Endogenous Control of Pain Flashcards

1
Q

what are nerve receptors of pain?

A

free nerve endings:

  1. nociceptors: detect noxious stimuli
    - ADelta: lightly myelinated
    - C fibers: no myelination
    - Silent: receptors that are not normally activated
  2. thermoreceptors
  3. mechanoreceptors
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2
Q

where do ALS fibers diverge?

A
  1. cortex - spinothalamic tract
  2. brainstem - spinoretriculr and spinomesencephalic tracts
  3. hypothalamus - spinohypothalamic tract
  4. limbic system via Rf and hypothalamus
  5. local reflex connections
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3
Q

hyperalgesia

A

increased pain in response to noxious stimulus

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4
Q

allodynia

A

pain perception to non-noxious stimulus

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5
Q

how is nociceptor modulated?

A

tissue injury results in release of inflammatroy mediators (i.e. PGs, LTs…)

  • decreases threshold of “regular” nociceptors
  • recruits silent nociceptors
  • axon reflex results in dilation of arterioles and edema
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6
Q

Axon reflex

A
  • peripheral modulation
  • if stimulus reaches the trigger zone and is intense enough it will be actuated and APs will flow back out to free nerve endings
  • glutamate will be released at free nerve endings causing further inflammation in periphery
  • the receptors threshold will be decreased and silent nociceptors will be recruited
  • this results in firing GP’s and increased population and overal. increased receptivity and strength of stimulus
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7
Q

modulation at the dorsal horn?

A
  • Spinal facilitation of pain “wind up”
  • central modulation
  • high intensity pain stimulus results in increased glutamate, substance P and BDNF being released onto second order neuron in dorsal horn.
  • glutamate activates AMPA: which is the fast pain and fast depolariztation
  • The high levels also activate NMDA channels which bring Ca2+ into the second order neuron.
  • Ca2+ activates G proteins which in turn affect the membrane sensitivity and change gene expression.
  • the G proteins make the membrane more sensitive to any glutamate released in the cleft thereafter.
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8
Q

Modulation by descending pathways?

A
  • inputs from hypothalamus, amygdala and Cx send projections to periaqueductal gray area and that will project to a few spots:
    1. Nucleus Raphe-Magnus (located in rostral medulla/caudal pons) receives descending fibers from PAgray and sends axons descending down cord to release opiods in dorsal horn to downregulate pain
    2. Locus Coeruleus
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9
Q

referred pain?

A

Angina pectoralis: pain on left side of chest due to pain coming from the heart. Intensity is great enough that primary affarent releases a large amount of NT that it activates a neuron that is receiving info of pain from a specific dermatome. The GVA will wire up to the same second order neuron that was receiving info about pain temp and crude touch from a patch of skin. This is convergence of the nervous system. The second order neurons decussate and head up to primary somatosensory cortex. It is used to the neuron being stimulated for bodily pain, thus the pain is perceived as being on the body.

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10
Q

“gait control theory”

A
  • when you smack your arm and rub it after, the pain is lessened….
  • wide dynamic range neurons (WDR) receive input from primary affarent of pain stimuli and primary affarent of tactile stimuli.
  • when the WDR fibers are stimulated they inhibit the pain coming in from the primary affarent pain fiber in the dorsal horn.
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