A patient receiving high-dose IV atropine for organophosphate poisoning develops flushed, hot, dry skin. The anhidrosis occurs because:
- A Eccrine sweat glands use sympathetic cholinergic transmission, blocked by atropine ✓
- B Atropine blocks sympathetic vasoconstrictor fibres to skin vessels
- C Atropine destroys the postganglionic sympathetic neurons to sweat glands
- D Atropine blocks alpha-1 receptors on sweat gland ducts
Explanation
Thermoregulatory eccrine sweat glands receive sympathetic fibres whose postganglionic transmitter is acetylcholine acting on muscarinic receptors, so atropine abolishes sweating even though the sympathetic pathway itself is anatomically intact. This is the classic exception to adrenergic sympathetic transmission. Atropine has no alpha-blocking action and does not damage neurons, and flushing results from cutaneous vasodilation rather than any effect on sweat glands.
Reference: Ganong Review of Medical Physiology, 26th ed.
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