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L30 - local anaesthetics Flashcards

1
Q

types of local anaesthetic

A

regional anaesthesia
local infiltration
topical

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2
Q

regional anaesthesia

A

loss of sensation to a region or body part

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3
Q

local infiltration anaesthesia

A

cuts, skin incisions

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4
Q

topical anaesthesia

A

eye / skin (venepuncture)

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5
Q

non-pharmalogical anaesthesia methods

A

cold (below 8-10 degrees)
pressure
hypoxia

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6
Q

how does hypoxia act as an anaesthetic

A

makes the area go numb

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7
Q

reversible local anaesthetic

A

loss of sensation to a localised area

after a period of time, the nerve impulse will become normal

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8
Q

non-reversible local anaesthetic

A

phenol, ethanol, radio frequency, surgical

once used, nerve conduction is blocked forever (patients with chronic pain)

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9
Q

LA definition

A

A drug which reversibly prevents transmission of the nerve impulse in the region which it is applied without affected consciousness

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10
Q

mechanism of LA

A

At the site of injury, LA block sodium channels opening by binding to subunits from inside the membrane

  • Na can no longer enter the cell
  • depolarisation
  • no action potentials = no pain flowing
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11
Q

endoneurium

A

a layer of connective tissue surrounding nerve fibres

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12
Q

fascicle

A

a bundle of nerves in the endoneurium

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13
Q

perineurium

A

surrounds the fascicles

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14
Q

epineurium

A

surrounds the perineurium

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15
Q

where does LS bind in a Na channel

A

S6 transmembrane domain from the inside, causing closure of the channel

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16
Q

how does LA travel across the membrane

A

only the unionised form can cross as it is liquid soluble (the majority is ionised)

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17
Q

which form of LA binds to the sodium channel

A

only the ionised / protonated form can bind to the channel

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18
Q

what determines speed of action of LA

A

% of unionised form of LA present

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19
Q

what does binding of LA to sodium channel do

A
  • slows the rate of AP
  • increases the threshold for stimulation
  • reduces rate of conduction
  • eventually blocks conduction completely
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20
Q

ideal LA

A
  • reversible
  • good therapeutic index (ratio of effective dose / legal dose)
  • quick onset
  • suitable duration
  • no irritation even on repeated application
  • no side effects
  • no potential to induce allergy
  • applicable by all routes
  • cheap, stable, soluble
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21
Q

structure of LA

A

aromatic (lipophilic part)
intermediate chain
hydrophilic substituted amino acid (protein acceptor)

22
Q

two types of LAs

A

amides

esters

23
Q

how to know if a LA is an amides

A

…i…caine

24
Q

how to know if a LA is an ester

A

…caine

25
Q

onset of action

A

depends on their ability to go into the nerve cell and cross the membrane
- drug must be unionised

26
Q

pH and onset of action

A

further away the pKa of LA from the body pH (7.4), there will be fewer in unionised form = slower onset

27
Q

pH in inflammation

A

low - so LA less effective

28
Q

differential block - type of nerve fibre

A

larger fibre = slower onset

29
Q

differential block - location of nerve fibre

A

nearer the centre of the mantle = takes longer to work

30
Q

what is commonly given with a LA

A

vasoconstrictors

31
Q

action of vasoconstrictors

A
  • prolong action
  • reduce plasma levels
  • greater anaesthesia or reduces dose
32
Q

when should vasoconstrictors not be used

A

not used with LAs which are supplied by end-vessels

e.g., fingers, toes, penis, ear lobe

33
Q

adrenaline

A

stimulation of alpha adrenoreceptors - constrict blood vessels

34
Q

examples of vasoconstrictors

A
  • adrenaline

- felypressin (less effective than adrenaline)

35
Q

adverse effects of LAs

A
  • hypersensitivity

- methaemoglobinaemia

36
Q

hypersensitivity

A
  • anaphylactic reaction

- ester> than amides

37
Q

methaemoglobinaemia

A

Main toxic effect of prilocaine due to its metabolic O-toluidine, which oxidises ferrous to ferric ions

38
Q

symptoms of methaemoglobinaemia

A

cyanosis, lethargy, respiration distress which does not respond to oxygen

39
Q

dose of lidocaine

A

3mg/kg

with adrenaline: 7mg/kg

40
Q

bupivacaine / levobupivacaine

A

2mg/kg

with adrenaline: 2mg/kg

41
Q

prilocaine

A

6mg/lg

with adrenaline: 8mg/kg

42
Q

treatment of LA toxicity

A
  • stop injection with LA
  • call for help
  • A: open the airway
  • B: give 100% oxygen and ensure adequate lung ventilation
  • C: confirm or establish IV access
  • D: control seizures
  • consider drawing
43
Q

treatment of LA toxicity - in circulatory arrest

A
  • start cardiopulmonary resuscitation
  • use standard ALS protocol
  • give IV lipid emulsion
44
Q

how do LA diffuse in to the body

A

outside the nerves - they then diffuse through the epineurium, perineurium and endometrium to act on the Na channels on nerve axons
(they are never injected into nerves)

45
Q

-COO- link

A

ester

46
Q

who initially used cocaine as a LA

A

Karl Koller

47
Q

examples of amide LAs

A

bupivacaine
ropivacine
prilocaine
ligocaine

48
Q

what determines potency of the LA

A

lipid solubility

49
Q

duration of action in a more protein binding LA

A

More protein binding = longer the duration of action

50
Q

potency

A

dose required to produce required effect

control (38 decks)

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