Sensory pathways; nociception Flashcards

1
Q

Explain how nociceptive receptors differ from those for touch and proprioception/features of nociceptors

A
Simple free nerve endings
High threshold and slow adapting fibres
Large receptive fields, low density
Small diameter
Aδ (IV) and C (IV) types
Polymodal; different types of nociceptors respond to different pain stimuli
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2
Q

Difference between nociceptive stimulus and interpretation

A

A nociceptive stimulus can be measured where pain is subjective and subject to other contextual influences

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3
Q

What are some examples of the ion channels which are stimulated by heat, cold, ph<7, intense pressure?

A

Heat: TRPV1
Cold: TRPM8
pH<7: Acid sensing channels
Intense pressure: K+ channels

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4
Q

What is the commonest cutaneous receptor?

A

Polymodal C fibre

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5
Q

What is the commonest skeletal muscle receptor?

A

Chemoreceptor

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6
Q

Which pathway carries visceral pain?

A

Peripheral: autonomic nerves
Central: Spinothalamic and dorsal columns

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7
Q

What is referred pain?

A

Occurs at sites of the body wall whose innervation enters the spinal cord at the same level as the organ

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8
Q

What are the features of visceral pain?

A

Poorly localised
Often referred to the body wall at the same spinal level
Characteristic midline pain (epigastric)
Visceral hyperalgesia may occur

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9
Q

Describe the features of the two sensory neurones which carry nociceptive information

A

Ad: large, fast adapting, fast conducting
C: smaller, slow conducting (unmyelinated), produces dull aching pain

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10
Q

Which neurotransmitters modulate nociceptive information?

A

Bradykinins, histamine, prostaglandins

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11
Q

Describe the pathway of how nociceptive information from the body and face travels to ‘higher centres’

A

Axon from primary sensory neurone synapses in dorsal column
Second order sensory neurone axon decussates and will ascend in the spinothalamic tract
[Info from limbs is lateral. Info from arms is medial.]
Primary sensory neurones from the face travels from trigeminal nerve fibres in the pons down to the spinal trigeminal nucleus in the medulla. Synapses here with second order neurone and cross to join spinothalamic tract.
Second order neurones travel to ventral posterolateral or venture posteromedial nucleus and tertiary sensory neurones relay info to primary somatosensory cortex

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12
Q

What is the use of SI when there is a nociceptive stimulus?

A

It detects the location and intensity of the stimulus.

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13
Q

What additional collateral branches are given off by the spinothalamic tract?

A

Brainstem (via reticular formation)
Thalamus (via intralaminar nuclei)
Hypothalamus
Limbic system

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14
Q

What is the purpose of collateral inputs from the spinothalamic tract?

A

By activating the reticular activating system, increases level of arousal so you will be more aware of danger.
The hypothalamus and limbic system will correlate to the emotional aspects of the stimulus.

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15
Q

What is central (descending) inhibition?

A

Neurones in the periaqueductal grey matter (surrounds the cerebral aqueduct) when there is high activity in the brain will send impulses down the reticular formation of the brainstem.
The descending neurones synapse with interneurones which release ENKEPHALIN which dampens down the activity between the first and second order neurones.

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16
Q

What is peripheral inhibition (gate control theory)?

A

C-fibres (primary nociceptive neurone) enters the dorsal column to synapse with a projection neurone to cross over and join the spinothalamic tract.
Non-nociceptive fibres (e.g. Aa, Ab mechanoceptors) also enter the dorsal columns and have collateral branches that can activate the inhibitory interneurones to inhibit the secondary nociceptive neurone.
Rubbing the area increases the intensity of the stimulus and less activation of second nociceptor neurone.

17
Q

What causes loss of pain sensation?

A

Damage to the spinothalamic tract and location of the lesion

18
Q

What are two examples of nociceptive disruption?

A

Syringomyelia; cyst forms in the cervical region and disrupts fibres from crossing the midline
Charcot joints; hereditary, lack of development of nociceptors, loss of perception of joint pain

19
Q

What are two examples of nociceptive dysfunction?

A

Wind up in dorsal horn: chronic stimulation leads to lowering of pain threshold which causes feelings of continuous pain due to AP from non-noxious stimuli
Thalamic syndrome: pain hypersensitivity

20
Q

How would you treat neuropathic pain?

A

Capsaicin patches
Binds to TRPV1 nerve endings
Direct toxicity on mitochondria which reduces hypersensitivity

21
Q

What is the definition of allodynia?

A

Pain due to stimulus that does not normally provoke pain

22
Q

Define hyperalgesia

A

Increased pain from a stimulus that usually does cause pain

23
Q

Define sensitisation

A

Increased responsiveness of nociceptive neurons to their normal input

24
Q

Define hypoalgesia

A

Diminished pain in response to a normally painful stimulus

25
Q

Define hyperpathia

A

Painful syndrome; abnormally increased pain response to a stimulus, especially one that is repetitive, as well as in increased threshold

26
Q

Define paraesthesia

A

Abnormal sensation (can be spontaneous or evoked)

27
Q

Define dysaethesia

A

Unpleasant abnormal sensation (can be spontaneous or evoked)