Local Anaesthetics Flashcards

1
Q

How do LA work

A

They stop nerve conduction by blocking the voltage gated sodium channels

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2
Q

What does LA work on

A

The first order afferent receptors - not the CNS but the PNS

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3
Q

What do the connective tissue barriers in the peripheral nerves act as

A

A diffusion barrier

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4
Q

What does a greater number of membrane mean for the LA

A

Will take longer to anesthetize

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5
Q

What is the general rule for weaning out

A

Nerves that will be anesthesized first will wean out first

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6
Q

What is the effect of position of the nerve in the bundle to LA

A

The further it is from the LA the longer it will take to be anaesthetised

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7
Q

What is the order of block in different fibres

A

Adelta, C, Abeta, Aalpha

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8
Q

What group do A alpha sensorial nerves belong to

A

group I

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9
Q

What group do A beta nerves belong to

A

group II

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10
Q

What group do Adelta nerves belong to

A

group III

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11
Q

What group do sensorial C nerves belong to

A

group IV

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12
Q

What is the function of A Alpha nerves

A

sensory (proprioception)

motor (skeletal muscle)

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13
Q

What is the function of A Beta nerves

A

sensory (mechanoreception)

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14
Q

What is the function of A gamma

A

Motor (muscle spindles)

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15
Q

What is the function of A delta

A

Sensory (mechanic-, thermo-, noci and chemoreceptors)

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16
Q

What is the function of C fibres

A

Sensory (noci-termo and chemoreceptors)

autonomic (post ganglionic)

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17
Q

What fibres do we want to anesthetize

A

Delta
A beta
C

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18
Q

What fibres do we not want to anaesthetise

A

autonomic

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19
Q

What is the mechanism of action of LA

A

binds to a site in the sodium channel
LA blocks the channel and prevents sodium influx
This blocks the action potential generation and propagation
Block persists so long as a sufficient number of NA channels are blocked

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20
Q

What other Na channels does LA block

A

in other excitable tissues e.g heart muscle

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21
Q

What are possible side effects of LA

A

bradycardia

hypotension

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22
Q

Do we need all sodium channels blocked

A

We don’t need to have absolutely all sodium channels blocked but enough to avoid AP reaching the maximum level

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23
Q

What are the 3 components of the organic molecule in lLA

A

aromatic region (hydrophobic)
ester or amide bond
basic amine side chain (hydrophilic)

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24
Q

How is LA presented as

A

hydrochloride (B.HCl)

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25
What does the B.HCl allow
renders the amine base more water soluble
26
Why are LA partly dissociated
As they are active in the ionized form | They can cross the membrane only in the unionized form
27
In what form is B.HCl pharmacologically active but non diffusible
B.H+
28
In what form is B.HCl diffusible but not active
B. + H+
29
What molecule binds the sodium channel
B.H+
30
Why are small diameter axons more susceptible to LA block
Same concentration of LA will act better on small diameter axons because there are less sodium channels to block
31
Why is a greater concentration of LA required for myelinated axons
NA channels and K channels are more concentrated at nodes of ranvier
32
What is the safety factor
To block the AP the LA needs to act on several nodes of ranvier along the axon
33
Why do several nodes need to be blocked
The local currents are strong enough to flow past the blocked region and to regenerate the AP at the nodes of ranvier
34
Why is the LA base present as hydrochloride
to increase solubility in aqueous solution
35
What is the volume of an LA cartilage in the UK
2.2ml
36
What is the concentration for LA injections
2-4%
37
What are other components present in LA
reducing agent preservative and fungicide +/- vasoconstrictor
38
Why do we use vasoconstrictor
prolongs the effect so lower conc of LA required
39
What is the reducing agent normally
sodium metabisulphide
40
What are the ester LA
cocaine and procaine (not really used) | benzocaine
41
What are the amide LAs
``` lignocaine (lidocaine) prilocaine articaine mepivacaine (not used much anymore) Bupivacaine Ropivacaine (not used much anymore) ```
42
What are most anesthetics regarding vasodilation/constriction
vasodilators
43
What is the issue with an LA being a vasodilator
Increased blood flow will increase the wash out of LA
44
What are the vasoconstrictors usually used in LA
adrenaline | felypressin (synthetic vasopressin)
45
What do vasoconstrictors act on
receptors on vascular smooth muscle
46
What are the adrenoreceptors
alpha receptors B2 receptors B1 receptors
47
What do alpha receptors do
vasoconstrictor
48
What do beta 2 receptors do
vasodilate
49
What do beta 1 receptors do
in cardiac muscle increase rate and force
50
Is adrenaline more effective on alpha or beta receptors
it is equally effective on both
51
If adrenaline is given locally what is the effect
vasoconstrictor (action on alpha receptors)
52
What is the effect of adrenaline if it is given systemically
it lowers the TPR (B>a) | adrenaline increases cardiac output however so overall adrenaline has no or little effect on the MABP
53
What will patients often feel with LA with adrenalin
palpitations
54
Is noradrenalin more effective on alpha or beta receptors
alpha
55
What is the effect of noradrenalin if given locally
vasoconstrictor effect on the alpha receptors
56
What is the effect of noradrenalin if given systemically
it increases TPR (a>B) increases cardiac output raise in MABP
57
How can noradrenalin result in a fall in BP
paradoxical effect
58
How are ester type LA broken down
by tissue esterase's making their action quite brief
59
How are amide type LA broken down
by liver amides | longer duration of action
60
What are the modes of administration of LA
``` surface application (topical) injection local infiltration regional nerve block nerve root block ('spinal', 'epidural') intravenous ```
61
What are the preparations for Lignocaine
2% lignocaine HCl | 2% lignocaine HCl + 1:80,000 adrenaline
62
What are the preparations for Prilocaine
4% prilocaine HCl | 3% Prilocaine HCl + felypressin (0.03U/ml)
63
What is the x% solution equivalent to
X mass/volume