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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
Q

Digoxin toxicity antidote

A

Normalize K+ and Mg+
Anti-digoxin Fab
Cardiac pacer
Lidocaine and/or phenytoin

25
Q

Cardiac glycosides - clinical use

A

CHF (increases contractility –> increases diuresis)

A-fib (decreases conduction at AV node, depression of SA node)

26
Q

CCB - clinical uses

A

Hypertension, angina
DHP: Raynaud’s phenomenon
Non-DHP: A-fib

Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm)

27
Q

Class 1a Antiarrythmics - name ‘em!

A

Na+ channel blockers

Quinidine, Procainamide, Disopyramide

28
Q

Mechanism of action of Class I antiarrythmics - general

A

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
Q

Class Ia antiarrythmics - effects, and clinical use

A

Increase AP duration, increase effective refractory period, and increase QT interval

Used for both atrial and ventricular arrythmias

30
Q

Class Ia antiarrythmics - toxicity

A

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
Q

Class Ib antiarrythmics - examples

A

Lidocaine, mexiletine, tocainide

32
Q

Class Ib antiarrythmics - mechanism and use

A

Decrease AP duration. Affects ischemic or depolarized Purkinje and ventricular tissue. Used for acute ventricular arrythmias, especially post-MI

33
Q

Class Ib antiarrythmics - toxicity

A

CNS toxicity, cardiovascular depression

34
Q

Class 1c antiarrythmics - examples

A

Moricizine, flecainide, propafenone

35
Q

Class Ic antiarrythmics - mechanism and use

A

Prolongs refractory period in AV node

Used only as last resort for PVCs, V-tach, a-fib

Proarrythmic, especially post MI!

36
Q

Class II antiarrythmics - examples

A

Beta blockers! Metoprolol, propanolol, esmolol, atenolol, timolol, carvedilol, ___olol

37
Q

Class II antiarrythmics - mechanism and uses

A

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
Q

Class II antiarrythmics - toxicity

A

Cardio symptoms: bradycardia, AV block, CHF
Impotence
Bronchospasm
CNS effects: sedation

Treat OD with glucagon

39
Q

Class III antiarrythmics - examples

A

K channel blockers

Amiodarone, ibutilide, dofetilide, sotalol

40
Q

Class III antiarrythmics: mechanism and uses

A

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
Q

Class III antiarrythmics - toxicity

A

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
Q

Class IV antiarrythmics - examples

A

CCBs: verapamil and diltiazem

43
Q

CCBs - antiarrythmic properties

A

Decrease SA/AV node automaticity, decrease conduction velocity, increase effective refractory period, increase PR interval

44
Q

Adenosine

A

Increases extracellular K, which hyperpolarizes the cell and decreases inward Ca current. Very short acting, can be used to abolish supraventricular tachycardia

45
Q

What are clinical indications for Mg?

A

Torsades de pointes

Digoxin toxicity

46
Q

What are the effects of Class 1a antiarrythmics on phase 0 depolarization, action potential?

A

DQP

Intermediate inhibition of phase 0 depolarization
Prolonged AP

47
Q

What are the effects of Class 1b antiarrythmics on phase 0 depolarization, action potential?

A

LTM

Weak inhibition of phase 0 depolarization
Shortened AP

48
Q

What are the effects of Class 1c antiarrythmics on phase 0 depolarization, action potential?

A

MFP

Strong inhibition of phase 0 depolarization
No change in AP length

49
Q

What cardiac meds DECREASE heart rate, contractility, conduction (negative chronotropic effects)?

A 
Beta blockers
Non-DHP calcium channel blockers
Cardiac glycosides
Amiodarone and sotalol
Cholinergic agonists (pilocarpine, rivastigmine)
50
Q

Calcium channel blockers - side effects

A

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
Q

What are all the class 1 antiarrythmics?

A

DQP, LTM, MorFP
Disopyramide, quinidine, procainamide
Lidocain, ticainide, mexiletine
Moricizine, flecainide, propafenone

52
Q

Antiarrythmic that significantly prolongs QT interval but is associated with a low incidence of torsade de pointes

A

Amiodarone

53
Q

Tx of beta blocker overdose

A

Glucagon: increases intracellular cAMP, increasing Ca release during muscle contraction. Improved rate and contractility

54
Q

What is the relative Na channel binding strength of class 1 antiarrythmics?

A

1C > 1A > 1B

55
Q

What antiarrythmics exhibit use dependence? Reverse use dependence?

A

Class 1c - faster HR = stronger effects (longer QRS)

Class 3 - slower HR = stronger effects (longer QT)

56
Q

Statins plus fibrates: what risk is increased?

A

Myopathy

57
Q

Fibric acid derivatives plus bile acid resins: what risk is increased?

A

cholesterol gallstones

Cardiology (2 decks)

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