Skeletal Muscle Relaxants and Neuromuscular Junction Physiology

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10 Questions

Where does acetylcholine bind after diffusing across the synaptic cleft?

Nicotinic cholinergic receptor

What is the main function of skeletal muscle relaxants?

Induce muscle relaxation

What enzyme destroys 80% of the released acetylcholine at the neuromuscular junction?

Neuronal acetylcholinesterase

What causes the release of the neurotransmitter acetylcholine into the synaptic cleft?

Ca2+ uptake into the terminal

What is the primary role of intracellular Ca+ in muscle contraction?

Binding to actin and myosin

How do depolarizing muscle relaxants like succinylcholine differ from Ach in terms of metabolism?

They are not metabolized by acetylcholinesterase

What is the mechanism of action of depolarizing muscle relaxants during Phase I Block?

Causing prolonged depolarization of muscle end-plates

What leads to Phase II Block in the action of depolarizing muscle relaxants?

Receptor desensitization and conformational changes

How is phase II block, produced by prolonged administration of succinylcholine, treated?

Using neostigmine, an anticholinesterase

Why should neuromuscular function be constantly monitored during the administration of succinylcholine?

To prevent over-dosing and phase II block

Study Notes

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.

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