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Pharmocolgy > P10: Local Anaesthetics > Flashcards

P10: Local Anaesthetics Flashcards

1
Q

What is the synthetic substitute of cocaine

A

Procaine

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2
Q

What are the major local anaesthetics in use

A

Lidocaine
Prilocaine
Articaine
Mepivacaine

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3
Q

What is the Infiltration method of local anaesthetic

A

Injection into tissues to reach nerve branches and terminals for minor surgery

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4
Q

What is the nerve block method of local anaesthetic

A

Injection close to the nerve trunk causes loss of peripheral sensation, used for surgery or dentistry - lidocaine, prilocaine

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5
Q

What is the surface method of local anaesthetic

A

Applied as a spray (lidocaine) or powder (benzocaine) to mucus membrnae of the nose, mouth and cornea

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6
Q

What is the spinal method of local anaesthetic

A

Injected into the subarachnoid space to act on spinal roots and cord - lidocaine

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7
Q

What is the epidural method of local anaesthetic

A

injected into the epidural space to block spinal roots.

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8
Q

What kind of molecule is lidocaine and describe its features

A

Amide, slow onset, medium duration of action, widely used

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9
Q

What kind of molecule is prilocaine and describe its features

A

Amide, rapid onset, low toxicity but can cause methaemoglobinaemia

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10
Q

Effects of cocaine on NA and DA

A

Blocks the uptake of these amines

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11
Q

What kind of molecule is bupivacaine and describe its features

A

Amide, slow onset, long duration of action, used for epidural anaesthesia

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12
Q

What kind of nerve fibres as more easily blocked

A

smaller myelinated fibres like Adelta fibres

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13
Q

Do local anaesthetics bind more strongly to active or inactive channels

A

Inactive

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14
Q

What is the order of nerve type blockade by increasing concs of LA

A 
Autonomic
Pain
Temperature
Touch
Proprioception
Skeletal muscle tone
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15
Q

Why are myelinated fibres easier to block than unmyelinated

A

Myelinated (autonomic etc) express clustered Na+ channels at nodes of ranvier

Unmyelinated (C fibres etc) expressed Na+ channels along length and yh

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16
Q

After voltage gated Na+ channels open what is used to close them

A

Slow acting inactivation gate that is refractory for 1-5ms

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17
Q

What side of an Na+ channel do LAs work on

A

Intracellular

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18
Q

As an LA must enter a neuron to work, what increases LA potency

A

Increased lipophilicty

Increased non-ionised fraction

19
Q

What is a use dependent block

A

This means that the more a nerve is stimulated, the faster the onset of the anaesthesia will be

20
Q

Where do all biological reaction take place

A

Aqueous solution

21
Q

What indicates whether a drug is protonated or not

A

If environmental pHpKa the drug will dissociate and release a proton

22
Q

Roughly what is the pKa of most LAs

A

Most LAs are weak bases with pKa - 8.9

23
Q

Are LAs often ionised at physiological pH

A

Mainly but not completely ionised as the physiological pH is below the pKa.

24
Q

What are the 2 main pathways that LAs can block Na+ channels with

A

Use Dependent - Hydrophilic

Use Independent - Hydrophobic

25
Q

Why do LAs need to have a weakly basic pKa

A

It is the ionised form of the drug that binds to the channel interior but only non-ionised forms of the drug can cross the membrane

26
Q

What happens to an LA is the pKa is too low

A

Drug will stay deionised inside and outside the cell - no blocking

27
Q

What happens to an LA is the pKa is too high

A

Drug will be ionised - no entry into the axon

28
Q

Due to a combo of pKa and lipophilicity what is a low potency LA

A

Procaine

29
Q

Due to a combo of pKa and lipophilicity what is an intermediate potency LA

A

Mepivacaine
Prilocaine
Chloroprocaine
Lidocaine

30
Q

Due to a combo of pKa and lipophilicity what is a high potency LA

A

Tetracaine
Bupivacaine
Etidocaine
Levobupivacaine

31
Q

What effect does vasodilation have on LAs

A

Enhanced blood flow at site of action leads to more rapid clearance of administered LA

32
Q

How do LAs cause vasodilation

A

blockade of sympathetic vasoconstrictive a1 stimulation

33
Q

Why is a low dose of adrenaline given with LAs

A

To cause vasoconstriction (activation of a1 receptors) preventing loss of anaesthetic

34
Q

Why shouldnt LAs be injected intravenously

A

Risk of systemic effects

35
Q

What are the 2 classes of LAs based on their structures

A

Amides or Esters

36
Q

Describe ester LAs metabolism, duration of action and toxic potential

A
  • Rapidly hydrolysed, short t1/2
  • Hydrolysed by plasma pseudocholinesterase
  • Almost no potential for accumulation
  • Toxicity is either by direct IV injection or repeated exposure
37
Q

Describe amide LAs metabolism, duration of action and toxic potential

A
  • More stable of hydrolysis
  • Primarily hepatic metabolism
  • Can accumulate on repeated dosage
  • Dose related toxicity, may be delayed by minutes to hours
38
Q

What is the easiest way to remember LAs are esters or amides

A

Amides have an ‘i’ before the ‘caine’ suffix

39
Q

What are the benefits and risks of amide LAs compared to esters

A

Amides have longer t1/2

Greater risk of toxicity

40
Q

What are early signs of CNS toxicity by LAs

A

Tinnitus
Dizziness
Light-headedness

41
Q

What are the symptoms of cardiovascular toxicity by LAs

A
  • Hypotension
  • Negative inotropism (reduced cardiac contractile force)
  • Vasodilation by direct actions on smooth muscle and blockade of SNS (except cocaine)
  • Bradycardia leading to asystole through block of cardaic Na+ channels (not always bad - lidocaine is anti-dysrhythmic cus of this)
42
Q

What usually occurs first CNS or CVS toxicity

A

CNS

43
Q

What is the key response method to acute toxicity

A

Maintain oxygenation and normal CO2

44
Q

What factors can increase risk of seizure and/or cardiovascular collapse with acute toxicity

A
  • Cold temperature (slows metabolism)
  • Metabolic or respiratory acidosis
  • Hypoxia
  • Pregnancy

Pharmocolgy (22 decks)

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