Cardiac Glycosides - Digoxin Flashcards

1
Q

Which of the following drugs is our core drug that is classed as cardiac glycoside?

1 - Digoxin
2 - Glyceryl trinitrate
3 - Isosorbide mononitrate
4 - Terlipressin

A

1 - Digoxin

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2
Q

Digoxin is the core drug that is classed as a cardiac glycoside. What is the mechanism of action of this drug?

1 - prodrug for lypressin (also known as lysine vasopressin) that is a vasoconstrictor and antidiuretic agent.
2 - inhibits Na+/K+ ATPase pump
3 - once metabolised released nitric oxide
4 - converted in mitochondria by aldehyde dehydrogenase in smooth muscle cells to nitric oxide

A

2 - inhibits Na+/K+ ATPase pump

  • Na+ and Ca+2 build up in the cell
  • causes more powerful cardiac contractions and cardiac output
  • slows AV node conduction
  • also increases renal blood-flow, urine output and reduced peripheral oedema
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3
Q

If b-blockers and Ca2+ channel blockers fail, digoxin is indicated in the treatment of atrial fibrilliation and atrial flutter. Why is digoxin a good medication to treat atrial arrhythmias?

1 - increased vagus nerve stimulation
2 - decreased vagus nerve stimulation
3 - inhibits AV node firing rate
4 - Increased AV node firing rate

A

1 - increased vagus nerve stimulation

  • increased vagus nerve = increased parasympathetic activity, which predominantly works on the atria
  • reduced conduction of AV node and subsequent impulses
  • this reduces heart rate and arrhythmias
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4
Q

The digoxin effect on AF arrhythmias is reliant on parasympathetic tone. Does exercise of stress have any affect on the effects of digoxin?

A
  • yes
  • reduces the effectiveness of digoxin, also the reason why it is not prescribed alone
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5
Q

Digoxin is indicated in severe heart failure, but is not the 1st line treatment. It is generally added an ACE inhibitor, B-blocker, aldosterone antagonist or angiotensin receptor blocker. Why is digoxin good for severe heart failure?

1 - increased Ca2+ and Na+ in cardiomyocytes, causing more efficient cardiac contraction
2 - increased sinus node activation to increase heart rate
3 - reduces O2 demand on the heart
4 - Increased AV node firing rate

A

1 - increased Ca2+ and Na+ in cardiomyocytes, causing more efficient cardiac contraction

  • this also increased renal flow and urine output
  • reduces peripheral oedema
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6
Q

Does digoxin have a negative or positive inotropic (relates to contraction force) effect?

A
  • positive
  • makes the heart pump more effectively
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7
Q

Does digoxin have a negative or positive chronotropic (relates to heart rate) effect?

A
  • negative
  • reduces heart rate
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8
Q

All of the following are adverse events of digoxin, EXCEPT:

1 - tachycardia
2 - GI upset
3 - rash
4 - dizziness
5 - visual disturbances

A

1 - tachycardia
- digoxin improves contractile efficiency so heart doesn’t need to beat as fast

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9
Q

Digoxin has a narrow therapeutic index, meaning there is a risk of toxicity. This toxicity could affect a number of organs and tissues, but what is the most dangerous?

1 - liver failure
2 - CKD
3 - GI ischaemia
4 - cardiac arrhythmias
5 - pulmonary fibrosis

A

4 - cardiac arrhythmias

  • can be life threatening
  • can cause bradycardia
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10
Q

When prescribing digoxin which of the following should be performed at baseline, prior to administering the medication?

1 - ECG
2 -

A
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11
Q

Which 3 of the following conditions is digoxin contraindicated in?

1 - seond degree heart block
2 - intermitent complete heart block
3 - renal failure
4 - ventricular arrythmias

A

1 - seond degree heart block
2 - intermitent complete heart block
4 - ventricular arrythmias

  • it can be used in renal failure, but the dose must be lowered as digoxin is removed via the kidneys
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12
Q

Specific electrolyte disturbances can increase the risk of digoxin toxicity. How can hypokalaemia increase the risk of arrhythmia?

1 - K+ binds with digoxin and increases digoxin effects
2 - if K+ is low then digoxin cannot bind to Na+/K+ ATPase
3 - digoxin competes with K+ to bind Na+/K+ ATPase, low K+ means effects of digoxin are enhances

A

3 - digoxin competes with K+ to bind Na+/K+ ATPase, low K+ means effects of digoxin are enhances

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13
Q

In addition to hypokalaemia, which 2 other electrolyte disturbances can increase the risk of digoxin toxicity?

1 - hypercalcaemia
2 - hypermagnesaemia
3 - hypocalcaemia
4 - hypomagnesaemia

A

1 - hypercalcaemia
4 - hypomagnesaemia

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14
Q

Loop diuretics and thiazide diuretics can increase the risk of digoxin toxicity, how?

1 - competes with digoxin binding
2 - causes hypercalcaemia
3 - causes hypokalaemia
4 - causes decreased sensitivity of clearance in the kidneys

A

3 - causes hypokalaemia

  • loop and thiazide diuretics increase Na+ excretion and K+ follows in collecting ducts
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15
Q

Caution should be used when prescribing digoxin alongside all of the following drugs, EXCEPT:

1 - amiodarone
2 - Ca2+ channel blockers
3 - sprionolactone
4 - quinine
5 - B-blockers

A

5 - B-blockers

  • all other drugs increase plasma concentration of digoxin and increase risk of toxicity
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16
Q

Digoxin can be given orally or IV, taking 2 hours and 30 minutes respectively to have an affect. Digoxin requires a loading dose to have a rapid effect. What is the standard loading dose?

1 - 50 micrograms
2 - 250 micrograms
3 - 500 micrograms
4 - 1mg

A

3 - 500 micrograms

  • followed by 250-500 micrograms 6 hours later
  • then maintenance does is 125-250 micrograms
  • should be monitored every 6 hours
17
Q

When prescribing digoxin all of the following should be routinely checked before and during administration, EXCEPT:

1 - renal function
2 - ECG
3 - echocardiogram
4 - U&Es

A

3 - echocardiogram

18
Q

The therapuetic effect of digoxin can affect an ECG in what way?

1 - flattened P wave
2 - inverted T wave
3 - ST segment depression
4 - QRS extension

A

3 - ST segment depression

  • often referred to as the reverse tick