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Cardiology > Pharmacology > Flashcards

Pharmacology Flashcards

0
Q

Calcium Channel Blockers - Examples

A

DHP: amlodipine, nimodipine, nifedipine

Non-DHP: diltiazem, verapamil

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1
Q

First line HTN therapy for diabetics or CHF

A

ACE inhibitors/ARBs

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2
Q

Calcium Channel Blockers - Mechanism

A

Block Ca++ channels, reducing muscle contractility of cardiac and smooth muscle.

Vascular smooth muscle: A=N>D>V
Cardiac muscle: opposite

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3
Q

Which calcium channel blocker acts like a beta blocker? Which one acts like a nitro drug?

A

Verapamil has much more activity on the heart than smooth muscle. Decreases afterload, similar to a beta blocker.

Nifedipine has more activity at smooth muscle, decreasing preload like a nitro.

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4
Q

Hydralazine - mechanism, clinical use, and toxicity

A

Increases cGMP –> smooth muscle relaxation. Affects arterioles, decreases afterload.

First line therapy for HTN in pregnancy. Also used for severe HTN and CHF.

Toxicity includes cardiac depression, AV block, edema, flushing, dizziness, hyperprolacinemia, constipation.

Often given with beta blocker for reflex tachycardia.

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5
Q

Nitroprusside

A

Short acting vasodilator for hypertensive emergency. Increases cGMP by direct release of NO. Also releases cyanide.

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6
Q

Fenoldopam

A

Dopamine D1 receptor agonist –> vasodilator.

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7
Q

Nitroglycerine, isosorbide dinitrate

A

Nitro drugs that increase NO, causing vasodilation in vascular smooth muscle via cGMP.

Affect veins preferentially –> decrease preload

Toxicity: reflex tachycardia (co administer with beta blockers), hypotension, flushing, headache.

Interacts with PDE inhibitors (ED drugs) to dangerously increase cGMP –> hypotension

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8
Q

Antianginal therapy

A

Nitrates and beta blockers

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9
Q

Statins - examples

A

lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin, and all sorts of thing that end with statin.

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10
Q

Statins - mechanism of action, effects on LDL, HDL, triglycerides

A

HMG-CoA reductase inhibitors (inhibit cholesterol synthesis)

LDL: large decrease
HDL: small increase
Triglycerides: small decrease

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11
Q

Statins - toxicity

A

Hepatotoxicity - check LFTs

Rhabdomyolysis

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12
Q

Niacin (B3) - mechanism, LDL, HDL, Triglycerides

A

Inhibits lipolysis in adipose tissue, lowers hepatic VLDL synthesis (a precursor to LDL)

LDL: moderate decrease
HDL: moderate increase
Triglycerides: small decrease

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13
Q

Bile acid resins - examples

A

Cholestyramine, colestipol, colesevelam

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14
Q

Niacin - toxicity

A

Red flushed face, hyperglycemia, hyperuricemia (bad for gout)

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15
Q

Bile acid resins - mechanism, LDL, HDL, triglycerides

A

Prevents intestinal reabsorption of bile acids so the liver must use up cholesterol to make more.

LDL: moderate decrease
HDL: slight increase
Triglycerides: slight increase

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16
Q

Cholestyramine, colestipol, colesevelam toxicity

A

GI discomfort, decreased absorption of fat-soluble vitamins, cholesterol gallstones

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17
Q

Ezetimibe

A

Cholesterol absorption blocker at small intestine brush border. Decreases LDL, no effect on HDL or triglycerides.

Toxicity = diarrhea

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18
Q

Fibrates - examples

A

gemfibrozil, clofibrate, vezafibrate, fenofibrate

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19
Q

Fibrates - mechanism and effects

A

Upregulates lipoprotein lipase, increasing triglyceride clearance. Also activates HDL synthesis.

Large decrease in triglycerides. Small increase in HDL, decrease in LDL.

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20
Q

Fibrates - toxicity

A

Myositis (especially with statins)
Hepatotoxicity
Cholesterol bile stones

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21
Q

Cardiac glycosides - examples and differences

A

Digitalis: long half life, eliminated by liver
Digoxin: shorter half life, eliminated by kidney
Digitoxin: longer half life, eliminated by liver

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22
Q

Cardiac glycosides - mechanism

A

Digitalis/digoxin

Competes with K+ at Na/K ATPase –> increased intracellular Na+ –> inhibition of Na+/Ca++ exchanger –> cell doesn’t pump Ca++ out, high [Ca++] –> positive inotropy, increased contractility. Stimulates vagus nerve to decrease HR.

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23
Q

Cardiac glycosides - Toxicity

A

Toxicity worsened by hypokalemia because digoxin/digitalis competes with K on pump. Digoxin toxicity worse in renal failure, digitalis in liver.

Cholinergic toxidrome: nausea, vomiting, diarrhea, blurry vision
Changes in color vision

ECG changes with increase PR, decreased QT, T wave inversion, arrhythmia, AV block

Electrolyte changes (K, Mg) -> ventricular tachyarrhythmias are potentially fatal!

Don’t use with verapamil, amiodarone, quinidine (decreases clearance)

24
Digoxin toxicity antidote
Normalize K+ and Mg+ Anti-digoxin Fab Cardiac pacer Lidocaine and/or phenytoin
25
Cardiac glycosides - clinical use
CHF (increases contractility --> increases diuresis) | A-fib (decreases conduction at AV node, depression of SA node)
26
CCB - clinical uses
Hypertension, angina DHP: Raynaud's phenomenon Non-DHP: A-fib Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm)
27
Class 1a Antiarrythmics - name 'em!
Na+ channel blockers Quinidine, Procainamide, Disopyramide
28
Mechanism of action of Class I antiarrythmics - general
All are Na+ channel blockers, and are "fast Na+ channel" dependent. All decrease slope of Phase 0 upstroke in ventricles, and phase 4 depolarization in nodal cells. All raise threshold for AP firing and decrease max rate of depolarization.
29
Class Ia antiarrythmics - effects, and clinical use
Increase AP duration, increase effective refractory period, and increase QT interval Used for both atrial and ventricular arrythmias
30
Class Ia antiarrythmics - toxicity
All: Torsades de pointes due to long QT interval, thrombocytopenia Disopyramide: heart failure, anticholinergic Quinidine: Cinchonism (headache and tinnitus) Procainamide: SLE-like syndrome (reversible) Hyperkalemia causes increased toxicity for all class I drugs
31
Class Ib antiarrythmics - examples
Lidocaine, mexiletine, tocainide
32
Class Ib antiarrythmics - mechanism and use
Decrease AP duration. Affects ischemic or depolarized Purkinje and ventricular tissue. Used for acute ventricular arrythmias, especially post-MI
33
Class Ib antiarrythmics - toxicity
CNS toxicity, cardiovascular depression
34
Class 1c antiarrythmics - examples
Moricizine, flecainide, propafenone
35
Class Ic antiarrythmics - mechanism and use
Prolongs refractory period in AV node Used only as last resort for PVCs, V-tach, a-fib Proarrythmic, especially post MI!
36
Class II antiarrythmics - examples
Beta blockers! Metoprolol, propanolol, esmolol, atenolol, timolol, carvedilol, ___olol
37
Class II antiarrythmics - mechanism and uses
Decrease sympathetic activity to heart, decrease cAMP, decrease decrease Ca currents (contractility), decrease the slope of phase 4 depolarization to suppress abnormal pacemakers. Increase PR interval. Used for treatment of supraventricular tachycardias, also slowing ventricles in a-fib and atrial flutter
38
Class II antiarrythmics - toxicity
Cardio symptoms: bradycardia, AV block, CHF Impotence Bronchospasm CNS effects: sedation Treat OD with glucagon
39
Class III antiarrythmics - examples
K channel blockers Amiodarone, ibutilide, dofetilide, sotalol
40
Class III antiarrythmics: mechanism and uses
Blocks K channels, prolonging repolarization. Increase AP duration and increase effective refractory period. Do not affect conduction velocity. Prolongs QT interval Used for a-fib, atrial flutter, ventricular tachycardia, and Wolff-Parkinson-White
41
Class III antiarrythmics - toxicity
Amiodarone: p450 inhibitor, pulmonary fibrosis, hepatotoxicity, thyroid disturbances, corneal and skin deposits, neurologic effects, constipation, cardio effects. PFTs and thyroid tests necessary! Ibutilide and sotalol: torsades de points, excessive b blockade (solatol only)
42
Class IV antiarrythmics - examples
CCBs: verapamil and diltiazem
43
CCBs - antiarrythmic properties
Decrease SA/AV node automaticity, decrease conduction velocity, increase effective refractory period, increase PR interval
44
Adenosine
Increases extracellular K, which hyperpolarizes the cell and decreases inward Ca current. Very short acting, can be used to abolish supraventricular tachycardia
45
What are clinical indications for Mg?
Torsades de pointes | Digoxin toxicity
46
What are the effects of Class 1a antiarrythmics on phase 0 depolarization, action potential?
DQP Intermediate inhibition of phase 0 depolarization Prolonged AP
47
What are the effects of Class 1b antiarrythmics on phase 0 depolarization, action potential?
LTM Weak inhibition of phase 0 depolarization Shortened AP
48
What are the effects of Class 1c antiarrythmics on phase 0 depolarization, action potential?
MFP Strong inhibition of phase 0 depolarization No change in AP length
49
What cardiac meds DECREASE heart rate, contractility, conduction (negative chronotropic effects)?
``` Beta blockers Non-DHP calcium channel blockers Cardiac glycosides Amiodarone and sotalol Cholinergic agonists (pilocarpine, rivastigmine) ```
50
Calcium channel blockers - side effects
Flushing, dizziness, hyperprolactinemia, constipation DHP: no effect on AV node. Reflex tachycardia Non-DHP: negative effects on HR, contractility, AV conduction. Sinus bradycardia, hypotension
51
What are all the class 1 antiarrythmics?
DQP, LTM, MorFP Disopyramide, quinidine, procainamide Lidocain, ticainide, mexiletine Moricizine, flecainide, propafenone
52
Antiarrythmic that significantly prolongs QT interval but is associated with a low incidence of torsade de pointes
Amiodarone
53
Tx of beta blocker overdose
Glucagon: increases intracellular cAMP, increasing Ca release during muscle contraction. Improved rate and contractility
54
What is the relative Na channel binding strength of class 1 antiarrythmics?
1C > 1A > 1B
55
What antiarrythmics exhibit use dependence? Reverse use dependence?
Class 1c - faster HR = stronger effects (longer QRS) Class 3 - slower HR = stronger effects (longer QT)
56
Statins plus fibrates: what risk is increased?
Myopathy
57
Fibric acid derivatives plus bile acid resins: what risk is increased?
cholesterol gallstones

Cardiology (2 decks)

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