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Questions and Answers
What is the correct sequence of muscle paralysis caused by neuromuscular blockers?
What is the correct sequence of muscle paralysis caused by neuromuscular blockers?
What is the primary effect of competitive neuromuscular blockers on the central nervous system?
What is the primary effect of competitive neuromuscular blockers on the central nervous system?
Which of the following is a clinical use of neuromuscular blockers during surgery?
Which of the following is a clinical use of neuromuscular blockers during surgery?
What is the duration of action of succinylcholine?
What is the duration of action of succinylcholine?
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Which of the following can potentiate the effects of neuromuscular blockers?
Which of the following can potentiate the effects of neuromuscular blockers?
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What is the primary mechanism by which competitive neuromuscular blockers function at the neuromuscular junction?
What is the primary mechanism by which competitive neuromuscular blockers function at the neuromuscular junction?
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How does the chemical structure of curare contribute to its usage in medicine and pharmacology?
How does the chemical structure of curare contribute to its usage in medicine and pharmacology?
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What is the required change in the endplate potential (EPP) value to ensure muscle action potential does not occur during neuromuscular blockade?
What is the required change in the endplate potential (EPP) value to ensure muscle action potential does not occur during neuromuscular blockade?
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What initial physiological effect do depolarizing neuromuscular blockers (NMBs) have on muscle tissue?
What initial physiological effect do depolarizing neuromuscular blockers (NMBs) have on muscle tissue?
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What differentiates the lifetime of acetylcholine (ACh) in the synapse from the duration of channel opening?
What differentiates the lifetime of acetylcholine (ACh) in the synapse from the duration of channel opening?
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Study Notes
Neuromuscular Blockers and Curare
- Curare was historically used as an arrow poison to immobilize animals and in early medicinal treatments for tetanus and spasticity.
- Studying curare's chemical structure led to the synthesis of similar compounds with varied properties.
- Neuromuscular blockers are classified into competitive and depolarizing blockers.
- Competitive blockers occupy nicotinic acetylcholine receptors (nAChRs), preventing acetylcholine (ACh) activation.
- Depolarizing blockers initially cause depolarization, leading to fasciculation, followed by blockade and paralysis.
- Acetylcholinesterase (AChE) inhibitors can enhance neuromuscular blocker effects by preventing ACh breakdown.
- Neuromuscular blockade causes muscle paralysis, starting with small muscles (eyes, jaw, larynx) and progressing to larger muscles and finally the intercostals, culminating in apnea.
- Succinylcholine has a short duration of action (approximately 5 minutes).
- Competitive neuromuscular blockers typically have no direct effect on the central nervous system (CNS).
- Older agents like D-tubocurarine and pancuronium can partially block autonomic ganglia, potentially leading to hypotension and tachycardia.
- Neuromuscular blockers are surgically used for muscle relaxation, allowing for easier surgical procedures and intubation.
- Neuromuscular blockade depth is assessed through techniques like ulnar nerve stimulation and thumb muscle contraction.
- Critically ill patients may benefit from neuromuscular blockers to facilitate intubation, control intracranial pressure, and reduce oxygen consumption.
- Drug interactions can occur, where some anesthetic agents can reduce the dose of competitive blockers required, aminoglycosides can potentiate their effect and calcium channel blockers may also enhance the effects of neuromuscular blockers.
- Adverse effects of neuromuscular blockers include apnea, cardiovascular collapse, respiratory depression, and potentially increased hypokalemia with succinylcholine.
Malignant Hyperthermia
- Malignant hyperthermia is a reaction to depolarizing neuromuscular blockers and inhalational anesthetics.
- Symptoms include muscle contracture, rigidity, heat production, metabolic acidosis, and tachycardia.
- Treatment involves cooling, managing acidosis, and using dantrolene.
Nicotine
- Nicotine initially stimulates ganglionic receptors (causing early EPSPs) but high concentrations cause persistent depolarization, and eventual blockade.
- Low doses of nicotine can stimulate the CNS, provide mild analgesia, and increase respiratory rate.
- Higher doses can cause tremors, seizures, and respiratory failure.
Ganglionic Blockers
- Ganglionic blockers are classified as depolarizing and competitive.
- Adverse effects can include dry mouth, postural hypotension, constipation, blurred vision, and urinary retention.
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Description
Explore the fascinating world of neuromuscular blockers, including the history and chemistry of curare, and their roles in medicine. Understand how competitive and depolarizing blockers function and their effects on muscle paralysis. This quiz covers essential concepts and mechanisms related to these critical pharmacological agents.
