Pain Management Flashcards

1
Q

What is the gate theory of pain?

A

That a non noxious stimuli e.g rubbing will inhibit/decrease ascending pain transmission/pathway

  • Non painful stimulus activates pascinian corpuscles of the skin and sensation travels via DCML
  • Activates inhibitory interneurones in substantia gelatinosa
  • Release inhibitory interneurones e.g encephalins that bind to opioid receptors on pre SN
  • Decreases Ca2+ channel opening + increases K+ conductance so AP chance decreases
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2
Q

What factors may affect pain perception?
What increases pain threshold?
What decreases pain threshold?

A
  • cultural factors
  • pain threshold
  • meanings of pain
  • sensory input
  • previous pain experience

Relaxation, relief, good sleep, sympathy + understanding

insomnia, anxiety, mood, fear, discomfort

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3
Q

How do we define pain ( 6 concepts)?

A
  • biopsychosocial impact of pain
  • protective but adverse effects
  • verbal communication not only way of expressing pain
  • emotional + sensory experience
  • experiences affect pain concept/perception
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4
Q

Compare acute vs chronic pain

A

Acute: < 3 months, normally protective
Chronic: > 3 months, not useful with adverse effects

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5
Q

What are the 5 main types of chronic pain?

A
Myofascial 
Musculoskeletal
Fibromyalgia 
Neuropathic
chronic headaches
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6
Q

What is neuropathic pain?

A

Pain caused by a disease or lesion of the somatosensory nervous system
lesion = known damage
disease = cause of damage is known e.g stroke, diabetes
It is anything that damages the nerves

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7
Q

What is nociceptive pain?

A

Pain in response to actual or potential tissue damage

Noxious stimuli -> electrical impulse which is relayed through the spinal cord

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8
Q

What is nociplastic pain?

A

Occurs due to altered nociceptive responses despite no evidence of actual/potential tissue damage or disease/lesion or somatosensory NS

Patient can be said to have more sensitive nerves

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9
Q

What is central pain?

A
Rare syndrome affecting the central nervous system
Includes strokes ( flaccid weakness -> UMN signs)
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10
Q

What is sensitisation?

What are the 2 main types?

A

Reduced threshold/ increased responsiveness of nociceptors to their normal input

Central
Peripheral

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11
Q

What maladaptive changes occur due to sensitisation?

A
  • Decreased descending inhibition
  • Glial cell activation ( transmission + storage of pain signals)
  • Chains in NT i.e increased glutamate, increased Ca2+ channels
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12
Q

What is the wind up phenomenon?

A

Exaggerated response to normal stimuli e.g touch/pressure

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13
Q

What is the MOA gabapentin?

How is it used to treat sensitisation?

A

Binds to alpha subunits og Ca2+ channels

Prevents Ca2+ influx and hence up regulation that occurs in sensitisation

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14
Q

What is allodynia?
What is hyperalgesia?
What is hypoalgesia?
What is hyperpathia?

A

Pain caused by a non painful stimulus ( lower threshold)
Increased pain from a painful stimulus ( increased response)
Low pain from a painful stimulus ( high threshold, low response)
Pain rxn to repetitie stimulus ( low threshold, high response)

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