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Pathophysiology > Neuropathic Pain > Flashcards

Neuropathic Pain Flashcards

1
Q

Define: pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or describe in terms of such damage

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2
Q

What are the 2 versions of pain?

A

Chronic (long term)

Acute (short term)

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3
Q

Is there treatment for chronic pain?

A

NO. you can only reduce the pain to a tolerable level that will not interfere with their daily function

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4
Q

What are the two main types of pain?

A

Nociceptive - pain associated with trauma, injury and inflammation (what we all think pain is)

Neuropathic - chronic pain syndrome that is associated with sensory abnormalities like numbness, tingling OR for example it may feel like you have a glove on (hand is warmer than the body)

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5
Q

Describe the pain processing loop in very basic terms.

A

Primary afferent (comes into the body) and carries pain impulse to the spinal cord, which relays info to brain. The brain then releases anti-pain sensing back to the spinal cord and then again to the site of injury.

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6
Q

What can chronic pain be caused by?

A

drug, disease, or injury that induces damage to the sensory fibres involved in the pain processing loop

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7
Q

What are some triggers of neuropathic pain?

A
  • alcoholism
  • amputation
  • diabetes
  • drugs
  • herpes zoster
  • HIV/AIDS
  • MS
  • spinal injury
  • stroke
  • tumor
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8
Q

What nerve fibres are associated with pain and temperature? Describe them as well please.

A

Aδ - small, myelinated
C - small, unmyelinated

*these are peripheral afferent fibres

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9
Q

What are the nerve fibres associated with touch and vibration?b Describe them as well please.

A

Aβ - large, myelinated

*Aβ in chronic pain start shooting chronic collaterals off of main root. Some of these hit the laminae 2 which means they are signalling the brain that the patient is in pain again.

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10
Q

Afferent = ?

A

coming into the spinal cord (dorsal)

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11
Q

Efferent = ?

A

leaving spinal cord (ventral)

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12
Q

Where are cortical neurons? When are they excitable?

A

In the brain.

In epilepsy.

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13
Q

Where are dorsal horn neurons? When are they excitable?

A

In spinal cord.

In neuropathic pain.

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14
Q

What is resting membrane potential of a cell?

A

-70 mV

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15
Q

Bc the cell membrane is actually more permeable to K+, the Ek is actually closer to -90 mV. How is this corrected back to the actual -70 mV?

A

Na-K pump
3 Na+ out
2 K+ in

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16
Q

At rest, what ion(s) are high intracellular ?

A

K+

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17
Q

At rest, what ion(s) are high extracellular ?

A

Ca2+, Na+ and Cl-

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18
Q

When the cell becomes more _____, that is what causes pain.

A

positive!

  • whatever happens to make the cell more POSITIVE is what causes the pain response.
  • whatever we can do to make the cell more NEGATIVE with stop the pain response.
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19
Q

So if we blocked Ca and Na channels, what would happen?

A

stop pain! :)

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20
Q

So if we blocked Cl channels, what would happen?

A

Pain would still be present :(

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21
Q

What would happen if we increased the flow of potassium (remember it flows from inside to outside of the cell)

A

stop pain! :)

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22
Q

What type of neurotransmitters bind to receptors and cause opening of Na and Ca channels?

A

Substance P

CGRP

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23
Q

How do anti-epileptic drugs work?

A

Block Ca and Na channels - therefore surpress pain

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24
Q

Describe the natural flow of ions.

A

K+ flows out.

Na+, Ca2+, Cl- flow in.

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25
Q

Describe action potential

A
  • a stimulus causes depolarization
  • Na+ channels open and Na+ flows into cell
  • cell becomes more positive (depolarizes)
  • if cell depolarizes to the threshold, an action potential will result
  • Na+ channels close, K+ channels open
  • Em returns to resting potential

*there is a refractory period following an AP when Na+ channels won’t open

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26
Q

What do excitatory neurotransmitters do?

Give examples please.

A
  • bind to post synaptic receptors and cause depolarization

ex. glutamate (Aδ fibres), Substance P (C fibres) and aspartate

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27
Q

What do inhibitory neurotransmitters do?

Give examples please.

A
  • bind to post synaptic receptors and cause hyper polarization
    ex. GABA, glycine (inter-neuronal fibres)
28
Q

What can hyper excitability be caused by?

A
  • enhancement of excitatory mechanisms

- loss or reduction in inhibition

29
Q

What happens when cell permeability increases?

A
  • Na+ increases intracellularly
  • Ca2+ increases intracellularly
  • when the intracellular conc of these ions increases, depolarization occurs and neutrons fire!
30
Q

Describe the pathophysiology of “windup” (slide 13)

A

Pretty much you want to treat early because one abnormal cell activates other cells which can turn into a big tumor.

*Windup occurs when adjacent neurons produce AP in response to ectopic firing therapy increasing the strength of the pain signal

31
Q

Again, what are the excitatory neurotransmitters?

A

aspartate

glutamate

32
Q

Again, what are the inhibitory neurotransmitters?

A

GABA A

GABA B

33
Q

What receptor does glutamate affect?

A

NMDA

34
Q

What receptor does aspartate affect?

A

AMPA

35
Q

Ca2+ and Na+ are affected by _____ transmission.

A

excitatory

36
Q

Cl- and K+ are affected by ________ transmission

A

inhibitory

37
Q

T or F: a GABA agonist is beneficial in pain management

A

True

  • GABA either increases Cl- influx or K+ efflux (both of these will make the cell less positive, resulting in pain suppression)
38
Q

T or F: a drug that was an NMDA receptor blocker is not beneficial in pain management

A

False

  • NMDA allows Na+ to flow into the cell (this would make the cell more positive so if we block this receptor, it is stopping a positive flow from coming into the cell so it would be beneficial in pain management)
39
Q

AMPA receptor causes leakiness of what ion into the cell?

A

Na+

40
Q

What effect does a GABA-A receptor have?

A

opens Cl- channels

41
Q

What effect does a GABA-B receptor have?

A

opens K+ channels

closes Ca2+ channels

42
Q

The neurotransmitters adrenalin, serotonin, and endogenous opioids all produce what effect?

A

Descending inhibition

43
Q

T or F: symptoms of neuropathic pain are extremely predictable

A

False man - they are very unpredictable

44
Q

What do neuropathic pain symptoms vary greatly depending on???

A
  • severity
  • intensity
  • location
45
Q

What are symptoms of neuropathic pain?

Note** - these are sensory symptoms, not nociceptive!

A
  • pins/needles
  • buring
  • shooting
  • stabbing
  • numbness,
  • tingling
  • jabbing
  • throbbing
  • aching
46
Q

Allodynia

A

pain due to stimulus that doesn’t normally provoke pain

*exaggerated pain symptoms from non-noxious stimuli

47
Q

Hyperalgesia

A

pain response greater than usual to a stimulus that is normally painful
*exaggerated pain symptoms from noxious stimuli

48
Q

Parasthesia

A

Abnormal numbing or prickling or skin

*pins and needles

49
Q

What are the 3 things involved in the pain triad?

A
  • neuropathic pain
  • psychological symptoms
  • sleep disturbances
50
Q

What additional disorders can chronic pain sufferers usually develop?

A
  • insomnia
  • fatigue
  • lack of conc
  • stress
  • depression
  • anxiety
51
Q

Describe the DN4 questionnaire used to diagnose neuropathic pain

A
  • Q’s with Y or N answer
  • total of 10 Q’s
  • Pt must score 4 or more to classify pain as NPP
52
Q

Describe the visual analogue scale used to diagnose neuropathic pain

A

Pt’s are asked to rate pain on a scale of 0-10
0 = no pain
5 = moderate pain
10 = worst pain

53
Q

What are the 4 main points of focus for treating NPP (neuropathic pain) ?

A

1 - inhibition of first order sensory afferent
2 - synaptic inhibition between 1st order sensory afferent and DRG
3 - synaptic inhibition between DRG and dorsal horn interneurons
4 - synaptic inhibition between dorsal horn interneurons and ?? (slide cut off)

54
Q

How can the action potential of a cell be regulated to treat NPP?

A

-decrease excitation
OR
-increase inhibition

55
Q

Describe decreasing excitation

A

Na channel blockers, inhibiting calcium channels or blocking excitatory receptors

56
Q

Describe increasing inhibition

A

GABA agonists, inhibition of serotonin and noradrenalin reuptake

57
Q

How do anti epileptics work to treat NPP?

A
  • reduce influx of Na+ and Ca2+
  • enhance inhibitory effects like GABA
  • reduces conc of glutamate and/or blocks NMDA receptor
58
Q

What is an example of an anti epileptic drug?

A

Gabapentin

*it blocks N type calcium channels

59
Q

How do tri-cyclic anti depressants work to treat NPP?

A
  • block reuptake of noradrenalin and serotonin
  • blocks Na+ and Ca2+ channels and NMDA receptors

ex. amitriptyline

60
Q

How do SSRI (selective serotonin reuptake inhibitors) anti depressants work to treat NPP?

A
  • inhibits serotonin reuptake without affecting noradrenalin

ex. sertraline

61
Q

Describe examples of topical anti-neuralgic agents and how they work to treat NPP.

A
  • exact mechanism is unclear however it has been proposed that these products desensitize afferent neutrons by depleting the release of substance P
    ex. capsaicin ointment or lidocaine
62
Q

What are first line treatments?

A
  • anti-epileptics
  • anti-depressants (tri-cyclic or SSRI)
  • topical anti-neuralgic agents
  • analgesics
63
Q

What are second line treatments?

A
  • analgesics
  • narcotics
  • refractory treatments
64
Q

What are third line treatments?

A
  • analgesics

- combination therapy

65
Q

What are fourth line treatments?

A
  • analgesics

- surgery

66
Q

What do noradrenalin reuptake inhibitors do?

A

suppress pain

Pathophysiology (15 decks)

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