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BAB > L05: Sensory Systems: Pain > Flashcards

L05: Sensory Systems: Pain Flashcards

1
Q

What is the definition of pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage

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2
Q

What is pain a combination of

A

Sensory (discriminative) and emotional

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3
Q

What is nociceptors

A

The sensory component of pain alone

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4
Q

What is the stimulus for pain

A 
Injury 
Heat
Cold 
Inflammation 
Low ph
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5
Q

What does the stimuli for pain cause to the tissues

A

Damage

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6
Q

What does the pain stimuli activate

A

Free nerve endings

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7
Q

Where are the free nerve endings found

A

Skin
Muscle
Viscera

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8
Q

What does nerve endings generate when they detect a stimulus

A

Action potential

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9
Q

What is a nociceptors

A

The free nerve ending

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10
Q

What are the 2 types of nociceptors

A

1) High threshold mechanical nociceptors/ mechanical nociceptors
2) polymodal nociceptors

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11
Q

What activates mechanical nociceptors

A

Strong shearing force in skin

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12
Q

What activates polymodal nociceptors

A

Multiple stimulus such as sharp stimulus, heart (above 46c) chemicals released by damaged tissue

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13
Q

What chemicals does damaged tissue release

A

Potassium
Hydrogen
Prostaglandins
Bradykinin

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14
Q

What type of pain does the activation of mechanical nociceptors result in

A

Sharp pain

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15
Q

What type of pain does the activation of polymodal nociceptors result in

A

Dull burning pain

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16
Q

What axons/fibres are mechanical nociceptors found on

A

A delta fibres

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17
Q

What axons/fibres are polymodal nociceptors found on

A

C fibres

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18
Q

Are a delta fibres and c fibres inhibitory or excitatory fibres

A

Excitatory

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19
Q

What happens to the primary neurone when it receives a stimulus

A

It generates and action potential

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20
Q

What happens to the primary neurone when it receives the AP

A

It sends the AP to the second order neurone at the dorsal horn of spinal cord

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21
Q

Where does the second order neurone terminate

A

Thalamus

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22
Q

What type of information does both c fibres and a delta fibres carry

A

Noxious information

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23
Q

If the a delta fibre results in sharp pain what is the structure of the axon

A

Myelinated

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24
Q

If a c fibre creates a dull burning pain what is the structure of the axon

A

Non-myelinated

25
Q

If the axon is myelinated what does it mean in terms of its propagation speed

A

Speed is fast / fast transmission

26
Q

If an axon is un-myelinated what does it mean in terms of its propagation speed

A

Speed is slow/ slower transmission

27
Q

What is first pain

A

The pain that quickly comes on and quickly off due to a delta fibres

28
Q

What is second pain

A

Pain that gradually builds up and slowly fades away due to c fibres

29
Q

What is the substantia gelatinosa

A

The region in the spinal cord where 2nd order neurone of cell body is for the dorsal columns

30
Q

In the dorsal horn what are the layers of organisation called

A

Lamina

31
Q

Which lamina are a delta fibres found in

A

Lamina 1 and 5

32
Q

Which lamina are c fibre found in

A

Lamina 2

33
Q

Which lamina are A beta fibre found in

A

Lamina 4

34
Q

How do interneurones inhibit ascending neurones

A

The interneurones are inhibitory and inhibit the ascending signal to the brain

35
Q

What is the gate theory of pain to non noxious input

A

1) Primary fibres i.e a beta that signal non noxious signal send an excitatory signal to the ascending signal
2) At the same time inhibitory neurones are sending an inhibitory signal to the ascending neurone
3) the primary fibres synapse with the inhibitory neurone so the inhibitory interneurone sends more inhibitory signal and overcomes the excitatory signal of the primary neurone
4) the gate is therefore closed for non-noxious info

36
Q

What happens to the gate when there is a noxious stimulus

A

1) a delta or c fibres synapse with the secondary neurone and send excitatory signal which is not sufficient to open the gate on its own
2) a delta or c fibres therefore synapse with another population of inhibitory interneurones
3) these inhibitory interneurones inhibit the other inhibitor interneurones that inhibit the ascending neurone
4) the inhibitor interneurones therefore are switched off and the gate opens
5) ascending neurone sends an excitatory signal to the brain that is for noxious info

37
Q

Give an example of the gate theory that comes into place in a real life scenario

A

1) You bang your knee (noxious info)
2) to stop the noxious info i.e pain to the brain You rub your knee
3) rubbing your knee is non-noxious info so beta fibres are activated and activate the inhibitory interneurones
4) gate is closes and you relive the pain

38
Q

After overcoming the gate control what tract does the signal travel in

A

Spinothalamic tract

39
Q

At what level of the brain do you add emotion to the pain that is perceived

A

Subcortical region

40
Q

Where does the signal feed into the brain to localise the pain in the spinothalamic tract

A

Cortex

41
Q

After the spinothalamic tract feeding into the brain which tract becomes activated

A

The descending pathways/tracts

42
Q

What does the descending pathways do to the gate

A

Close the gate

43
Q

How does descending pathway close the gate

A

Release 5HT, Noradrenaline, enkephalin

44
Q

What is the close of the gate by the descending tract called

A

Intrinsic analgesia system

45
Q

What is facilitated pain

A

The sensation of pain= afferent input duration and intensity

46
Q

To experience pain what does the stimulus have to reach

A

a threshold

47
Q

When can the threshold to cause pain decrease

A

After an injury

48
Q

What happens after an injury when you apply a continous stimulus

A

You experience more pain i.e hyperalgesia

49
Q

What happens when you get a pain that you previously did not get

A

Allodynia

50
Q

What is the mechanism for getting hyperalgesia and allodynia

A

Sensitation of peripheral nociceptors

51
Q

What is the processes involved in the sensitisation of peripheral nociceptors

A

1) nerve ending will have a stimulus of damaged cells
2) the stimulus causes action potential to be fired which propagates antidramic so the ap goes down the branches of the axon
3) this causes the release of substances of substance P and CGRP at the peripheral ending
3) subtance P and CGRP diffuse away from the nerve ending and interval with receptors on the blood vessel
4) as a result you get , vasodilation, plasma extravasate on and immune cell migrating and activation
5) immune cell activation causes the release of: prostaglandins, h+, bradykinin, NGF and cytokines (all referred to as inflammatory soup)
6) nerve endings that have receptors for the inflammatory soup are detected and this lowers the threefold for the AP
7) you are now sensitised

52
Q

What is the process described previously for sensitisation of peripheral nociceptors called

A

Neurogenic inflammation

53
Q

What is alloydina

A

Lower threshold mean more ap is fired and more noxious info is perceived from a smaller stimulus

54
Q

What is hyperalgesia

A

A nerve ending with peripheral sensitisation has a lower threshold so when you apply a big stimulus (that also previously caused pain) causes a more pain

55
Q

Where does primary hyperalgesia occur in

A

In the damaged tissue

56
Q

Where does secondary hyperalgesia occur in

A

Around the site of injury

57
Q

Describe the process that occurs at the dorsal horn between the primary afferent and second order neurone for normal pain (acute pain)

A

1) glutamate from the primary afferent is released in response to low AP firing
2) on the post synaptic membrane, AMPA (a glutamate receptor) receives glutamate
3) pain is sensed by the second neurone for signal to the brain

58
Q

Which fibres/axons foes this signalling occur in

A

A delta

C fibre

59
Q

Describe the process that occurs at the dorsal horn between the primary afferent and second order neurone in facilitated pain i.e central sensitisation

A

1) in facilitated pain there is lots of AP at high frequency so more glutamate is released from the primary neutrons
2) substance P is also released from the primary neurone
3) subtance P binds to NK-1 receptor on the post synaptic membrane of the second order neurone
4) glutamate binds to AMPA receptor on the post-synaptic membrane of the second order neurone
5) nk-1 and AMPA activation activates another glutamate receptor called NMDA
6) NMDA has its magnesium iron removed to glutamate can bind to it
7) NMDA causes calcium influx
8) the calcium influx triggers second messenger cascades to send a bigger signal to the brain

BAB (21 decks)

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