Cholinesterase Health Dictionary

An acetic-acid ester of the organic base choline, acetylcholine is one of the substances which mediates the transmission of nerve impulses from one nerve to another, or from a nerve to the organ it acts on, such as muscles. It acts on both muscarinic receptors (blocked by ATROPINE and responsible for ganglionic and parasympathetic transmission and also for sympathetic innervation of sweat glands – see under AUTONOMIC NERVOUS SYSTEM) and nicotinic receptors (responsible for the transmission of nerve impulses to muscles and blocked by curare, thus causing paralysis). Acetylcholine is rapidly destroyed by cholinesterase, an ENZYME present in the blood. ANTICHOLINERGIC drugs such as PHYSOSTIGMINE prolong the action of acetylcholine.... acetylcholine

Any compound that inhibits the activity of CHOLINESTERASE, thus permitting ACETYLCHOLINE to continue its function of transmitting nerve impulses. Drugs with anticholinesterase properties include distigmine, NEOSTIGMINE and PHYSOSTIGMINE.... anticholinesterase

A serious disorder in which the chief symptoms are muscular weakness and a special tendency for fatigue to come on rapidly when e?orts are made. The prevalence is around 1 in 30,000. Two-thirds of the patients are women, in whom it develops in early adult life. In men it tends to develop later in life.

It is a classical example of an autoimmune disease (see AUTOIMMUNITY). The body develops ANTIBODIES which interfere with the working of the nerve endings in muscle that are acted on by ACETYLCHOLINE. It is acetylcholine that transmits the nerve impulses to muscles: if this transmission cannot be e?ected, as in myasthenia gravis, then the muscles are unable to contract. Not only the voluntary muscles, but those connected with the acts of swallowing, breathing, and the like, become progressively weaker. Rest and avoidance of undue exertion are necessary, and regular doses of neostigmine bromide, or pyridostigmine, at intervals enable the muscles to be used and in some cases have a curative e?ect. These drugs act by inhibiting the action of cholinesterase – an ENZYME produced in the body which destroys any excess of acetylcholine. In this way they increase the amount of available acetylcholine which compensates for the deleterious e?ect of antibodies on the nerve endings.

The THYMUS GLAND plays the major part in the cause of myasthenia gravis, possibly by being the source of the original acetylcholine receptors to which the antibodies are being formed. Thymectomy (removal of the thymus) is often used in the management of patients with myasthenia gravis. The incidence of remission following thymectomy increases with the number of years after the operation. Complete remission or substantial improvement can be expected in 80 per cent of patients.

The other important aspect in the management of patients with myasthenia gravis is IMMUNOSUPPRESSION. Drugs are now available that suppress antibody production and so reduce the concentration of antibodies to the acetylcholine receptor. The problem is that they not only suppress abnormal antibody production, but also suppress normal antibody production. The main groups of immunosuppressive drugs used in myasthenia gravis are the CORTICOSTEROIDS and AZATHIOPRINE. Improvement following steroids may take several weeks and an initial deterioration is often found during the ?rst week or ten days of treatment. Azathioprine is also e?ective in producing clinical improvement and reducing the antibodies to acetylcholine receptors. These effects occur more slowly than with steroids, and the mean time for an azathioprine remission is nine months.

The Myasthenia Gravis Association, which provides advice and help to sufferers, was created and is supported by myasthenics, their families and friends.... myasthenia gravis

In clinical practice, the transmission of impulses at the NEUROMUSCULAR JUNCTION may be blocked to paralyse temporarily a patient for a surgical procedure, or to assist treatment on the intensive care unit. There are two main types of drug, both of which competitively block the ACETYLCHOLINE receptors on the motor end plates. (1) Depolarising neuromuscular blocking agents: these act by ?rst producing stimulation at the receptor, and then by blocking it. There are characteristic muscle fasciculations before the rapid onset of paralysis which is of short duration (less than ?ve minutes with the commonly used drug, suxamethonium). The drug is removed from the receptor by the enzyme, CHOLINESTERASE.

(2) Non-depolarising neuromuscular blocking agents: these drugs occupy the receptor and prevent acetylcholine from becoming attached to it. However, in su?ciently high concentrations, acetylcholine will compete with the drug and dislodge it from the receptor; the e?ect of these drugs is reversed by giving an anticholinesterase, which allows the amount of acetylcholine at the neuromuscular junction to build up. These drugs have varying durations of action, but all are slower in onset and of longer duration than the depolarisers.... neuromuscular blockade

n. see cholinesterase.... acetylcholinesterase

n. an organic phosphorus compound, used as a pesticide, that causes poisoning when inhaled, ingested, or absorbed through the skin. Like several other organic phosphorus compounds, it attacks the enzyme *cholinesterase and causes excessive stimulation of the parasympathetic nervous system. The symptoms are headache, sweating, salivation, lacrimation, vomiting, diarrhoea, and muscular spasms. Treatment is by administration of *atropine.... parathion

n. an enzyme found in the blood and other tissues that – like *cholinesterase – breaks down acetylcholine, but much more slowly. Not being localized at nerve endings, it plays little part in the normal breakdown of acetylcholine in synapses and at neuromuscular junctions.... pseudocholinesterase

Organophosphorus insecticides act by inhibiting the action of cholinesterase (see ACETYLCHOLINE). For this reason they are also toxic to humans and must therefore be handled with great care. The most widely used are PARATHION and MALATHION. Organophosphorus has also been used to make nerve gases (see BIOLOGICAL WARFARE).

Treatment After contamination with insecticides, decontaminate (remove clothes, wash skin). Those treating should wear gloves, mask, apron and goggles. For symptoms give 2 mg of ATROPINE IV every 30 minutes until full atropinisation (dry mouth, pulse >70). Up to three days’ treatment may be needed. Severe poisoning may require pralidoxine mysalate: available from designated centres, this drug should be given intravenously within 24 hours of exposure.... organophosphorus

any one of a class of drugs that block the action of acetylcholinesterase (see cholinesterase), an enzyme that quickly breaks down the neurotransmitter acetylcholine. This neurotransmitter is central to the functional interconnection between nerve cells in the outer layer (cortex) of the brain; the early impairment of cognitive function found in Alzheimer’s disease is associated with a reduction in acetylcholine levels. By inhibiting acetylcholine breakdown, acetylcholinesterase inhibitors have been found helpful in slowing down the rate of cognitive decline in mild to moderate dementia; they do not halt the progress of the disease. The group includes donepezil, galantamine, and rivastigmine... acetylcholinesterase inhibitor