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Kaplan Qbank USMLE



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First of all, can someone please check if my notes are right...

- Nictonic acetylcholine receptors are found at skeletal neurmomuscular junctions and at autonomic ganglia

- Hexamethonium is an antagonist to nicotinic acetylcholine receptors (nAChRs) on autonomic ganglia. It prevents innervation from the autonomic nervous system.

- Antagonists to nAChRs at skeletal neuromuscular junctions come in two types. Both types cause muscle relaxation.

- Type 1: Competitive antagonists (e.g. tubocurarine). These compete with acetylcholine for the nicotinic acetylcholine receptor.

- Type 2: Depolarisation antagonists (e.g. suxamethonium). These bind to nAChRs for a long time preventing muscular contraction.

- Cholinesterase inhibitors. These inhibits the enzyme acetylcholinesterase, which breaks down the acetylcholine on nAChRs.


Questions:

- My notes says that cholinesterase inhibitors causes activation of the parasympathetic nervous system. Why is this? Why doesn't the sympathetic nervous system gets innervated?

- My notes also say that the drugs that inhibit nAChRs act as muscle relaxants, which means that less anasthetic is required. I don't understand this at all. I thought anasthetics put you to sleep - why would muscle relaxants have an effect?

Thanks...







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