L25 Pain Flashcards

1
Q

what are the 2 types of pain

A

nociceptive pain

neuropathic pain

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2
Q

what are the 2 types of pain

A

nociceptive pain

neuropathic pain

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3
Q

define nociceptive pain

A

direct stimuli of nociceptors and have the potential to cause tissue damage

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4
Q

define neuropathic pain

A

CANNOT be explained by a simple activation of nociceptors by tissue damage
includes pain where the mechanism is a site of atypical somatosensory processing the PNS or CNS

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5
Q

define first pain

A
  • sharp and quick pain resulting form the activation of mechanical or thermal receptors
  • receptors use A delta fibers = myelinated and very fast
  • this is known as the “ouch effect”
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6
Q

define second pain

A
  • much slower onset pain, more like a burning sensation resulting from polymodal nociceptors
  • these receptors use unmyelinated C fibers that have a much slower velocity this a slower onset
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7
Q

does the brain have nociceptors?

A

no

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8
Q

how do headaches arise?

A

irritation of neighboring tissue, most often the meninges

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9
Q

describe visceral pain

A

visceral organs have nociceptors

results from the stimulation of visceral and deep somatic nociceptors - conduct signal via unmyelinated C fibers

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10
Q

describe referred pain

A

visceral nociceptive activation is perceived as a cutaneous painful sensation

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11
Q

how can referred pain be explained?

A

neurons in the dorsal gray matter of the spinal cord receive convergent input from both somatic and visceral afferents at the same location and are projected into the ALS

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12
Q

in the event of tissue damage, what chemical are released that can activate chemical nociceptors?

A
  • bradykinin - from blood
  • histamine - from mast cells
  • potassium - from damage cells (remember increase extracellular K+ depolarized membrane potential)
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13
Q

define hyperalgesia

A

enhanced sensitivity and responsivity to an area around damaged tissue

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14
Q

what causes hyperalgesia

A

increasing nociceptor sensitivity cause by chemicals released at site of trauma

  • prostaglandins and leukotrienes from damaged cells
  • substance P from primary afferent pain fibers
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15
Q

define second pain

A
  • much slower onset pain, more like a burning sensation resulting from polymodal nociceptors
  • these receptors use unmyelinated C fibers that have a much slower velocity this a slower onset
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16
Q

does the brain have nociceptors?

A

no

17
Q

how do headaches arise?

A

irritation of neighboring tissue, most often the meninges

18
Q

describe visceral pain

A

visceral organs have nociceptors

results from the stimulation of visceral and deep somatic nociceptors - conduct signal via unmyelinated C fibers

19
Q

describe referred pain

A

visceral nociceptive activation is perceived as a cutaneous painful sensation

20
Q

how can referred pain be explained?

A

neurons in the dorsal gray matter of the spinal cord receive convergent input from both somatic and visceral afferents at the same location and are projected into the ALS

21
Q

define hyperalgesia

A

enhanced sensitivity and responsivity to an area around damaged tissue

22
Q

what causes hyperalgesia

A

increasing nociceptor sensitivity cause by chemicals released at site of trauma

  • prostaglandins and leukotrienes from damaged cells
  • substance P from primary afferent pain fibers
23
Q

explain gate control in the spinal cord

A

if a touch fiber is stimulated, it will meet the pain fiber in the dorsal horn (similar to referred pain) and will activate interneurons that will inhibit the synapse between the first and second order pain fibers

24
Q

what does the stimulation of the touch fiber cause the interneuron to release?

A

enkephalin (endogenous opiod) = inhibits pain fibers

25
Q

what is the mechanism of opiods (to AP duration, EPSP durations, polarization)

A

decrease AP duration
decrease EPSP duration
hyperpolarize the second order neuron

26
Q

what is the role of serotonergic and noradrenergic fibers in modulating pain

A

they act the same as gate control pathway

they both synapse on the opiodergic interneuron where they control the transmission of the pain fibers

27
Q

what is the MOA of aspirin

A

decrease COX resulting in decrease of prostaglandins (which normally sensitize sensory afferent fibers)

28
Q

what is a dorsal rhizotomy

A

in extreme cases (terminal cancer etc) DRG is removed to stop pain transmission

29
Q

is acupuncture beneficial to pain relief

A

its a bunch of crap - it may release opiod peptides that could decrease pain fiber transmission, but there are serious adverse effects that are BAD