RNFA MASTER Exam With Correct Answers.

RNFA MASTER Exam With Correct u u u u




Answers
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Neuromuscular blockers - Correct Answer - Tubocurarine Atracurium Cisatracurium Mivacurium
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Rocuronium Pancuronium Vecuronium Succinylcholine
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AchE inhibitors - Correct Answer - Neostigmine Edrophonium
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Muscarinic Antagonists - Correct Answer - Glycopyrrolate
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Spasmolytics - Correct Answer - Dantrolene Diazepam Baclofen Tizanidine Gabapentin Progabide
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Glycine Idrocilamide Riluzole Dantrolene Botulinum toxin Cyclobenzaprine
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Neuromuscular blockers. - Correct Answer - Used during surgical procedures and in intensive care
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units to cause paralysis.
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NONDEPOLARIZING BLOCKERS - Correct Answer - • They are competitive antagonists. In small clinical
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doses they act predominantly at the nicotinic receptor site by competing with acetylcholine. Their
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action can be overcome by increasing the concentration of acetylcholine in the synaptic cleft; this can
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be achieved, for example, by administration of acetylcholinesterase inhibitors such as neostigmine or
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edrophonium. Anaesthesiologists use this strategy to shorten the duration of the neuromuscular
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blockade.
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• In larger doses, nondepolarizing blockers also enter the pore of the ion channel to cause a more
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intense motor blockade. This further weakens neuromuscular transmission and diminishes the ability
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of acetylcholinesterase inhibitors to antagonize the action of nondepolarizing blockers.
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,• Nondepolarizing blockers may also block prejunctional sodium channels. As a result, they reduce the
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release of acetylcholine at the nerve ending.
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• During anesthesia, the IV administration of a nondepolarizing blocker first causes motor weakness;
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ultimately, skeletal muscles become totally flaccid and inexcitable to stimulation. Larger muscles (e.g.
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those of the trunk) are more resistant to block and recover more rapidly than smaller ones (e.g.
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muscles of the hand).
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DEPOLARIZING BLOCKERS - Correct Answer - Succinylcholine is the only depolarizing neuromuscular
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blocker used clinically in the USA. succinylcholine remains popular because it is the only ultrarapid
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onset/ultrashort duration neuromuscular blocker available.
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• Succinylcholine binds to the nicotinic receptor and acts like acetylcholine to cause depolarization of
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the end plate. This in turn spreads and depolarizes adjacent membranes, causing transient
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fasciculations, especially in chest and abdomen, though general anesthesia and prior administration of
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a small dose of a nondepolarizing muscle relaxant tends to attenuate them. Succinylcholine is not
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metabolized effectively at the synapse, therefore the membrane remains depolarized and
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unresponsive to additional impulses. A flaccid paralysis results. This is called Phase I block, or
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depolarization block. Phase I block is augmented, not reversed, by acetylcholinesterase inhibitors.
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• The onset of neuromuscular blockade is very rapid, usually within 1 minute. Because of its rapid
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hydrolysis by plasma butyrylcholinesterase (pseudocholinesterase), duration of neuromuscular block is
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5-10 minutes.
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• With a single large dose, repeated doses, or prolonged continued infusion of succinylcholine (30-60
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minutes) the membrane repolarizes; despite this repolarization, the membrane can't be depolarized
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again because it is desensitized.
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The channels behave as if they are in a prolonged closed state. This is called phase II block or
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desensitization block. Phase II block may be reversed by acetylcholinesterase inhibitors.
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PHARMACOKINETICS OF NEUROMUSCULAR BLOCKERS - Correct Answer - • All neuromuscular blocking u u u u u uu u u u u u


agents contain one or two quaternary ammonium
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groups, which makes them highly polar and very poorly soluble in lipid.
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,• Neuromuscular blockers are inactive if given by mouth. They are always given IV or IM. They
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penetrate membranes very poorly and do not enter cells or cross the blood-brain barrier.
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NON-DEPOLARIZING BLOCKERS - Correct Answer - Highly ionized. They don't cross membranes well
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and have limited volume of distribution of 80-140 mL/Kg -not much larger than blood volume.
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They have durations of action that range from 20 to 90 minutes, which can be extended by
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supplemental dosing.
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Non-depolarizing blockers can be classified into: long-, intermediate-, and short-acting.
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SHORT-ACTING

Mivacurium



INTERMEDIATE-ACTING



Atracurium

Rocuronium

Cisatracurium

Vecuronium




LONG-ACTING

Tubocurarine

Pancuronium



METABOLISM - Correct Answer - The duration of neuromuscular blockade produced by
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nondepolarizing relaxants is strongly correlated with the elimination half-life.
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, Drugs that are excreted by the kidney typically have longer half-lives, leading to longer durations of
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action.
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Drugs eliminated by the liver tend to have shorter half-lives and durations of action.
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Atracurium is inactivated by hydrolysis by non-specific plasma esterases and by a spontaneous reaction
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(Hoffman elimination). Duration of neuromuscular block produced by atracurium is not altered by the
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absence of renal function.
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One of atracurium metabolites is laudanosine. Laudanosine may cause transient hypotension and, in
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higher doses, seizures.
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Cisatracurium, a stereoisomer of atracurium, undergoes Hoffman elimination to form laudanosine.
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Because cisatracurium is more potent than atracurium and lower doses are required, laudanosine
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concentrations following cisatracurium administration are lower. Cisatracurium also causes less
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histamine release. Therefore, cisatracurium has largely replaced atracurium in clinical practice.
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Mivacurium has short duration of action. Hydrolysis by butyrylcholinesterase is the primary mechanism
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for inactivation of mivacurium. Not dependent on liver or kidney.
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Rocuronium has the most rapid onset among nondepolarizing blockers. Can be used as alternative to
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succinylcholine for rapid sequence intubation.
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DEPOLARIZING BLOCKERS - Correct Answer - The extremely short duration of action of succinylcholine
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(5-10 minutes) is due to its
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rapid hydrolysis by plasma (and hepatic) butyrylcholinesterase.
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Neuromuscular blockade by succinylcholine (and mivacurium) may be prolonged in patients with an
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abnormal variant of butyrylcholinesterase. Prolonged paralysis from succinylcholine caused by
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abnormal butyrylcholinesterase should be treated with continued mechanical ventilation until muscle
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function returns to normal.
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Because of the rarity of these variants, butyrylcholinesterase testing is not routine clinical procedure.
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ADVERSE EFFECTS - Correct Answer - ...
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