Pain Flashcards

1
Q

definition of pain
acute
chronic

A

unpleasant sensory and emotional experience which we associate with actual or potential tissue damage
acute <3/12
Chronic >3

Though more recent definitions are chronic pain occurs when the original injury is no longer acting

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2
Q

Types of pain

A
  1. nociceptive (nerves intact_
  2. neuropathic (damage or dysfunction to any part of the nervous system)
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3
Q

how does pain perception occur?

A
  1. nociceptors are stimulated
  2. mixed nerves carry impulse to spinal cord via dorsal root and cross the the spinothalamic tract.
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4
Q

What fibres does high intensity pain stimulus travel down?

A

A-delta myelinated fast fibres (mechano-thermal, 0.5-2sec short lasting)

& C unmyelinated slow fibres(polymodal, 6-30m/s, dull, burning pain)

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5
Q

what fibres do low intensity pain stimuli travel down?

A

A-beta fibres

NB Clinical pain can differ from physiological where even low intensity stimuli can stimulat A-Delta & C fibres together with A-beta inducing pain

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6
Q

What is peripheral sensitisation & how does it occur?

A

Peripheral sensitisation is a process where chemical & inflammatory factors can sensitise peripheral nociceptors to lower their threshold in eliciting a painful response from a reduced stimulus. Common following trauma or surgery

  1. direct activation: nociceptor is activated by cell damage, which triggers release of K+ + bradykinin & synthesis of prostaglandins-> increase in sensitivity of the terminal (lower threshold nociception)
  2. secondary activation: impulse propagates to nearby terminal which stimulate release of substance P-> vasodilation & further bradykinin release & release of histamine & serotonin
  3. Spread of hyperalgesia: histamine & serotonin increase sensitises nearby nociceptors.
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7
Q

What happens to opioid receptors as a result of tissue damage?

A

Dorsal root ganglion pain fibre cell bodies produce more opioid receptors which are passed peripherally and acted on by endogenous opioids release by inflammatory cells. Exogenous opioids eg morphine also act on these

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8
Q

What occurs in the dorsal horn (in context of pain)

A

the dorsal horn is where afferent fibres synapse with ascending afferent neurones in the pain pathway

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9
Q

Substances involved in nociception:

A

-Glutamate (plays major role acting at NMDA & non-NMDA receptors)
-substance P
-Neurokinin A
-CRGP

Opiod, GABA, Catecholamines & glycine all modulate the doral root ganglion nociceptive transmission

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9
Q

Role of glutamate & substance P in pain

A

Glutamate & substance P are released from afferents to activate the appropriate receptors, allowing Na+ influx and secondary messenger activation. This primes the NMDA receptor by removing its Mg2+ plug, allowing Na+ & Ca2+ influx.

NMDA receptor activation produces secondary effects in the cell, increasing nociceptive responsiveness of the system.

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10
Q

What happens with sustained activation of NMDA receptors

A

Chronic pain

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11
Q

how is pain transmitted to CNS

A

lateral spinothalamic tract -> thalamus
unmyelinated C fibres
myelinated A delta fibres

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