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AI Exam 2 > General Anaesthesia > Flashcards

General Anaesthesia Flashcards

1
Q

What anaesthetics can be inhaled?

A

-Ether
-Halothane
-Methoxyflurane
-Nitrous oxide

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2
Q

What channels/receptors does anaesthetic work through?

A

-NMDA receptors
-Voltage-gated Na+ channels
-Two-pore domain K+ channels
-GABAa receptors

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3
Q

What are the three main sub-types of Nicotinic receptors?

A

Muscle
Ganglionic
CNS

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4
Q

What type of channels are nicotinic receptors?

A

Ligand-gated ion channels - mediate fast excitatory synaptic transmission

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5
Q

What does Nicotine mimic at receptors?

A

Nicotine mimics the action of ACh, therefore acts as an agonist

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6
Q

ACh receptor is selective and only cations can pass through, when opens sodium passes through into the cell causing a depolarisation, what does this cause?

A

Contraction of skeletal muscle

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7
Q

What are examples of non-selective for nAChR?

A

ACh, Nicotine

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7
Q

Inhibition of transmission at the NMJ as well as autonomic ganglia can be achieved by two mechanisms, what are they?

A

1) Competitive inhibition of the nicotinic receptor = non-depolarising block
2) Depolarising block

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7
Q

What drug is selective for the muscle nAChRs?

A

Suxamethonium

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8
Q

Give an example of a nAChR antagonist?

A

Tubocurarine

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8
Q

What does Tubocurarine cause in a human?

A

Paralysis due to a small depolarisation, no action potential = no contraction occurs!

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8
Q

Give an example of a nicotinic agonist?

A

Nicotine

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9
Q

If you increase an agonist ACh what happens to inhibition which is competitive?

A

Increase of ACh = overcome inhibition

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10
Q

What does persistent stimulation of nAChR cause?

A

Phase 2 block due to desensitisation of nAChRs

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11
Q

Why isn’t Tubocurarine not used?

A

-Hypotension = ganglion block
-Release of histamine

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12
Q

What is the duration of action of non-depolarising Pancuronium?

A

1 hour

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13
Q

What is the duration of action of non-depolarising Vencuronium?

A

Intermediate duration of action

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14
Q

What is the duration of action of non-depolarising Atracurium?

A

Intermediate duration of action

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15
Q

What is the duration of action of non-depolarising Mivacurium?

A

Short duration of action (15 mins)

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16
Q

What are depolarising blocking agents which act at the NMJ?

A

Suxamethonium

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17
Q

If cholinesterase inhibitors are present ACh produces a ____________ at the NMJ?

A

Depolarising block

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18
Q

Duration of action of Suxamethomium?

A

10 minutes as it is hydrolysed by plasma cholinesterase’s

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19
Q

When would prolonged paralysis be a worry for a patient given Suxamethomium?

A

-Neonates
-Patient’s with liver disease
-Patients with genes lacking cholinesterase activity

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20
Q

What does general anaesthetic affect?

A

The synaptic transmission and neuronal excitability

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21
Q

What type of molecule is General Anaesthetic?

A

Small, lipid soluble molecules that readily get access to the brain by crossing the BBB

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22
Q

Why can general anaesthetic cause Amnesia?

A

Hippocampal inhibition

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23
Q

What is the reticular formation responsible for?

A

Wakefulness

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24
Q

What is stage 1 of Anaesthesia?

A

Cortical inhibition. Voluntary eye movements still occur

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25
Q

What is stage 2 of Anaesthesia?

A

Excitation/inhibition of reticular neurones, delirium, involuntary movements.
Depression of reticular formation = involuntary movements.

26
Q

What is stage 3 of Anaesthesia?

A

Surgical anaesthesia. Gradual loss of respiration, reflexes, larynx + Pharynx decrease.

27
Q

What is stage 4 of Anaesthesia?

A

Overdose: reparatory and circulatory paralysis. No Cardiac Output. = death!

28
Q

Why do IV anaesthetics have a slow elimination from the body compared to inhalation anaesthetics?

A

-Resides in the lean tissues and fat for longer than the brain, viscera and blood.
It builds up in the fat slowly = accumulates over time.

29
Q

What drug distributes into the fat and can cause a ‘hangover’ feeling?

A

Thiopental = not used!

30
Q

What type of kinetics does Thiopental display?

A

Saturation kinetics
-Large doses or repeated doses can cause the plateau in the blood concentration to become more and more elevated as more drug accumlates in the body and the metabolism saturates = big disadvantage and why is it not used!

31
Q

As thiopental cannot be used, what drug can?

A

Propofol

32
Q

Is there a hangover phase with Propofol?

A

No, it is rapidly metabolised and has a limited cumulative effect

33
Q

What kinetics does Propofol display?

A

First order kinetics

34
Q

What are the unwanted affects of Propofol and Thiopental?

A

Cardiovascular and Respiratory depression

35
Q

What drug acts differently to other anaesthetics, as it increases blood pressure and heart rate but doesn’t effect respiration?

A

Ketamine

36
Q

What is the onset of Ketamine?

A

1-2 mins, slower than other anaesthetics

37
Q

What are the unwanted side effects of Ketamine?

A

Can increase intracranial pressure, cause hallucinations, delirium during recovery.

38
Q

An ideal general anaesthetic should be readily controllable so that induction and recovery of anaesthesia can be rapid, true or false?

A

True

39
Q

What inhalation anaesthetics are used in the maintenance of anaesthesia?

A

Isofuorane, sevofluorane, desfulrane and nitrous oxide

40
Q

What events occur at induction of anaesthesia?

A

1) Anaesthetic equilibrates with the alveoli
2) Equilibration in the blood this should be RAPID; an ideal inhalation anaesthetic rapidly reaches the required arterial blood concentration and vice versa
3) Blood must become saturated for transfer to the tissues to occur –> SLOW

41
Q

What events occur at induction of anaesthesia SIMPLE?

A

Inhaled gas –> Alveoli (FAST) –> Blood –> Tissues (SLOW)

42
Q

Why do the kinetic behaviour of inhaled anaesthetics vary?

A

Solubility

43
Q

What are the two different solubility ratios?

A

Blood : gas coefficient
Oil : gas coefficient (fat solubility)

44
Q

What kinetics determine the pharmacologic effect of the blood : gas coefficient?

A

Kinetics in arterial blood

45
Q

What is the Oil : gas partition coefficient

A

Transfer of anaesthetic between the blood and the tissues which affect the kinetics of equilibration

46
Q

What percent of anaesthetic after equilibrium will be in the fat?

A

95%

47
Q

What drug if used is extremely fat soluble and if a patient has a high fat content will have a slower recovery, with more chance of a hangover feeling?

A

Halothane

48
Q

What sedative premedication is used in surgery?

A

Benzodiazepine

49
Q

What IV anaesthetic is used for rapid induction?

A

Propofol

50
Q

What muscarinic antagonists are used to reduce bronchial and salivary secretions?

A

Atropine

51
Q

What analgesia is used for pain relief in surgery?

A

Morphine

52
Q

What physiological factors determine the induction and recovery of inhalation anaesthesia?

A

1) Alveolar ventilation rate
2) Cardiac output

53
Q

Explain Alveolar ventilation rate?

A

The greater the minute volume i.e, the amount of air that the patient breaths in 1 min (tidal volume x RR) = faster the equilibration

54
Q

Explain Cardiac output

A

Reduction of alveolar perfusion reduces alveolar absorption of the anaesthetic so speeds up induction

55
Q

If there is fast ventilation what does this allow for?

A

Quicker delivery to the alveolus

56
Q

What is minimal alveolar concentration used for?

A

A measure of potency for individualised GA

57
Q

What is the latest theory of the MOA of aesthetic?

A

Anaesthetic molecules bind to hydrophobic pockets within specific membrane protein targets

58
Q

How could GABAa be responsible for Anaesthesia?

A

GABAa receptors increase activity
-Bind to hydrophobic pockets within different GABAa receptor subunits = v complex

59
Q

How could Glutamate receptors be responsible for anaesthesia?

A

Decrease in activity, eg, ketamine blocks NDMA receptors

60
Q

Can Voltage-gated sodium, potassium and calcium channels be responsible for anaesthesia?

A

Yes

61
Q

What is the effect of mutations at Ser270, Ala291 and Thr294 on GABAa receptors?

A

Decreased sensitivity to volatile anaesthetics but not to IV anaesthetics.
The β subunit is important for the effects of both midazolam and propofol

62
Q

How does the β3(N265M) mutation affect the response to etomidate and neurosteroids?

A

NO response to neurosteroids, but the receptors still respond to general anesthetics like etomidate

63
Q

What is glutamate?

A

Major excitatory neurotransmitter in the CNS

64
Q

What drugs at the NMDA receptors?

A

Nitrous oxide, xenon, isoflurane

65
Q

Where can a mutation reduce alcohol-induced inhibition of glutamate receptors?

A

Domain 3 and 4

66
Q

Xenon and Isoflurane inhibit NMDA R by competing with what for its regulatory site?

A

Glycine

67
Q

Why are two pores essential for the role of a voltage-gated sodium and potassium channels?

A

To regulate resting membrane potentials

68
Q

What do mutations in TM3 result in?

A

Alters the response to general mutations, therefore we can see where GA’s target and can be used to determine MOA.

AI Exam 2 (16 decks)

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