RNFA MASTER EXAM 2023 WITH 100% CORRECT ANSWERS

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