Somatosensory Pathology Flashcards

1
Q

2 tests of THE INTEGRITY OF THE ASCENDING SOMATOSENSORY PATHWAYS

A
  • Quantitative sensory testing (QST)

- Electrical perceptual thresholds (EPT)-

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2
Q

What is an Electrical perceptual thresholds (EPT) test

A

like QST but semi-automated Electrical current sent to skin and the patient either feels it or doesn’t

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3
Q

What is a Quantitative sensory testing (QST) test

A

a set of various tools we can use to look into the integrity of all of the different modalities e.g. using a brush to stroke someone’s arm 13 different tests can be done

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4
Q

what causes nociceptive pain?

A

Tissue damage, typically acute e.g. skin cut

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5
Q

what causes muscle pain?

A

Lactic acidosis, ischaemia e.g. stretching, fibromyalgia)

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6
Q

what causes somatic pain?

A

Well-localised e.g. inflammation, infection

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7
Q

what causes visceral pain?

A

Deep, poorly localised e.g. stomach, colon, IBS

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8
Q

what causes referred pain?

A

From an internal organ/structure e.g. angina

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9
Q

what causes neuropathic pain?

A

PAIN CAUSED BY A LESION OR DISEASE OF THE SOMATOSENSORY NERVOUS SYSTEM

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10
Q

How does ACUTE AND CHRONIC PAIN manifest

A

hyperalgesia and allodynia

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11
Q

What comorbidities can you get with acute and chronic pain

A

anxiety and depression as secondary comorbidities

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12
Q

What does neuropathic pain feel like

A

Sharp, burning, electric shocks

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13
Q

Success of analgesic opiated in neuropathic pain?

A

Poor

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14
Q

3 types of neuropathic pain?

A

 Sciatica (most common)- spinal nerves compressed in intervertebral foramen
Diabetic neuropathy
 Post-hepatic neuralgia can be caused by shingles
HIV induced neuropathy
 CRPS = pain around the whole body that spreads spontaneously

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15
Q

What types of neuropathic pain can you get (5)

A
ALLODYNIA
Hyperalgesia
Sensitisation
Hypoalgesia
Paraesthesia
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16
Q

What is ALLODYNIA

A

Pain due to a stimulus that does not normally provoke pain e.g. brush

17
Q

What is Hyperalgesia

A

Increased pain from a stimulus that normally provokes pain

18
Q

What is Sensitisation

A

Increased responsiveness of nociceptive neurons to their normal input

19
Q

What is Hypoalgesia

A

Diminished pain in response to a normally painful stimulus

20
Q

What is Paraesthesia

A

Abnormal sensation, whether spontaneous or provoked

21
Q

How do we diagnose and asses neuropathic pain (2)

A

Clinically we use a combination of questionnaires and simple sensory tests e.g. brushing etc.

22
Q

What is central sensitization in chronic pain

A

Increased amount of pain was found not to just be from sensitization in the periphery but in the spinal cord

23
Q

What do NMDA receptors do and how does result in central sensitisation and chronic pain

A

(mechanism for central hypersensitisation) they allow a big post-synaptic depolarisation which allows calcium into the neuron- this activates intracellular signalling and increases synaptic strength and our sensitivity

Persistent activation of NMDA receptor can result in development of chronic pain

24
Q

What happens in hyperalgesia

A

Central sensitisation via persistent NMDA activation which causes a lack of inhibitor from interneurons

25
Q

What happens in allodynia

A

Almost a rewiring of neurons so mechanoreceptors can stimulate nociceptive fibres

26
Q

What sort of shape is curve of a stimulus intensity against pain intensity graph

A

sigmoidal

27
Q

What is descending modulation of chronic pain

A

Monoamines released from the brainstem that work to inhibit spinal cord excitability (and thus reduce pain)

28
Q

What are 2 methods of descending modulation of pain

A
THE PAG-RVM AXIS
LOCUS CERELEUS (LC):
29
Q

The LOCUS CERELEUS (LC) in descending pain modulation (location, NT,

A

This is in the pons

This uses noradrenaline as its main neurotransmitter

30
Q

The PAG-RVM AXIS in descending pain modulation (names of nuclei, locations, NT)

A

Periaqueductal gray - midbrain
rostral ventral medial medulla - Pons
serotonin (5-HT)

31
Q
  • The PAG and RVM contain high concentrations of X RECEPTORS
A

Mew opioid

32
Q

How does the PAG-RVM axis inhibit pain

A
  • The PAG and RVM contain high concentrations of  OPIOID RECEPTORS
  • Endogenous opioids enhance descending inhibition from the PAG-RVM axis
  • Reduce pain transmission from the dorsal horn by inhibiting glutamate release i.e. activation of spinothalamic neurons
  • Forms part of an ENDOGENOUS ANALGESIC SYSTEM
33
Q

Drugs used to target descending pain modulation?

A
  • Opioids
  • Antidepressants (Tri-cyclic Antidepressants (TCAs), Serotonin Noradrenaline Reuptake Inhibitors (SNRIs) and Selective Serotonin Reuptake Inhibitors (SSRIs)
34
Q

Effectiveness of SSRIs as analgesics?

A

low analgesic efficacy

35
Q

Effectiveness of SNRI as analgesics?

A

Effective

36
Q

MoA of SNRIs in pain inhibition?

A
  • If you give an SNRI e.g. duloxetine, it binds to the presynaptic or postsynaptic terminal in the dorsal horn and inhibits NA reuptake from the synaptic cleft
  • This means NA acts on inhibitory 2 receptors for longer and inhibitory influence is increased (pain is reduced)
37
Q

3 neuropathic pain patient clusters?

A
  1. SENSORY LOSS
  2. THERMAL HYPERALGESIA
  3. MECHANICAL HYPERALGESIA