characteristics of somatic ns
drugs that block neuromuscular response
uses of neuromuscular blockers
depolarizing agents
succinylcholine apnea
malignant hyperthermia
mutation in SR Ca channel protein => excessive Ca release
=muscle spasm + elevated body temp
lethal
treat with SR Ca channel blockers
competitive (non-depolarising) antagonists of Ach
how do responses of DA/NDA agents differ
DA: phase 1+2
1: prolonged opening of nicotinic r channel = twitches
2. muscle paralysis
NDA: phase 2 only
- duration of opening of channels unaffected
DA mechanism
DA = longer duration of action than ach = higher affinity for receptor + resistance to degradation by AChE
sk remains depolarised with high level of Ca in cytoplasm
pumped back eventually into SR - muscle relaxes but DA remains bound to receptor preventing binding of ach = contractions => paralysis
receptors become desensitized to ach during phase 2 = fail to respond to binding even if not bound to DA
AChE inhibitor with DA vs NDA
DA = block of sk reversed enhanced
NDA = block of sk contraction reversed
noncompetitive ACh antagonists
BOTOX - inhibits ACh release from pre neuron
highly toxic if ingested
myasthenia gravis
autoimmune disease - antibodies against ACh r
EDROPHONIUM - competitive AChE inhibitor = temporarily restores muscle function
PYRIDOSTIGMINE - AChE substrate inhibitor