Cardiac Glycosides Flashcards

(36 cards)

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
Effect of digoxin on magnesium
Mechanism: Antagonizes the effect of calcium Effect: Hypomagnesemia sensitizes the heart to digitalis-induced arrythmia
26
Which drugs increase the serum concentration of CG?
Verapamil amiodarone spironolactone Quinidine propafenone warfarin cyclosporine Macrolides
27
What is the drug interaction of CG with diuretics?
Hypokalaemia, with increased risk of digitalis arrhythmias
28
Treatment of acute digoxin toxicity
- 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
Treatment of chronic digoxin toxicity
- Supportive therapy - Symptomatic bradycardia or heart block : Atropine/Digoxin specific Fab fragment - Arrythmia: Lidocaine / Phenytoin
30
Which drugs are used to treat arrhythmias from chronic digoxin toxicity?
Lidocaine / Phenytoin
31
How to treat digoxin-induced hypokalaemia and hyperkalaemia
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
What is digoxin-specific Fab fragment (digibind fragment)?
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
Meaning of increased PR interval
Slower HR, dromotropy
34
Shortened QT interval meaning
Depolarisation and repolarisation take longer
35
Depressed ST segment meaning
Impaired blood flow
36
Abnormal QRS wave meaning
Conduction abnormalities