TEMA 24. BLOQUEANTES NEUROMUSCULARES

Prescription on fermera.com Topic 24 Neuromuscular Blockers

This section discusses neuromuscular blockers, their mechanism of action, classification, and clinical implications.

Mechanism of Action

• Neuromuscular blockers act at the motor endplate by interfering with acetylcholine.

• Interaction between acetylcholine and nicotinic receptors generates a motor endplate potential leading to muscle contraction.

Classification

• Divided into non-depolarizing blockers like tubocurarine and depolarizing blockers like succinylcholine.

• Non-depolarizing blockers competitively antagonize acetylcholine, while depolarizing ones act as agonists initially.

Clinical Implications

• Non-depolarizing blockers can be reversed by neostigmine at normal doses but worsen at high doses.

• Depolarizing blockers like succinylcholine can lead to muscle paralysis and have rapid onset but prolonged effects.

Neuromuscular Blockers - Clinical Considerations

This section covers the administration, metabolism, adverse effects, interactions, and contraindications of neuromuscular blockers.

Administration and Metabolism

• Administered intravenously due to poor bioavailability.

• Metabolism varies among different drugs affecting onset and duration of action.

Adverse Effects and Interactions

• Common adverse effects include ganglionic blockade-related symptoms.

• Interactions with anesthetics or other drugs may potentiate or diminish the blocking effect.

Depolarizing Neuromuscular Blockers - Succinylcholine

Succinylcholine's mechanism of action, administration, metabolism, effects, contraindications are discussed in this section.

Succinylcholine Details

• Acts as an agonist initially causing muscle contractions before inducing paralysis.

• Metabolized rapidly through hydrolysis by cholinesterases affecting its duration of action.

Clinical Considerations

• Preoperative assessment for cholinesterase levels is crucial for surgical procedures involving succinylcholine.