Anaesthetic Drugs Flashcards
Contemporary Use of Anaesthesia:
Unconsciousness: Potential Drug Targets:
- cerebral cortex
- thalamus
- reticular activating system
- spinal cord
- GABA receptors
- glutamate receptors
- glycine receptors
- serotonin receptors
All anaesthetic agents affect tissues by
depressing all excitable tissues to variable sensitivities
All anaesthetic drugs are lipid soluble.
True or False?
True
Proprofol: Method of Delivery:
IV
Proprofol:
- lipid soluble
- rapidly perfuses the brain, relaxes the larynx
- rapidly metabolised by liver
- does not accumulate
- offset (wears off) by redistribution)
Proprofol: Drug Class:
- antiemetic
- antiepileptic
Proprofol: Side Effects:
- pain on injection
- abnormal movements
- hypotension
Inhaled Anaesthetics:
- are
- side effects
- halogenated ethers
- post-op nausea and vomiting
- if irritant, makes gas induction difficult
- emergence phenomena
Idea proporties of inhaled agents:
- stable, non-corrosive
- liquid
- vapourisable at room temp
- pleasant to inhale, bronchodilator, non-
irritant - low blood:gas solubility
- not metabolised
General Anaesthesia:
- IV induction
- gas maintenance
NMBAs
- neuromuscular blocking agents
- only given to unconscious patients
Akinesia/Muscle reaction by
NMBAs
Two classes of NMBAs:
- depolarising
- non-depolarising
Label
insert diagram
Depolarising NMBAs:
- eg
- receptors?
- location?
- molecular effect
- onset and offset
- half life
- metabolised by
- side effects
- succinylcholine
- acts on muscarinic and nicotinic receptors
- at post-synaptic membrane
- 2 Ach joined together; minimises Ach
available to bind - rapid onset and offset
- half life = 2mins
- metabolised by plasma cholinesterase
- multiple side effects: twitchy at first, only
lasts for five mins (effects), muscle pains
post-op, bradycardia because harshly
affecting muscarinic receptors but we want
effect of inhibition of nicotinic
stuck at receptors, can not restimulate muscle
Non-Depolarising NMBAs:
- eg/are
- receptors?
- location?
- molecular effect
- onset and offset
- half life
- metabolised by
- side effects
- aminosteriod/ quaternary ammonium
compounds - nicotinic receptors: alpha subunit
- synaptic cleft/post-synaptic neuron
- competes with Ach by binding and blocking
Na+ channel on nicotinic receptor - slow onset and offset (30-40mins)
When can prolonged paralysis during the use of succinylcholine (depolarising NMBA) as an akinesic agent?
cholinesterase deficiency
anything that inhibits cholinesterase
Botulinum Toxin:
- intracellular toxin
- prevents vesicles of Ach binding to
intracellular membrane preventing release
of Ach into the synaptic cleft - relieves muscle spasms and contractions,
neuropathic pain and used for aesthetic
purposes
Are depolarising or non-depolarising more receptor-specific?
Non-depolarising only nicotinic
succinylcholine both muscarinic and nicotinic
Non-depolarising NMBAs require reversal agents eg
- neostigmine: binds to acetylcholinesterase
and prevents the break down of Ach in the
synaptic cleft; will increase ach at muscarinic
and nicotinic; activates sympathetic so given
with atropine to block muscarinic receptors - sugammadex: selective relaxant binding
agent (SRBA), binds to aminosteriod non-
depolarising NMBAs, preventing action of
the akinesic agent (aminosteriod)
