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Neurological, neuromuscular and musculoskeletal disease > Anaesthesia > Flashcards

Anaesthesia Flashcards

1
Q

Sleep =

A

Period of rest of body and mind. Rapidly reversible with external stimuli

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2
Q

Sedation =

A

Allows patients to tolerate unpleasant diagnostic/surgical procedures.

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3
Q

What is maintained in sedation?

A

Verbal contact

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4
Q

Coma =

A

State of extreme unresponsiveness in which an individual exhibits no voluntary movement or behaviour

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5
Q

Anaesthesia is classified into:

A

General

Local

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6
Q

Triad of balanced anaesthesia =

A

Hypnosis
Areflexia
Analgesia

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7
Q

Areflexia =

A

no response to surgical stimuli

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8
Q

Undesirable effects of anasthesia =

A

Decreased cardiac contractility
Sympathetic inhibition
Respiratory depression

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9
Q

At too high concentrations, anasthesia can cause =

A

All brain functions to be depressed

Respiratory failure - death

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10
Q

Classes of general anasthetics

A

Inhalation

Intravenous

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11
Q

Inhalational anasthetics:

A

Gas

Liquids

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12
Q

Ex of gas GA

A

N2O

Cyclopropane

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13
Q

Ex of liquid GA

A

Halothanes: halothane, isoflurane

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14
Q

Intravenous GA:

A

Inducing
Dissociative
Neurolept

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15
Q

Inducing GA ex:

A

Propofol
Thipentane
Etomidate

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16
Q

Dissociative DA ex;

A

Ketamine

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17
Q

MoA of inducing GA

A

GABA agonist, increase GABA sensitivity

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18
Q

MoA of ketamine:

A

NMDA antagonist

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19
Q

Thiopentane is a

A

Barbituate

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20
Q

Side effects of thiopentane

A
  • CVS depression
  • Resp depression
  • Bronchoconstrictions
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21
Q

What shouldn’t be given to asthmatics?

A

Thiopentane

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22
Q

MoA of inhalational GA

A

NMDA antagonist

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23
Q

Onset of IV vs inhalational

A

Inhalation: slow, alveolar gas exchange
IV: rapid

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24
Q

Offset of IV vs inhalational:

A

Inhalational: alveolar gas exchange
IV: redistribution, metabolism

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25
Q

Metabolism of inhalational vs IV

A

Inhalational: almost none
IV: liver

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26
Q

Types of local anaesthetics:

A

Esters

Amides

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27
Q

MoA of LA:

A

Voltage gated Na+ antagonists

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28
Q

Effect of LA depends on:

A

Diffusion graident
Fiber size
Myelination

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29
Q

Which fibers do LAs work on?

A

Alpha delta

C fibers

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30
Q

Alpha delta fibers nociceptors:

A

Mechanical

Thermal

31
Q

C fiber nociceptors:

A

Polymodal

32
Q

1st pain vs 2nd pain

A

1st pain = alpha delta, sharp, localised

2nd pain = c fibers, dull, diffuse

33
Q

LA are less effective in what type of tissue?

A

Acidic

34
Q

Due to LAs being weak bases, what do they not work on

A

Abscesses

35
Q

LA toxicity occurs when

A

Sodium channels in ALL excitable tissue potentially blocked

36
Q

What organ shows the first sign of LA toxicity?

A

Brain

37
Q

First signs of LA toxicity =

A

Perioral tingling

Feeling of doom

38
Q

LA toxicity is initially

A

Excitory =
agitation
confusion
perioral tingling

39
Q

After excitatory LA toxicity becomes

A

Depressive:
CNS = LOC, respiratory arrest
Heart = cardiac arrest

40
Q

General management of LA toxicity -

A
  • Recognise
  • Stop injecting
  • ABC, oxygen, crash call
  • Intralipid
41
Q

Intralipid =

A

20% lipid solution provides lipid load to vascular space. LA absorbed into lipid solution.

42
Q

2 types of neuromuscular blocking agents =

A
  1. Depolarising

2. Non-depolarising

43
Q

Neostigmine =

A

AChE

44
Q

Tubcurarine =

A

Non-depolarising blocking agent

45
Q

Suxamethonium =

A

Depolarising blocking agents

46
Q

Succinylcholine =

A

Depolarising blocking agents

47
Q

Depolarising NMB agent =

A
  • Binds to nicotinic cholinergic receptor and causes depolarisiation
48
Q

What patient should you not give depolarising NMB agent to?

A

Hyperkalaemic

49
Q

Effects of depolarising NMB on parasympathetic NS:

A

Muscle fasiculations
Bradycardia
Hyperkalaemia

50
Q

Moa of non-depolarising NMB agent =

A

Competes with Ach for binding site. Doesn’t stimulate receptor

51
Q

Non-depolarising NMB agent has no=

A

K+ efflux

No fasiculations

52
Q

Novochock is =

A

AchEi

53
Q

Side effects of nerve agents:

A 
Bradycardia
Increase secretions (saliva, bronchial, GI - foaming at mouth)
54
Q

Treatment for nerve agents =

A

Atropine

55
Q

Risks of GA

A
  • CNS, CVS, RS depression
  • Aspiration of gastric contents
  • Awareness
  • Postop nausea and vomiting, respiratory complications
  • death
56
Q

Why are patients of GA nil by mouth?

A

Apiration of gastric contents

57
Q

Benefits of GA

A

Unconscious
Optimal access
Total control of RS< CVS, CNS
Complications easy to treat

58
Q

Risks of LA

A

Not suitable for operation
Fails
Nerve injury
Toxicity

59
Q

Benefits of LA

A

Avoid GA complications
Less GI disturbance
Less risk of DVT

60
Q

4 stages of anasthesia:

A
  1. Induction
  2. Excitement
  3. Surgical
  4. Danger
61
Q

Induction stage:

A

Analgestia –> LOC

62
Q

Pupils in induction stage:

A

Reflex present

63
Q

Excitement phase:

A

FOllows LOC.

Irregular respiration, HR, uncontrolled movement, vomiting, breath holding, pupil dilation

64
Q

Pupils in excitement phase:

A

Dilated, reflex present

65
Q

Surgical phase:

A

Resp depression, skeletal muscles relax

66
Q

Pupils in surgical phase:

A

dilate , no reflex

67
Q

Overdose phase:

A

Severe brainstem and medullary depression

68
Q

Pupils in overdose phase:

A

Dilated

69
Q

MAC:

A

Measures exhaled concentration

70
Q

BIS =

A

Bispectral index monitor

71
Q

What does BIS do?

A

Interprets EEG into wakefulness scale

72
Q

BIS when fully awake =

A

100

73
Q

BIS when no EEG activity

A

0

74
Q

BIS scale for surgical anaesthesia =

A

45-60

Neurological, neuromuscular and musculoskeletal disease (22 decks)

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