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Pharmacology > 05 Antidysrhythmic drugs > Flashcards

05 Antidysrhythmic drugs Flashcards

1
Q

5.01 CLASS 1a ANTIDYSRHYTHMIC

Disopyramide (similar: quinidine, procainamide) - actions

A

antidysrhythmic

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2
Q

5.01 CLASS 1a ANTIDYSRHYTHMIC

Disopyramide (similar: quinidine, procainamide) - MOA

A

belongs to class Ia of the Vaughan Williams classification
blocks open and inactivated Na+ channels in the cell membrane (‘use-dependent’ action) to reduce the rate of phase 0 depolarisation, causing an increase in the effective refractory period and slowed AV conduction
also produces some slowing of action potential repolarisation (a class III action)

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3
Q

5.01 CLASS 1a ANTIDYSRHYTHMIC

Disopyramide (similar: quinidine, procainamide) - abs/distrib/elim

A

given orally or IV
half-life 5-10h
half is excreted unchanged by the kidney, half is metabolised in the liver

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4
Q

5.01 CLASS 1a ANTIDYSRHYTHMIC

Disopyramide (similar: quinidine, procainamide) - clinical use

A

supraventricular and (more usually) ventricular dysrhythmia

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5
Q

5.01 CLASS 1a ANTIDYSRHYTHMIC

Disopyramide (similar: quinidine, procainamide) - adverse effects

A

atropine-like effects: blurred vision, dry mouth, constipation, urinary retention
negative inotropic action

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6
Q

5.02 CLASS 1c ANTIDYSRHYTHMIC

Flecainide (similar: propafenone, encainide) - actions

A

antidysrhythmic

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7
Q

5.02 CLASS 1c ANTIDYSRHYTHMIC

Flecainide (similar: propafenone, encainide) - MOA

A

belongs to class Ic of the Vaughan Williams classification
preferential block of open Na+ channels
reduces the rate of phase 0 depolarisation, causing an increase in the effective refractory period and slowed AV conduction
associates with and dissociates from Na+ channels more slowly than either Ia or Ib agents

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8
Q

5.02 CLASS 1c ANTIDYSRHYTHMIC

Flecainide (similar: propafenone, encainide) - abs/distrib/elim

A

given orally or IV
half-life 20h
mostly excreted unchanged in urine
propafenone is metabolised more rapidly by the liver and has a shorter half-life (5-10h)

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9
Q

5.02 CLASS 1c ANTIDYSRHYTHMIC

Flecainide (similar: propafenone, encainide) - clinical use

A

prevention and treatment of atrial fibrillation
ventricular tachyarrhythmias

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10
Q

5.02 CLASS 1c ANTIDYSRHYTHMIC

Flecainide (similar: propafenone, encainide) - adverse effects

A

increases likelihood of dysrhythmia
may increase mortality due to ventricular fibrillation post-infarction
needs careful use and is suitable only for patients who do not have ischaemic or structural heart disease
negative inotropic action

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11
Q

5.03 CLASS II ANTIDYSRHYTHMIC

β-adrenoceptor antagonist (bisoprolol, esmolol, propanolol, etc.) - actions

A

β-adrenoceptor antagonists
antidysrhythmic (also antihypertensive, antianginal)
block actions of catecholamines on β-adrenoceptors

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12
Q

5.03 CLASS II ANTIDYSRHYTHMIC

β-adrenoceptor antagonist (bisoprolol, esmolol, propanolol, etc.) - MOA

A

block sympathetic drive, reducing pacemaker activity (phase 4) and increasing AV conduction time
reduce the slow inward Ca2+ current, which affects phase 2 of the action potential
propranolol has additional class I action

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13
Q

5.03 CLASS II ANTIDYSRHYTHMIC

β-adrenoceptor antagonist (bisoprolol, esmolol, propanolol, etc.) - abs/distrib/elim

A

given orally or IV

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14
Q

5.03 CLASS II ANTIDYSRHYTHMIC

β-adrenoceptor antagonist (bisoprolol, esmolol, propanolol, etc.) - clinical use

A

paroxysmal atrial fibrillation and other tachyarrhythmias
reduction of mortality after infarct (where dysrhythmias have a sympathetic input)

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15
Q

5.03 CLASS II ANTIDYSRHYTHMIC

β-adrenoceptor antagonist (bisoprolol, esmolol, propanolol, etc.) - adverse effects

A

bronchoconstriction in asthmatic patients
cardiac slowing with possible heart block

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16
Q

5.04 CLASS III ANTIDYSRHYTHMIC

Amiodarone (similar: sotalol, dronedarone, ibutilide) - actions

A

antidysrhythmic

17
Q

5.04 CLASS III ANTIDYSRHYTHMIC

Amiodarone (similar: sotalol, dronedarone, ibutilide) - MOA

A

class III drugs block K+ channels in the cell membrane to delay repolarisation and increase action potential duration
this increases the refractory period
amiodarone also blocks Na+ channels and β adrenoceptors so has class I and class II actions
sotalol is a β-adreno­ceptor antagonist that also has class II actions

18
Q

5.04 CLASS III ANTIDYSRHYTHMIC

Amiodarone (similar: sotalol, dronedarone, ibutilide) - abs/distrib/elim

A

long-acting
extensive tissue binding
half-life of several weeks
sotalol and ibutilide have half-lives of 5-10h

19
Q

5.04 CLASS III ANTIDYSRHYTHMIC

Amiodarone (similar: sotalol, dronedarone, ibutilide) - clinical use

A

atrial fibrillation and flutter
ventricular ectopic beats and ventricular tachyarrhythmias
ibutilide IV for acute treatment of atrial fibrillation and flutter

20
Q

5.04 CLASS III ANTIDYSRHYTHMIC

Amiodarone (similar: sotalol, dronedarone, ibutilide) - adverse effects

A

torsades de pointes (less likely with amiodarone than other class III drugs)
amiodarone may cause pulmonary fibrosis, liver damage, photosensitive skin rashes, thyroid malfunction

21
Q

5.05 CLASS IV ANTIDYSRHYTHMIC

Verapamil (similar: diltiazem) - actions

A

antidysrhythmic (also antihypertensive, antianginal)
blocks Ca2+ channels in both cardiac and smooth muscle so has both negative inotropic and smooth muscle relaxant actions

22
Q

5.05 CLASS IV ANTIDYSRHYTHMIC

Verapamil (similar: diltiazem) - MOA

A

blocks L-type voltage-gated Ca2+ channels, which are important in the action potential plateau, and in particular affects action potential propagation in the SA and AV nodes
shows use-dependence so is more active in tachyarrhythmias
decreases automaticity and slows AV conduction

23
Q

5.05 CLASS IV ANTIDYSRHYTHMIC

Verapamil (similar: diltiazem) - abs/distrib/elim

A

given orally (less commonly IV)
half-life 6-8h

24
Q

5.05 CLASS IV ANTIDYSRHYTHMIC

Verapamil (similar: diltiazem) - clinical use

A

supraventricular tachycardias
control of ventricular rate in atrial fibrillation

25
Q

5.05 CLASS IV ANTIDYSRHYTHMIC

Verapamil (similar: diltiazem) - adverse effects

A

side effects due to smooth muscle relaxation: hypotension and dizziness, ankle oedema, constipation
unwanted cardiac actions include heart block and bradycardia

26
Q

5.06 ADENOSINE RECEPTOR AGONISTS

Adenosine (similar: regadenoson) - actions

A

antidysrhythmic

27
Q

5.06 ADENOSINE RECEPTOR AGONISTS

Adenosine (similar: regadenoson) - MOA

A

activates G protein-coupled adenosine receptors
action (on A1 receptors) is due to inhibition of Ca2+ channel opening and increased K+ channel opening (the effect is analogous to the action of ACh on cardiac muscarinic receptors)
important actions are its negative chronotropic action on the SA node and slowed AV conduction

28
Q

5.06 ADENOSINE RECEPTOR AGONISTS

Adenosine (similar: regadenoson) - abs/distrib/elim

A

given IV
short duration of action
half-life 10sec

29
Q

5.06 ADENOSINE RECEPTOR AGONISTS

Adenosine (similar: regadenoson) - clinical use

A

termination of paroxysmal supraventricular tachycardia
slowing of AV conduction to enable more precise diagnosis of supraventricular tachycardias
coronary vasodilator to enable radionuclide myocardial perfusion imaging and cardiac stress testing

30
Q

5.06 ADENOSINE RECEPTOR AGONISTS

Adenosine (similar: regadenoson) - adverse effects

A

side effects (e.g. flushing, chest pain, dyspnoea, bronchospasm) are short-lived because of rapid elimination of adenosine
interacts with other drugs that exert effects on adenosine pathways (dipyridamole, theophylline)

31
Q

5.07 CARDIAC GLYCOSIDE

Digoxin - actions

A

slows heart
slows AV conduction
prolongs AV node refractory period
increases force of contraction in failing heart

32
Q

5.07 CARDIAC GLYCOSIDE

Digoxin - MOA

A

inhibits Na+/K+ ATPase in plasma membrane
the increased intracellular Na+ reduces Ca2+ extrusion, thus increasing intracellular Ca2+

33
Q

5.07 CARDIAC GLYCOSIDE

Digoxin - abs/distrib/elim

A

given orally, usually with an oral or IV loading dose if rapid action is needed
renal excretion
plasma half-life ~36h

34
Q

5.07 CARDIAC GLYCOSIDE

Digoxin - clinical use

A

atrial fibrillation
heart failure (if diuretics and ACE inhibitors have not worked)

35
Q

5.07 CARDIAC GLYCOSIDE

Digoxin - adverse effects

A

dysrhythmias, due to block of AV conduction and ectopic pacemaker action
yellow vision
nausea and vomiting

36
Q

5.07 CARDIAC GLYCOSIDE

Digoxin - special points

A

narrow margin between effective dose and toxic dose
decreased plasma K+ increases toxicity due to competition between K+ and digoxin for the Na+/K+ ATPase

Pharmacology (34 decks)

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