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systemic Pharma- week 3/4 Anti-arrythmics/ Anti-couagulants/Anti-platelets > Anti-arrythmic drugs > Flashcards

Anti-arrythmic drugs Flashcards

1
Q

Anti-Arrythmic drugs

A

 Class I: Na+ channel blockers
 Class II: Beta-blockers
 Class III: K+ channel blockers
 Class IV: Ca2+ channel blockers

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2
Q

——————- : is the period in which the heart cannot start a new depolarisation cycle. This prevents ectopic beats (irreglualr heart beat) from happening

A

ERP (Effective Refractory Period

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3
Q

MoA of Class I: Na+ channel
blockers “Use-Dependent”

A

-Inhibit AP propagation in excitable cells.
-They reduce the max depolarisation rate at phase 0.
-Bind to activated and inactivated (rather than closed channels).
-Block high frequency excitation of the myocardium w/o affecting HR at normal frequencies!

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4
Q

Contraindications of Class I: Na+ channel
blockers “Use-Dependent”

A

Hyperkalaemia
–> causes increased toxicity for all class I
drugs

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5
Q

Class IA: Na+ channel
blockers Examples

A

Procainamide (weak Anticholinergic- short half-life)
Quinidine (Moderate Antichlinergic)
Disopyramide (Strong Anticholinergic)
(Pro-Qui-Di)

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6
Q

MoA of Class IA: Na+ channel
blockers

A

-They mostly block channels in the open or activated state.
-Prolong repolarisation ( K+ CHANNEL BLOCKED , less than class III).
-Increase APD & ERP

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7
Q

AE of Class IA: Na+ channel
blockers (generally not each drug)

A

QT interval associated w/ torsade and syncope
(because class IA cause prolonged repolarization so they prolong QT interval)

* torsade –> (Polymorphic ventricular arrythmias)

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8
Q

Clinical uses of Class IA: Na+ channel
blockers

A

Atrial flutter, fibrillation, Supraventricular and ventricular Tachyarrthmias

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9
Q

AE of Procainamide

A

Lupus-like sy in
25-30% of patients

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10
Q

AE of Quinidine

A

Cinchonism (blurred vision, tinnitus, headache, psychosis)

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11
Q

AE of Disopyramide

A

Negative intropic effects = Less contraction force and HR
contraindicated in HF

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12
Q

Class IB: Na+ channel blockers Examples

A

1) Lidocaine (IV)
2) Mexiletine (Oral)

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13
Q

MoA of Class IB: Na+ channel blockers

A
  • Bind selectively to inactivated channels in ventricular and Purkinje fiber cells
  • Decrease APD
  • supresses excitability in hypoxic areas of the heart
  • Block preamture beats
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14
Q

Clinical uses of Class IB: Na+ channel blockers

A
  • Ventricular arrythmias, particularly post-MI
  • Digoxin toxicity
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15
Q

AE of Class IB: Na+ channel blockers

A

1) Drowsiness,
2) disorientation,
3) convulsions (seizures)
4) CV depression
5) tremor

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16
Q

Class IC: Na+ channel
blockers Examples

A

Flecainide (oral)
Propafenone

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17
Q

MoA of Class IC: Na+ channel
blockers

A
  • Inhibit conduction through His Purkinje system.
  • Suppress ventricular ectopic beats
  • No effect on APD or on ANS
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18
Q

AE of Class IC: Na+ channel
blockers

A

Increased risk of sudden death when:
-Vfib after MI
-VT
* no longer used

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19
Q

Clinical uses of Flecainide

A

Prophylaxis against paroxysmal atrial fibrillation (for patients w/o structural and ishemic heart disease- dilated cardiomyopathy).

* Class IC: Na+ channel blockers

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20
Q

AE of Flecainide (oral)

A

Limited use as it is a Proarrythmic –> increased risk in sudden death post MI and when used prophylactically in VT

*Class IC: Na+ channel

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21
Q

Contraindications of Flecainide (oral)

A

HF -> structural and Ischemic heart disease (Dilated cardiomyopathy)

Class IC: Na+ channel blockers

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22
Q

Clinical uses of Propafenone

A

SVT & VT w/o sturctural ischemia
(supraventricular tavhyarrthmias and ventricualr tachyarrythmias)

* Class IC: Na+ channel blockers

23
Q

Contraindiactions of Propafenone

A

HF –> β-blocking and Ca+ channel blocking activity can worsen HF

* Class IC: Na+ channel blocker

24
Q

Class II: B-Blockers Examples

A

Propranolol (non-selective), with minor class I activity
Metoprolol (β1-selective)
Esmolol - IV (β1-selective: used in acute SVT via IV route: very short-acting)

25
Q

MoA of Class II: B-Blockers

A
  • Decrease SA and AV nodal activity.
  • Decrease slope of phase 4 (diastolic currents) of AP in pacemakers
  • increase cAMP
26
Q

Clinical uses of Class II: B-blockers

A
  • Reduce mortality following MI (prophylaxis)
  • SVTs
27
Q

Contraindications of Class II: B-Blockers

A

1) Caution in diabetics
since it may mask hypoglycaemia
2) WPWS

28
Q

Class III: K+ channel blockers Examples

A

AMIODARONE (IV)
Dronedarone
Sotalol

29
Q

MoA of Class III: K+ channel
blockers

A
  • Block K+ channels including the outward rectifier current
  • Prolong APD (QT interval)
  • Greater refractory period may interrupt reentrant arrhythmias and suppress ectopic beats
  • Especially active in Purkinje and ventricular
    fibers
30
Q

AE of Class III: K+ channel
blockers

A

Prolonging APD may lead to
torsade de pointes

31
Q

Contraindications of Class III: K+ channel
blockers

A

1) antipsychotics.
2) Increased risk with hypokalaemia,
3) hypercalcaemia
4) hereditary prolonged QT

* Monitor electrolyte levels, especially K+

32
Q

MoA of Amiodarone

A
  • K+/ Ca+2 channel blocker –> decreases AV activity
  • prolongs APD –> Prolongs QT interval –> torsade

->Long half-life = 10-100 days!
–> Because it accumulates in the body (can cause toxicity)

* Class III: K+ channel blockers

33
Q

Clinical uses of Amiodarone

A

1) Tachycardia associated w/ Wolf-Parkinson-White Syndrome
2) SVT/ VT

34
Q

Administration of Amiodarone

A

IV

*Class III: K+ channel blockers (

35
Q

AE of Amiodarone

A
  • Photosensitive skin rashes (phototoxicity)
  • blue pigmentation of the skin
  • Thyroid dys.
  • Pulmonary fibrosis
  • Corneal deposits
  • Heapatic necrsosis
  • bradycardia, heart block, heart failure.
  • Rarely VT or torsade de pointes

*Class III: K+ channel blockers

36
Q

Clinical uses of Dronedarone

A

Used instead of Amiodarone as it has less sever AE (New drug)

*Class III: K+ channel blockers

37
Q

Clinical uses of Sotalol

A

Life threatening VT
(Less effective than amiodarone in preventing chronic VT)

* Class III: K+ channel blockers

38
Q

AE of Sotalol

A

can cause Torsades de pointes

* Class III: K+ channel blockers

39
Q

Class IV: Ca+ channel blockers Examples

A

Verapamil (oral/IV)

40
Q

MoA of Class IV: Ca+ channel
blockers

A

1) Decrease phases 0 and 4 (decreases HR) in the SA and AV nodes = increases ERP
2) Decrease phase 2 in fast response fibres:
° shorten AP plateau,
° decrease contractility,
° reduces after depolarisation→ suppresses premature ectopic beat

41
Q

AE of Class IV: Ca+ channel
blockers

A

1) Constipation (Verapamil)
2) dizziness
3) flushing
4) hypotension
5) AV block
6) Oedema

42
Q

Clinical uses of Verapamil?

A

Prevention of paroxysmal SVT (Atrial tachy) and Afib

*CCB

43
Q

Contraindications of Verapamil

A

1) Wolff-Parkinson-White Syndrome;
2) VTs;
3) Beta-blockers –> AV block
4) Digoxin –> displaces digoxin from tissue -binding sites (Digoxin toxicity)

44
Q

Anti-Arrythmic drugs NOT CLASSIFIED +clinical uses

A

1) Atropine (IV) (M2 receptor Antagonist) –> sinus Bradycardia
2) Adenosine (IV)- short half-life –> Acute SVT
3) Digoxin –> Afib

45
Q

AE of Atropine

A
  • Dry mouth
  • Constipation
  • Urinary retention
  • Mydriasis (pupil dilatation)
  • Tachycardia
  • Blurred vision
46
Q

AE of Digoxin

A

Yellow vision

47
Q

MoA of Adenosine

A
  • Increase K outward current (IKAch) and decreases Ca2+ inward current
  • Activates Adenosine receptors: causes Gi-coupled decreases in cAMP
     * Shorter lived than Verapamil, thus safer,
           only lasts **20-30s after a bolus**.
48
Q

AE of Adenosine

A

1) Chest pain,
2) SOB (shortness of breath),
3) dizziness,
4) nausea,
5) flushing.

49
Q

Contraindications of Adenosine

A

Important interactions:
1) Theophylline and other xanthines (caffeine) block adenosine receptors and thus inhibit the actions of adenosine.
2) Dipyrimadole (anti-platelet) blocks the nucleoside uptake mechanism, prolonging the adverse effects of adenosine

50
Q

Ivabradine Class?

A

Selective inhibitor of “If” channles

*if : funny channels

51
Q

MoA of Ivabradine

A

Selective demandsor of “If” channels:
- prolongs slow depolarisation phase
- Decreases SA node firing
- Reduces oxygen demands

52
Q

Clinical uses of Ivabradine

A

1) Chronic stable angina.
2) Chronic HF for patients:
- in sinus rhythm
- HR>70bpm
- LVEF<35%
- who have a B-blocker contraindication

53
Q

AE of Ivabradine

A

1) Bradycardia,
2) visual disturbances,
3) hypertension
4) Long QT
5) Atrial fibrillation

systemic Pharma- week 3/4 Anti-arrythmics/ Anti-couagulants/Anti-platelets (3 decks)

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