L14: Pain Flashcards

1
Q

What are the 3 types of pain?

A

acute, chronic and intermittent

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2
Q

What is the disorder associated with loss of pain sensation?

A

CIPA

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3
Q

What causes CIPA?

A

mutation in gene for a nerve growth factor so sensory nerves don’t develop properly

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4
Q

What are the 3 classes of nociceptor? What are they activated by?

A
  • thermal: activated by v high or low temps
  • mechanical: activated by intense pressure
  • polymodal: activated by high intensity mechanical, thermal, or chemical stimuli
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5
Q

What are C fibres and what signal travels along them?

A

unmyelinated axons - signal ongoing slow dull pain (polymodal receptors)

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6
Q

What are A∂ fibres and what signal travels along them?

A

thinly myelinated axons - signal acute onset (thermo & mechanoreceptors)

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7
Q

What type of receptors are usually featured on nociceptors? What stimuli are they sensitive to?

A

TRP (Transient Receptor Potential) channels - sensitive to lots of different stimuli

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8
Q

Describe the ascending somatosensory pathways for pain

A

dorsal root → synapse on dorsal horn of spinal cord projection neurons → cross midline → ascend to thalamus (via spinothalamic tract) → thalamic neurons project to somatosensory cortex and other nuclei involved in pain response ⇒ allows us to locate pain

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9
Q

What is hyperalgesia? What causes it?

A
  • enhanced pain
  • usually due to previous injury
  • often due to inflammation and release of chemicals from damage site
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10
Q

What is allodynia?

A
  • Pain in response to innocuous sensory stimuli
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11
Q

What is substance P? What does it do?

A
  • local transmitter
    • activates mast cells to release histamines → inflammation
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12
Q

How can hypergesia result in chronic pain?

A

strength of synapses in CNS changes→ sensitisation of networks in nervous system and brain → chronic pain [very complex]

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13
Q

Describe the gate control model, with examples

A

Pain signalling can be “gated” by stimulation of non-pain sensory fibres from same area which activates inhibitory interneurons in dorsal horn, reducing output of projection neurons = less excitable, less APs
- e.g. rubbing site of injury
- e.g. TENS (provides different signal from area → decreases pain system)

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14
Q

Are opioid receptors generally excitatory or inhibitory?

A

Inhibitory -> activation can lead to analgesic effects

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15
Q

How do NSAIDs work?

A

inhibit cyclooxyrgenase enzymes to reduce prostaglandin synthesis, have pain suppression effects both at site of injury and in sensory neurons in dorsal root ganglion (DRG) and CNS

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16
Q

what do prostaglandins do?

A
  • involved in producing inflammation and pain
  • bind to lots of different receptors in free nerve ending → e.g. TRP channel family
17
Q

What is referred pain?

A

poor localisation of pain bc not able to differentiate between skin and viscera

18
Q

What is thought to cause phantom limb sensation/pain?

A
  • amputation may cut peripheral nerve but cell body stays alive in dorsal root ganglia
  • still have activation of this nerve, brain interprets that limb is still there