## Core Concept
Organophosphorus poisoning occurs due to the inhibition of acetylcholinesterase, an enzyme responsible for the breakdown of acetylcholine. This results in an accumulation of acetylcholine in the synaptic cleft, leading to overstimulation of muscarinic and nicotinic receptors. The treatment involves administering antidotes that can counteract this effect.

## Why the Correct Answer is Right
Atropine is used as an antidote for organophosphorus poisoning because it acts as a muscarinic receptor antagonist. By blocking muscarinic receptors, atropine can effectively counteract the muscarinic effects of excessive acetylcholine, such as bradycardia, salivation, and bronchial secretions. Atropine does not affect nicotinic receptors, so it is often used in conjunction with pralidoxime (2-PAM), which reactivates acetylcholinesterase.

## Why Each Wrong Option is Incorrect
* **Option A:** This option is incorrect because, although pralidoxime (2-PAM) is indeed used in the treatment of organophosphorus poisoning, it works by reactivating acetylcholinesterase and is not the primary antidote that directly counteracts the muscarinic effects.
* **Option B:** This option is incorrect as it seems to be a blank or not specified.
* **Option C:** This option is incorrect because, while oximes like pralidoxime are crucial in treating organophosphorus poisoning, the question seems to be looking for a direct antidote that can immediately counteract the effects, which involves muscarinic blockade.

## Clinical Pearl / High-Yield Fact
A key point to remember is that the treatment of organophosphorus poisoning typically involves the administration of atropine and pralidoxime (2-PAM). Atropine is specifically used to counteract the muscarinic effects (e.g., bradycardia, increased salivation), while pralidoxime helps in reactivating the inhibited acetylcholinesterase enzyme.

## Correct Answer: D. Atropine