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)
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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
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2
Q

General anaesthetic drug administration

A
  • inhalation: isoflurane, sevoflurane, enflurane, desflurane, Nitric oxide
  • intravenous:
    Commonest= propofol, thiopental,etomidate,ketamine
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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
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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
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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
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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

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7
Q

How do you treat malignant hyperthermia?

A
  • give ryanodine receptor 1 antagonist: DANTROLENE
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8
Q

What are the main routes of anaesthetic drug administration?

A
  • inhalation and IV
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9
Q

What are the anaesthetic drugs administered by inhalation? (5)

A
  • isofluarne, desflurane, sevoflurane, enflurane, NO
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10
Q

What are the anaesthetic drugs administered by IV? (4)

A
  • propofol, thiopental, etomidate, ketamine
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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
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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
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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
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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
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15
Q

What are the non depolarising neuromuscular blockers?

A
  • atracurium, vecuronium, pancuronium
  • they are antagonists at NMJ nicotinic receptors
  • respiratory muscles are last to be paralysed and first to be recovered
  • lasts 20-40 mins
  • can be reversed by neostigmine (anticholinesterase) and glycopyrolate to prevent musarinic effects
  • side effects can be caused due to acting on autonomic ganglia= tachycardia and hypotension
16
Q

What is important to maintain when administering neuromuscular blockers?

A
  • secure the airway by using endotracheal tube to incubate the patient