Lecture 14 - Anaesthetics Flashcards

1
Q

What is the mechanism of anaesthetic related to?

A

Disruption of lipid membrane of cells

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2
Q

What is the potentiation of GABA A receptor?

A

Inhibitory receptor for the inhibitory amino acid transmitter GABA amino butyric acid

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3
Q

What are examples of certain anaesthetics?

A

Isoflurane

Propofol

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4
Q

What is GABA A receptor?

A

Chloride Ion channel

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5
Q

What examples of potentiation?

A

GABA A

Glycine

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6
Q

What are examples of inhibition?

A

NAChR
5HT3
NMDA

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7
Q

What is NMDA?

A

Receptor for excitatory amino acid neurotransmitters

Acted upon by Glutamate

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8
Q

What is the result of receptor mediated mechanism?

A

Dampening down/quester effect on the cell

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9
Q

What is the effect of nervous system?

A

Enhancement of tonic inhibition

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10
Q

What is anaesthesia?

A

Constellations of effects which incorporate but not limited to Analgesia

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11
Q

What happens when depth of Analgesia increases?

A

Pass through stages of unconsciousness and loss of reflexes

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12
Q

What are various parts of the brain affected by?

A

Anaesthetic compounds

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13
Q

What do many anaesthetics lead to?

A

Some form of Amnesia

Interference with the hippocampal function

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14
Q

What is the hippocampal function closely tied up with?

A

Processes of short-term memory

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15
Q

What is the stage I of anaesthesia?

A

Analgesia

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16
Q

What is the effects produced by stage 1 of anaesthesia?

A

Analgesia without amnesia or loss of touch sensation

Consciousness retained

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17
Q

What is stage II of anaesthesia?

A

Excitation

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18
Q

What are the effects produced of stage II of anaesthesia?

A

Excitation and delirium with struggling
Respiration rapid and irregular
Frequent eye movements with increased pupil diameter
Amnesia

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19
Q

What is stage III of anaesthesia?

A

Surgical anaesthesia

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20
Q

What are the effects produced of stage III of anaesthesia?

A

Loss of consciousness
Plane I: decrease in eye movements and some pupillary constriction
Plane II: loss of corneal reflexes
Plane III and IV: increasing loss of pharyngeal reflex
Progressive decrease in thoracic breathing and general muscle tone

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21
Q

What is IV of anaesthesia

A

Medullary depression

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22
Q

What are the effects produced of stage IV of anaesthesia?

A

Loss of spontaneous respiration and progressive depression of cardiovascular reflexes

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23
Q

What is intravenous anaesthetics used for?

A

Induction

Rapidly induce anaesthesia than inhalational/gaseous anaesthetics

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24
Q

What is Thiopental?

A

Capable of quickly inducing anaesthesia
It’s use is widespread
It is a barbiturate
Largely replaced by Propofol

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25
Q

What is ketamine?

A

Dissociative anaesthesia
Patient retains some degree of consciousness but dissociated from their environment
Causes perceptual disturbance

26
Q

What compound can maintain anaesthesia?

A

Propofol

With slow infusion

27
Q

What compound is used during endoscopy procedure?

A

Midazolam

28
Q

What are some examples of drugs of intravenous anaesthetics?

A
Propofol 
Thiopental
Etomidate
Ketamine 
Midazolam
29
Q

What is the speed of induction and recovery of Propofol?

A

Fast onset

Very fast recovery

30
Q

What is the main unwanted effect of Propofol?

A

Cardiovascular and respiratory depression

31
Q

Propofol

A

Rapidly metabolised
Continuous infusion
Causes pain at injection site

32
Q

What is the speed of induction and recovery of Thiopental?

A

Fast
Accumulation occurs
Slow recovery
‘Hangover’

33
Q

What is the main unwanted effects of Thiopental?

A

Cardiovascular and respiratory depression

34
Q

Thiopental

A

Largely replaced by Propofol
Causes pain at injection site
Risk of precipitating porphyria I’m susceptible patients

35
Q

What is the speed of induction and recovery of Etomidate?

A

Fast onset

Fairly fast recovery

36
Q

What is the main unwanted effects of Etomidate?

A

Excitatory effects during induction and recovery

Adrenocortical suppression

37
Q

Etomidate

A

Less cardiovascular and respiratory depression than with Thiopental
Causes pain at injection site

38
Q

What is the speed of induction and recovery of ketamine?

A

Slow onset

After effects common during recovery

39
Q

What is the main unwanted effects of ketamine?

A

Psychotomimetic effects following recovery
Postoperative nausea, vomiting and salivation
Raised intracranial pressure

40
Q

Ketamine

A

Produces good Analgesia and amnesia

41
Q

What is the speed of induction and recovery of Midazolam?

A

Slower than other agents

42
Q

Midazolam

A

Little respiratory or cardiovascular depression

43
Q

Inhalational anaesthetics

A

Ranges from nitrous oxide to Ether

44
Q

What is the most commonly used compound for inhalational anaesthetics?

A

Isoflurane

45
Q

How is certain concentration of inhalational anaesthetics within bloodstream achieved?

A

Low blood: gas coefficient (relatively low solubility in blood)

46
Q

What does the oil:gas coefficient dictate?

A

How easily an anaesthetic once in body passes to blood into fat and other tissues

47
Q

What are the factors affecting the rate of induction and recovery?

A

Solubility in blood

Solubility in fat

48
Q

Why is induction/recovery quicker with low blood solubility?

A

Equilibrium is reached quicker

49
Q

What does oil:gas coefficient determine?

A

Potency

50
Q

What happens when there is a small partition coefficient?

A

Small proportion of anaesthetic passing into fat/lean tissue

51
Q

What are the properties of the ideal anaesthetics?

A
Inherently stable
Non-flammable 
Non-explosive 
Potent
Low blood solubility (rapid induction)
Rapid emergence from anaesthesia 
Rapid adjustment of depth of anaesthesia 
Non-irritant to the airways 
Non-toxic 
Lack of sensitisation of the heart to catecholamines
Analgesic 
Easily reversible 
Minimal interaction with other drugs 
Inexpensive
52
Q

What do local anaesthetic do?

A

Stop the local propagation of action potentials along the neuron

53
Q

What are local anaesthetics?

A

They are all weak bases

54
Q

Why is it crucial to have some unionised form of local anaesthetics?

A

No penetration through axonal membrane

55
Q

How do anaesthetics become ionised?

A

Significant inflammation that will lower the local PH

56
Q

What happens at normal physiological PH?

A

Anaesthetics can cross axonal membrane

57
Q

What does the ionised form block?

A

Sodium channel

58
Q

What happens if the sodium channel gate remain closed?

A

The local anaesthesia can’t get in

59
Q

What is the use-dependent pathway?

A

Local anaesthetics is reversing axonal membrane and getting inside and existing in equilibrium with ionised form which can block the sodium channel

60
Q

What is inhibited when a local anaesthetic is administered?

A

All fibres