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Block 12 Ellen > L25: Anaesthesia > Flashcards

L25: Anaesthesia Flashcards

1
Q

2 ways GA is given

A
  • intravenous

- inhaled

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2
Q

2 types of local anaesthetic agent

A

esters

amides

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3
Q

2 types of neuromuscular blocking drugs

A

depolarising

non-depolarising

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4
Q

analgesia=

A

opioids

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5
Q

3 commonly used inhalational GA

A
  • nitrous oxide
  • isoflurane
  • sevoflurane
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6
Q

4 intravenous GAs

A
  • propofol
  • sodium thiopentone
  • etomidate
  • ketamine
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7
Q

what may effect how potent a GA is

A 
lipid solubility 
(the more soluble= more potent)
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8
Q

MAC=

A

minimal alveolar concentration of specified substance

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9
Q

what do GAs work on

A

potentiate GABAa receptors

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10
Q

which GABA receptor subunit do intravenous GAs work on

A

beta subunit

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11
Q

how does increasing levels of GABA work

A

GABA is inhibitory neurotransmitter so potentiating it will induce a decreased level of consciousness

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12
Q

3 desirable effects of anaesthesia

A
  • unconsciousness
  • loss of reflexes
  • analgesia
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13
Q

most important brain area for unconsciousness

A

reticular formation

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14
Q

side effects of anaesthesia (3)

A
  • decreased cardiac contractility
  • sympathetic inhibition
  • respiratory depression
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15
Q

What is a volatile substance

A

one that is very close to boiling point -quickly turns into gaseous state

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16
Q

in which patients does inhaled GA work fast

A

kids- as they breath more

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17
Q

in which patients does GA work slower

A

anyone with impaired breathing - e.g COPD

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18
Q

are inhaled drugs metabolised

A

no

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19
Q

what metabolises intravenous drugs

A

liver

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20
Q

which form of GA is faster onset

A

intravenous

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21
Q

what are IV drugs dependant on for onset

A

cardiac output (need to be carried from blood stream to brain)

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22
Q

what time do all IV drugs work in

A

one arm-brain circulation time

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23
Q

what makes you wake up with IV drugs

A

when the drugs are redistributed around the body (not metabolised till after this)

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24
Q

what determines when the Inhalation drugs stop working

A

how quickly you breath of the gases

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25
Q

what do local anaesthetics do

A

block voltage sensitive Na+ channels

26
Q

where are voltage sensitive Na+ channels found

A

on all peripheral and central nerves

27
Q

what pH are all local anaesthetics

A

weak bases

28
Q

which tissues do local anaesthetics work worse in

A

acidic tissues (e.g absess)

29
Q

A fibres=

A

large diameter, myelinated

30
Q

B fibres

A

small diameter, myelinated

31
Q

C fibres=

A

small diameter

unmyelinated

32
Q

which fibres are first affected by local anaesthetic

A

C-fibres

33
Q

what C-fibres are first effected

A

postganglionic autonomic fibres

34
Q

what does blocking of the Na channels in postganglionic autonomic neurons do

A
  • vasodilation
  • warm dry feet
  • systemic hypotension
35
Q

second C-fibres to be affected

A

sensory fibres

36
Q

what fibres are the final ones to be anaesthetised

A

alpha fibres

37
Q

what are alpha fibres

A

motor

38
Q

antagonist neuromuscular drugs=

A
  • non-depolarising

- competitive

39
Q

e.g of 3 non-depolarising neuromuscular blocking drugs

A
  • atracurium
  • rocuronium
  • vecuronium
40
Q

agonist neuromuscular drugs=

A
  • depolarising

- non-competitive

41
Q

e.g of agonist neuromuscular blocking drugs

A

suxamethonium

42
Q

reversal agent for neuromuscular blocking drugs

A

anticholinesterase

43
Q

MOA of nondepolarizing muscle relaxants

A

they bind to the ACh receptors but are unable to induce ion channel openings preventing ACh binding

44
Q

MOA of depolarizig muscle relaxants

A

bind to ACh receptors causing an action potential but aren’t broken down meaning extended depolarization so the end plate can’t repolarize

45
Q

how do anticholinesterases reverse the effects

A

by inhibiting cholinesterase so it can’t break down ACh increaseing conc of ACh

46
Q

e.g of 2 anticholinesterases

A
  • pyridostigmie

- Neostigmine

47
Q

what happens first with suxamethonium

A

muscle fasciculations (and then relaxation)

48
Q

how long does suxamthonium last

A

-short acting normally

49
Q

side effects of anticholinesterases

A
  • increase parasympathetic increased:
  • saliva
  • bronchial secretions
  • GI
50
Q

what needs to be taken with anticholinesterases to counteract the side effects

A

atropine

51
Q

what new drugs can be used instead of anticholinesterase

A

cyclodextrin

52
Q

how many stages of anaesthesia

A

4

53
Q

what stage 1 also called

A

induction

54
Q

what is stage 1 between

A

initial administration and loss of consciousness

55
Q

what is stage 2 also known as

A

excitement stage

56
Q

what is stage 2

A

period following loss of consciousness marked by excited and delirious activity

57
Q

what may happen in stage 2

A
  • respirations and heart rate may become irregular

- may be uncontrolled movement, vomiting, pupillary dilation

58
Q

why are rapidly acting drugs used to minimise stage 2

A

as the combination of spastic movements, vomiting and irregular respirations may lead to airway compromise

59
Q

what happens in stage 3

A
  • the skeletal muscles relax, vomiting stops and respiratory depression occurs
  • eye movement slow then stop
60
Q

what stage are patients ready for surgery

A

stage 3

61
Q

what is stage 4

A

overdose stage- where too much medication has been given relative to the amount of surgical stimulation

62
Q

reliable clinical signs to use in anaesthetics (5)

A
  • muscle tone
  • light reflex
  • eyelid reflex
  • lacrimation
  • eye position

Block 12 Ellen (25 decks)

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