Anticholinesterases Succinylcholine

The effect of administering different botulinum neurotoxin serotypes at the same time or within several months of each other is unknown. Excessive neuromuscular weakness may be exacerbated by administration of another botulinum toxin prior to the resolution of the effects of a previously administered botulinum toxin. Aminoglycosides Cautiously perform coadministration of botulinum toxin type A and aminoglycosides or other agents interfering with neuromuscular transmission (eg, curare-like nondepolarizing blockers, lincosamides, polymyxins, quinidine, magnesium sulfate, anticholinesterases, succinylcholine chloride) because the effect of the toxin may be potentiated. 

Because anticholinesterase agents also inhibit plasma pseudo-ChE, they will potentiate the effects of succinylcholine by inhibiting its breakdown. This is important, for example, when succinylcholine is to be employed in patients who have previously received cholinesterase inhibitors for the treatment of myasthenia gravis or glaucoma. 

May occur when anticholinesterase agents are not discontinued before use of succinylcholine during elective surgery. 

Contrary to their expected action, anticholinesterases potentiate the blockade produced by succinylcholine when used with non-depolarizing agents. The continued presence of succinylcholine results in repolarization of the end plate. However, despite repolarization, the end plate remains refractory to stimulation as long as succinylcholine is present. With continued exposure, the end plate begins to respond as it does to non-depolarizing agents, a non-sustained response to tetanic stimulus, which is reversed by anticholinesterases. 

Chole- Relating to the biliary system, cholestasis The failure of the normal bile flow to the intestine, causing cholestatic jaundice, cholinergic Nerve fibres that release ACETYLCHOLINE, cholinesterases Enzymes that hydrolyse choline esters, especially ACETYLCHOLINE of which there are two main forms acetylcholinesterase ( true cholinesterase ) is specific for acetylcholine, rapid in this action, and has a discrete distribution being especially located near cholinergic nerve terminals (and in erythrocytes) butyrylcholinesterase ( pseudo cholinesterase) is less selective and is able to hydrolyse some drugs (e.g. SUCCINYLCHOLINE CHLORIDE). Many drugs are known that inhibit the action of these enzymes. See anticholinesterases. chromatin A protein found in the nucleus which stains with basic dyes. It is used in the study of the behaviour of... 

B. Recovery from succinylcholine-induoed neuromuscular blockade may be slightly delayed (5-10 minutes). Similarly, esmolol metabolism may be inhibited by anticholinesterase agents (eg, organophosphates). 

Anticholinesterases oppose the actions of competitive neuromuscular blockers (e.g. tubocurarine) and can therefore be used as an antidote to restore muscular activity following their use. Conversely, anticholinesterases increase and prolong the actions of the depolarising neuromuscular blockers (e.g. suxamethonium (succinylcholine)). Anticholinesterases used to treat Alzheimer s disease may also interact with neuromuscular blockers. 

The depolarising blockers (such as suxamethonium (succinylcholine)) act like acetylcholine to depolarise the motor endplate, but unlike acetylcholine, they are not immediately removed by cholinesterase. The anticholinesterase drugs increase the concentration of acetylcholine at the neuromuscular junction, which enhances and prolongs this type of blockade, and therefore anticholinesterases cannot be used as an antidote for this kind of blocker. Care should be taken if an anticholinesterase has been given to antagonise a competitive neuromuscular block prior to the use of suxamethonium, as the duration of the suxamethonium block may be prolonged. ... 

The manufacturer warns that irinotecan could possibly prolong the neuromuscular blocking effects of suxamethonium (succinylcholine) and antagonise the neuromuscular blockade of competitive (non-depolarising) drugs. This is based on the fact that irinotecan has anticholinesterase activity (see also Neuromuscular blockers + Anticholinesterases , p. 114, for an explanation of this mechanism). 

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