General Anaesthetics Flashcards
0
Q
Mechanism of action of anaesthetics.
A
- reticular activating system complex polysnaltic pathway in brain stem.
- diffuse projections to cortex to regulate arousal
- inhibition of glutamate receptors (excitatory pathway)
- enhance GABA pathway (inhibitory pathway)
1
Q
What is anaesthesia?
A
- reversible loss of consciousness with absence of sensation
- depresses excitable tissues, ie nerves and muscle
- could be fatal if too much so depress the CVS and respiratory control centres
2
Q
General anaesthetic drug administration
A
- inhalation: isoflurane, sevoflurane, enflurane, desflurane, Nitric oxide
- intravenous:
Commonest= propofol, thiopental,etomidate,ketamine
3
Q
What do inhalation agents do?
A
- speed of induction depends on the solubility in blood and inspired concentration (only soluble anaesthesia takes effect)
- low solubility means the blood becomes more saturated so quicker onset of anaesthetics (also means shorter duration)
- minimum alveloar concentration is the conc that produces surgical anaesthesia in 50% of patients. No movement in response to the surgical incision
4
Q
Nitric oxide (inhalation)
A
- vapour in room temp
- can only produce anaesthetic effects along with other agents.
- low solubility in blood so blood can quickly become saturated= rapid onset and recovery
- can be a good analgesic when given with 50% of O2 in entonox
- Entonox= 50% of O2 and 50% of NO
- prolonged exposure can inactivate vitamin B12 causing sensory neuropathy and encephalopathy
5
Q
Halogenated ethers
A
- no longer used because of potential fatal liver toxicity
- newer agents are: isoflurane, desflurane, sevoflurane and enflurane
- can precipitate malignant hyperthermia in an anaesthetic emergency
6
Q
What is malignant hyperthermia?
A
- abnormal activity of ryanodine receptor leads to an increase in release of calcium ions from sacroplasmic reticulum. This drives up body temp (pyrexia), like cooking itself
- increased in partial pressure of CO2
- Rhabdomyolysis= increase in creatine level due to breakdown of muscle. Can also be identified by increase in potassium level (lots of K intracellular)
- acidosis
-TO TREAT: give a ryanodine receptor 1 antagonist= DANTROLENE
7
Q
How do you treat malignant hyperthermia?
A
- give ryanodine receptor 1 antagonist: DANTROLENE
8
Q
What are the main routes of anaesthetic drug administration?
A
- inhalation and IV
9
Q
What are the anaesthetic drugs administered by inhalation? (5)
A
- isofluarne, desflurane, sevoflurane, enflurane, NO
10
Q
What are the anaesthetic drugs administered by IV? (4)
A
- propofol, thiopental, etomidate, ketamine
11
Q
Propofol
A
- family of alkylphenol
- 1.5-2.5mg/kg
- onset: 10-20 seconds( one arm brain circulation) single dose lasts 2-4 mins and then drug is redistributed to other tissues
- is metabolised in liver and excreted in urine
- SIDE EFFECTS: burning at injection site, hypotension, bradycardia and apoea
12
Q
Thiopental
A
- a rapid (< 30s) onset and short acting barbiturate generl anaesthetic
- metabolised by liver
- may depress myocardium and respiratory centre
- can contradict in patients with acute porphyria
- blocks 11 beta0 hydroxylation in adrenal cortex= suppress cortisol production for 24 hours
- ‘truth serum’
- can be used in epilepsy when several fits occurred or when fits dont stop
13
Q
Ketamine
A
- NMDA receptor antagonist
- stimulates respirtory and cardiovascular centres so used in emergency induction in shocked patients and in asthmatic (as it can bronchodilate)
- can produce dissociative states and hallucinations
- abuse of ketamine can lead to induced ulcerative cystitis
14
Q
What is the only clinically used depolarising neuromusclar blocker?
A
- suxamthonium (1mg/kg)
- binds to nicotinic receptor at NMJ and leads to inactivation of Na channels
- can cause fasciculations
- half life is short (4 mins)
- metabolised by pseudocholinesterase ( found in plasma)
- side effects can be caused due to binding to M2 receptor at SA node= bradycardia and potential cause of malignant hyperthermia
