Week 3 - Nociception Flashcards Preview

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Flashcards in Week 3 - Nociception Deck (35)
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1
Q

what is the difference between pain and nociception?

A

pain is a conscious, emotional, psychological perception associated with noxious stimuli

nociception is any process in PNS or CNS associated with noxious or highly-unplesant stimulus

both pathways rely on different sets of structures

2
Q

what are nociceptors? what are they activated by?

A

peripheral endings of primary sensory neurons whose cell bodies are located in dorsal root and trigeminal ganglia (like somatosensory receptors)
-harmful stimuli applied to skin or subcutaneous tissue

3
Q

how do nociceptors differ from mechanoreceptors and other sensory receptors on skin?

A

least differentiated sensory receptors on skin

-exist as free nerve endings that don’t have peripheral structures that transduce and filter peripheral stimuli

4
Q

what are the 2 types of nociceptors that mediate pain? what kind of fibers do they have? what are they activated by?

A

thermal/mechanical - small diameter, thinly myelinated A-delta fibers that conduct at 5-30 m/s
-activation associated with sharp, pricking pain
polymodal - small-diameter, unmyelinated C fibers that conduct at 0.5-2 m/s
-activated by high-intensity mechanical, chemical, and hot (over 45 C) or cold stimuli

5
Q

how does a noxious stimulus activate a nociceptor?

A

depolarizing membrane of a sensory ending

  • mechanisms of which are unknown
  • nociceptors discharge only when stimulus is intense enough to cause damage
6
Q

what does “noxious” mean?

A

high intensity and potentially tissue damaging or life threatening

7
Q

what is the “first and second” pain? what happens if stimulation is intense enough?

A

stimulus intensity has to be raised to a level to activate corresponding fibers

1st: A-delta fibers in peripheral nerve = tingling
- if stimulation is intense enough, there is sharp pain
2nd: C fiber axons activated if stimulus intensity is increased further = duller, longer-lasting sensation of pain

8
Q

can A-delta and C-fibers be separated?

A

yes, by anesthetic blocking experiments

-can selective anesthetize C and A-delta fibers

9
Q

what is the receptor on both C and A-delta fibers? what is it activated by? how are APs triggered?

A

vanilloid receptor TrpV1

  • activated by stimuli like capsaicin, head, acids, and anandamine (endogenous cannabanoid receptor stimulus)
  • respond to endogenous chemicals similar to capsaicin that are released with peripheral injury
  • AP Na+ voltage gated channels
10
Q

what is hyperalgesia?

A

enhanced sensitivity and responsivity to stimulation of area in and around damaged tissue

  • so if burn point A, near point B and C, all 3 of them will have decreased threshold sensitivity
  • AKA if peripheral tissues are damaged, sensation of pain in response to subsequent stimuli is enhanced
11
Q

what causes hyperalgesia?

A

sensitization of nociceptors by various substances released when tissue is damaged

  • release of bradykinin, histamine, prostaglandins, and other agents from site of injury enhances responsiveness of nociceptive endings
  • electrical activity in nociceptors stimulates local release of chemical substances that cause vasodilation, swelling, and release of histamine from mast cells
12
Q

how do aspirin and other NSAIDs act?

A

inhibit cyclooxygenase (for biosynthesis of prostaglandins)

13
Q

can pain be sensed if nociceptive pathways are damaged?

A

yes, pain can arise spontaneously in absence of activity in nociceptors
-pain due to peripheral nerves is important clinical problem with several etiologies

14
Q

what is brachial plexus avulsion an example of? what is the pain from?

A

referred pain when nociceptive pathways are damaged; patients feel burning pain in dermatomes corresponding to denervated area (dorsal roots have been torn away)
-pain is from hyperactivity of dorsal horn neurons in deafferented region of cord

15
Q

where do most nociceptive fibers terminate?

A

superficial dorsal horn (lamina I and II) projection neurons

-some A-delta nociceptive fibers project more deeply into lamina V

16
Q

what do lamina I neurons contain? what are they called?

A

high density of projection neurons that process pain information
-excited solely by A-delta and C nociceptive fibers, thus called nociceptive specific (NS) projection neurons

17
Q

what kind of input do lamina V neurons receive?

A

both mechanoreceptors and nociceptors, thus called wide dynamic range neurons (WDR)

  • respond to both somatosensory and noxious stimuli
  • have much larger receptive fields than NS neurons
18
Q

in general, where do mechanoreceptor A-alpha, A-beta fibers, and nociceptor A-delta and C fibers synapse?

A
A-alpha/beta = lamina IV
A-delta = lamina I and V
C = lamina II
19
Q

what is referred pain?

A

displacement of pain from visceral structure (organ) to a somatic area of the body b/c fo convergence of visceral and cutaneous cociceptors onto same dorsal horn projection neurons

20
Q

where is anginal pain referred to?

A

upper chest wall and radiation of arm

21
Q

where is esophageal pain referred to?

A

chest wall

22
Q

where is ureteral pain referred to?

A

lower abdomen and back (happens if passing a kidney stone)

23
Q

where is bladder pain referred to?

A

perineum

24
Q

where is prostate pain referred to?

A

characteristic distribution above and below affected side

25
Q

how is nociceptive input from lower and upper body (excluding face) relayed to brain?

A

projection neurons that cross midline and ascend all the way to brainstem and thalamus in anterolateral spinothalamic pathway

26
Q

how is nociceptive input from face relayed to brain?

A

axons from trigeminal ganglion cells and VII, IX, and X ganglia carry info from facial nociceptors and thermoreceptors into brainstem, cross midline, and ascend trigeminothalamic tract

27
Q

what is the major target nuclei of ascending pain and temperature axons?

A

ventral posterior nuclear complex of thalamus, esp. VPM (face) and VPL (rest of body)

  • similar arrangement for mechanosensory and noxious stimuli responsible for discriminative aspects of pain
  • although close together, comprise separate systems
28
Q

what doe the somatosensory cortex receive from VPN of thalamus?

A

nociceptive information

  • no orderly arrangement of input to cortex similar to tactile inputs
  • clinical studies indicate damage to large areas of somatosensory cortex doesn’t cause impaired responses to noxious stimuli or loss of pain
29
Q

what are the zones of loss if there’s a lesion in the spinal cord?

A
  1. right next to it is zone of complete loss of sensation
  2. reduced epicritic/somatosensory sense below ipsilaterally
  3. reduced nocioception below contralaterally

referred to dissociated sensory loss

30
Q

what happens to the dorsal horn of the spinal cord if brain stem is stimulated?

  • what do experimentally induced lesions of dorsolateral funiculus do?
  • what does administration of low doses of opiates do?
A

brain stem stimulation inhibits nociceptive neurons in dorsal horn of spinal cord

  • neurons in periaqueductal gray matter make excitatory connections in rostroventral medulla
  • neurons in rostroventral medulla make inhibitory connections in laminae of I, II, and V of dorsal horn (also termination of nociceptive afferent neurons)
  • electrical stimulation in either site causes inhibition of dorsal horn neurons that respond to noxious stimulation
  • experimentally induced lesions of DF (pathway carrying descending info) abolished effect of electrical stimulation
  • opiates directly into same specific regions produced powerful analgesia
31
Q

what are the interactions between primary afferents, interneurons, and descending neurons in dorsal horn?

A

descending axons of serotonergic and noradrenergic neurons from nucleus raphe magnus contact dendrites of spinothalamic tract neurons and local enkephalin-containing inhibitory interneurons in superficial dorsal horn
-descending inhibition of spinothalamic tract neurons is mediated by activation of enkephalin interneurons in dorsal horn

32
Q

where is the nucleus raphe magnus?

A

the rostroventral medulla (where PAG neurons make excitatory connections)

33
Q

what does the superficial dorsal horn contain?

A

high density of enkephalin- and dynorphin-containing interneurons close to terminals of cocicceptive afferents, and to the dendrites of the dorsal horn neurons that receive nociceptive afferent input

34
Q

where are opiate receptors located?

A

terminals of nociceptive afferents and on the dendrites of postsynaptic neurons

35
Q

how do opiates and opioid peptides regulate nociceptive transmission?

A

inhibit release of glutamate, substance P, and other transmitters from sensory neurons
-opiates also act possynaptically at afferent synapses to suppress activity of nociceptive dorsal horn neurons