Muscle Relaxants Flashcards
Acetylcholine
Neurotransmitter at NMJ
Formation
________ + ________ ( enyzme
_________________ ) → Ach
Destruction
Action of ________ present in ________
Choline + acetyl co A
choline acetyl transferase
acetyl cholinesterase
synaptic cleft
Neuromuscular Transmission :
Depolarisation of motor nerve→ ____ propagated to _______→↑permeability to ________ & ________ of vesicles→Ach release
Ach cross synaptic cleft & bind to receptors →Dep. of _________________ & generation of AP →_____ channels open→_____ release→ _______ + _________ coupling → CONTRACTION
AP; NMJ; calcium; exocytosis
muscle end plate; Na; Ca
actin + myosin
Factors which influence NMT
Prevent Ach SYNTHESIS
_______________
Prevent Ach RELEASE
_______________, _______________, ____________, _______________
Deplete Ach STORES
______________
Hemicholinium
↓calcium, ↑magnesium Botulism Aminoglycosides
Tetanus
Factors which influence NMT
Block Ach RECEPTORS
_______,________________
Block action of acetyl- cholinesterase
_______________,______________
Muscle relaxants Myasthenia gravis
Anticholinesterases
Organophosphorus
What are Muscle Relaxants?
Drugs used to impair _______________ and used to provide skeletal muscle _________ during anaesthesia or critical care.
neuromuscular transmission
relaxation
Indications for Muscle Relaxants :
To Facilitate :
_________
__________
____________
Tracheal intubation
Ventilation
Surgical access
Classification
DEPOLARISING MR ( Competitive or Non-Competitive?))
Resemble Ach →bind to receptors → _____________ (_____________)
Not metabolised by _____________.
Concentration in synaptic cleft remains high.
Reversal by _____________ from ________ & ___________ by _____________ Phase ___ block
No ___________
No _____________
Non-Competitive
initial depolarisation ; fasiculations
acetylcholinesterase ; diffusion ; NMJ
Hydrolysis ; pseudocholinesterase Phase I
fade; post tetanic potentiation
Depolarizing Block
Because _______ resembles Ach it stimulates the receptors first causing _________
•It then stays fixed on receptors as it is not metabolised by ____________.
•It therefore prevents Ach from reacting with the receptors and allowing NMT.
suxamethonium; fasiculations
acetylcholinesterase
NON DEPOLARISING MR(Competitive or Non-Competitive?)
Bind to Ach receptors (with or without?) initial depolarisation; (fasciculation or no fasiculations?) .
Phase ___ block
Exhibit ______
Exhibit _______________
Competitive ; without
II; fade; post tetanic potentiation
Non-Depolarising MR
Reversal- redistribution, metabolism, excretion.
_______________ - inhibits ______________→ ↑ Ach.
Potentiated by __________,__________ agents, (alkalosis or acidosis?) , ↓ K, ↑ Mg, ↓ Ca.
Anti cholinesterase; acetyl cholisterase
aminoglycosides ; volatile
Acidosis
Monitoring the NMJ Peripheral nerve stimulator
Assess _______ , _______, _______ or _______ response to electrical stimulus.
Use _______, _______ or _______ nerve
visual, tactile, mechanical or EMG
ulnar, facial or tibial nerve
Monitoring the
Patterns of stimulation.
Single twitch (_____ – ______ Hz).
Tetanic stimulation (____ - ____ Hz. x ______ s)
Post tetanic stimulation using single twitches
Train of four —____ twitches at ____ hz.
0.1 – 1.0 Hz
50 - 100 Hz. x 3- 5s
4 twitches at 2 hz.
Train of Four (TOF) twitches:
Only 3 twitches → ____% block
Only 2 twitches → ____%
Only 1 twitch → ____%
No twitch →____%
75% ; 80% ; 90% ; 100%
Train of Four (TOF) twitches:
____ % reqd for intubation
____ –____% for maintenance
___ –____% before attempting reversal
100
90-100
75-80
Train of Four (TOF) twitches:
100 % reqd for __________
90 –100% for __________
75 –80% before __________
intubation
for maintenance
before attempting reversal
BefORE MR(NO BLOCK)
No MR given, Ach crosses NMJ and stimulates the receptors causing NMT •Nerve stimulator produces ______ twitches
•Also applicable to ________ of ________
full
reversal of NDMR
After MR (Complete block)
•NDMR blocks the Ach receptors and prevents further NMT
•Nerve stimulator produces ______ twitches on stimulation
•__________ can be carried out.
no; Intubation
Partial Block
•NDMR gets ______________ and few Ach molecules can now stimulate the receptors •Nerve stimulator produces __________ amplitude.
metabolised
reduced twitch
FADE
With a partial block- _____ MR show a _________↓ amplitude – No fade
•With a partial block- ________ MR show a __________ ↓ in amplitude from the 1st to the 4th twitch in a TOF - Fade
Dep; uniform
non-dep; gradual
Post-Tetanic Facilitation
With a partial _______ block, tetanic stimulation recruits Ach molecules to
the synaptic cleft
•Subsequent twitches have __________ – Post tetanic facilitation/stimulation
non-dep; ↑amplitude
Suxamethonium
Clinical Practice in 1951
____ Ach molecules
Dose
_______ mg/kg ____
____ mg/kg ___/____
Onset: __________
Indicated in (slow or rapid?) sequence induction
Duration ________________
2
1–2; I.v
2; I.m/s.c
30-45 secs; rapid
2 –5 mins
Suxamethonium
Best for anticipated ________________
difficult intubation
Suxamethonium
CVS - _____cardia
More frequent in (children or adults?)and with a ______ dose given within ________.
MSS - ________ → Postoperative __________
↑ ————-,______,__________ pressures
Hyperkalaemia-↑K by 0.5meq/L x3–5 mins
↑with _________ injuries , ______
Brady; children; 2nd ; 5 mins
Fasiculations; myalgia
Intragastric, intraoccular, intracranial
Denervation; burns
Suxamethonium
Can cause ________________, a
Premonitory sign of ________________
Myoclonus
Adverse drug reaction
Malignant hyperthermia
masseter spasm
Suxamethonium is metabolised by ______________ which has a reduced Conc in : ?????(list 4)
pseudo- cholinesterase
Pregnancy
- Liver disease,
- Malnutrition,
- ↓ protein states
