Anaesthesia Flashcards

1
Q

Give 3 examples of inhalational anaesthetic agents

Give 2 IV

A
Inhalational:
- Nitrous oxide
- Isoflurane
- Sevoflurane
IV:
- Propofol
- Ketamine
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2
Q

What is the general theory behind anaesthesia?

A

Principal anaesthetic agent plus adjuvant drugs

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3
Q

What is regional anaesthesia?

A

Affects larger regions of the body by blocking transmission between that region and the spinal cord

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4
Q

What is local anaesthesia?

A

Affects small region via peripheral nerve block

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5
Q

Where does general anaesthesia act in terms of anatomical locations?

A
  • Reticular activating system
  • Brainstem
  • Spinal cord
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6
Q

List 4 molecular targets of anaesthetic agents

A
  • GABA chloride channels
  • Glycine chloride channels
  • Nicotinic ACh receptors
  • NMDA receptors
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7
Q

What is the mechanism of action of Propofol?

Binding to which other channel works exactly the same way?

A

Acts via GABA chloride channels - bind to channel and increase its sensitivity to GABA - in turn increases chloride currents so cell is hyperpolarised - less excitable

Glycine chloride channels

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8
Q

What is the theory behind targeting nicotinic ACh receptors in anaesthesia?

A

Inhibiting nACh receptors reduces excitatory currents - contributes to amnesia and analgesia

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9
Q

What is the mechanism of action of nitrous oxide and ketamine?

A

Bind to glutamate NMDA receptors, which reduces calcium currents and therefore reduces neurotransmission

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10
Q

In terms of pharmacodynamics, what is the mechanism of action of anaesthetic agents which bind to inhibitory ligand-gated channels (GABA/glycine)?
(Mention potency and efficacy)

A

They are positive allosteric modulators - they decrease the EC50, meaning less GABA/glycine needs to bind in order to exert the same level of effect
Therefore there is increased ligand potency and efficacy

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11
Q

In terms of pharmacodynamics, what is the mechanism of action of anaesthetic agents which bind to excitatory ligand-gated ion channels?
(Mention potency and efficacy)

A

Non-competitive allosteric antagonism -
once agent binds, receptor is inactivated. Therefore fewer receptors available for binding, so decreased efficacy.
BUT affinity for the unbound receptors is still just as high - no change in potency.
Therefore potency (i.e. EC50) is unchanged but efficacy decreases

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12
Q

How are the inhalational anaesthetic agents administered?

A

Volatile liquids at room temperature - vaporised and mixed with “carrier” of O2/air/nitrous oxide
Breathed in via mask

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13
Q

What is the MAC?

A

Minimum alveolar concentration - alveolar concentration at which 50% of patients fail to move to a surgical stimulus

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14
Q

How is MAC linked to potency?

A

The lower the MAC, the more potent the agent is -

MAC is related to lipid solubility, and the higher the lipid solubility, the more potent the anaesthetic

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15
Q

What is the normal MAC dose needed?

A

1.2 - 1.5

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16
Q

How could you reduce the MAC needed?

A

Give a MAC-sparing drug alongside the inhalational such as nitrous oxide or fentanyl

17
Q

Give 4 factors that affect MAC

A

Age - MAC needed decreases with age
Temperature - increases with temp
Pregnancy - increases MAC needed
Other anaesthetics/sedatives/opioids - decrease MAC needed

18
Q

How are inhalational agents absorbed?

A

Pass down concentration gradient from alveoli into bloodstream

19
Q

What determines the absorption of inhalational anaesthetic agents?

A

Blood:gas coefficient - describes volume of gas in litres that can dissolve in 1L of blood

20
Q

What does a high blood:gas coefficient signify?

A

Agent will enter blood more readily

21
Q

What does the tissue: blood coefficient signify?

A

Specific uptake capacity of certain tissues for each agent - i.e. how readily anaesthetic will move from blood into that tissue

22
Q

How are inhalational agents eliminated?

A

Basically reverse of absorption and distribution:

  • Anaesthetic withdrawn slowly
  • Blood conc drops so agent moves from tissues into venous blood, then removed at alveoli unchanged
23
Q

Why might a patient take quite a while to recover from a GA?

A

Drug continues to circulate - may get reabsorbed into arterial blood when it reaches lungs

24
Q

Which tissue takes longest for inhalational anaesthetics to clear from?

A

Fat - highly lipophilic

25
Q

Is induction of anaesthesia with IV agents more rapid than with inhalationals?

A

Yes - seconds rather than minutes

26
Q

Where do IV agents distribute to mostly?

A

CNS initially, where it has a transient effect, but then redistributes to muscle/fat. Need repeated dosing to keep CNS levels high

27
Q

Why is the metobolism of Propofol unusual?

A

Undergoes hepatic and extrahepatic conjugation

28
Q

List 3 common ADRs of GA

A
  • Post-op N+V
  • Hypotension
  • Post-op cognitive dysfunction
29
Q

Give 2 rare ADRs of GA

A
  • CVS depression

- RICP

30
Q

Which drug classes are used as adjuvants alongside the principal agents?

A
  • Benzos
  • Propofol
  • N2O
  • Opioids
  • Neuromuscular blocking agents
31
Q

What determines the onset speed of local anaesthesia?

A

Dissociation constant - lower = faster

32
Q

What is a possible ADR of local anaesthesia?

A

Systemic spread can result in arrhythmias/cardiac toxicity as Na+ channel blockers