**Core Concept**
Acute organophosphorous poisoning affects the cholinergic system by inhibiting acetylcholinesterase, the enzyme responsible for breaking down acetylcholine. This leads to an accumulation of acetylcholine in the synaptic cleft, causing overstimulation of muscarinic and nicotinic receptors.

**Why the Correct Answer is Right**
The accumulation of acetylcholine results in overstimulation of muscarinic receptors, leading to excessive parasympathetic activity. This manifests as increased salivation, sweating, lacrimation, urination, and defecation. The overstimulation of nicotinic receptors at the neuromuscular junction causes muscle fasciculations, muscle weakness, and eventually, respiratory failure.

**Why Each Wrong Option is Incorrect**
* **Option A:** This option is not provided.
* **Option B:** This option is not provided.
* **Option C:** This option is not provided.
* **Option D:** This option is not provided.

**Clinical Pearl / High-Yield Fact**
In acute organophosphorous poisoning, atropine is used to counteract the muscarinic effects by competing with acetylcholine for receptor binding. Pralidoxime is used to re-activate acetylcholinesterase.

**Correct Answer:** None provided