Pain Flashcards

1
Q

What is pain?

A

Subjective unpleasant sensory experience associated with nociception

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2
Q

What is nociception?

A

Information indicating tissue damage

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3
Q

Where are nociceptive signals first perceived as pain?

A

Thalamus

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4
Q
What does the following describe?
simple naked nerve ending
high threshold mechanoreceptor
responds to intense mechanical stimulus
thinly myelinated axon (5-30m/s)
responsible for first sharp, well-localised pain
A

A delta fibre

- nociceptor

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5
Q

What does the following describe?
simple naked nerve ending
responds to intense mechanical stimulation, temperatures >42 degrees & irritant chemicals
unmyelinated axon (0.5-3m/s)
responsible for slow, second, poorly localised pain

A

c fibre

– polymodal nociceptor

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6
Q

What ion channel does capsaicin and high temperature act on?

A

Trpv1

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7
Q

How do high doses of capsaicin makes us more tolerant to hot chillis?

A

It desensitises pain fibres and deplete them of substance P

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8
Q

What do most sensory neurones - including nociceptors - use as their principle fast (excitatory) transmitter?
What else to many nociceptive sensory neurones also contain?

A

glutamate

peptides such as substance P and CGRP

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9
Q

When is substance P released?

A

when nociceptive axons carry high frequency trains of action potentials
The release of substance P is required for stimuli to be perceived as moderate to intense pain

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10
Q

Substance P is released peripherally from sensory neurones as well as in the spinal cord where it…….

A

induces mast cells to release histamine – promoting inflammation 5HT – acvtivates nociceptors
causes vasodilation

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11
Q

How do histamine, compounds generated by enzymatic break-down of cell membranes (prostaglandins) and extracellular molecules (bradykinin) act as primary hyperalgesia?

A

increases nociceptor sensitivity

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12
Q

Non-steroidal anti-inflammatory (NSAIDs) painkilliers (e.g. aspirin, ibuprofen) block enzymes that produce what?

A

prostaglandins

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13
Q

How can chronic stimulation of nociceptors from trauma lead to secondary hyperalgesia?

A

Peptides like substance P accumulate in the dorsal horn
There is a progressive increase neuronal responsiveness
Low threshold mechanoreceptors that normally respond to light touch start to generate pain responses (allodynia)

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14
Q

Explain the gate theory of pain

principle Transcutaneous Electrical Nerve Stimulation (TENS) operates on

A

Many spinothalamic interneurones are contacted by both nociceptive and touch sensory fibres

The mechanoreceptors drive them at low frequency and this signal is not perceived by the brain as pain

The nociceptors drive them at high frequencies and this is perceived as pain

When the nociceptive fibre is active it excites the spinothalamic interneurone and blocks inhibitory activity in the neurone that could reduce interneurone responsiveness

During a painful stimulus, mild mechanical stimulation (e.g. rubbing) of the painful region activates the neuron that inhibits the spinothalamic interneurone carrying the pain signal

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15
Q

How do endorphins and enkephalins (opiate-like peptides present naturally in the dorsal horn neurones) produce an analgesic (pain relieving) effect?

A

They block the release of substance P from nociceptive fibres
suppressing activity in sensory interneurones

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16
Q

Name an opiate antagonist

A

naloxone

17
Q

How do the axons of serotonin (5HT) containing neurones in the brainstem (descend to the dorsal horn) block pain pathways?

A

They act on inhibitory GABAergic neurones

18
Q

What is the ascending pathway involved in visceral pain called?

A

Spinoreticular tract
Runs to the reticular formation in the brainstem
Visceral pain often referred

19
Q

What can alleviate an itch?

When is it ineffective?

A

Antihistamine acts on histamine receptors on C and A delta fibres
No effect if itch caused by spinal circuitry
m-opiod antagonists may alleviate itch caused by epidural/ spinally administered morphine (may block effect of morphine)
or K-opiod antagonists (do not block effect of morphine)

20
Q

Which fibres are involved in an itch?

A

C and A delta

21
Q

Which pathway is visceral pain carried in?

A

Dorsal column pathway

22
Q

What can be carried out for viceral cancer pain that is not responsive to drug treatment?

A

Midline myelotomy

23
Q

Consequences of nerve damage on axons?

A

Under the influence of growth factors released by glial cells, axons sprout from the cut end may re-innervate targets if still present

24
Q

Consequences of nerve damage if outward growth is blocked?

A

a neuroma (a tangled mass of axons) develops – this may occur even if some axons grow out successfully

25
Q

What do nociceptive fibres in the neuroma start to express?

A

a-adrenergic receptors

26
Q

What do a-adrenergic receptors respond to?

A

noradrenalin released from peripheral sympathetic axons which results in pain

27
Q

Other than NA, what do neuromas be sensitive to?

A

May be very sensitive to pressure and temperature - generate massive spontaneous impulse discharges in the nociceptors, resulting in severe pain

28
Q

Are there are nociceptive endings within central nervous tissue?

A

no