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BDS2 LA > Local Anaesthetic > Flashcards

Local Anaesthetic Flashcards

1
Q

What do local anaesthetics do?

A

-stop nerve conduction by blocking the voltage-gated Na+ channels

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2
Q

What nerve in nerve pathways do local anaesthetics work on?

A

The first order afferent nerve receptors (we dont touch the CNS)

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3
Q

What acts as a diffusion barrier for local anaesthetics in a peripheral nerve?

A

Connective tissue layers

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4
Q

What connective tissue layers are found in a peripheral nerve and where?

A
  • Epineurium = around full nerve
  • Perineurium = around bundles of axons
  • endoneurium = found around the myelin shealth in myelinated nerve fibres (axons)
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5
Q
A

A will be blocked first because it is closer to the injection site but also because the number of membranes it has to diffuse through are the same as B (or possibly less)
Those in close proximity to the LA are anaethetised first

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6
Q

Which nerve from the previous card will the LA wear out on first?

A

A - in general the nerve that is anaesthetised first will wear out first
NOTE: however, there can be other factors

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7
Q

What characteristic does LA need to have to be able to cross the membranes?

A

Lipophilic

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8
Q

Nerve axons differ in their susceptibility to block by LA. What is the order of block of different nerve fibres by LA?

A
  • Aδ
  • C
  • Aβ
  • Aα
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9
Q

Describe Aα nerve axons.

A

-myelinated
Function = sensory (proprioception) Motor (skeletal muscle)

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10
Q

Describe Aβ axons.

A

-myelinated
Function = sensory (mechanoreception)

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11
Q

Describe Aδ nerve axons.

A

-myelinated
Function = sensory (mechano- thermo-, noci- and chemo-receptors)

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12
Q

Describe C-fibres.

A

-unmyelinated
Function = sensory (noci-, thermo- and chemo-receptors) Autonomic (post-ganglionic)

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13
Q

Due to the order of block of different axons, what senses are therefore blocked first and last?

A 
Sensory functions (A-delta) [mechano-, thermo-, noci- and chemoreception]
Proprioception blocked last (A -alpha) - some patients feel movement but wont feel pain but this can make some P's anxious
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14
Q

What is the mechanism of action for local anaesthetics?

A
  • LA binds to a site in the Na+ channel
  • LA blocks the channel and prevents Na+ influx
  • This blocks action potential generation and propagation
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15
Q

How long does the block on axons from LA persist?

A

As long as a sufficient number of Na+ channels are blocked on the axon

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16
Q

Do all the Na+ channels on an axon need to be blocked to stop AP generation and propagation?

A

No - just a sufficient number

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17
Q

Where else can local anaesthetics block Na+ channels and what can this cause?

A
  • Can block Na+ channels in other excitable tissues such as heart muscle
  • can cause bradycardia and hypotension
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18
Q

What might happen to a patient if they get hypotension as a result of an LA injection?

A

Could faint

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19
Q

What are local anaesthetics made up from?

A

Organic molecules

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20
Q

What are the 3 components of LA’s?

A
  • aromatic region (hydrophobic)
  • ester or amide bond
  • basic amine side chain (hydrophilic)
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21
Q

In what form is the local anaesthetic presented? (comes in)

A

-hydrochloride (B.HCL)

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22
Q

Whatsd fn

A

renders thte base more water soluble

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23
Q

The LA is partly what?

A

Dissociated

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24
Q

In what form is the LA active?

A

ionised form (B.H+)

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25
Q

In what form can the LA diffuse across membranes?

A

un-ionised form only

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26
Q

Describe LA’s mechanism of action. (getting to the sodium channels)

A

basically the B.H+ needs to become un-ionised to cross the membrane then activate again (ionise)

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27
Q

Why are smaller diameter axons more susceptible to LA blocks?

A

They have less Na+ channels so takes less LA to sufficiently block the nerve

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28
Q

In myelinated axons, where are the Na+ channels found?

A

The Na+ channels (and K+) are concentrated at the Nodes of Ranvier

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29
Q

To be able to block a myelinated axon, what needs to be done? Why?

A

The LA needs to act on several nodes of Ranvier along the axon
This is because the local currents are stronge enough to flow past a blocked Node of Ranvier and regenerate the AP at the next Node of Ranvier

30
Q

The LA base is present as a hydrochloride, why?

A

To increase solubility in aqueous solution

31
Q

For dental injections, what % solutions are the preparations?

A
32
Q

What cartridge size is normally used? Why is knowing the cartridge size important?

A

Get 1.8 and 2.2 - 2.2 normally used
Important as it changes how you calculate the max dosage

33
Q

What else is present in an LA injection other than the hydrochloride?

A

-reducing agent (sodium metabisulphide) -preservatives an fungicide - + or - a vasoconstrictor

34
Q

What does a vasoconstrictor in LA do/provide?

A
  • used to prolong the effect of the LA
  • means you can use less LA
  • BUT reduces blood flow
35
Q

**you will hear about P’s that are allergic to LA History of P - they have has LA before without an allergic reaction They could be allergic to a brand This is the reducing agent and the preservative is what differs between brands Presence of these 2 components - important to know risk of allergic reaction to them If have a reaction make sure to note the brand, batch and manufacture - could be the key to identify the real cause of the allergic reaction

A
36
Q

What are the 2 subtypes of LA?

A
  • esters
  • amides
37
Q

What do ester LA’s tend to be?

A

Topical anaesthetics

38
Q

What is an ester used for topical anaesthetic?

A

Benzocaine

39
Q

What amides are used as LA’s?

A
  • lignocaine (lidocaine)
  • Prilocaine
  • Articaine
  • Bipivacaine
40
Q

In terms of vasodilation/vasoconstriction, what are most local anaesthetics?

A

Vasodilators

41
Q

What is the problem with local anaesthetics being vasodilators?

A

-will cause increased blood flow and will increase the ‘wash-out’ of LA

42
Q

How can the duration of action of an LA be increased?

A

-including a vaso-constrictor

43
Q

What are some vasoconstrictors that can be used in LA?

A
  • adrenaline (most common)
  • Felypressin (synthetic vasopressin)
44
Q

What do vasoconstrictors act on?

A

On receptors on vascular smooth muscle

45
Q

What different adrenoreceptors do you get?

A
  • α receptors and β2 receptors on blood vessels
  • β1 receptors on cardiac muscle
46
Q

What do alpha receptors cause?

A

Vasoconstriction

47
Q

What is the effect of activation of beta-2 receptors?

A

Vasodilation

48
Q

What are the effects of beta-1 receptor activation?

A
  • positive chrontropic effect (increased heart rate)
  • positive inotropic effect (increased force of heart)
49
Q

What adrenoreceptors is adrenaline more effective on?

A

Is equally effective on both alpha and beta receptors

50
Q

Adrenaline given locally has what effect?

A

Vasoconstrictor effect (action on alpha receptors)

51
Q

Systemically, what effect does adrenaline have?

A

works on beta 2 receptors and lowers total peripheral resistance

52
Q

What effect does adrenaline have on cardiac output?

A

increases caridac output

53
Q

What might the patient complain of due to increased cardiac output?

A

feelings of palpitations due to increased HR and force

54
Q

What effect does adrenaline have on mean arterial BP?

A

has little or no effect on mean arterial BP

55
Q

What adrenoreceptor is noradrenaline more effective on?

A

More effective on alpha receptors than beta

56
Q

What effect does noradrenaline have when given locally?

A

vasoconstrictor effect (alpha receptors)

57
Q

What does noradrenaline do systemically?

A

Increases total peripheral resistance (works on alpha recptors)

58
Q

What effect does noradrenaline have on cardiac output?

A

increases CO

59
Q

What effect does noradrenaline have on mean arterial blood pressure?

A

raises it

60
Q

The raise in mean arterial BP from noradrenaline can lead to a fall of BP. Why?

A

Bodys response to the increase in mean arterial BP to compensate for this change

61
Q

How is LA inactivated?

A

Washes out from the tissues by the blood supply to then be broken down

62
Q

How are ester LA’s broken down?

A

Broken down by tissue esterases

63
Q

How are amide type LA’s broken down?

A

By liver amidases

64
Q

Which type of LA has a longer duration of action?

A

Amides (esters action is quite brief)

65
Q

What might be problem with LA’s in a patient with a liver problem?

A

Liver important for breakdown of amide LA’s so safe doses will need to adjusted

66
Q

What are the modes of administration for LA?

A
  • surface application (topical)
  • injection
  • local infiltration
  • regional nerve block
  • nerve root block (spinal, epidural)
  • intravenous
67
Q

What is the formula for percentage solution?

A

X% solution = X mass/volume

68
Q

How much prilocaine HCl will be in a 2ml cartridge of a 3% solution?

A

e.g. 3% prilocaine HCl solution: 3% = 3g/100ml =30mg/1ml A 2ml cartridge of 3% prilocaine HCL will contain 2x30 = 60mg of prilocaine HCL

69
Q

As the solution of vasoconstrictors are very dilute in LA, how are they expressed?

A

As ratios
e.g. 1:80,000 1 part of adrenaline in 80,000 parts liquid

70
Q

What is the maximum dose for Lignocaine?

A

Approx. 4mg per kg body weight

71
Q

What is the maximum dose of adrenaline?

A

500 ug (B.N.F.)

72
Q

some missed stuff

A

BDS2 LA (4 decks)

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