flushed face, which is decreased by aspirin or long term use hyperglycemia (acanthosis nigricans) hyperuricemia (exacerbates gout)
38
What effects does niacin have on the different types of cholesterol?
large decrease LDL largest increase HDL decrease TGs
39
What is the mechansim of action of bile acid resins?
prevent intestinal reabsoption of bile acids; liver must use cholesterol to make more
40
What are the names of the bile acid resins?
cholestyramine, colestipol, colesevelam
41
What are the side effects of bile acid resins?
patients hate it-taste bad and causes GI discomfort decreased absorption of fat soluble vitamines cholesterol gallstones
42
What effects do bile acid resins have on the different types of cholesterol?
large decrease LDL slight increase HDL slight increase TGs
43
What is the name of the cholesterol absorption blocker?
ezetimibe
44
What is the mechanism of action of ezetimibe?
prevents cholesterol reabsorption at the small intestine brush border
45
What are the side effects of ezetimibe?
rare increased LFTs diarrhea
46
What are the effects of ezetimibe on the different kinds of cholesterol?
large decreased LDL only
47
What are the names of the fibrates?
gemfibrozil clofibrate bezafibrate fenofibrate
48
What is the mechanisim of action of the fibrates?
upregulate LPL, leading to increased TG clearance
49
What are the side effects of fibrates?
myositis hepatotoxicity (increased LFTs) cholesterol gallstones
50
What are the effects of fibrates on the different kinds of cholesterol?
decrease LDL increase HDL largest decrease TGs
51
What is the name of the cardiac glycoside?
digoxin
52
What is the mechanism of digoxin?
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
What is digoxin used for?
CHF (increase contractility) | AFib (decrease conduction at AV node and depression of SA node)
54
What are the effects of cardiac glycoside toxicity?
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
What factors predispose someone to cardiac glycoside toxicity?
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
What is the antidote for cardiac glycoside (digoxin) toxicity?
``` slowly normalize K+ lidocain cardiac pacer anti-digoxin Fab fragments Mg2+ ```
57
What are the class 1A antiarrhythmics?
Quinidine Procainamide Disopyramide
58
What are the class 1B antiarrhythmics?
Lidocaine Mexiletine Tocainide
59
What are the class 1C antiarrhythmics?
Flecainide | propafenone
60
What are the class 2 antiarrhythmics?
B blockers | -metoprolol, propranolol, esmolol, atenolol, timolol
61
What are the class 3 antiarrhythmics?
amiodarone ibutilide dofetilide sotalol
62
What are the class 4 antiarrhythmics?
Calcium channel blockers | -verapamil, diltiazem
63
What are 2 antiarrhythmics that don't fall into the 4 main classes?
adenosine | Mg2+
64
How do class 1A antiarrhythmics work?
increase AP duration, increase effective refractory period, increase QT interval affect both atrial and ventricular arrhythmias, esp reentrant and ectopic SVT and VT
65
What occurs in class 1A toxicity?
quinidine: (cinchonism-headache, tinnitus) procainamide: (reversible SLE-like syndrome) disopyramide: (heart failure); thrombocytopenia, torsades de pointes
66
How do class 1B antiarrhythmics work?
decrease AP duration | affect ischemic or depolarized purkinje and ventricular tissue preferentially
67
When are class 1B antiarrhythmics useful?
in acute ventricular arrhythmias (esp post MI) and in digitalis-induced arrhythmias (1B is Best post-MI)
68
What occurs in class 1B toxicity?
local anesthetic CNS stim/depression cardiovascular depression
69
How do class 1C antiarrhythmics work?
no effect on AP duration
70
When are class 1C antiarrhythmics useful?
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
What occurs with class 1C antiarrhythmic toxicity?
proarrythmic, especially post-MI | significantly prolongs refractory period in AV node
72
When are class 1C drugs counterindicated?
Post-MI and structural heart disease
73
What is the mechanism of action of the class 2 antiarrythmics?
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
Which B blocker is very short acting?
esmolol
75
What are class 2 antiarrhythmics used for?
VT, SVT, slowing ventricular rate during AFib and Aflutter
76
What occurs with class 2 antiarrhythmic (B blocker) toxicity?
``` impotence exacerbation of asthma CV effects (bradycardia, AV block, CHF) CNS effects (sedation, sleep alterations) may mask the signs of hypoglycemia ```
77
Which beta blocker can cause dyslipidemia?
metoprolol
78
Which B blocker can exacerbate vasospasm in Prinzmetal's angina?
propranolol
79
What can you treat B blocker overdose with?
glucagon
80
How do the class 3 antiarrhythics work?
increase AP duration increase ERP used when other antiarrhythmics fail increase QT interval
81
What is the toxicty of Sotalol?
torsade de pointes, excessive B block
82
What is the toxicity of ibutilide?
torsades de pointes
83
What is the toxicity of amiodarone?
``` 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
Why does amiodarone have all the side effects of class I, II, III, and IV effects?
it alters the lipid membrane
85
When are Ca2+ channel blockers used as antiarrythmics?
prevention of nodal arrhythmias (SVT)
86
How does adenosine work?
increases K+ out of cell, leads to hyperpolarizine of the cell + decreases ICa
87
When is adenosine the drug of choice?
diagnosing/abolishing SVT
88
How long does adenosine have an effect?
15s
89
What are the effects of adensoine toxicity?
flushing, hypotension, chest pain
90
What drugs can block the effects of adenosine?
theophylline and caffiene
91
When is Mg2+ used?
torsades de pointes | digoxin toxicity

FIRST AID (8 decks)

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