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15 Cards in this Set
- Front
- Back
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Name some non-depolarizing neuromuscular blockers |
Atracurium, cisatracurium, mivacurium, pancuronium, rocuronium, tubocurarine, vecuronium |
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Name some depolarizing neuromuscular blockers
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Succinylcholine/suxamethonium |
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Name the drug which can reverse the effect of vecuronium and rocuronium. |
Sugammadex |
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What are the indications for the use of botulinum toxin? |
- Cosmetic procedures - Blepharospasm - Strabismus - Spasticity - Hyperhydrosis - Overactive bladder |
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What is the prototype of non-depolarizing neuromuscular blockers? |
Tubocurarine |
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What are the indications of neuromuscular blockers? |
- Surgical procedures - Electroconvulsive therapy - Intubation - Joint reposition - To turn off spontaneous ventilation during artificial ventilation |
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What is the mechanism of action of non-depolarizing neuromuscular blockers?
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Non-depolarizing neuromuscular blockers bind to postsynaptic nicotinic acetylcholine receptors, preventing acetylcholine from binding to them. This prevents the depolarization of muscle.
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How can we reverse the effect of non-depolarizing neuromuscular blockers?
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By giving reversible acetylcholinesterase inhibitors like neostigmine. If vecuronium and rocuronium were used, sugammadex can reverse their effect. |
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What are the side effects of non-depolarizing neuromuscular blockers? |
- Ganglion-blocking -> hypotension, tachycardia Atracurium and mivacurium are highly basic drugs, which stimulates histamine release. This causes side-effects like bronchospasm, itching and hypotension |
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Name some drugs which non-depolarizing neuromuscular blockers interact with |
General anaesthetics, aminoglycosides, tetracyclines |
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In which disease is the effect of non-depolarizing neuromuscular blockers increased? |
Myasthenia gravis |
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Describe the special mechanism by which atracurium is eliminated. |
Atracurium is broken down by spontaneous non-enzymatic hydrolysis in plasma, called Hofmann elimination. |
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Describe the mechanism by which most non-depolarizing neuromuscular blockers are metabolized.
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By enzymatic hydrolysis by butyrylcholinesterase in plasma. |
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What is the mechanism of action of succinylcholine? |
Succinylcholine is a nicotinic receptor agonist which is not deactivated by acetylcholinesterase. When binding to the postsynaptic nicotinic receptors succinylcholine causes depolarization, but it doesn't leave the receptor so the muscles stay depolarized.
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What is the treatment of malignant hyperthermia? |
Dantrolene, bicarbonate and cooling. |
