Week 4: Pain Flashcards

1
Q

Pain is classified as 3 different types. What are they?

A

Nociceptive – archetypal mechanism, the experience of pain is evoked by damage to somatic or visceral tissues e.g.,
Neurogenic / Neuropathic arises from abnormal activity in nerves that transmit nociceptive pain
Psychogenic: from influences in the subjects mind, such as memory, association with
past events and malingering

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2
Q

Pain generation. what are the 4 key components?

A
  1. Transduction
  2. Peripheral Transmission 3. Central Transmission
  3. Modulation
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3
Q
  1. Transduction
A
  • tissue damaged is detected by free nerve endings
  • stimulated by creating a change in the body
  • chemically (e.g. bradykinins, serotonin, inflammation response)
  • mechanically (e.g. stretch caused by swelling from hemmorage or tumor)
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4
Q
  1. Peripheral transmission of pain
A

-pick up and relay the info from the free nerve endings
-C fibres= transmit, thermal and chemical stimuli
A-delta= mechanical sensations at low stimulus intensity but pain at higher levels
Note: there aren’t specialised nerve fibres for pain transmission. ts mediated by nerves that have other functions.
Pathway of the afferents:
a) info picked up mostly by dorsal roots-depending
-depending on volume of information it will run up or down a couple of levels which is why we feel pain in broader areas.

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5
Q
  1. Central transmission of pain?
A

Spinothalamic tract:

  • control/ modulation in Rexes Laminae
  • then goes up to the thalamus were it is processed by 3 components
    1. Limbic system- emotional dimensions of stimulus (brain will process pain in different ways for different people)
  • allodynia= lowering of the pain threshold
  1. Parietal lobe for location/ origin of stimulus
  2. Reticular formation of brainstem (anterolateral funiculus= spinothalamic tracts)
    - reticular formation filters incoming stimuli to discriminate from relevant and irrelevant.
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6
Q
  1. Modulation of Pain
A

Its the feedback loop that modulates the level, intensity and severity of pain

  • send info down into spinal cord to excerpt inhibitory effects on ascending traffic
  • in chronic pain, pain is processed in smaller areas due to CNS changes
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7
Q

What are some of the pain Interventions?

A
  1. Transduction - at level of the skin- corticosteroids or NSAIDS
  2. Peripheral transmission -nerve relaying
    - anaesthetic blocks (cut the nerve, knock out the receptors)
  3. central transmission- spinal cord
    - SC stimulators (disturb afferent pain signals), spinal opoids
  4. change the patients perception of pain
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8
Q

Complex regional pain syndrome

There are 2 types

A
  • previously called Reflex sympathetic dystrophy
  • the whole system goes into overdrive
  • central sensitisation (The brain has learnt how to process pain so efficiently that any sensation experienced is interpreted as pain)

Type 1:
-develops after a tissue trauma- not related to a single nerve
-allodynia with spontaneous burning, continuous pain not proportional to trauma made worse by movement, cold and touch
-will get skin vasomotor changes- temp, colour, focal oedema, moisturiser.
Phase1: (wees- 3 months)
-involved extremity is warm, oedematous and joints are tender
-increased sweating and hair growth
Phase 2 (3-6 months)
-thin, shiny, coll skin

Phase 3

  • atrophy of the skin and subcutaneous tissue
  • flexion contractures

Type 2 (causalgia):

  • after injury to a specific peripheral nerve (usually a major nerve trunk)
  • spontaneous pain develops within the nerve territory then spreads outside it.
  • paroxysms of sharp, shooting or deep pain (similar to neuropathic Pain)
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9
Q

Treatment of pain syndromes

A
  • course of glucoocorticosteroids with early mobilisation and physical therapies
    2. NSAIDS
    3. Ca channel blockers
    4. Opioids- slippery path
    5. Stellate Ganglion blocks
    6. Psychological factors
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