Pain Flashcards

1
Q

Hyperalgesia vs allodynia?

A

Hyperalgesia = increased response to noxious stimuli

Allodyna = painful response to non-noxious stimuli

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2
Q

Describe and give the differences in transmission (axons + NTs) of fast and slow pain.

A

Fast

  • Sharp, well localised
  • Myelinated axons (alpha-delta fibres)
  • Glutamate NT (rapid acting, short duration)

Slow

  • Dull, not localised
  • Unmyelinated axons (C fibres)
  • Substance P NT (slower acting, longer duration)
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3
Q

What specific channels do we have for hot/cold pain and how do they function?

A

Transient receptor potential (TRP) channels.

Temperature sensitive ion channels - Na+ and Ca2+ excitatory channels.

Cold receptor channels = TRPM8 (firing rate DECREASES as temp decreases)

Hot receptor channels = TRPV1/3 (firing rate INCREASES as temp increases)

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4
Q

What type of receptor channels are involved in mechanical nociception?

A

Stretch gated ion channels - excitatory.

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5
Q

What are polymodal nociceptors?

How do they function (fibres, NT)

A

Receptive to all painful stimuli:

  • C fibres
  • Glutamate and/or substance P
  • Response to heat/cold/physical/chemical stimuli
  • Express multiple receptors

Tell us pain no matter waht the stimulus is.

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6
Q

How does hyperalgesia develop in the context of inflammation?

A

Inflammation creates abundance of stimuli (bradykinin, H+, prostaglandin, lipids, heat) that stimulates and sensitises nociceptors.

Turns high-threshold nociceptors into low-threshold nociceptors.

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7
Q

Describe the different tracts of fast and slow pathways of pain

A

Neospinothalamic tract - Fast

  • Alpha-delta fibres (myelinated)
  • Ascend anterolateral spinothalamic tract into the brainstem
  • Almost no branching - straight from thalamus into CORTEX

Paleospinothalamic tract - Slow

  • C fibres (unmyelinated)
  • Ascent anterolateral spinothalamic tract to the brainstem
  • Lots of branching in the brain
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8
Q

What is the efferent analgesic system and how does it function?

A

Role is to inhibit afferent pain signals.

Pain afferent signals stimulate neurons in periaqueductal gray (PAG) region (midbrain) and nucleus raphe magnus (medulla)

THis activates anti-nociceptive pathways resulting in release of NTs to create analgesia.

Messengers:

  • Serotonin
  • NA

Opioids:

  • Enkephalins
  • Endorphins

Reuslts in suppressed pain going up the spinal cord

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9
Q

What is the gate-control theory?

A

Pain can be suppressed at the dorsal horn level.

Normally, inhibitory neurones inhibit ascending pathways for pain.

Upon painful stimulus, fibres from nociceptors override interneuron inhibition, and pain travels to brain.

Lateral inhibition from sensory fibres activates inhibitory interneurones.

If both pain and non painful stimulus arrive at same time (e.g. rubbing a painful spot), there will be partial inhibition of pain transmission.

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10
Q

How do local anaesthetics work, giving an exmaple

A

BLock action potential conduction in nociceptive nerve fibnres

E.g. cation channel blockers like Lidocaine

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