Pain Flashcards

1
Q

How can pain be defined?

A

‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage’

  • a combination of sensory and affective components
  • pain is always subjective
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2
Q

What is nociception?

A

The sensory component of pain alone

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3
Q

What is the pathway by which pain is perceived?

A
  • Free nerve endings in skin, muscle, viscera
  • Activated by intense (noxious) stimuli
  • Generates AP
  • Stimulus intensity encoded through firing rate
  • Propagated centrally
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4
Q

What are the 2 types of nociceptors?
What are they activated by?
What pain fibres are they associated with?

A

Mechanical
- activated by strong shearing force in skin
- e.g cut, strong blow
- A delta fibres
Polymodal
- respond to many stimuli e.g. sharp blow, damaging heat, chemicals released by damaged tissue (e.g. K+, H+, histamine, prostaglandins, bradykinin)
- C fibres

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5
Q

Are primary sensory neurones inhibitory or excitatory?

A

All excitatory

Synapse in dorsal horn

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6
Q

Describe structural and functional differences between C and Adelta fibres
What kind of pain are they responsible for?

A

Adelta fibres
- myelinated
- fast transmission/conduction velocity
- responsible for first, sharp pain, quickly after stimulus
C fibres
- unmyelinated
- slower tranmission/conduction velocity
- responsible for the second, dull, burning pain, present longer after stimulus

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7
Q

How are nociceptive inputs organised in the dorsal horn?

A

laminar and somatotopic organisation

-

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8
Q

Where do C fibres terminated in the dorsal horn of the spinal cord?

A

substantia gelatinosa

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9
Q
  • What makes up the vast majority of dorsal horn neurones?
  • What is their function?
  • Are they inhibitory or excitatory?
  • What must the pain signal do, in order to be sent to the brain?
A
  • local interneurones
  • modulate activity of projection neurones
  • majority are inhibitory, spontaneously active, or stimulated by primary afferent input
  • pain signal must overcome inhibition to be sent to brain
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10
Q

Describe the gate control theory of pain in terms of the neurones involved in the following:

  • Gate closed to non-noxious input
  • Arrival of noxious stimulus, opening of gate
A

Gate closed to non-noxious input
- Abeta mechanoreceptor (non-nonxious) fibres are primary afferent neurones and are therefore excitatory
- Inhibitory interneurones in the dorsal horn inhibit the output neurones and prevent pain signals to the brain
- The Abeta fibres are excitatory and synapse with these interneurones so that no pain signals are sent if the mechanoreceptors are stimulated
Gate open, noxious stimulus
- Now there is excitatory input from Adelta/C fibres directly onto the output neurone
- But also onto another inhibitory interneurone that inhibits the other inhibitory neurone (connected to mechanoreceptors) and therefore disinhibits the output neurone and so pain signals can ascend to the brain

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11
Q

What is the clinical significance of the gate control theory

A
  • increased non-noxious afferent input to the spinal cord for analgesic effect
  • TENS, electrical signal through skin activated Abeta fibres but not Adelta/C.
  • Abeta are big and quite easy to excite
  • Abeta input is capable of closing the gate at the spinal level
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12
Q

What are the ascending pathway involved in the reception of pain and what are their roles?

A

Ascending spinothalamic pathway - C fibres mostly

  • synapses in the thalamus
  • perceived at a subcortical level
  • localised at the cortical level
  • limbic system important in feeding in affective component (emotion)
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13
Q

What are the descending pathways involved?

What is their role?

A
  • feedback control
  • cortical input can trigger descending fibres which could reduce the pain
  • brain stem nuclei (rich in opioids), released of 5-HT from RV medulla, noradrenaline from PAG, ekephalin from locus coereleus
  • closing the spinal gate
  • Intrinsic Analgesia System
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14
Q

What is the idea of facilitated pain?

What are the two mechanisms that will do this?

A

normal physiological pain is directly proportional to afferent input duration and intensity
- however in chronic/persistent pain state, sensitivity to pain can be increased
Two mechanisms
1. peripheral sensitisation
2. central sensitisation

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15
Q

What is hyperalgesia?

A

enhanced painful response to a normally painful stimulus

–> more pain

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16
Q

What is allodynia?

A

painful response to a normally non-painful stimulus

17
Q

What is the pain threshold?

A

The stimulus intensity at which an innocuous stimulus because noxious

18
Q

Describe the changes in pain sensation induced by injury

A

Injury shift the pain sensation curve to the left
Results in allodynia and hyperalgesia
Pain threshold also shifted down

19
Q

Describe the mechanism of peripheral sensitisation

A
  • noxious stimulation activates nociceptor directly and causes release of various factors in damaged skin/underlying tissue
  • antidromic action potential propagation (NT release at receptor) can occur along the primary afferent fibre branches that innervate injured tissue
  • this stimulates substance P and CGRP realise from peripheral nerve ending that acts on the vacularture to cause plasma extravasation and immune cell migration into tissue
  • Immune cells release pro-inflammatory substances that act on nociceptors to lower threshold for AP generation
  • lower threshold = sensitisation
  • antidromic AP propagation along fibre branches that innervate inured AND neighbouring uninjured tissue. Result in sensitisation of neurones that also innervate the neighbouring uninjured tissue.
  • This depends on the overall of sensory territories - contributes to sensory hyperalgesia
20
Q

What is primary hyperalgesia?

What is secondary hyperalgesia?

A

Primary hyperalgesia = increase pain sensitivity that occurs in the damaged tissue
- peripheral sensitisation promotes central sensitisation
Secondary hyperalgesia = increased pain sensitivity sudan from the site of injury (surrounding tissues)

21
Q

Describe the mechanism of central sensitisation and secondary hyperalgeis

A
  • mechanism in the spinal dorsal horn
  • high frequency afferent input (possibly as a result of peripheral sensitisation) invades presynaptic terminal
  • stimulates substance P release (high frequency is required, so not involved in acute pain signalling) as well as increasing glutamate release
  • combination of substance P –> Nk1 receptor and glutamate –> AMPA receptor
  • produces sufficient depolarisation of the post synaptic membrane to relieve voltage-dependent Mg2+ block of NMDA receptor
  • glutamate can then bind to the NMDA receptor resulting in Ca2+ entry
  • Ca2+ entry activates intracellular mechanisms increasing neurone responsiveness and amplification of rate of action potential efferent firing long ascending nociceptive pathway