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Cardiology > Antiarrhythmic Drugs - Miscellaneous > Flashcards

Antiarrhythmic Drugs - Miscellaneous Flashcards

1
Q

What is Adenosine.

A

Adenosine is a naturally occurring purine nucleoside that forms from the breakdown of adenosine triphosphate (ATP).

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2
Q

Effect of Adenosine on the coronary vascular smooth muscle.

A
  • Binds to adenosine type 2A Purinergic receptor.
  • This receptor is coupled to Gs-protein.
  • Activation of G-protein stimulates adenylyl cyclase = ⬆️ cAMP
  • This triggers protein kinase activation.
  • Thus kATP channels are stimulated.
  • Smooth muscle hyperpolarises causing it to relax.
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3
Q

Effects of Adenosine in cardiac tissue.

A
  • Adenosine binds to type 1 (A1) receptor.
  • This receptor is coupled to Gi-protein.
  • Activation of Gi-protein decreasing cAMP.
  • This inhibits L-type calcium channels and therefore calcium entry into the cell.
  • This leads to a decrease in the conduction velocity (Negative Dromotropic effect) particularly at the AV nodes.
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4
Q

Effects of Adenosine in SA node.

A
  • Adenosine acting through A1 receptors inhibits the pacemaker current (If).
  • This decreases the slope of phase 4 of the pacemaker action potential.
  • This leads ⬇️ in its spontaneous firing rate (negative chronotropy).
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5
Q

State the half-life of Adenosine.

A

Less than 10 seconds.

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6
Q

How is Adenosine excreted from the body.

A

It is taken up by RBCs (and other cells).

There, it is rapidly deaminated by adenosine deaminase to inosine.

It is further broken down to hypoxanthine, xanthine and uric acid, which is excreted by the kidneys.

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7
Q

Therapeutic indication of Adenosine.

A

Paroxysmal Supraventricular Tachycardia:

Its suppression of AV conduction makes it very useful in treating paroxysmal supraventricular tachycardia in which the AV node is part of the re-entry pathway (as in Wolff-Parkinson-White Syndrome).

Given either as an i.v. bolus or i.v. Infusion

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8
Q

Side effects of Adenosine as an anti-arrhythmic drug.

A
  • Flushing and Headache

[In relation to the vasodilation effect]

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9
Q

State a competitive inhibitor of adenosine’s binding at its purinergic receptor.

A

Methylxanthines:

  • Caffeine
  • Theophylline
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10
Q

Contraindication of the use of Adenosine.

A

Patients with pre-existing second or third degree AV block.

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11
Q

Hypomagnesemia values.

A

Serum concentration < 1,5 mg/dL.

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12
Q

Hypokalaemia values.

A

Serum concentration < 3,5 mg/dL.

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13
Q

Therapeutic indications of i.v. Magnesium Sulfate.

A
  • Torsades de pointes VT.

- Digitalis induced ventricular arrhythmias.

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14
Q

Use of Vernakalant.

A

Novel drug.

Blocks Na channels and K channels.

Used intravenously for rapid conversion of acute onset of AF (lasting 3 - 72 hrs).

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15
Q

Therapeutic indication of Isoprenaline.

A

It is a beta-1 and beta-2 agonist,

Positive Dromotropic effect.

Used to treat AV block.

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16
Q

Therapeutic indication of Adrenaline.

A

Intra-cardiac injection.

For treatment of Cardiac Arrest.

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17
Q

Therapeutic indication of Calcium Chloride.

A

Ventricular tachycardia due to hyperkalaemia.

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18
Q

Cardiac glycosides are derived from which plant?

A

Foxglove plant (Digitalis purpurea)

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19
Q

Describe briefly the mechanism of action of digitalis.

A
  • Inhibits cellular Na+/K+ ATPase.
  • This pump is responsible for moving THREE sodium out and TWO potassium in against their concentration gradient = An ELECTROGENIC PUMP.
  • Loss of these ion gradients leads to cellular depolarization and loss of negative membrane potential (required for normal cell function).
  • Cardiac myocytes also have Na+-Ca+++ exchanger (Not an active energy-requiring pump).
  • Three Na in exchange for one calcium.
  • Increase in intracellular Na+ would lead to increase in intracellular Ca++ due to decreased exchanged pump activity (due to loss of conc. gradient driving force).
20
Q

How does digitalis compounds induce positive inotropic action?

A
  • Increased intracellular calcium causes more calcium to be released from the sarcoplasmic reticulum.
  • As a result, more calcium is available to bind to troponin-C
  • This increases the contractility.
21
Q

State the effect of digitalis compounds in the vascular smooth muscle.

A

Inhibition of the Na+/K+ - ATPase causes the vascular smooth muscle to depolarise.

This results in smooth muscle contraction and vasoconstriction.

22
Q

How does digitalis compounds produce a negative chronotropic and negative dromotropic effects?

A
  • Digitalis compounds increase vagal efferent activity of the heart.
  • This parasympathomimetic action reduces SA firing rate and reduces the conduction velocity of electrical impulses through the AV node.
23
Q

Half life of digoxin.

A

40 hours.

24
Q

Half-life of digitoxin.

A

160 hours.

25
Q

Half life of Ouabain.

A

20 hours.

26
Q

Route of elimination of Digoxin.

A

Kidneys.

27
Q

Route of elimination of Digitoxin.

A

Liver.

28
Q

Route of elimination of Ouabain.

A

Kidneys.

29
Q

Therapeutic plasma concentration of digoxin.

A

0,5 - 1,5 ng/ml

30
Q

What is implied by the term “digitalization”

A

A special dosing regimen involving “loading doses” that is used to rapidly increase digoxin plasma levels due to the long half-life.

The long half-life would require several days of constant dosing to reach steady-state.

31
Q

Plasma concentrations of Digoxin must not rise above? And why?

A

> 2,0 ng/ml.

Concentrations above this can lead to arrhythmias, some of which may be life-threatening.

32
Q

Antidote of digoxin intoxication.

A

Immune Fab (Digibind)

Potassium supplement can also reverse toxic effects of Digoxin if the toxicity is due to hypokalemia.

33
Q

Therapeutic indications of Digitalis compounds.

A

Arrhythmias:

  • Supraventricular arrhythmia

Heart Failure:

  • ⬆️ Inotropy
  • ⬆️ Ejection Fraction
  • ⬇️ Preload
    _ ⬇️ Pulmonary congestion/oedema
34
Q

Many commonly used drugs interact with digitalis compounds. Provide a list of examples.

A

Quninidine:

Competes with Digoxin for binding sites and depresses renal clearance of digoxin.

Ca-Channel Blockers

NSAIDs

Diuretics (can cause hypokalaemia)

35
Q

The role of HYPOKALAEMIA in Digoxin Intoxication.

A

Increases binding of Digoxin to the Na+/K+ -ATPase.

This possibly occurs through increased phosphorylation of the enzyme.

36
Q

The role of HYPOCALCEMIA in Digoxin intoxication.

A

It enhances the digitalis-induced increases in intracellular calcium, which can lead to calcium overload and increased susceptibility to digitalis-induced arrhythmias.

37
Q

Role of HYPOMAGNESEMIA in Digitalis Intoxication.

A

It sensitises the heart to the digitalis-induced arrhythmias.

38
Q

State two main side effects of cardiac glycosides.

A

Atrial tachycardias.

AV blocked.

39
Q

Contraindications of Digitalis Compounds.

A

Patients with:

Hypokalaemia

AV block

Wolff-Parkinson-White syndrome

40
Q

Two precautious measures when employing the use of digoxin in therapeutic interventions.

A

Impaired renal function.

Lean muscular mass because muscle Na+/K+ -ATPase acts as a large binding reservoir for digitalis.

41
Q

Explain the effects of atropine on the heart.

A

Atropine blocks the binding of Ach on M2 receptors that are found primarily in the SA and AV nodes.

Muscarinic receptors are couples to the Gi-protein; therefore, vagal stimulation decrease cAMP.

This leads to activation of K channels —> increased potassium efflux and hyperpolarisation.

42
Q

Vagal activity on SA node.

A

Decreases the firing rate of pacemaker cells by decreasing phase 4 slope = ⬇️ Chronotropy.

Hyperpolarisation increase the cell’s threshold for firing, contributing to the reduction of the firing rate.

43
Q

Vagal activity on AV node.

A

Reduced CONDUCTION VELOCITY = ⬇️ Dromotropy

44
Q

Effect of atropine on muscarinic receptors.

A

Blocks the effect of vagal nerve activity on the heart.

Make the sympathetic effect on the heart stronger.

⬆️ Chronotropy

⬆️ Dromotropy

45
Q

Therapeutic Indication of Atropine.

A

Sinus bradycardia

AV block

46
Q

Contraindication of Atropine.

A

Glaucoma

47
Q

Described the anticholinergic effects of atropine.

A

Tachycardia

Pupil dilation

Dry mouth

Urinary retention

Inhibition of sweating (anhidrosis)

Blurred vision

Constipation

Cardiology (2 decks)

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