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BAMS > Oral Biology- Action Potentials and LA > Flashcards

Oral Biology- Action Potentials and LA Flashcards

1
Q

What is RMP due to?

A

Mainly due to diffusion of K+ from cell interior through K+ channels

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2
Q

What is the diffusion potentionals of sodium and potassium?

A

Na+ would diffuse into cell, but ‘resting’ membrane is impermeable to Na+

K+ would diffuse out of cell, and ‘resting’ membrane is very permeable to K+

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3
Q

How does the sodium/potassium pump contribute to the resting membrane potential?

A

Exchanges unequal numbers of K+ and Na+

Pump moves 3 Na OUT
And 2 K IN

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4
Q

What is the AP thresholds?

A

-55mV

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5
Q

What is the ‘rising’ phase AP due to?

A

Na influx

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6
Q

What is falling AP stage due to?

A

K efflux

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7
Q

What are the 3 voltage-gated sodium channel positions?

A

Channel closed
- m-gate closed, h-gate open

Channel open
- m-gate open, h-gate open

Channel closed
- m-gate open, h-gate closed (refractory period)

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8
Q

What is the first stage of AP?

A

Stimulus applied– depolarisation
MP moves towards ‘threshold’
Gated ion channels closed

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9
Q

What happens when MP reaches threshold?

A

MP reaches -55mV

  • Na channels start to open
  • Na influx
  • More depolarisation

K channels remain closed

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10
Q

What happens after MP reaches 0mV

A

MP overshoots 0mV

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11
Q

What happens when MP reaches +35mV?

A

Na channels shut
Inactivation (‘h’) gate closes

K channels open
K efflux begins

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12
Q

What happens after K efflux begins?

A

AP downstroke
Refractory period

MP returns to ‘resting’ level
Ion channels return to resting stage

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13
Q

What is independent of stimulus?

A

Amplitude is independent of stimulus

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14
Q

What causes refractory period?

A

Due to inactivation of voltage-gated sodium channels

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15
Q

What are 4 consequences of the refractory period?

A
  1. Limits maximum firing frequency of AP in axons
  2. Ensures unidirectional propagation
  3. Prevents summation of APs
  4. Prevents summation of contractions in cardiac muscle- the cardiac AP lasts as long as ventricular contractions
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16
Q

What lays down myelin?

A

Glial cells

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17
Q

What is the function of myelin sheaths?

A

Forms insulating layer, decreases leakage of current from axon

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18
Q

Name the interruptions in myelin sheath

A

Nodes of Ranvier

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19
Q

What are the 3 axon types present in ‘cutaneous’ nerves?

Give function

A

Aβ- myelinated- mechanoreceptors

Aδ- myelinated- mechanoreceptors, thermoreceptors, nociceptors, chemoreceptors

C- UNmyelinated- mechanoreceptors, thermoreceptors, nociceptors

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20
Q

How do LAs work?

A

Blocks voltage-gated Na+ ion channels, preventing generation of AP

21
Q

What are the 3 connective tissue layers surrounding nerves?

A

Epineurium- outer sheath

Perineurium- sheath surrounds bundles (fasicles) of nerves

Endoneurium- sheath around individual fibres within nerve

22
Q

What is the order of block in different fibres?

A

Aδ
C
Aβ
Aα

23
Q

What is the mechanism of LA actions?

A

LA binds to site in Na channel
Blocks channel and prevents Na influx

This blocks AP generation and propagation

24
Q

What are the 3 components of LA molecule

A

Organic molecules:

Aromatic region (hydrophobic)
Ester or amide bond
Basic amine side chain (hydrophilic)

25
Q

Why is LA partly dissociated

A

Active in ionised form

Can only cross membrane in un-ionised form

26
Q

Why is the LA base present as and why?

A

Hydrochloride

Increases solubility in aqueous solution

27
Q

What 4 other components are added to LA preparations?

A

Reducing agent (e.g. Sodium metabisulphide)
Preservative(s)
Fungicide
Vasoconstrictor

28
Q

Name 3 ester LAs

A

Cocaine
Procaine
Benzocaine*

29
Q

Name 6 amide LAs

A 
Lignocaine (lidocaine)*
Prilocaine*
Articaine*
Mepiracaine
Bupiracaine*
Ropiracaine
30
Q

Name 2 types of vasoconstrictors in LA

A

Adrenaline

Felypressin (synthetic vasopressin)

31
Q

What receptors does adrenaline act on and what effects are there?

A

Act on receptors on vascular smooth muscle

α receptors: vasoconstriction
β2 receptors: vasodilation
β1 receptors: cardiac muscle
- positive chonotropic effect (increases HR)
- positive inotropic effect (increases force of heart)

32
Q

What receptors does felypressin act on?

A

ADH receptors

33
Q

What effect does adrenaline have locally?

A

Vasoconstrictor (α receptors)

34
Q

What effect does adrenaline have systemically?

A

Lowers TPR (β > α)

35
Q

What effect does adrenaline have on CO?

A

Increases CO

36
Q

What effect does adrenaline have on arterial blood pressures?

A

Little or no effect

37
Q

What effect does noradrenaline have locally?

A

Vasoconstrictor effect

38
Q

What effect does noradrenaline have systemically?

A

Increased TPR (α > β)

39
Q

What effect does noradrenaline have on CO?

A

Increases

40
Q

What effect does noradrenaline have on arterial BP?

A

Increases

41
Q

What causes inactivation of LA?

A

‘Washout’ from tissues by blood supply

42
Q

How are ester type LAs broken down and how long is their action?

A

Broken down my tissue esterases

Action quite brief

43
Q

How are amide type LAs broken down and how long is their action?

A

Broken down by liver amidases

Longer duration of action

44
Q

Name 6 modes of administration of LA

A 
Surface application ('topical')*
Injection
Local infiltration*
Regional nerve block*
Root nerve block (spinal, epidural)
IV
45
Q

What are the 2 LA preparations for lignocaine and prilocaine?

A

2% lignocaine HCl
2% lignocaine HCl + 1:80,000 adrenaline

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

46
Q

What is max dose of lignocaine?

A

Approx 4mg per kg body weight

47
Q

What is max adrenaline dose?

A

500 μg

48
Q

How much adrenaline is in a cartridge?

A

27.5 μg

49
Q

What usual values are the resting membrane potential?

A

20-90 mV

BAMS (9 decks)

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