MUSCLE RELAXANT Flashcards
What is muscle relaxant?
Muscle relaxant is the drug used to relax the muscle contraction. Hence, it will interferes with the mechanism of the muscle contraction.
The classification of muscle relaxant and its subtypes.
- Centrally acting
- Peripherally acting
- Depolarising muscle blocker (DMB)
- Non- depolarising muscle blocker (NMB)
State the prototypes for depolarising and non depolarising muscle relaxant.
Depolarising: succinylcholine
Non depolarising: Tubocurarine
Mechanism of action in tubocurarine.
- Tubocurarine is a non depolarising muscle blocker.
- It acts as a competitive antagonist.
- Tubocurarine will bind to the same receptor as the ACh at the same site.
- This causes the receptor unable to open and allow the Na+ ion to pass through
- Hence, depolarising cannot happen.
- However, the binding of tubocurarine is surmountable.
- If the amount of ACh is increased, then it can prevent the binding of tubocurarine.
Mechanism of action of Succinylcholine.
- Succinylcholine is a depolarising muscle blocker.
- When succinylcholine bind to the receptor. the receptor will remain open the channel and allow the Na+ to pass through.
- This is succinylcholine is not regulated by the neuron
- Hence, this will lead to disorganisation of MEP depolarisation and desensitised MEP.
- This causes fasciculation and flaccid paralysis to happen.
What happen during phase 1 and phase 2 NM block?
- During phase 1 NM block, succinylcholine is permanently depolarised at the motor end plate.
- Ca2+ will be transported back into the cytoplasmic reticulum.
- Hence the muscle will be relax.
- However, if succinylcholine is used in a prolonged time, then phase 2 NM block will happen where Nm receptor is desensitised.
- Hence, ACh will bind to the Nm and causes no Ca2+ to be released.
COMPARE TUBOCURARINE AND SUCCINYLCHOLINE.
- Tubocurarine is a competitive antagonism.
- It does not causes motor end plate to depolarise because it is a non-depolarising muscle blocker.
- However, it can cause flaccid paralysis.
- Tubocurarine also have antagonistic on neostigmine.
- It required long time of action
- WHILE, Succinylcholine is an agonist.
- It does effect on motor endplate by disorganised and permanently depolarised at first and when it is a prolonged exposure, Nm receptor desensitisation.
- It will cause fasciculations initially then flaccid paralysis.
- Succinylcholine will cause addictive on neostigmine during the phase 1 block.
- It give a short time of action.
- Both succinylcholine and tubocurarine have action on Nm cholinergic receptor at MEP.
- They can be given through IV administration and both have low Vd.
List therapeutic uses of neuromuscular blockers
- Endotracheal intubation for srugery
2. Adjunct to general anaesthesia during surgery.
List the adverse effects of NMB.
- Histamine release causing flushing, hypotension or bronchial constriction.
- Ganglion blockade which lead to hypotension.
List the adverse effects of DMB.
- Hyperkalaemia
- Myalgia
- Malignant hyperthermia
Desc the causes, symptoms, and treatment of malignant hyperthermia.
Causes:
Mutations in Ryanodine receptor on sarcoplasmic reticulum causing excessive Ca2+ release.
Symptoms:
- Elevated plasma CO2
- Generalised muscle rigidity
- Elevated body tempature
- Acidosis
- Tachycardia + arrhythmias
- Hyperthermia
Treatment:
Dantrolene - it is a ryanodine receptor inhibitor - inhibit excessive Ca2+ release - lowering intracytoplasmic Ca2+ - relaxes muscle - reversal of MH changes
The uses of centrally acting muscle relaxant.
- Baclofen
- Diazepam
- Cyclo-benzaprine
- Baclofen
- Selective GABA-B agonist
- Inhibit action of excitatory NT
- Occur at spinal cord
- Example: Spasticity of spinal cord injury, control muscle spasm d/t acute pain
- Oral
- Half life short
- Excreted unchanged in urine - DIAZEPAM
- Benzodiazepine class
- + allosteric modulator of GABA-A
- Occur at brain
- Example: Perioperative muscle relaxation
- Acute spasms and spastic conditions
- Oral
- Long duration of action
- Liver metabolism and excretion - Cyclobenzapine
- Inhibit serotonin
- Occur at brainstem and spinal cord
- Example: acute spasms and spastic conditions like cerebral palsy
- Oral
- Liver metabolism, excreted mostly in urine
TRUE/FALSE
REGARDING NPB:
A. BLOCK NICOTINIC RECEPTOR AT NMJ
B.METABOLISED BY PLASMA CHOLINESTERASE
C. D- TUBOCURARINE IS AN EXAMPLE
D. PRALIDOXIME IS AN ANTIDOTE
E. CAUSED FLACCID PARALYSIS
NPB = TUBOCURARINE
A. TRUE
B. FALSE (IT IS NON METABOLISED. SUCCINYLCHOLINE (DMB) IS METABOLISED BY THE PLASMA CHOLINESTERASE)
C. TRUE
D. FALSE
(PRALIDOXIME AND ATROPINE IS USED IN ORGANOPHOSPHATE POISONING - ATROPINE IS AN ANTICHOLINERGIC CAUSING THE AMOUNT OF ACETYCHOLINE TO DECREASE. NPB WILL CAUSE MUSCLE RELAXANT -> NOT MUCH ACETYCHOLINE IS BIND TO THE RECEPTOR -> PRALIDOXIME IS SYNERGIST)
E. TRUE (SUCCINYLCHOLINE WILL CAUSED FASCICULATION IN THE 1ST PHASE THEN FLACCID IN THE 2ND PHASE)
