A genetic disease called myasthenia gravis causes the body to produce antibodies that block acetylcholine receptors on the motor end plate preventing acetylcholine from binding. Patients with this disease exhibit varying degrees of muscle weakness and flaccid paralysis in the affected muscles. We use a drug that blocks the acetylcholinesterase. Why do we do that?
In myasthenia gravis antibodies are formed against the receptors for acetylcholine in the motor end plate. So the acetylcholine activity is blocked. We know that acetylcholine esterase will degrade the acetylcholine releases to the synaptic cleft. So if we use a drug that blocks acetylcholine esterase the degradation of acetylcholine is inhibited. So the action big acetylcholine will increase. As only few receptors are available the prolonged action of acetylcholine will help to withstand the muscle weakness caused by myasthenia gravis
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