Neuromuscular blocking drugs Flashcards
what branch of the NS is neuromuscular transmission dealing with?
- SOMATIC
describe NM transmission
- production of ACh using CAT
- AP propagation
- Ca2+ influx
- ACh exocytosis
- ACh binds to receptors and Na+ influx
- ACh esterase breaks down ACh
- recycling by uptake
name the 3 most important NM-blocking drugs
competitive - tubocurarine, atracurium
depolarising - suxamethonium
what makes up the nicotinic acetylcholine receptor?
5 subunits: alpha 1, alpha 2, beta, delta, gamma
ACh only binds to alpha receptor
where is the density of these receptors high?
motor end plate
give examples of spasmolytics and their MoA
e. g. Diazepam, Baclofen
- target central processes within nerve cell
- spasmolytics relieve spasm of muscles
what is the MoA of local anaesthetics?
inhibit influx of Na and so reduce propagation of AP along nerve
what does Hemicolinium do?
- Ca2+ entry blockers
- neurotoxins
- inhibit re-uptake of choline
what are non-depolarising NM-blocking drugs?
competitive antagonists
e.g. Tubocurarine, Atracurium
what are depolarising NM- blocking drugs?
- agonists
- cause depolarising block
- Suxamethonium
- good at stimulating due to its VERY similar structure to ACh
what is important to remember with these drugs?
- do not affect consciousness or pain sensation
- respiration must always be assisted
what is the MoA of suxamethonium?
- causes a long depolarising block (takes a long time to break down in synaptic cleft)
- causes fasciculations –> flaccid paralysis
what are the pharmacokinetics of suxamethonium?
- IV admin
- duration of paralysis is short (around 5 mins)
- metabolised by a pseudo-cholinesterase in liver and plasma
what are the uses of suxamethonium?
- intubation (relaxes vocal chords)
- muscle relaxant for ECT
what are the unwanted effects of suxamethonium?
- post op muscle pains
- bradycardia
- hyperkalaemia
- inc. in IOP
what is the MoA of tubocurarine?
- competitive nAChR antagonist
- block of 70-80% needed to cause effect of skeletal muscle relaxation
what are the effects of tubocurarine?
- flaccid paralysis
- flaccid paralysis affects muscles in specific order
what is the order in which muscles are affected?
- extrinsic eye muscles
- small muscles of face, limbs, pharynx
- resp muscles
- recovery of this effect works backward
what are the uses of non-depolarising NM-blockers?
- relaxation of skeletal muscles during surgical operations
- permits artifical ventilation
how are these effects reversed?
using anticholinesterases
what are the pharmacokinetics of tubocurarine?
- administered via IV
- does not cross BBB or placenta
- paralysis lasts long time (60 mins)
- not metabolised, excreted 70% urine, 30% bile
what are the unwanted effects of tubocurarine?
causes ganglion block and histamine release
- hypotension (ganglion blockade lowers TPR and histamine release = vasodilation)
- tachycardia (reflex tachycardia)
- bronchospam, excessive secretions (histamine release causing bronchoconstriction)
- apnoea
