Skeletal Muscle Relaxants and Neuromuscular Junction Physiology

Neuromuscular Junction

• Acetylcholine binds to nicotinic receptors on the muscle endplate after diffusing across the synaptic cleft.

Skeletal Muscle Relaxants

• The main function of skeletal muscle relaxants is to reduce muscle tone and facilitate surgical procedures.

Acetylcholine Metabolism

• The enzyme acetylcholinesterase destroys 80% of the released acetylcholine at the neuromuscular junction.

Neurotransmitter Release

• The release of acetylcholine into the synaptic cleft is caused by an action potential reaching the nerve terminal.

Muscle Contraction

• The primary role of intracellular Ca+ is to initiate muscle contraction by binding to troponin and tropomyosin.

Depolarizing Muscle Relaxants

• Depolarizing muscle relaxants like succinylcholine differ from Ach in terms of metabolism, as succinylcholine is not metabolized by acetylcholinesterase.

Mechanism of Action

• The mechanism of action of depolarizing muscle relaxants during Phase I Block involves persistent depolarization of the muscle endplate, making it unresponsive to further stimulation.

Phase II Block

• Phase II Block is caused by prolonged administration of succinylcholine, leading to desensitization of the nicotinic receptors.

Treatment of Phase II Block

• Phase II Block can be treated by administering anticholinesterases to increase the availability of acetylcholine.

Neuromuscular Function Monitoring

• Neuromuscular function should be constantly monitored during the administration of succinylcholine to prevent complications.

This quiz covers the classification of skeletal muscle relaxants, including peripherally acting and centrally acting ones like Baclofen and Diazepam. It also delves into the physiology of the neuromuscular junction, discussing the release of Acetylcholine and the mechanisms involved when an impulse reaches the terminal of a motor neuron.