L25: Anaesthesia Flashcards

(62 cards)

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
what do local anaesthetics do
block voltage sensitive Na+ channels
26
where are voltage sensitive Na+ channels found
on all peripheral and central nerves
27
what pH are all local anaesthetics
weak bases
28
which tissues do local anaesthetics work worse in
acidic tissues (e.g absess)
29
A fibres=
large diameter, myelinated
30
B fibres
small diameter, myelinated
31
C fibres=
small diameter | unmyelinated
32
which fibres are first affected by local anaesthetic
C-fibres
33
what C-fibres are first effected
postganglionic autonomic fibres
34
what does blocking of the Na channels in postganglionic autonomic neurons do
- vasodilation - warm dry feet - systemic hypotension
35
second C-fibres to be affected
sensory fibres
36
what fibres are the final ones to be anaesthetised
alpha fibres
37
what are alpha fibres
motor
38
antagonist neuromuscular drugs=
- non-depolarising | - competitive
39
e.g of 3 non-depolarising neuromuscular blocking drugs
- atracurium - rocuronium - vecuronium
40
agonist neuromuscular drugs=
- depolarising | - non-competitive
41
e.g of agonist neuromuscular blocking drugs
suxamethonium
42
reversal agent for neuromuscular blocking drugs
anticholinesterase
43
MOA of nondepolarizing muscle relaxants
they bind to the ACh receptors but are unable to induce ion channel openings preventing ACh binding
44
MOA of depolarizig muscle relaxants
bind to ACh receptors causing an action potential but aren't broken down meaning extended depolarization so the end plate can't repolarize
45
how do anticholinesterases reverse the effects
by inhibiting cholinesterase so it can't break down ACh increaseing conc of ACh
46
e.g of 2 anticholinesterases
- pyridostigmie | - Neostigmine
47
what happens first with suxamethonium
muscle fasciculations (and then relaxation)
48
how long does suxamthonium last
-short acting normally
49
side effects of anticholinesterases
- increase parasympathetic increased: - saliva - bronchial secretions - GI
50
what needs to be taken with anticholinesterases to counteract the side effects
atropine
51
what new drugs can be used instead of anticholinesterase
cyclodextrin
52
how many stages of anaesthesia
4
53
what stage 1 also called
induction
54
what is stage 1 between
initial administration and loss of consciousness
55
what is stage 2 also known as
excitement stage
56
what is stage 2
period following loss of consciousness marked by excited and delirious activity
57
what may happen in stage 2
- respirations and heart rate may become irregular | - may be uncontrolled movement, vomiting, pupillary dilation
58
why are rapidly acting drugs used to minimise stage 2
as the combination of spastic movements, vomiting and irregular respirations may lead to airway compromise
59
what happens in stage 3
- the skeletal muscles relax, vomiting stops and respiratory depression occurs - eye movement slow then stop
60
what stage are patients ready for surgery
stage 3
61
what is stage 4
overdose stage- where too much medication has been given relative to the amount of surgical stimulation
62
reliable clinical signs to use in anaesthetics (5)
- muscle tone - light reflex - eyelid reflex - lacrimation - eye position