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block 12 anna > lecture 24 analgesia > Flashcards

lecture 24 analgesia Flashcards

1
Q

local anaesthetics are

A

esters and amides

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2
Q

common intravenous general anaethetic

A

propofol

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3
Q

common inhaled egeneral anaesthetic

A

isoflurine

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4
Q

how is potency affected

A

how lipid soluble they are

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5
Q

three principals of anaesthetics

A

loss of reflex
unconscious
analgesia

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6
Q

why do you want to stop the reflexes

A

so you can put tubes down

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7
Q

where is the RAS

A

brainstem

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8
Q

what does RAS control

A

sleep/wake

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9
Q

barbituates work on

A

GABA receptor

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10
Q

how do inhaled drugs affect the GABA receptor

A

change the phospholipid bilayer around it

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11
Q

volatile onset in general

A

slow

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12
Q

volatile onset in children

A

fast

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13
Q

volatile onset in COPD

A

slow

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14
Q

what is volatile

A

close to boiling point

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15
Q

common volatile drugs

A

NO, isoflurane and sevoflurane

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16
Q

volatile metabolism

A

none

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17
Q

volatile side effects

A

depression of cardiovascular and respiratory

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18
Q

volatile abnormal reaction

A

malignant hyperpyrexia and bone marrow suppression (in staff also)

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19
Q

Intravenous onset in general

A

rapid

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20
Q

how long does it take for intravenous to work

A

one arm heart brain cycle

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21
Q

intravenous examples

A

propofol, Thiopental, and ketamine

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22
Q

intravenous metabolism

A

in the liver

23
Q

intravenous abnormal reaction

A

anaphylaxis

24
Q

local anaesthetics block

A

sodium channels

25
Q

how do local anaesthetics stop depolarisation

A

stop the influx of sodium

26
Q

chemical of local aneasthetics

A

alkaline

27
Q

what tissue cant local anesthetics work in

A

acidic

28
Q

example of a tissue local anaesthetics cant work on

A

absess

29
Q

why may a local anaesthetic take longer to work

A

if the nerve is myelinated

30
Q

first group of nerves to be anaesthatised under local

A

C fibres

31
Q

what does the patiet first expreience with local

A

tingling

dryness

32
Q

why do the patients get the first experience with local

A

vasodilation

33
Q

second fibres local affacts

A

C again

34
Q

second experience by the patient

A

touch and pain

35
Q

last fibers the local affects

A

A delta

36
Q

last experience with local

A

loss of motor function

37
Q

describe anaesthesia of the brain

A

stimulatory period: fit

unconsciousness

38
Q

what chemical roperty should drugs have to stop them affecting the brain

A

heavier than water

39
Q

neuromuscular blocking drugs are divided into

A

antagonist and agonist

40
Q

describe neuromuscular blocking drugs atagonists

A

non depolarising

competative

41
Q

describe neuromuscular blocking drugs agonists

A

depolarising

non competative

42
Q

example of neuromuscular blocking drugs antagonist

A

atracurium

43
Q

eample of neuromuscular blocking drugs agonist

A

suxamethonium

44
Q

Anticholinesterases reverse

A

non depolarising

45
Q

Suxamethonium

A

depolarising muscle relaxant

46
Q

Suxamethonium molecule

A

two acetylecholines stuck together

47
Q

Suxamethonium binds to

A

acetylecholine receptor

48
Q

MOA of Suxamethonium

A

binds to receptor
causes firing until the nerve is exhausted
not broken down

49
Q

how do you know when you give Suxamethonium

A

twithcing then relaxation

50
Q

Suxamethonium wears of after

A

5-10 mins

51
Q

where is Suxamethonium broken down

A

plasma

52
Q

rare side effect of Suxamethonium

A

Suxamethonium apnoea - people dont have the enzymes to break it down

53
Q

name a drug that inhibits acetylecholine esterase

A

pyridostigmine

block 12 anna (24 decks)

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