Pain Flashcards

1
Q

What is the receptive field ?

A

An area that a particular nerve responds to a stimulus in.

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2
Q

What is a stimulus turned into ?

A

Depolarisation - Receptor potential - Generator potential

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3
Q

What determines acuity ?

A
  • Area of receptive field

- Density of neurones in the area

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4
Q

What are Ab fibres ?

A

Large myelinated axons that carry information on touch, vibration and pressure

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5
Q

What are Aℑ fibres ?

A

Small myelinated axons that carry information on fast , sharp pain and cold

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6
Q

What are C fibres ?

A

They are unmyelinated axons that carry information on dull, slow pain and warmth

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7
Q

Which fibres mediate proprioception ?

A

Aa and Ab

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8
Q

Where do Aa get signals from ?

A

Extrafusal muscle spindles and GTO’s

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9
Q

Where do Ab get signals from ?

A

Secondary receptors of muscle spindles

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10
Q

What 3 things do sensory pathways do ?

A
  • Converge
  • Adapt
  • Laterally inhibit
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11
Q

Definition of nociception

A

The detection of noxious harmful stimuli by Aℑ and C fibres that have the ability to cause tissue damage.

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12
Q

What is the gate control theory ?

A

Aa and Ab fibres activate inhibitory interneurones by releasing endorphins that inhibit transmitter release in Aℑ and C fibres. Descenind inhibition from PAG and NRM also activate these inhibitory interneurones and hence close the gate.

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13
Q

Which is the name of the neurotransmitter release ?

A

Substance P

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14
Q

How do NSAID’S work ?

A

They stop COX from converting arachidonic acid into prostaglandins. Less prostaglandins less sensitisation to bradykinin, less depolarisation and so less pain.

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15
Q

How do local aesthetics work ?

A

Block all Na+ - axonal transmission is stopped

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16
Q

How does TENS (Transcutaneous Electrical Nerve Stimulation) work ?

A

Some method as closing the gate. Aa and Ab fibres are activated and they activate inhibitory interneurones which prevent signals passing up through Aℑ and C fibres.

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17
Q

How do opiates work ?

A
  • Reduce the amount of neurotransmitter release
  • Activate the descending inhibitory pathways
  • Reduce the sensitivity of nociceptors
18
Q

What is Neuropathic pain ?

A

Pain caused by nerve damage. Usually a burning or prickling sensation. There is no obvious tissue damage, usually resistant to medical treatment.

19
Q

Why does referred pain occur ?

A

The visceral and somatic nerve fibres enter the spinal cord at the same level. This can sometimes lead to misinterpretation of incoming signals by higher brain centres.

20
Q

Where does the LST terminate ?

A

In the ventroposteior thalamic nuclei

21
Q

Where does the AST terminate

A

In the medial thalamic nuclei

22
Q

Where are signals sent from the thalamus ?

A

The cortex, brainstem and limbic system

23
Q

Where does pain perception occur ?

A

In the somatosensory cortex

24
Q

What is involved in the descending control of pain

A

The medial thalamus, hippocampus and amygdala are involved and they relay this to the brainstem.

25
Q

Where do descending pathways go ?

A

Via the PAG

26
Q

Definition of Hyperalgesia

A

Increased perception of pain

27
Q

Allodynia

A

Decreased threshold of pain response

28
Q

What happens during peripheral sensitisation ?

A

The nociceptive receptors have an increased sensitivity to stimuli

29
Q

What is central sensitisation ?

A

Increases the response of the 2nd order neurone in the CNS to normal input of both noxious and noxious stimuli.

30
Q

What can central sensitisation lead to ?

A

The development and maintenance of chronic pain.

31
Q

What are the 3 stages of central sensitisation ?

A
  1. Wind up
  2. Classical
  3. Long-term potentiation
32
Q

What is wind up ?

A

Occurs only during the stimulus, and causes an increase in the number of AP’s that are fired due to a stimulus. Substance P and CGRP are involved.

33
Q

What is classical ?

A

Classical involves opening up new synapses. Starts with the stimulus and outlasts it. It results in secondary hyperalgesia.

34
Q

What is secondary hyperalgesia ?

A

Secondary hyperalgesia is defined as an increase in pain sensitivity when a noxious stimulus is delivered to a region surrounding, but not including, the zone of injury.

35
Q

What is long-term potentiation ?

A

Involved both AMPA and NMDA receptors activated by glutamate. Synapses are strengthened.

36
Q

Features of acute pain

A
  • < 1 month
  • Tissue damage
  • Has a protective function
  • Pain resolves upon healing
  • Usually nociceptive
  • Responds to conventional analgesics
37
Q

Features of chronic pain

A
  • > 3 months
  • Pain beyond the expected timeframe of healing
  • No protective function
  • Degrades health and function
  • Usually neuropathic
  • Doesn’t respond well to conventional analgesics
38
Q

What is neuropathic pain ?

A

Damage or disease affecting the somatosensory NS, it causes pain.

39
Q

What can block transduction ?

A
  • Ice
  • Rest
  • NSAID’s
40
Q

What can block transmission ?

A
  • Nerve block
  • Opiates
  • Cordotomy
41
Q

What can help with reducing pain perception ?

A
  • CBT
  • Relaxation
  • Distraction
42
Q

What helps control descending modulation ?

A
  • Opioids

- Anti-depressants