In organophosphorus compound poisoning atropine can reverse all the following signs except –
**Core Concept**
Organophosphorus compound poisoning inhibits acetylcholinesterase, leading to an accumulation of acetylcholine in the synaptic cleft. This results in overstimulation of muscarinic and nicotinic receptors, causing various systemic effects.
**Why the Correct Answer is Right**
Atropine, a muscarinic receptor antagonist, reverses signs of organophosphorus poisoning mediated by muscarinic receptors. These signs include bradycardia, excessive salivation, bronchospasm, and abdominal cramps. Atropine works by competing with acetylcholine for muscarinic receptor binding sites, thereby reducing the effects of excessive acetylcholine.
**Why Each Wrong Option is Incorrect**
* **Option A:** Atropine does not reverse nicotinic receptor-mediated effects such as muscle weakness and paralysis. This is because atropine does not cross the blood-brain barrier and therefore cannot affect nicotinic receptors in the central nervous system.
* **Option B:** Miosis (pupillary constriction) is a sign of organophosphorus poisoning mediated by nicotinic receptors. Atropine does not reverse miosis, which is why it's an exception to the other signs.
* **Option C:** Option C is not provided so we are unable to explain why it would be incorrect.
**Clinical Pearl / High-Yield Fact**
In organophosphorus poisoning, atropine is most effective when administered early, before the development of severe systemic effects. However, atropine does not reverse the effects of organophosphorus compounds on the neuromuscular junction, which can lead to prolonged muscle weakness and paralysis.
**Correct Answer: B. Miosis**