Neuromuscular Blocking Drugs Flashcards
What are NMBD??
These are drugs that impair neurotransmission and cause muscle relaxation.
NMBD are classified into two namely??
Agonists… Depolarizing, non competitive blockers.
Antagonists… Non depolarizing, competitive blockers.
Examples of depolarizing NMBD agents?
Succinylcholine.
Steroid based Non depolarizing NMBD include?
Pancuronium
Vercuronium
Rocuronium
Examples of synthetic non depolarizing agents?
Atracuronium
Doxacuronium
Mivacuronium
Examples of curare alkaloids non depolarizing agents?
Metocuraine
Another name for succinylcholine is?
Suxamethonium.
What is the mechanism of action of suxamethonium
Read your note
Suxamethonium is hydrolysed by plasma cholinesterase to?
Succinyl monochlonine and chlonine
Suxamethonium is stored at?
4°C
IV infusion of suxamethonium is given at?
5-15mg/kg/hr
Suxamethonium is given intramuscularly at which dose?
3-5mg/kg
What are the blocking phases of suxamethonium?
Depolarization block.
Desensitisation block.
Phase II block.
What happens in depolarization phase or phase I block recovery?
Preceded by muscle fasiculation.
Occurs as a result of suxamethonium stimulating the ach receptors causing repetitive firing.
Phase I block recovery occurs as the suxamethonium diffuses away from the NMJ down a conc gradient
It is metabolised by plasma cholinesterase.
What happens during Desensitisation block?
Occurs when ach receptors are insensitive to the channel opening effects of agonists and ach.
What happens during phase II block??
Occurs after repeated boluses or prolonged infusion of suxamethonium.
After initial depolarization, the membrane potential returns to the resting stage even when the NMJ is exposed to the drug.
What are the indications for suxamethonium?
Drug of choice for anesthesia and also when rapid trachea intubation is required.
What are the side effects of suxamethonium?
Hyperkalamia- it increases k levels by 0.5mmol/L… And it’s worse in burns pts and people with muscle dystrophy cause of proliferation of extra junctional receptors.
Bradycardia.
Muscle pains.
Increased intragastric pressure.
Anaphylaxis.
What are the two main causes of reduced plasma cholinesterase activity?
Can be congenital or acquired
Plasma cholinesterase has 3 variants which are?
Atypical
Flouride resistant
Silent
Non depolarizing NMBDs are not metabolised at the NM junctions
T/F
True
How are non depolarizing NMBDs blocks resolved?
By dilution with time.
There are two groups of non depolarizing NMBDs which are??
Benzylisoquinolinum compounds.
Aminosteriods.
Examples of benzylisoquinolinum drugs are??
Note: curium
Atracurium.
Mivacurium.
Tubocurarine.
Which benzylisoquinolinum causes ganglion blockade?
Tubocurarine
Which benzylisoquinolinum has no direct cardiovascular effects?
Atracurium
Which benzylisoquinolinum does not release histamine?
Cisatracurium
Which benzylisoquinolinum has a short duration of action?
Mivacurium
What is the first steroid NMBD in clinical use?
Pancuronium
Which Aminosteriods does not release histamine or have any cardiovascular effect?
Vercuronium
What are anticholinesterases
They are acetylcholineestetase inhibitors
What are the side effects of anticholinesterases?
Bradycardia
Nausea
Bronchospasm
Sweating and salivation
GI upset
