Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.

Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the carbamylated enzyme, making it difficult for the enzyme to regenerate. Over time, the phosphorylated enzyme can undergo a process called aging, where it loses an alkyl group and becomes less reactive. This aging process prevents enzyme regeneration, resulting in an accumulation of acetylcholine in the synaptic cleft. This exacerbates cholinergic actions and contributes to the toxic effects of irreversible anticholinesterases.

Treating anticholinesterase poisoning involves several measures. Gastric lavage is performed to remove any ingested poison. Maintaining hydration, blood pressure, and airway patency is essential. Diazepam is administered to control convulsions in patients. The muscarinic side effects can be managed by administering intravenous atropine; however, muscle paralysis caused by nicotinic actions cannot be reversed by atropine. In cases of organophosphate poisoning, cholinesterase reactivators such as pralidoxime and obidoxime are used to restore neuromuscular transmission. However, these reactivators are only effective if administered before the aging process begins.