AcetylcholinesteraseHemmer

Acetylcholinesterase inhibitors, or Acetylcholinesterase-Hemmer, are drugs that block the enzyme acetylcholinesterase, which normally breaks down the neurotransmitter acetylcholine at cholinergic synapses. By inhibiting this enzyme, they increase acetylcholine levels at both muscarinic and nicotinic receptors, enhancing cholinergic signaling in the central and peripheral nervous systems.

Most therapeutic uses rely on reversible inhibitors with short to intermediate duration, such as edrophonium (short-acting), neostigmine and pyridostigmine (intermediate-acting), and physostigmine (central-acting). Irreversible inhibitors, including certain organophosphates, form covalent bonds with acetylcholinesterase and cause prolonged inhibition; these are associated with toxicity and require different management.

Clinical uses include the treatment of myasthenia gravis (neostigmine, pyridostigmine), reversal of nondepolarizing neuromuscular blockade after anesthesia (neostigmine), and symptomatic treatment of Alzheimer’s disease in the form of donepezil, rivastigmine, and galantamine. Topical acetylcholinesterase inhibitors such as physostigmine have been used in glaucoma, though they are less common today. Historically, echothiophate and other inhibitors were employed for intraocular pressure reduction; their use has declined with safer alternatives.

Adverse effects reflect excess cholinergic stimulation and include sweating, salivation, lacrimation, miosis, bradycardia, diarrhea, bronchoconstriction, muscle fasciculations, and weakness. Overdose can lead to a cholinergic crisis. Management of organophosphate poisoning involves atropine to counter muscarinic effects and pralidoxime to reactivate acetylcholinesterase if administered promptly. Drug interactions with other cholinergic or anticholinergic agents can modify effects.