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Pharmacology · Toxicology: yellow oleander poisoning
Sample itemA 24-year-old woman in South India is brought after chewing seeds of the yellow oleander (Thevetia peruviana). She has vomiting, a pulse of 42 per minute with first-degree atrioventricular block and serum potassium of 6.2 mmol/L. Which mechanism explains the hyperkalaemia and conduction block?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Inhibition of the sodium-potassium ATPase pump by cardiac glycosides
Thevetia seeds contain cardenolides, which inhibit the sodium-potassium ATPase and so raise extracellular potassium and intracellular calcium, as in digoxin toxicity. Increased vagal tone and direct nodal depression cause bradycardia and AV block. Treatment includes activated charcoal, atropine and digoxin-specific Fab fragments where available.
Option by option
A. Inhibition of the sodium-potassium ATPase pump by cardiac glycosides (correct)
Cardiac glycoside pump inhibition raises potassium and slows nodal conduction.
B. Activation of beta-1 receptors
Beta-1 activation would increase the heart rate and not cause AV block.
C. Inhibition of acetylcholinesterase
Acetylcholinesterase inhibition is seen in organophosphate poisoning, which causes miosis and secretions.
D. Blockade of sodium channels in the His-Purkinje system
Sodium channel blockade is the mechanism of class I antiarrhythmics and tricyclic overdose, which give wide QRS rather than hyperkalaemia.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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