Cardiac Glycosides Flashcards

1
Q

Causes of heart failure

A

HEART PMI

Hypertension
pulmonary embolism
anaemia
arrhythmia
rheumatic heart disease
thyrotoxicosis
pregnancy
myocardial infarction
medication
infection

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2
Q

Symptoms of right sided heart failure

A

Peripheral oedema
jugular vein distension
increased peripheral venous pressure
weight gain
Ascites
hepatosplenomegaly
fatigue

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3
Q

Symptoms of left sided heart failure

A

Cyanosis
dyspnoea
tachypnoea
pulmonary congestion
tachycardia
restlessness

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4
Q

Source of thevetin

A

Thevetia neriifolia (nut)

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5
Q

Source of strophanthus G (ouabain)

A

Strophanthus gratus (seed)

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6
Q

Source of convallotoxin

A

Lily of the Valley (Convallaria majalis)

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7
Q

Examples of semi synthetic glycosides

A

Acetyl digoxin
Acetyl strophanthidin
Desacetyl lanatoside

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8
Q

Plant families of cardiac glycosides

A

Scrophulariaceae
Apocyanaceae
Liliceae

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9
Q

Effects of cardiac glycosides on cardiac function

A

Reduced chronotropy
Increased inotropy
Reduced dromotropy
Increased lusitropy

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10
Q

What are the effects of increased inotropy on the cardiovascular system?

A

a. Increased cardiac output
b. Decreased heart size
c. Decreased venous pressure
d. Decreased circulating blood volume
e. Diuresis

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11
Q

How does digoxin bring about reduced chronotropy

A

Via its vagal and extra vagal action by
- amplifying parasympathetic discharge to the heart via baroreceptors:
- direct stimulation of vagal center
- sensitization of SA node to acetylcholine

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12
Q

Electrophysiological effects of cardiac glycosides

A

Decrease amplitude or inversion of T wave
Increased PR interval
Shortening QT interval
Depression of ST segment
Abnormal QRS wave

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13
Q

Cardiac glycosides on Blood vessels

A

Mild direct vasoconstriction

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14
Q

Effect of CG on Kidney

A

Causes diuresis in CHF patients

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15
Q

Effect of CG on CNS

A

High doses stimulate the vomiting center causing nausea and vomiting and much higher doses causes hyperapnoea, mental confusion, visual disturbances, disorientation.

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16
Q

What portion of the Na-K-ATPase pump does digoxin bind to?

A

Extracellular

17
Q

In high doses, digoxin toxicity is reversed by what? How?

A

K+ infusion

Binding of digoxin to the pump is slow, and the inhibition further depletes intracellular K+.

18
Q

Low potassium levels will reduce digoxin binding. True or false?

A

False. It increases it. Potassium infusion is used to treat toxicity, remember.

19
Q

What are other effects of low potassium levels?

A

Prolonged AP
Arrythmia

20
Q

What are the extracardiac adverse effects of cardiac glycosides?

A

Anorexia
nausea and vomiting
abdominal pain
visual disturbances
fatigue
Weakness
confusion
gynaecomastia
diarrhoea

21
Q

What are the cardiac adverse effects of cardiac glycosides?

A

Ventricular arrhythmias
atrioventricular block
Atrial arrhythmia
sinus bradycardia

22
Q

Precautions and contraindications for CG

A

Hypokalemia- Low K increases the binding to Na- K -ATPase
Elderly, renal or hepatic disease – More sensitive
Thyrotoxicosis – More prone to develop arrythmia.
Ventricular tachycardia – More prone to ventricular fibrillation
Myxoedema – Eliminate digoxin slowly and prone to toxicity

23
Q

Effect of digoxin on potassium

A

Mechanism: Digoxin & K inhibit each other binding to Na K ATPase

Effect: Hyperkalemia reduces digoxin activity
Hypokalemia potentiates digoxin toxicity

24
Q

Effect of digoxin on calcium

A

Mechanism: Enhances calcium absorption into the myocytes and accelerates overloading of calcium stores

Effect: Hypercalcemia potentiates digitalis-induced arrythmias

25
Q

Effect of digoxin on magnesium

A

Mechanism: Antagonizes the effect of calcium

Effect: Hypomagnesemia sensitizes the heart to digitalis-induced arrythmia

26
Q

Which drugs increase the serum concentration of CG?

A

Verapamil
amiodarone
spironolactone
Quinidine
propafenone
warfarin
cyclosporine
Macrolides

27
Q

What is the drug interaction of CG with diuretics?

A

Hypokalaemia, with increased risk of digitalis arrhythmias

28
Q

Treatment of acute digoxin toxicity

A
  • STOP DIGOXIN administration!!!
  • Acute toxicity in <2hrs: Decrease absorption by administering Activated Charcoal or Cholestyramine to decontaminate the GIT
  • Supportive therapy: Rehydrate to increase renal clearance
29
Q

Treatment of chronic digoxin toxicity

A
  • Supportive therapy
  • Symptomatic bradycardia or heart block : Atropine/Digoxin specific Fab fragment
  • Arrythmia: Lidocaine / Phenytoin
30
Q

Which drugs are used to treat arrhythmias from chronic digoxin toxicity?

A

Lidocaine / Phenytoin

31
Q

How to treat digoxin-induced hypokalaemia and hyperkalaemia

A

Treat with Potassium chloride (KCl) and therapeutic drug monitoring of digoxin and potassium.

Hyperkalemia: Digoxin specific Fab fragment , insulin and dextrose / sodium bicarbonate use.

32
Q

What is digoxin-specific Fab fragment (digibind fragment)?

A

Used in severe cases of life threatening digoxin toxicity, it was developed for measuring plasma concentration of digoxin by radioimmunoassay.

It acts by cross reacting with digitoxin. It is non-immunogenic with the digoxin-fab fragment rapidly excreted by kidney.

33
Q

Meaning of increased PR interval

A

Slower HR, dromotropy

34
Q

Shortened QT interval meaning

A

Depolarisation and repolarisation take longer

35
Q

Depressed ST segment meaning

A

Impaired blood flow

36
Q

Abnormal QRS wave meaning

A

Conduction abnormalities