Organophosphorus Poisoning and Atropine - Article Example

This essay declares that The muscarinic effects are bradycardia, hypotension, rhinorrhea, bronchorrhea, bronchospasm, cough, severe respiratory distress, hypersalivation, nausea and vomiting, abdominal pain, diarrhea, fecal incontinence, blurred vision, miosis, increased lacrimation, and diaphoresis. The nicotinic effects are muscle fasciculations, cramping, weakness, and diaphragmatic failure. The autonomic nicotinic effects are hypertension, tachycardia, mydriasis, and pallor. The CNS effects include anxiety, emotional lability, restlessness, confusion, ataxia, tremors, seizures, and coma.

This paper stresses that organophosphates mainly inhibit carboxyl ester hydrolases, especially acetylcholinesterase (AChE), which is an enzyme that degrades acetylcholine (ACh) into choline and acetic acid. This inactivation of AChE occurs by the phosphorylation of the serine hydroxyl group located at the active site of AChE. The inactivation of AChE results in the accumulation of acetylcholine and subsequent overstimulation of the muscarinic and nicotinic receptors. In animal studies, a few potential treatments that have been identified, which include organophosphate hydrolases, reversible anticholinesterases like carbamate pyridostigmine, which reduce re-inhibition of acetyl cholinesterase; and glutamate antagonists and agonists for adenosine and -2 adrenergic receptors, which limit damage to the CNS