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Cardio Pharm Flashcards

0
Q

What are the l-type channels?

A

On cardiac and smooth muscle

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1
Q

What are the L-type calcium channel blockers?

A

Nifedipine
Verapamil
Diltiazem
Amylodipine

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2
Q

What is the toxicity of calcium channel blockers?

A 
Cardiac depression
AV block
Peripheral edema
Flushing
Dizziness
Constipation
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3
Q

What is the MOA of hydralazine?

A

Increase cGMP causing smooth muscle relaxation –> reduces afterload

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4
Q

What is hydralazine used for?

A

Severe HTN
First line for HTN in pregnancy with methyl dopa (alpha 2 agonist)
Frequently used with beta blockers to prevent reflex tachycardia

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5
Q

What is the toxicity of hydralazine?

A 
Compensatory tachycardia 
Fluid retention
Nausea
Headache
Angina
Lupus-like syndrome
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6
Q

What is the MOA of nitroprusside?

A

Increases cGMP via direct release of NO

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7
Q

What is the draw back to nitroprusside?

A

Releases cyanide!

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8
Q

What is hydralazine contraindicated in?

A

CAD and angina because it causes reflex tachycardia increases the need for oxygen of the heart

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9
Q

What is the MOA of fenoldopam?

A

D1 agonist –> vasodilation of coronary, peripheral, renal, splanchnic arteries
Decreases BP and increases natriuresis

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10
Q

What is the MOA of nitroglycerin?

A

Vaso and venodilator by releasing NO in smooth muscle causing an increase cGMP
Decreases preload and afterload

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11
Q

What is the clinical use of nitroglycerin?

A

Angina

Pulmonary edema

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12
Q

What is the toxicity of nitroglycerin?

A 
Reflex tachycardia 
Hypotension
Flushing 
Headache
Monday disease - due to build up of tolerance during the week, lose it over the weekend (because not using it) and then come Monday causes side effects: tachycardia, dizziness, headache
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13
Q

Which beta blockers are contraindicated in angina?

A

Pindolol and acebutolol - Partial B agonist

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14
Q

Which calcium channel blocker is similar to beta blockers in effect?

A

Verapamil

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15
Q

What is the mech of action of a statin?

A

HMG-CoA reductase inhibitors - inhibit conversion of HMG-CoA to mevalonate

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16
Q

What are the side effects of statins?

A

Hepatotoxicity

Rhabdomyolysis

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17
Q

What is the effect of niacin on lipids?

A

Inhibits lipolysis in adipose tissue
reduces hepatic VLDL secretion into circulation
Effect: decreases circulating lipids

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18
Q

What are the side effects of niacin?

A

Flushing (counteract with aspirin because due to prostaglandins)
Hyperglycemia
Hyperuricemia

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19
Q

What are the bile acid resins?

A

Cholestyramine
Colestipol
Colesevelam

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20
Q

What is the MOA of bile acid resin?

A

Prevents intestinal reabsorption of bile acids

Liver must use cholesterol to make more!

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21
Q

What is the side effect?

A

Bad taste
GI discomfort
Decrease absorption of fat soluble vitamins
Cholesterol gallstones

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22
Q

What is ezetimibe?

A

Cholesterol absorption blocker - prevents absorption at small intestine brush border

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23
Q

What are the side effects of ezetimibe?

A

Increase in LFTs

Diarrhea

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24
What is the MOA of fibrates?
Upregulates LPL to increase TG clearance
25
What are the fibrates?
Gemfibrozil Clofibrate Bezafibrate Fenofibrate
26
What are the side effects of fibrates?
Myositis Hepatotoxicity Cholesterol gallstones
27
What lipid med had the best effect on LDL?
HMG- CoA reductase
28
What lipid med has the greatest effect on TGs?
Fibrates
29
Which med has the most effect on HDL?
Niacin
30
What is half life of digoxin?
40 hours
31
What is the bioavailability of digoxin?
75%
32
What percent of digoxin is protein bound?
20-40%
33
What is the MOA of digoxin?
Inhibition of the Na/K pump leading to indirect inhibition of Na/Ca exchanger --> increase intracellular calcium (not pumping it out anymore because no more ATP to run antiport) Positive inotropic Stimulates vagus --> decrease HR, depresses SA node and decreases conduction at AV node
34
What is the digoxin used for?
A-fib | CHF
35
What is the toxicity of digoxin?
Cholinergic - N/V, diarrhea, blurry yellow vision | ECG - increased PR interval, decreased QT interval, ST scooping, T-wave inversion, arrhythmias, AV block
36
What conditions predispose to digoxin toxicity?
Renal failure (because excreted in urine) Hypokalemic Quinidine (displaces digoxin from tissue binding sites, decreases clearance)
37
What is the antidote for digoxin?
``` Normalize K Lidocaine Cardiac pacer Anti-digoxin Fab fragments Magnesium ```
38
What are the class I anti arrhythmics?
Quinidine, procainamide, disopyramide
39
What are the effects of the class I anti arrhythmics?
Increase action potential duration Increase effective refractory period Affect atrial and ventricular arrhythmias especially reentrant and ectopic SVC and VT
40
What is the tox of quinidine?
Cinchonism - tinnitus, headache
41
What is the tox of procainamide?
Reversible SLE-like syndrome
42
What is the tox of disopyramide?
Heart failure
43
What are the toxicities of class I?
TCP Torsades de pointes Hyperkalemia increases the toxicity of these drugs
44
What are the class b anti-arrythmics?
Lidocaine Mexilitine Tocainamide
45
What are the effects of class b?
Decrease action potential duration | Affect ischemic or de polarized Purkinje and ventricular tissue
46
What are class b used for?
Post MI arrhythmias | Digitalis arrhythmias
47
What are the toxicities of class b?
Local anesthetic, CNS stimulation/depression, CV depression
48
What are the class c antiarrythmics?
Flecainide, propafenone
49
What are class c used for?
Intractable SVT VT that progresses to VF Last resort - only for patients without structural abnormalities
50
What are the tox of class c?
Pro arrhythmic especially post MI | Significantly prolongs refractory period in AV node
51
What are the class II antiarrythmics?
Beta blockers
52
What do beta blockers do?
Decrease SA and AV nodal activity by decreasing camp and calcium. Decrease slope of phase 4 Increase PR interval. Esmolol is short acting
53
What are class II used for?
VT, SVT | slowing ventricular rate during a-fib, a-flutter
54
What is the tox of class II?
Impotence, exacerbation of Asthma, bradycardia , AV nodal block, CHF, sedation, masks hypoglycemia
55
What can metoprolol cause?
Dyslipidemia - tx OD with glucagon
56
What can propranolol do?
Exacerbate spasm in Prinzmetal's
57
What are the class III?
Amiodarone Ibutilide Dofetilide Sotalol
58
What is the MOA of class III?
Increase AP duration increase ERP Increase QT interval Used when other antiarrythmics
59
What is the tox of sotalol?
Torsades de pointes | Excessive beta block
60
What is the tox of ibutilide?
Torsades
61
What is the tox of amiodarone?
``` Pulmonary fibrosis Hepatotoxicity Hypothyroidism/hyperthyroid Corneal deposits Blue/gray Skin deposits Photodermatitis Constipation Bradycardia AV nodal block CHF ```
62
What is unique about amiodarone?
Has class I-iV effects because it alters the lipid membrane
63
What are the class IV?
Calcium channel blockers: verapamil, diltiazem
64
What is the MOA of class IV?
Decreases conduction velocity, increases ERP, increase PR,
65
What are class IV used for?
In prevention of nodal arrythmias
66
What is the MOA of adenosine as an antiarrythmic?
``` Increase K efflux hyper polarizing the cell and decreases spontaneous calcium channels Short acting (15 seconds) ```
67
What is the DOC for diagnosing/taxing SVT?
Adenosine
68
What is the tox of adenosine?
Flushing Hypotension Chest pain
69
What blocks adenosine?
Caffeine | Theophylline
70
What is magnesium used for?
Effective in torsades and digoxin tox
71
Which antiarrythmic causes bradycardia and QT prolongation?
Sotalol - class 3 K-blocking and beta blocker
72
How do beta blockers work as antiarrythmics?
Slow AV nodal conduction and phase 4 depolarization of cardiac pacemaker cells Phase 4 is mediated by sodium channels that depolarize spontaneously
73
What phase do calcium channel blockers slow?
Phase 0 of pacemaker cells - the opening of voltage gated calcium channels Phase 2 of myocyte action potential - calcium influx through calcium channels that balances K efflux
74
What side effects is verapamil associated with?
Gingival hyperplasia Constipation AV nodal block
75
What is ergonovine?
An ergot alkaloid that stimulates serotonin and alpha adrenergic receptors
76
What is ergonovine used for?
Testing for Prinzmetal's angina by provoking an attack
77
How is procainamide metabolized?
By acetylation
78
What is the MOA of an ARB?
Blocks Ang I receptors thereby blocking the effects of angiotensin II Will have increased renin and Ang I and Ang II but decreased aldosterone and vasodilation. No change in bradykinin
79
How does metoprolol work in lowering bp?
Blocks B1 in heart and in Jg apparatus thereby decreasing the level of circulating renin.
80
What is the MOA of nesirtide?
Recombinant form of BNP - dilates arterioles and venules by activating guanylate cycle and increasing cGMP. Also causes diuresis/natriuresis and decreases bp
81
What can nesirtide be used for?
Decompensated left ventricular dysfunction leading to CHF
82
On which part of the EKG do beta blockers act?
Increase the PR interval
83
Which phase of the ventricular depolarization graph do class IA agents act on?
Prolong phase 0 - decrease sodium influx so that the upstroke isn't as rapid Prolong phase 3 - slow K efflux for slow repolarization Increase AP duration, ERP, and QT interval
84
What effects do class IB agents have on the ventricular action potential graph?
Shorten phase 3 - so increase efflux of K and repolarization, also decreases ERP Decreases duration of the action potential Have affinity for rapidly de polarizing cells (best for ischemic cells)
85
What effect do class IC agents have on the ventricular action potential curve?
Slows phase 0 - slow the opening of sodium channels so the upstroke isn't as rapid. Has no effect on action potential duration Works within the QRS interval May significantly prolong the refractory period in the AV node (PR interval) Have highest affinity for non-resting sodium channel - have more effect on normal myocardium
86
What phase do beta blockers act in?
Prolong phase 4 - decreases current through funny sodium channels so decreases rate of depolarization Also decreases calcium influx thru channels that usually augment phase 4 by decreasing camp Slows conduction through the SA and AV node (increases PR interval)
87
What effects do class 3 agents have on the ventricular action potential curve?
Increase phase 3 - decrease potassium efflux | Increases AP duration, QT interval and ERP
88
What is the toxicity of sotalol?
Torsades and excessive beta block
89
What is the toxicity of ibutilide?
Torsades
90
What phases do calcium channel blockers act on?
Slow phase 0 - calcium influx causing the upstroke in the SA node Slow phase 4 - decreasing calcium flow that normally augments this period - slows diastolic depolarization Decreases conduction velocity, increases ERP, increases PR interval

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