General anaesthesia Flashcards

1
Q

What are the clinical objectives of anaesthesia?

A
  • Loss of consciousness (at low conc)
  • Suppression of reflex responses (at high conc)
  • Analgesia (relief of pain)
  • Muscle relaxation
  • Amnesia
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2
Q

What other drugs are used to facilitate general anaesthesia?

A
  1. Opioid (e.g. IV fentanyl) - analgesia
  2. NM blocking drug (e.g. suxamethonium) for muscle relaxation
  3. Benzodiazepines - amnesia
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3
Q

What is the Meyer-Overton theory? What was assumed because of it?

A
  • The potency of a G.A. increases in proportion to its oil:water partition coefficient
  • Therefore – site of action of G.A.s was the lipid bilayer portion of nerve membranes
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4
Q

What is the problem with the Meyer-Overton theory

A
  • At pharmacologically relevant concentrations, changes to the lipid bilayer are minute
  • No-one could understand why is a change in the lipid bilayer would result in a dysfunctional membrane protein
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5
Q

How are the effects of GAs produced?

A
  • Reduced neuronal activity

- Altered synaptic function

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6
Q

How do intravenous anaesthetics work?

A

E.g. etomidate, propofol

  • Potentiate GABA A receptor function (altered synaptic function) – most abundant, fast inhibitory, ligand-gated ion channel in CNS
  • B3 subunits present - suppress reflex responses
  • a5 subunits - amnesia
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7
Q

How do inhaled anaesthetics work?

A
  1. Potentiate GABA A receptor function (and glycine receptors) - NOTE: glycine = inhibitory NT
    - Show no subunit selectivity (altered synaptic function)
    - a1 subunits present - suppression of reflex responses
  2. Inhibits nAChRs (altered synaptic function) - analgesia
  3. Facilitate TREK (background leak) potassium channel opening (reduced neuronal excitability) - loss of consciousness
  4. Reduced NMDA receptor function (altered synaptic function) - nitrous oxide
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8
Q

Are intravenous or inhaled anaesthetics more potent?

A

Intravenous

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9
Q

What is unconsciousness?

A

Massive decrease in cortical activity

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10
Q

How do GAs cause loss of consciousness?

A

Depression of thalamocortical neurones caused by:

  • Background leak K+ channels –> hyperpolarisation
  • Enhanced GABA function

Results in disconnection of periphery from brain - thalamus acts as relay station for info btwn cortex + rest of CNS

Affect RAS - decreased firing of RAS, decreased level of arousal

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11
Q

How do GAs suppress reflex responses?

A
  • Depression of reflex pathways in the dorsal horn of the spinal cord
  • Anaesthetic agents that enhance GABA and glycine function in dorsal horn will decrease activity of dorsal pathways
  • Disconnects brain from sensory info from periphery
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12
Q

How do GAs cause amnesia?

A
  • At low dose
  • Lots of GABA receptors in hippocampus w/a5 subunit
  • Leads to decrease in synaptic transmission in hippocampus (memory formation)
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13
Q

How does route of administration influence the induction/maintenance of anaesthesia?

A

IV:

  • Fast induction
  • Difficult to control rate of excretion as injected straight into blood

Inhalation:

  • Large amount of inhaled gas is excreted back into lungs
  • Gives rapid control of depth of anaesthesia
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14
Q

What is the ideal blood:gas partition coefficient for inhaled anaesthetics?

A

LOW:

  • The majority of the drug that crosses into the blood remains in gaseous form
  • Can easily enter brain
  • Also much easier to clear from brain if poorly dissolved in blood

If it’s high, majority of drug becomes liquid in blood and struggles to enter brain

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15
Q

How is anaesthesia usually induced?

A

Intravenous agent - propofol

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16
Q

How is anaesthesia usually maintained?

A

Inhalational agent - enflurane