10: Neuromuscular blocking drugs Flashcards
What kind of drug groups can be differentated within the neuromuscular blocking drugs?
What are the drugs for each?
- Non-depolarising (competittive antagonist)
- Or depolarising (agnoist) Suxaemethonium = succinylcholine
What is succinylcholine?
The same drug as suxamethonium
–> action at the Motor end plate AP initiasation
What is the mechanism of action of suxamethonium?
It is a muscular ACh receptor agonist
It causes an
- overstimmulation causing
- extended depolerisation –> fasciculations
- Leading to shut down of receptors –> depolerisation block (phase 1)
What is the mechanims of action of Tubocurarine?
How much of is is needed to get an effect (on molecular level)
Is a competittive nictinic AChR antagoist
–> 70-80% must be blocked to achieve flaccid paralisis
What is flaccid paralsisi?
Paralysis due to reduced muscle tone
What are FASCICULATIONS?
Twitching of muscles due to overstimmulation and hence generation of AP
What is the effect of suxamethonium?
Extended depolerisation on the muscular end plate –> (ACh agonist)
Causes overstimmulation
- fasciculations
Shut down of receptors
- causes flaccid paralysis
No interference with conciousness and no analgesic effect
What is the effect of Tubocuranine?
Flaccid paralysis in following order
- of the extrinsic eye muscles causing double vision
- Small muscles of face, limbs, larynx
- Respiratory muscles
(Also recoverers in reverse order)
No analgesic or nor interference with conciousness
What is the clinical use of Tubocurarine?
What do you always have to provide when administering tubocurarine?
- Relaxation of skeletal muscle during surgical operations–> reduces dose of required anesthetic (reduces risk)
- Permits artificial ventilation
Always assist ventilation!
What is the clinical use of suxamehtonium?
What do always need to provide when administering it?
- To allow endotracheal intubation
- Relaxation for Electroconvulsive therapy (ECT)
- used in very severe deppression
- provide electric impulses over brain
Always assist ventilation
Explain the pharmacokinetic administration and properties of Suxamethonium
- IV administration (highly charged)
- short action (about 5 min)
- Metabolised by pseudo-cholinesterases (cholinesterase is too selevtiv efor ACh) in plasma and liver
Explain the pharmacokinetic properties and route of administration of Tubocurarine
- IV adminstration (highly charged)
- long paralytic action (1-2h)
- does not cross BBB or placenta
- not metabolised
- excretion 70% via kidney, 30% via bile (important in renal/ hepatic disfunction)
How could you treat an overdosation of Tubocurarine?
because it is a competitive antagonist–> effects can be reversed by increased ACh
- Neostigme (Anticholinesterases)
- (In combination with Atropine to not cause overstimmulation of muscarenic receptors)
What are the side effects of Tubocurarine?
It is a muscular nicotinicAChR antagonist–> only limited selectivity for muscular nicotinic R
Occuring side effects are because of Ganglion bloockage and histamine release (because of basic properties of Tubocurarine)
- Hypotension
- Tachycardia (may trigger arrythmias)
- Reflex
- inhibition of vagal ganglia (less PNS to heart)
- Bronchospasm + excessive bonchiosecretion (histamine release)
- Apnoe –> always assist respiration
What are the side effects of suxamehtonium?
- Post-opperative muscle pains
- Bradycardia (direct muscarenic action on heart –> for prevention Atropine is normally given as pre-medication)
-
Hyperkalaemia
- Expecially in patients with soft-tissue injury or burns –> nerve damage–> no innervation to these tissues –> receptor upregulation
- When receptors are stimmulated–> More NA+ inflow + K+ outlow
- Migh trigger arrythmias, cardiac arrest
- increase in Intra-occular pressure
- avoid in eye injuries and glaucoma
