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C&M Neuroanatomy > Week 10: Local Anaesthetics > Flashcards

Week 10: Local Anaesthetics Flashcards

1
Q

What are the 3 types of local anaesthesia?

A
  1. Regional anaesthesia –> loss of sensation to a region or part of body
  2. Local infiltration –> anaesthetic is injected where the injury is
  3. Topical –> eye, skin (no injection
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2
Q

What is a local anaesthetic?

A

a drug which reversibly prevents transmission of the nerve impulse in the region to which it is applied, without affecting consciousness

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3
Q

What are the non-pharmacological methods of local anesthesia?

A
  • cold temperature (neuroconduction is blocked if temp falls below 8 degrees)
  • pressure
  • hypoxia
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4
Q

What are the 2 types of pharmalogical local anaesthesias?

A
  1. reversible e.g local anaesthetics block nerve conduction for a variable period of time
  2. irreversible e.g ethanol, surgical –> once you use these, the nerve conduction is blocked forever
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5
Q

How does an injury cause pain?

A
  1. At the site of injury, the Na+ channels open and Na+ moves inside the cell so the membrane depolarises and generates an action potential
  2. 1st order neuron takes information from site of injury to spinal cord
  3. 2nd order neuron takes information from spinal cord to thalamus
  4. 3rd order neuron takes information from the thalamus to the somatosensory cortex
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6
Q

Where is the severity of pain analysed?

A

the somatosensory cortex

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7
Q

How do local anaesthetics work?

A
  • local anaesthetics block the alpha subunit of the voltage-gated sodium channel so the impulse cannot cross the areas
  • so the brain is not receiving information about the pain so you cannot feel it
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8
Q

What is the endoneurium?

A

each nerve fibre (axon) is surrounded by a layer of connective tissue called the endoneurium

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9
Q

What does the perineurium surround?

A
  • bundles of nerves are called vesicles

- each vesicle is surrounded by perineurium

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10
Q

Many vesicles join together to form a nerve covered by what?

A

epineurium

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11
Q

Where are LAs injected?

A
  • LAs are injected outside the nerves and then they diffuse through epineurium, perineurium and endoneurium to act on the sodium channels on nerve axons.
  • LAs are never injected into the nerves as this will cause damage to the nerves
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12
Q

What two forms does local anaesthetic exist in

A
  • ionised/protonated

- unionised/ unprotinated

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13
Q

Which form of LA can:

  1. Cross the cell membrane
  2. Can bind to the sodium channel
A
  1. Unionised

2. Protonated

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14
Q

If there is an injury of the hand, explain how the information about pain reaches the somtosensory cortex

A
  • the information will be carried from the site of injury to the spinal cord by the median nerve
  • The information will synapse at the grey horn
  • then travel in the lateral spinothalamic tract to the thalamus
  • then to the somatosnesory cortex
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15
Q

What is the ideal local anaesthetic?

A
  • reversible
  • good therapeutic index
  • quick onset
  • suitable duration
  • no local irritation
  • no side effects
  • no potential to induce allergy
  • cheap, stable and soluble
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16
Q

What was the first local anaesthetic used?

A

cocaine

17
Q

What are the 3 parts of every LA?

A
  1. the lipophilic part
  2. the intermediate chain
  3. the hydrophillic part
    the intermediate chain connects the lipophilic and hydrophilic parts
18
Q

What determines the type of anaesthetic?

A
  • the bond that connects the intermediate chain with the benzene ring
  • determines whether the LA is an ester or an amide
19
Q

How can you tell which LA is an amide and which is an ester?

A
  • all LAs end in ‘caine’
  • if there is an i earlier in the word, the LA is an amide
  • if there is no i in it its an ester
20
Q

What does the onset of action of an LA depend on?

A
  • Depends on the ability of the LA to go into the nerve cells and block the Na+ channel from the inside
  • unionised form of the drug crosses the membrane
  • so more of the unionised form the faster the action
21
Q

When does pKa = pH?

A

unionised form = ionised forms of local anaesthetics

22
Q

When is pKa > pH

A

when unionised form > ionised form

23
Q

What is the relationship between pKa and body pH?

A

further away the pKa of local anaesthetic from body pH the lesser the unionised form, therefore the slower in onset

24
Q

Why is an LA less effective in inflamed tissue?

A

inflammation results in local acidosis which decreases the surrounding pH of tissue

25
Q

What does the duration of action of an LA depend on?

A
  1. Protein binding
    More protein binding = the longer duration of action
  2. Length of the intermediate chain joining the aromatic and amine group
26
Q

What is potency?

A

dose required to produce the desired effect

27
Q

What does potency depend on?

A
  • Lipid solubility –> more lipid soluble drugs penetrates the cell membrane
  • smaller amount required to produce a given effect
28
Q

What does the ability to block nerve conduction depend on?

A
  1. Type of fibre
    larger fibre = slower onset
    smaller fibres get blocked first
  2. Location of nerve fibre
    outside or in the mantle (if the nerve is in the centre, the LA has to go all the way through the nerve so onset is longer)
29
Q

What does ability to block neuronal conduction depend on?

A

type of nerve fibre

30
Q

sensory functions are lost in which order after an LA is injected?

A

In order of length of fibre (from shorter to longer):

  1. Cold, warmth
  2. Pain (‘first pain’ = A delta fibres then ‘second pain’ = C fibres)
  3. Touch, deep pressure
  4. Motor function
31
Q

Why are LAs frequently given with a vasoconstrictor?

A
  • prolong action
  • reduce plasma levels (less risk of CNS effects) –> less blood supply so LA can stay in desired area for longer
  • reduced operative haemorrhage
32
Q

When are vasoconstrictors not used with LAs?

A

when the area is supplised by end vessels:

  • fingers and toes
  • penis
  • ear lobule, ala of nose
33
Q

What are the two vasoconstrictors used?

A
  1. Adrenaline

2. Felypressin

34
Q

How does adrenaline increase the safe dose of LAs?

A

by causing vasoconstriction and delaying the absorption of local anaesthetic agents

35
Q

What are the adverse effects of LAs?

A
  • hypersensitivity (allergic response)
  • anaphylactic reaction (this is a problem with ester LAs but rare with amides)
  • may be a reaction to preservatives, not the LA itself
36
Q

What is methemoglobinaemia?

A
  • Main toxic effect of prilocaine due to its metabolite 0-toluidine, which oxidises ferrous to ferric ions so haemoglobin cannot transport oxygen
  • Symptoms – cyanosis, lethargic and respiratory distress which does not respond to oxygen
  • Treatment is i.v methylene blue 1.5mg/kg
37
Q

What does the systemic effects of toxicity of an LA depend on?

A
  • route of administrration

- speed at which the blood toxicity levels rise

38
Q

How do we treat LA toxicity?

A
  1. stop injecting the LA
  2. airway
  3. give 100% oxygen and ensure adequate lung ventilation
  4. control seizures with drugs

C&M Neuroanatomy (44 decks)

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