Pain Flashcards

1
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage.
It acts as a protective sense.
Always subjective as the unique process is experienced in the brain.
Combines discriminative sensory and affective / emotional components.

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2
Q

What is nociception and what do nociceptors do?

A

The sensory component of pain detected by free nerve endings in skin, muscle and viscera.
Nociceptors are activated by noxious stimuli that are sufficient to cause tissue damage. They generate an AP which is propagated centrally.

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3
Q

How is stimulus intensity coded?

A

Stimulus intensity is encoded though firing rate. Stimulus determines the quality of pain experienced.

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4
Q

What are the two types of nociceptors and what does each respond to?

A

Mechanical receptors respond to strong shearing force in skin e.g. cut, strong blow, to induce a sharp pain via A delta fibres.

Polymodal receptors respond to heat >46, sharp blow, chemicals from damaged tissue (K, H, Histamine, PGs, bradykinin) to cause a dull burning pain via C fibres.

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5
Q

How is the stimulus modulated in the dorsal horn?

A

The excitatory primary afferents travel to the dorsal horn where the AP circulates whilst interneurons modulate the stimulus, using descending information from the brain.

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6
Q

What type of fibres are C? (speed and myelination)

A

Unmyelinated, slow conducting fibres.

Majority of pain fibres are C

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7
Q

What type of fibres are A delta? (speed and myelination)

A

Fast conducting, myelinated fibres.

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8
Q

What causes a second pain response?

A

The two types of nociceptors have different conducting velocities. The fast A delta fibres produce the first response = sharp pain.The slow C fibres produce a second pain response = dull burning pain.

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9
Q

How does a pain stimulus trigger a motor reflex?

A

As the secondary fibre arises in the dorsal horn, it decussates into the contralateral lateral spinothalamic tract. This triggers alpha motor neurons in the ventral horn.

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10
Q

What tract is used to carry sensory information to the brain?

A

Lateral spinothalamic tract - bundle of sensory axons ascending through the white matter of the anterolateral system to the brain. Passes through the limbic system of the thalamus and perceived at subcortical level for experience and localised on the cortex to determine origin of pain.

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11
Q

What is the zone of Lissauer / dorsolateral tract?

A

Located at the entrance of the posterior nerve root into the dorsal horn carrying crude touch and pressure. It allows the entering nerve to ascend or descend to other spinal levels via unmyelinated fibres for interconnecting segments.

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12
Q

What and where is substansia gelatinosa?

A

Located at the apex of dorsal horn, receiving input from pain and temperature sensory afferents. It connects fibres to different laminar areas within the grey matter via interneurons for modulation of pain perception.

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13
Q

What kind of organisation is present in the grey matter of the dorsal horn?

A

Laminar organisation - groups neurons with the same structure and function. The afferents will synapse either directly or indirectly via interneurons, to second order neurons.
Allows modulation.

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14
Q

In which laminae are the following fibres located:
A beta -
A delta -
C fibre -

A

A beta - III to V (cutaneous mechanoreceptor)
Cutaneous A delta (pressure and temperature) and C (chemical, mechanical, thermal) - I to II
Visceral A delta and C - I, V, X (diffuse fibres so less easy to identify specific origin of pain).

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15
Q

What is the gate theory?

A

A pain signal will only be passed onto second order neurons if it can overcome the inhibition exerted by inhibitory interneurons. The interneurons either spontaneously release inhibitory NT in a tonic manner or are stimulated by primary afferent to prevent second order neurons from firing unless signalled to. Keeps excitability low.

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16
Q

How does a non-noxious stimulus create an analgesic effect?

A

Pain afferents, A delta and C, disinhibit the inhibiton of a second order neuron. Increasing a non-noxious stimulus will increase the activity of the inhibitory interneuron to prevent the pain stimulus from disinhibiting. e.g. rubbing, TENs, acupuncture, physiotherapy.

17
Q

How does the descending pathway reduce the level of pain experienced?

A

The descending pathway arises from the brainstem nuclei and causes release of 5-HT, NAd and enkephalin. This creates an intrinsic analgaesic system by stimulating the inhibitory interneurons and closing the spinal gate.

18
Q

Which brainstem nuclei are involved in the descending pathway?

A

Rostroventral medulla/ ventromedial nuclues, periaqueductal gray (Primary control centre for pain containing enkephalin producing cells), locus coereleus (pons).

19
Q

How does the state of chronic pain alter sensitivity to pain?

A

It increases sensitivity due to peripheral and central sensitisation through the modification of neurotransmission and nociceptor plasticity (response is determined by previous experience)

20
Q

What is hyperalgesia?

A

An enhanced pain response to a noxious stimulus.

21
Q

What is allodynia?

A

A pain response to a previously non-noxious stimulus due to central sensitisation

22
Q

What is primary hyperalgesia?

A

Increased pain sensitivity that occurs directly in damaged tissue through peripheral sensitisation. Promotes central sensitisation.

23
Q

What is secondary hyperalgesia?

A

Increased pain sensitivity in a distant site from the injury via central sensitisation.

24
Q

What is the process of peripheral sensitisation leading to primary hyperalgesia?

A

1) Noxious stimulus causes release of factors from damaged tissue.
2) Causes antidromic AP (travelling in opposite direction to normal) in the fibres innervating the tissue.
3) Stimulates release of substance P and CGRP from nerve ending.
4) These act on vasculature for plasma extravasation and immune cell migration into tissue.
5) Immune cells release pro-inflammatory factors = redness and swelling
6) Inflammatory factors act on nociceptor to lower the threshold of AP = sensitisation = primary hyperalgesia.

25
Q

What is the process of peripheral sensitisation that results in secondary hyperalgesia?

A

Antidromic AP travel along axons innervating neighbouring uninjured tissue due to overlap in sensory territories = increased sensitivity in surrounding tissues.

26
Q

What is the process of central sensitisation?

A

Occurs in dorsal horn.

1) High frequency afferent input invades presynaptic terminal (may be due to peripheral sensitisation)
2) Stimulates release of substance P and glutamate.
3) Sub. P acts at NK-1 R and glutamate at AMPA R to depolarise post synaptic membrane
4) Sufficient depolarisation releases the voltage dependent Mg block on NMDA R.
5) Glutamate interaction at NMDA results in Ca entry into neuron
6) Ca increases neuron’s responsiveness and amplifies rate of AP firing of the ascending pathway = ascending pain signal enhanced