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Pharmacology > module 6 > Flashcards

module 6 Flashcards

1
Q

Heart Failure Drugs

A 
The heart is unable to pump blood in
sufficient amounts from the ventricles to meet
the body’s metabolic needs
 Symptoms depend on the cardiac area
affected
 Systolic dysfunction
 Diastolic dysfunction
• Less common
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2
Q

Heart Failure: Causes

A 
Cardiac defect
 Myocardial infarction
 Valve deficiency
 Defect outside the heart
 Coronary artery disease
 Pulmonary hypertension
 Diabetes
Supraventricular dysrhythmias
 Atrial fibrillation
 Atrial flutter
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3
Q

Drug Therapy for Heart Failure

A 
Positive inotropic drugs
 Increase the force of myocardial contraction
 Positive chronotropic drugs
 Increase heart rate
 Positive dromotropic drugs
 Accelerate cardiac conduction
 Used to treat heart muscle failure
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4
Q

Drug Therapy for Heart Failure

A 
ACE inhibitors
 Angiotensin II receptor blockers
 B-type natriuretic peptides
 Phosphodiesterase inhibitors
 Cardiac glycosides
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5
Q

ACE inhibitors

end in pril

A

Prevent sodium and water resorption by
inhibiting aldosterone secretion
Diuresis results, which decreases preload, or
the left ventricular end-volume, and the work
of the heart
Examples: lisinopril, enalapril, captopril

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6
Q

lisinopril(Prinivil, Zestril) (C in women in 1st trimester; D in 2nd & 3rd can cause fetal death in these trimesters)

A

Ace inhibitor; used for HTN, HF & acute MI;
Hyperkalemia ma occur with any ACE inhibitor & K+ supplmentaion or K+ sparing diuretics need to be used with caution. SE-dry cough & possible decreased renal function

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7
Q

enalapril,

A

Hyperkalemia ma occur with any ACE inhibitor & K+ supplmentaion or K+ sparing diuretics need to be used with caution. SE-dry cough & possible decreased renal function

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8
Q

captopril

A

Hyperkalemia ma occur with any ACE inhibitor & K+ supplmentaion or K+ sparing diuretics need to be used with caution. SE-dry cough & possible decreased renal function

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9
Q

Angiotensin II Receptor Blockers(ARB)

end in artan

A

Potent vasodilators; decrease systemic
vascular resistance (afterload)
Examples: valsartan, candesartan, losartan

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10
Q

valsartan(Diovan) (D)

A

ARBS are potent vasodilators; used alone or in combo with other drugs such as diuretics in tx of HTN & HF.Most commonly used; Less likely to cause cough or hyperkalemia

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11
Q

candesartan(Atacand)(D)

A

ARBS are potent vasodilators; used alone or in combo with other drugs such as diuretics in tx of HTN & HFMost commonly used; Less likely to cause cough or hyperkalemia

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12
Q

losartan(Cozaar) (D)

A

ARBS are potent vasodilators; used alone or in combo with other drugs such as diuretics in tx of HTN & HFMost commonly used; Less likely to cause cough or hyperkalemia

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13
Q

B-type Natiuretic Peptides

A

nesiritide (Natrecor)
Used in se ere life threatening heart fail re
severe, life-failure

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14
Q

B-type Natiuretic Peptides:

Mechanism of Action

A

Vasodilating effects on arteries and veins
Indirectly increases cardiac output
Suppresses renin-angiotensin system
Diuresis

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15
Q

Phosphodiesterase Inhibitors

A 
Work by inhibiting the enzyme phosphodiesterase
 Results in:
 Positive inotropic response
 Vasodilation
 Two drugs (inodilators)
 Inamrinone and milrinone
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16
Q

Inamrinone

A

Phosphodiesterase Inhibitors,Work by inhibiting the enzyme phosphodiesterase
Results in:
Positive inotropic response
Vasodilation(inodilators)

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17
Q

milrinone

A

Phosphodiesterase Inhibitors,Work by inhibiting the enzyme phosphodiesterase
Results in:
Positive inotropic response
Vasodilation(inodilators)

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18
Q

Phosphodiesterase Inhibitors:

Indications

A

Short-term management of heart failure
Given when patient does not respond to treatment with digoxin, diuretics, and/or vasodilators
AHA and ACC advise against weekly infusions
No improvement of clinical status

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19
Q

Phosphodiesterase Inhibitors:

Adverse Effects

A 
*inamrinone
 Thrombocytopenia
 Dysrhythmia, nausea, hypotension
 Elevated liver enzymes with long-term use
* milrinone
 Dysrhythmia, mainly ventricular
 Hypotension, angina, hypokalemia, tremor,
thrombocytopenia
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20
Q

Cardiac Glycosides

A

No longer used as first-line treatment
Originally obtained from Digitalis plant,
foxglove
Digoxin
Used in heart failure and to control ventricular
response to atrial fibrillation or flutter

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21
Q

Cardiac Glycosides:

Mechanism of Action

A 
Increase myocardial contractility
 Change electrical conduction properties of the heart
Decrease rate of electrical conduction
 Prolong the refractory period
• Area between SA node and AV node
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22
Q

Cardiac Glycosides:

Drug Effects

A

Positive inotropic effect
Increased force and velocity of myocardial contraction
Negative chronotropic effect
Reduced heart rate
Negative dromotropic effect
Decreased automaticity at SA node, decreased AV nodal
conduction

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23
Q

Cardiac Glycosides:

Drug Effects

A

Increased stroke volume
Reduction in heart size during diastole
Decrease in venous BP and vein engorgement
Increase in coronary circulation
Promotion of diuresis due to improved blood circulation
decreased exertional and paroxysmal nocturnal dyspnea, cough, and cyanosis

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24
Q

Cardiac Glycosides:

Indications

A

Heart failure
Supraventricular dysrhythmias
Atrial fibrillation and atrial flutter

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25
Q

Cardiac Glycosides:

Adverse Effects

A 
digoxin (Lanoxin)
 Very narrow therapeutic range and low TI
 Drug levels must be monitored
• 0.5 to 2 ng/mL
 Hypokalemia increases its toxicity
 Electrolyte levels must be monitored
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26
Q

Digoxin:

Adverse Effects

A

digoxin (Lanoxin) (cont’d)
Cardiovascular
• Dysrhythmias, including bradycardia or tachycardia
CNS
• Headaches, fatigue, malaise, confusion, convulsions

27
Q

Digoxin Toxicity

A

digoxin immune Fab (Digibind) therapy
Life-threatening digoxin overdose
Life-threatening cardiac dysrhythmias

28
Q

Digibind

A

Used in digoxin overdose

Life-threatening cardiac dysrhythmias

29
Q

Antidysrhythmic Drugs

A

Dysrhythmia
Any deviation from the normal rhythm of the heart
Antidysrhythmics
Used for the treatment and prevention of
disturbances in cardiac rhythm

30
Q

Cardiac Cell

A

Inside the resting cardiac cell there exists a
net negative charge relative to the outside of
the cell
This difference in the electronegative charge
results from an uneven distribution of ions
(sodium, potassium, calcium) across the cell
membrane
Resting membrane potential (RMP)

31
Q

Resting Membrane Potential

A

An energy-requiring pump is needed to
maintain this uneven distribution of ions
Sodium-potassium ATPase pump

32
Q

Action Potential

A

A change in the distribution of ions causes cardiac cells to become excited
The movement of ions across the cardiac cell’s membrane results in an electrical impulse spreading
across the cardiac cells
This electrical impulse leads to contraction
of the myocardial muscle

33
Q

Action Potential Duration

A

Absolute or effective refractory period
Relative refractory period
Threshold potential
Automaticity or pacemaker activity

34
Q

Electrocardiogram

A 
ECG or EKG
 P wave
 PR interval
 QRS complex
 ST segment
 T wave
35
Q

Common Dysrhythmias

A

Supraventricular dysrhythmias
Ventricular dysrhythmias
Ectopic foci
Conduction blocks

36
Q

Vaughan Williams Classification

A

System commonly used to classify
antidysrhythmic drugs
Based on the electrophysiologic effect of
particular drugs on the action potential

37
Q

Vaughan Williams

Classification

A 
Class I
    Class Ia
    Class Ib
    Class Ic
 Class II
 Class III
 Class IV
 Other
38
Q

Vaughan Williams Classification:

Mechanism of Action

A 
Class I
 Membrane-stabilizing drugs
 Fast sodium channel blockers
 Divided into Ia, Ib, and Ic drugs, according
to effects
39
Q

Vaughan Williams Classification:

Mechanism of Action and Indications

A

Class I: moricizine
General class I drug
Has characteristics of all three subclasses
Used for symptomatic ventricular and life-threatening dysrhythmias

40
Q

Vaughan Williams Classification:

Mechanism of Action and Indications

A

Class Ia: quinidine, procainamide,
disopyramide
Block sodium (fast) channels
Delay repolarization
Increase the APD
Used for atrial fibrillation, premature atrial
contractions, premature ventricular contractions, ventricular tachycardia

41
Q

quinidine(C)

A

Antiarrhythmic;Class Ia:Sodium channel blocker;decrease myocardial excitability & slow conduction velocity. tx restoration & maintenance of sinus rhythm in pt with a.fib.or flutter & prevention of recurrent ventricular arrhythmias

42
Q

procainamide,(C)

A

Antiarrhythmic;Class Ia:Sodium channel blocker;decrease myocardial excitability & slow conduction velocity;tx wide variety of ventricular & atrial arrhythmias & maintance of normal sinus rhythm

43
Q

disopyramide(C)(Norpace, Norpace CR)

A

Antiarrhythmic;Class Ia:Sodium channel blocker;decrease myocardial excitability & slow conduction velocity. Has anticholinergic properties.Little effect on HR but has a direct neg. inotropic effect.tx ventricular tachycardia

44
Q

Vaughan Williams Classification:

Mechanism of Action and Indications

A 
Class Ib: phenytoin, lidocaine
 Block sodium channels
Accelerate repolarization
Increase or decrease the APD
 Used for ventricular dysrhythmias only
 Premature ventricular contractions, ventricular tachycardia,ventricular fibrillation
45
Q

phenytoin(D) (Dilantin,Phenytek)

A

lidocaine(also used as anticonvulsant) Class 1b:Limits seizure progagation by altering ion transport, may also decrease synaptic transmission, antiarrhythmic porerties as a result of shortening the action potentenial & decreasein automaticity. tx termination of ventricular arrhythmias

46
Q

lidocaine(B)(Lido Pen, Xylocaine, Lindoderm,etc)

A

lidocaine(also used anesthetic topical local) Class 1b: given IV suppresses automaticity & spontaneous depolarization of the ventricles during diastole by altering the flux of sodium ions across cell membranes with little or no effect on HR. tx control of ventricular arrhythmias

47
Q

Vaughan Williams Classification:

Mechanism of Action and Indications

A

Class Ic: flecainide, propafenone
Block sodium channels
Little effect on APD or repolarization
Used for severe ventricular dysrhythmias
May be used in atrial fibrillation/flutter,
supraventricular tachycardia dysrhythmias

48
Q

flecainide(C)(Tambocor)

A

Antiarrhythmic Class 1c; Slows conduction in cardiac tissue by altering transport of ions across cell membrane. tx ventricular arrhythmias & ventricular tachycardia

49
Q

propafenone(C)(Rythmol, Rythmol SR)

A

Antiarrhythmic Class 1c;Slows conduction in cardiac tissue by altering transport of ions across cell membrane. tx ventricular arrhythmias & ventricular tachycardia(immediate release only)

50
Q

Vaughan Williams Classification:

Mechanism of Action and Indications

A

Class II: Beta-blockers: atenolol, esmolol,
metoprolol, propranolol
Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in the heart’s conduction system
General myocardial depressants for both
supraventricular and ventricular dysrhythmias
Also used as antianginal & drugs

51
Q

atenolol(D)(Tenormin)

A

antihypertensive,antianginal,Atihypertensive ClassII Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in the heart’s conduction system
General myocardial depressants for both
supraventricular and ventricular dysrhythmias

52
Q

esmolol(C)(Brevibloc)

A

antihypertensive,antianginal,Atihypertensive ClassII. Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in the heart’s conduction system
General myocardial depressants for both
supraventricular and ventricular dysrhythmias

53
Q

metoprolol(C)(Lopressor, Toprol-XL)

A

antihypertensive,antianginal,Atihypertensive Class II Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in the heart’s conduction system
General myocardial depressants for both
supraventricular and ventricular dysrhythmias

54
Q

propranolol(C)(Inderal, InnoPran)

A

Antiarrhythmic, antianginals, antihypertensives vascular HA suppressant ClassII; Beta Blocker-decrease HR & BP, suppression of arrhythmias, prevention of MI.tx mgnt HTN,angina, arrhythmias hypertrophic cardiomyopathy, thyrotoxicossis, pheochromocytoma(a tumor on andrenal gland),preventn & mgnt of MI and vascular HA

55
Q

Vaughan Williams Classification:

Mechanism of Action and Indications

A

Class III: amiodarone, sotalol*, ibutilide
Increase APD
Prolong repolarization
Used for dysrhythmias that are difficult to
treat
Life-threatening ventricular tachycardia or
fibrillation, atrial fibrillation or flutter—resistant to other drugs
Sustained ventricular tachycardia
*Sotalol also exhibits Class II properties

56
Q

Sotalol(B)(Betapace, Sorine)

A

Antiarrhythmia Class III;Blocks stimulation of beta1 & beta 2 ; tx mgnt of ventricular arrhythmia; Betaspace AF-maintence of normal sinus rhythm in pt with highly symptomatic A.Fib. who are currently in sinus rhythm.

57
Q

Vaughan Williams Classification:

Mechanism of Action and Indications

A

Class IV: verapamil, diltiazem
Calcium channel blockers
Inhibit slow-channel (calcium-dependent) pathways
Depress depolarization
Reduce AV node conduction
Used for paroxysmal supraventricular tachycardia;rate control for atrial fibrillation and flutter

58
Q

verapamil(C)(Calan, Covera-HS, IsoptinSR, Verelan)

A

Antihypertensive, antiarrhythmic, antianginals, vascular HA suppressant; Calcium Channel Blocker- inhibits the transport of Ca+ into myocardial & vascular smooth muscle cells, resulting inhibition of exitation and contraction coupling & subsequent contraction; decreases SA& AV conduction & prolongs AV refactory period in conduction tissue. tx mgnt HTN, angina. mgnt suprventricular arrhythmia, rapid ventricular rates in a. fib.

59
Q

diltiazem(C)(Cardizem, Cartia, Dilacor, Taxtia etc.)

A

Antihypertensive, antiarrhythmic, antianginals, vascular HA suppressant; Calcium Channel Blocker- inhibits the transport of Ca+ into myocardial & vascular smooth muscle cells, resulting inhibition of exitation and contraction coupling & subsequent contraction; decreases SA& AV conduction & prolongs AV refactory period in conduction tissue.tx HTN, angina, suprventricular tachyarrhymias, rapid ventricular rates in a. fib.

60
Q

Vaughan Williams Classification:

Other Antidysrhythmics

A

digoxin, adenosine

Have properties of several classes and are not placed into one particular class

61
Q

digoxin(C)(Lanoxin)

A

Antidysrhythmics; increaeses the force of myocardial contraction, prolongs refractory period of the AV node, decreases conduction through the SA & AV node. tx HF, A. Fib & flutter, parosysmal atrial tachycardia

62
Q

adenosine(C)(Adenocard, Adenoscan)

A

Antidysrhythmics;restores normal sinus rhythm by interrupting re-entrant pathways in the AV node, slows conduction time through AV node, produces coronary artery vasodialation.tx paroxysmal supraventicular tachycardia(PSVT), used as diagnostic agent for myocardial perfusion defects as result of coronary artery disease

63
Q

Unclassified Antidysrhythmic

A

adenosine (Adenocard)
Slows conduction through the AV node
Used to convert paroxysmal supraventricular
tachycardia to sinus rhythm
Very short half-life—less than 10 seconds
Only administered as fast IV push
May cause asystole for a few seconds

64
Q

Antidysrhythmics: Adverse

Effects

A 
ALL antidysrhythmics can cause dysrhythmias!
 Hypersensitivity reactions
 Nausea
 Vomiting
 Diarrhea
 Dizziness
 Blurred vision
 Headache

Pharmacology (7 decks)

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