Pain Flashcards

1
Q

What inflammatory mediators are released if an injury continues to deteriorate?

A

Prostaglandin
Bradykinin
Nerve growth factors

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2
Q

What is the role of prostaglandin?

A

Controls inflammation and blood flow

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3
Q

What is the role of Bradykinin?

A

Involved in blood-clotting processes

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4
Q

What is the role of Nerve growth factors

A

They make the nerve endings more sensitive.

Released more the injury deteriorates or gets irritated. Nociceptive output will also increase

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5
Q

How are free nerve endings activated when tissue is damaged?

A

Inflammatory mediators are released by tissues.

Histamine and serotonin activate free nerve endings.

Prostaglandin acts as a sensitiser, increasing activation.

The free nerve endings are acting as nociceptors and send these signals to the brain via spinal cord

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6
Q

What is the spinothalamic tract?

A

A pathway in which pain signals to the brain. Carries temperature, pain and crude touch signals.

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7
Q

What are the two sides to the spinothalamic tract?

A

Direct spinothalamic

Indirect spinothalamic

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8
Q

What are the characteristics of the direct spinothalamic tract?

A

Faster Aδ fibres

Contains cortical areas

Better spatial discrimination

Discriminatory sense of pain sensations

Where on the body the damage or danger is happening.

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9
Q

What are the characteristics of the indirect spinothalamic tract?

A

Slower C fibres

Limbic system, hypothalamus, reticular activating system.

Poorer spatial discrimination.

Linked to emotional aspects of pain, understanding salience, memory of previous painful experiences and autonomic responses.

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10
Q

What are the two main types of nociceptor fibre?

A

Aδ Fibre

C Fibre

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11
Q

What sensation of pain do you feel from a mechanical Aδ fibre?

A

Sharp
Pricking
Fast pain

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12
Q

What sensation of pain do you feel from a thermal Aδ fibre?

A

Slow burning
Cold sharp
Pricking

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13
Q

What sensation of pain do you feel from a C fibre?

A

Burning
Cold
Slow, deep pain

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14
Q

What is a Aδ fibre?

A

A myelinated and larger diameter axon, rapid conduction speed.

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15
Q

What is a C fibre?

A

Unmyelinated and smaller diameter axon. Slow conduction speed.

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16
Q

Describe the descending inhibitory pathway

A

Neurons in the brain stem send efferent fibres to the spine. They pass downward in the spine.

The descending modulatory fibres release serotonin and norepinephrine. Releasing powerful endorphins (enkephalins) which reduce the incoming nociceptive signals and therefore reduce central perception of pain.

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17
Q

When is glutamate released?

A

Glutamate is released when the 1st order neuron reaches the synapse and it activates a series of receptors on the polysynaptic cell called AMPA receptors.

18
Q

What is the NDMA receptor?

A

The more glutamate is being activated, a second receptor is activated - NMDA.

This receptor sensitises the neuron and possible long-term changes to excitability.

19
Q

What is central sensitisation?

A

Nociceptive signals are pumped to the brain from the 2nd order neuron due to the changes in excitability from the AMPA and NDMA receptor being activated from glutamate production.

20
Q

What is the function of the 1st order neuron in transient sensitisation?

A

Transient stimulation of the 1st order neuron leads to the activation of AMPA receptors on 2nd order neurons

21
Q

WHEN does central sensitisation happen?

A

When NMDA receptors are activated on the 2nd order neuron

22
Q

What is the effect of central sensitisation?

A

Nociceptive signals become more sensitive, a stronger signal is sent to the brain, making the pain experience worse

23
Q

What is peripheral sensation?

A

Persistent activation of free nerve endings which hence releases substance P (a powerful vasodilator)

24
Q

Why is peripheral sensation a vicious cycle?

A

If you keep damaging the same damaged tissue, it will hurt more and more and more. Causes a positive feedback loop and hence a vicious cycle.

25
Q

Peripheral compared to central sensitisation.

A

PS - substance P mediated feedback loop. (presynaptic neurons sensitised)

CS - NMDA receptors activated with strong/activated activation. (postsynaptic neurons sensitised)

26
Q

What is nociception vs pain perception?

A

Nociception is the warning signal, they are not pain.

Pain is our brain telling us how important those signals are. The brain generates the pain experience.

27
Q

What psychological states ‘open’ the pain experience gate?

A
Stress
Depression 
Boredom 
Worry 
Lack of activity
28
Q

What psychological states ‘close’ the pain experience gate?

A

Relaxation
Optimism
Distraction
Positive sense of control

29
Q

What are 4 key psychological factors that can affect pain perception?

A
  1. Attention
  2. Experience
  3. Expectation
  4. Perceived threat
30
Q

What affect does perceptual filtering have on pain perception?

A

Perceptal filtering of incoming nociceptive information can amplify or attenuate pain perception. (Wiech et al. 2008)

31
Q

What is the Neuromatrix theory of Pain States?

A

Many different areas in the brain get involved in processing this nociceptive information. What goes on in your brain affects this processing.

32
Q

What factors affect how the neuromatrix of our brain respond to nociceptive signals?

A
Learned responses 
Attitudes/fears 
Perception of danger 
Health beliefs 
Psychological status
33
Q

What are the 3 types of pain?

A

Somatic (superficial)
Somatic (deep)
Visceral (deep)

34
Q

What areas of pain is affected (somatic/visceral)

A

Somatic (superficial = skin)

Somatic (deep = deeper skin, muscles, joints)

Visceral (deep = organs)

35
Q

What does somatic/visceral pain feel like?

A

S superficial = sharp fast pain

S deep = burning/itching/aching

Visceral = dull ache/burning

36
Q

What is the 1st order neuron?

A

1st order neuron carries the action potentials up the spinal cord

37
Q

What is the 2nd order neuron?

A

2nd order neuron carries the information up the spine, to the thalamus

38
Q

What is the 3rd order neuron?

A

3rd order neuron carries the signal further into the CNS from the thalamus to the somatosensory cortex which makes up aware of pain

39
Q

What is hyperalgesia?

A

Increased sensitivity following tissue injury

Primary = localised 
Secondary = extending to undamaged sites
40
Q

What is Allodynia?

A

Increased sensitivity to non-noxious stimulus