**Core Concept**
Organophosphorus poisoning occurs due to the inhibition of acetylcholinesterase enzyme, 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**
The antidote for organophosphorus poisoning is pralidoxime (2-PAM), which acts by reactivating the inhibited acetylcholinesterase enzyme. This is achieved through a nucleophilic attack on the phosphorylated enzyme, restoring its activity and allowing for the breakdown of acetylcholine. Pralidoxime is most effective when administered early in the course of poisoning.

**Why Each Wrong Option is Incorrect**
**Option A:** Atropine is used as an adjunct therapy in organophosphorus poisoning, but it is not the primary antidote. It helps to counteract the muscarinic effects of excess acetylcholine.
**Option B:** Physostigmine is an acetylcholinesterase inhibitor and would exacerbate the effects of organophosphorus poisoning, rather than treating it.
**Option C:** Sodium bicarbonate is used to treat acidosis, which can be a complication of organophosphorus poisoning, but it is not an antidote.

**Clinical Pearl / High-Yield Fact**
In cases of organophosphorus poisoning, atropine should be administered in conjunction with pralidoxime to effectively manage symptoms and prevent respiratory failure.

**Correct Answer: D. Pralidoxime (2-PAM)**