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BDS2 - BAMS > Local Anaesthetics > Flashcards

Local Anaesthetics 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

where on the nerve pathway does LA affect

A

first order afferent neuron

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3
Q

where can you get information on the toxicity of LA and the maximum dosage

A

BNF

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4
Q

where are blood vessels found within the peripheral nerve

A

within the bundles but also surrounding the nerve and whole structure

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5
Q

what nerves are anaesthetised first

A

Nerves in the proximity of the local anaesthetic will be anaesthetised first
the number if membranes the LA has to pass through plays a part as well

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6
Q

molecules that cross membranes need to be what

A

> lipophilic

> have an aromatic ring - this is in LA which gives the characteristics of being lipophilic

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7
Q

what benefit is there to having fat in the nerve bundles

A

Allows LA to remain for longer
LA Cannot be too hydrophilic as it will stay in the fat and not really reach the nerve
Needs to have an affinity but not a great affinity

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8
Q

if the LA acts fast then does it tend to leave the space faster or stay longer

A

leave the space faster

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9
Q

which axons are most affected by LA (most to least)

A

A delta
C
A beta
A alpha

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10
Q

describe the structure and function of a alpha axons

A

group I

myelinated

Sensory (proprioception)
Motor (skeletal muscle)
Last ones for LA to work on
Important to reassure patient that the tooth is numb but can still feel a pressure

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11
Q

describe the structure and function of a beta axons

A

group II

myelinated

Sensory (mechanoreception)

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12
Q

describe the structure and function of a gamma axons

A

myelinated

motor (muscle spindles)

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13
Q

describe the structure and function of a delta axons

A

group III

myelinated

Sensory (mechano-, thermo-, noci- & chemo-receptors)
Most affected - as they are sensorial they are what we are looking for the LA to work on along side the a delta and c

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14
Q

describe the structure and function of c axons

A

group IV

unmyelinated

Sensory (noci-, thermo- & chemo-receptors)
Autonomic (post-ganglionic) [we do not want to anaesthetise these]

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15
Q

describe the mechanism of the action of LA

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
• Block persists so long as a sufficient number of Na+ channels are blocked
○ This is important - don’t need to have all the Na channels blocked but you do need to have enough blocked to stop the AP from reaching the maximum level

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16
Q

what happens when LA blocks Na channels in other excitable tissues like the heart muscle

A

• NB: LA block Na+ channels in other excitable tissue eg heart muscle
• LA can cause bradycardia and hypotension
○ This is a worrying / stressing side effect / symptom
○ Injecting LA with or without vasoconstriction - want to stop it entering the main system due to this
○ Can cause the patient to faint
§ Hypotension is what is generated for the fainting but bradycardia is what you want to look out for?

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17
Q

what is in LA

A

• Organic molecules, three components:
○ Aromatic region (hydrophobic)
○ Ester or amide bond
○ Basic amine side chain (hydrophilic)

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18
Q

what is LA presented as

A

• Presented as hydrochloride (B.HCl)
○ Renders the amine base more water soluble
B = base, HCl = hydrochloride

• Partly dissociated
○ Active in ionised form
Can cross membrane only in un-ionised form

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19
Q

describe B.H+ in the LA

A 
pharmacologically active
non-diffusible 
base hydrogen can dissociate
both B and B.H can bind
BH has greater affinity
20
Q

describe B. in the LA

A

diffusible
non-active
no way for LA to cross membrane to be active if it is ionised - membrane will not allow this

21
Q

LA mechanisms of action picture

A

dont think i understand this enough to ask a question about it in words cos it looks so confusing but go look at it and test that you know where everything goes cos i havent a clueeee hhahaha sorry xoxo

22
Q

why are small diameter axons more susceptible to LA block

A
  • Due to the number of channels that are blocked
    ○ Don’t need to block all the channels but need to block a great proportion to stop the signal
  • Small diameter axons = have less number of channels
    ○One molecule per blocking will act better on a smaller diameter than a larger diameter as there are less channels to block
23
Q

how does LA work on myelinated axons

A

• Na+ channels (and K+ channels) are concentrated at the nodes of Ranvier
Nodes = have a greater concentration of channels as they need to generate AP in a saltatory way - so it can jump from one to another

24
Q

what is the safety factor for using LA on myelinated axons

A

• The local currents are strong enough to flow past the blocked region and to regenerate PA at the next node of Ranvier
Ie: blocking one node of Ranvier will not be enough the block the whole axon / nerve because the jumping is so strong it can just by pass the LA

To block the AP, the LA needs to act on several nodes of Ranvier along the axon

25
Q

what is included in LA preparations

A

• LA base present as hydrochloride, to increase solubility in aqueous solution
• For dental injections, 2-4% solutions ○ UK: 2.2% but cannot guarantee this
• Reducing agent ○ Sodium metabisulphide
• Preservative(s) and fungicide
± vasoconstrictor

26
Q

what is the vasconstrictor used for

A

Used to prolong the effects of the anaesthetic and reduces the need for a higher concentration of LA

27
Q

what are the disadvantages of using vasoconstrictors

A

§ There are problems with adrenaline
□ Reduces blood flow

This is a problem when doing a procedure like moving a piece of gingiva tissue to another area (flap / periodontal treatment) and it is not beneficial to have less blood flow as it might mean the tissue won’t survive

28
Q

can patients be allergic to LA

A

yes but these are very rare situations (usually have other allergies)

usually ingredients in the LA are what cause the allergic reaction
such as the preservative or the reducing agent

some LA use latex and patients can be allergic to these but a lot of places are latex free now a days

29
Q

name local anaesthetics that are esters

A

○ Cocaine
§ Good topical anaesthetic
§ not usually used
§ Hard to use

○ Procaine
§ Toxic effects
§ not usually used

○ Benzocaine 
§ Topical anaesthetic we use
	□ Stings 
	□ Bad taste
	□ But does reduce pain

○ Some clinicians don’t like to use topical anaesthetics and wouldn’t use it but others wouldn’t do LA without it
Technique is more important than topical anaesthetics to reduce sensitivity without the need for topical as it doesn’t really solve the problem anyway

30
Q

name local anaesthetics that are amides

A

○ Lignocaine (lidocaine)
§ Used

○ Prilocaine
○ Articaine
§ These 2 above are used more in specific situations

○ Mepivacaine
§ not usually used

○ Bupivacaine
§ Used in certain procedures

○ Ropivacine
§ not usually used

31
Q

what is the problem with most LA being vasodilators

A

increase blood flow

increases the wash out of LA

32
Q

what are the vasoconstrictors included in the LA preparations

A

○ Adrenaline
§ Usually

○ Felypressin (synthetic vasopressin)
§ Used in prilocaine

33
Q

where do vasoconstrictors act

A

act on receptors on vascular smooth muscle

34
Q

what are the adrenoreceptors where adrenaline acts

A

○ Alpha receptors: vasoconstriction
○ Beta2 receptors: vasodilation
○ Beta1 receptors:
§ Cardiac muscle:
□ Positive chronotropic effect = increase heart rate
□ Positive inotropic effect = increase heart force

35
Q

what are the receptors that the felypressin (synthetic vasopressin) acts on

A

ADH receptors

36
Q

explain adrenaline effect on alpha and beta receptors

A

• Adrenaline is equally effective on alpha and beta receptors
○ Ie works on both receptors

• Given locally, it has a vasoconstrictor effect (action on alpha receptors)

• Systemically, it lowers total peripheral resistance (TPR) (beta > alpha)
○ There are more beta than alpha receptors there

• Adrenaline increases cardiac output
○ Works on cardiac beta receptors
○ More force, more flow, less TPR = blood pressure is not affected that much with adrenaline

• Overall, adrenaline has little or no effect on mean arterial BP
Patient has increase heart rate and heart force

37
Q

explain noradreanline effect on alpha and beta receptors

A

• Noradrenaline (NA) is more effective on alpha than on beta receptors
○ Has a preference to alpha over beta
○ Works better in alpha receptors
○ Has local vasoconstrictor effect

  • Given locally, it has vasoconstrictor effect (alpha receptors)
  • Systemically, it increases TPR (alpha > beta)
  • NA increases cardiac output
  • Overall, NA raises mean arterial BP

• This can result in a fall of BP - Why?
○ Fall in blood pressure but increase cardiac output = paradoxical effect
○ Response of body when you have the increase in blood pressure due to things that are not physiological is to compensate for that by driving the blood flow to other areas
○ So by compensating it goes too low

38
Q

how is LA inactivated

A
  • ‘washout’ from tissues by blood supply
  • Countered by presence of vasoconstrictor agent

• Ester types broken down by tissue esterases
○ Action is quite brief (topicals)

• Amide types broken down by liver amidases
○ Longer duration of action
○ This means the liver is important in the break down
○ Medical history important
§ Patient present with liver disease then you need to consider if the dose of LA is safe for the patient as the process of removing the amides might be affected

39
Q

what are the different modes of administration for LA

A
  • Surface application (‘topical’)
  • Injection
  • Local infiltration
  • Regional nerve block
  • Nerve root block (‘spinal’, ‘epidural’)
  • Intravenous
40
Q

what are the LA preparations for lignocaine

A

Lignocaine
○ 2% lignocaine HCl
○ 2% lignocaine HCl + 1:80,000 adrenalin

41
Q

what are the LA prepartions fir prilocaine

A

Prilocaine
○ 4% prilocaine HCl
○ 3% prilocaine HCl + felypressin (0.03U/ml)

42
Q

what are percentages solutions

A
  • Percentages are still widely used in clinical practise
  • X% solution = X mass / volume

○ Eg 3% prilocaine HCl solution
○ 3% = 3g / 100ml
○ = 30mg / 1ml
= A 2ml cartridge of 3% prilocaine HCl will contain 2 x 30mg = 60mg prilocaine HCl

43
Q

how are very dilute solutions expressed in LA

A

• Very small amounts of vasoconstrictor are present in LA preparations
• Confusing if given as %
○ Eg adrenaline content is <0.001%

• Instead, adrenaline content is expressed as a ratio:
○ Eg 1:80,000
§ 1 part of adrenaline in 80,000 parts of liquid

§ For similar reasons, fluoride concentrations are given as “parts per million” (1:1,000,000)

44
Q

what is the maximum dose of lignocaine

A

Approx 4mg per Kg of body weight

45
Q

what is the maximum dose of adrenaline

A

○ 500μg (BNF)

○ Cartridge contains 27.5μg adrenaline
○ If this entire amount was injected into 5 litres of blood = 5μg/L
○ Plasma levels of adrenaline following dental injections increase with the amount injected
○ The plasma levels following ‘normal’ injections are within the physiological range (up to 0.5μg/litre)
○ Maximum physiological levels (intense exercise) can reach 0.5μg/litre

Reach LA maximum dose before adrenaline maximum dose but the adrenaline symptoms are more

BDS2 - BAMS (18 decks)

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