**Core Concept**
Acute organophosphorus poisoning occurs due to inhibition of acetylcholinesterase, leading to an accumulation of acetylcholine in the synaptic cleft. This results in overstimulation of muscarinic and nicotinic receptors, causing a range of systemic effects.

**Why the Correct Answer is Right**
The correct answer is related to the inhibition of acetylcholinesterase, which leads to an accumulation of acetylcholine. This causes overstimulation of muscarinic receptors, resulting in increased salivation, sweating, lacrimation, and bronchial secretions. The inhibition of acetylcholinesterase also affects the autonomic nervous system, leading to bradycardia, hypotension, and respiratory failure.

**Why Each Wrong Option is Incorrect**
**Option A:** This option is not directly related to the acute effects of organophosphorus poisoning. While it may be a consequence of prolonged exposure, it is not the most immediate or characteristic effect.

**Option B:** This option is incorrect because the primary effect of organophosphorus poisoning is on the muscarinic receptors, not the nicotinic receptors. While nicotinic receptors may be affected, the primary manifestation is muscarinic in nature.

**Option C:** This option is incorrect because the primary effect of organophosphorus poisoning is on the autonomic nervous system, leading to bradycardia and hypotension, rather than tachycardia and hypertension.

**Clinical Pearl / High-Yield Fact**
Atropine is the antidote of choice for organophosphorus poisoning because it competitively inhibits the muscarinic receptors, counteracting the effects of excessive acetylcholine.

**Correct Answer:** D.