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Flashcards in Neuropathic Pain Deck (66):
1

Define: pain

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

2

What are the 2 versions of pain?

Chronic (long term)
Acute (short term)

3

Is there treatment for chronic pain?

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

4

What are the two main types of pain?

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)

5

Describe the pain processing loop in very basic terms.

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.

6

What can chronic pain be caused by?

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

7

What are some triggers of neuropathic pain?

-alcoholism
-amputation
-diabetes
-drugs
-herpes zoster
-HIV/AIDS
-MS
-spinal injury
-stroke
-tumor

8

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

Aδ - small, myelinated
C - small, unmyelinated

*these are peripheral afferent fibres

9

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

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.

10

Afferent = ?

coming into the spinal cord (dorsal)

11

Efferent = ?

leaving spinal cord (ventral)

12

Where are cortical neurons? When are they excitable?

In the brain.
In epilepsy.

13

Where are dorsal horn neurons? When are they excitable?

In spinal cord.
In neuropathic pain.

14

What is resting membrane potential of a cell?

-70 mV

15

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?

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

16

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

K+

17

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

Ca2+, Na+ and Cl-

18

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

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.

19

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

stop pain! :)

20

So if we blocked Cl channels, what would happen?

Pain would still be present :(

21

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

stop pain! :)

22

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

Substance P
CGRP

23

How do anti-epileptic drugs work?

Block Ca and Na channels - therefore surpress pain

24

Describe the natural flow of ions.

K+ flows out.
Na+, Ca2+, Cl- flow in.

25

Describe action potential

-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

26

What do excitatory neurotransmitters do?
Give examples please.

-bind to post synaptic receptors and cause depolarization
ex. glutamate (Aδ fibres), Substance P (C fibres) and aspartate

27

What do inhibitory neurotransmitters do?
Give examples please.

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

28

What can hyper excitability be caused by?

-enhancement of excitatory mechanisms
-loss or reduction in inhibition

29

What happens when cell permeability increases?

-Na+ increases intracellularly
-Ca2+ increases intracellularly

* when the intracellular conc of these ions increases, depolarization occurs and neutrons fire!

30

Describe the pathophysiology of "windup" (slide 13)

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

Again, what are the excitatory neurotransmitters?

aspartate
glutamate

32

Again, what are the inhibitory neurotransmitters?

GABA A
GABA B

33

What receptor does glutamate affect?

NMDA

34

What receptor does aspartate affect?

AMPA

35

Ca2+ and Na+ are affected by _____ transmission.

excitatory

36

Cl- and K+ are affected by ________ transmission

inhibitory

37

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

True

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

38

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

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

AMPA receptor causes leakiness of what ion into the cell?

Na+

40

What effect does a GABA-A receptor have?

opens Cl- channels

41

What effect does a GABA-B receptor have?

opens K+ channels
closes Ca2+ channels

42

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

Descending inhibition

43

T or F: symptoms of neuropathic pain are extremely predictable

False man - they are very unpredictable

44

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

-severity
-intensity
-location

45

What are symptoms of neuropathic pain?

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

-pins/needles
-buring
-shooting
-stabbing
-numbness,
-tingling
-jabbing
-throbbing
-aching

46

Allodynia

pain due to stimulus that doesn't normally provoke pain
*exaggerated pain symptoms from non-noxious stimuli

47

Hyperalgesia

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

48

Parasthesia

Abnormal numbing or prickling or skin
*pins and needles

49

What are the 3 things involved in the pain triad?

-neuropathic pain
-psychological symptoms
-sleep disturbances

50

What additional disorders can chronic pain sufferers usually develop?

-insomnia
-fatigue
-lack of conc
-stress
-depression
-anxiety

51

Describe the DN4 questionnaire used to diagnose neuropathic pain

-Q's with Y or N answer
-total of 10 Q's
-Pt must score 4 or more to classify pain as NPP

52

Describe the visual analogue scale used to diagnose neuropathic pain

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

53

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

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

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

-decrease excitation
OR
-increase inhibition

55

Describe decreasing excitation

Na channel blockers, inhibiting calcium channels or blocking excitatory receptors

56

Describe increasing inhibition

GABA agonists, inhibition of serotonin and noradrenalin reuptake

57

How do anti epileptics work to treat NPP?

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

58

What is an example of an anti epileptic drug?

Gabapentin
*it blocks N type calcium channels

59

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

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

ex. amitriptyline

60

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

-inhibits serotonin reuptake without affecting noradrenalin

ex. sertraline

61

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

-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

What are first line treatments?

-anti-epileptics
-anti-depressants (tri-cyclic or SSRI)
-topical anti-neuralgic agents
-analgesics

63

What are second line treatments?

-analgesics
-narcotics
-refractory treatments

64

What are third line treatments?

-analgesics
-combination therapy

65

What are fourth line treatments?

-analgesics
-surgery

66

What do noradrenalin reuptake inhibitors do?

suppress pain