LO6 Temp and pain [8] Flashcards

(37 cards)

1
Q

Temps outside which range elicits as pain? What is the thermoneutral point?

A

outside 10-48 C

33 = thermoneutral

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2
Q

Cold vs Warm receptor range

A

Cold: 10-37

Warm: 30-48

(note: 33 = thermoneutral point)

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3
Q

How is Temp information from periphery received?

A

Temp info from periphery →
transduced into receptor potential → trigger AP

(stronger intensity = more AP freq)

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4
Q

Cool receptors on free nerve endings of neurons are typically found on _____ fibers and warm receptors are found on ____ fibers

A

Aδ fibers - cool

C fibers

(note the switch:

  • nociceptors that are activ. by extreme HOT temp (>43) are associated with Aδ fibers
  • Nociceptors associated that signal extrememely COLD temp (
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5
Q

Difference between the spinothalamic tract and the spinoreticular tract

A

spinothalamic tract: carries info that provides conscious awareness of skin temp

SPinoreticular tract: carries info (ie pain) via reticular formation → forebrain/hypothalamus (imp for body temp control/autonomic fxn) → elicits emotional/behavioral response

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6
Q

The anterolateral pathway includes which tracts? List the structures that these tracts convey info to.

A
  1. spinothalamic
    - thalamus
  2. spinoreticular
    - forebrain → medulla/pons
  3. spinomesencephalic
    - midbrain PAG
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7
Q

Two other cortical regions that are activated when pain info is processed (other than thalamus+forebrain+hypothalamus) and why they are imp.

A
  1. cingulate gyrus: part of limbic system → emotional component of pain sensation
  2. Insular cortex → processes info (autonomic component of pain)
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8
Q

The DRG is to the Trigeminal ganglion as the dorsal horn is to the _______

A

Spinal Trigeminal nucleus

only it receives input form the head/neck via trigeminal ganglion instead of trunk and limbs from DRG

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9
Q

Thermal nociceptors that are activated by extreme temps are associated with which fibers?
Cold?
Hot?

A
  • nociceptors that are activ. by extreme HOT temp (>43) are associated with Aδ fibers
    (note: Aδ for Hot and C for warm)
  • Nociceptors associated that signal extrememely COLD temp are associated with C fibers)
    (note: Aδ for cool, C for Cold)
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10
Q

Intense pressure (not touch) activates which receptors?

A

mechanical nociceptors (which are assoc w/ Aδ fibers)

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11
Q

____ fibers for Hot and ____ fibers for warm

A

Aδ for Hot and C for warm

(remember the warm cunt?)

(Aδ fibers - cool and HOT)

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12
Q

____ fibers for cool, ____ fibers for Cold

A

Aδ for cool, C for Cold

C fibers - warm and COLD

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13
Q

Polymodal nociceptors have ____ fibers as their afferents.

What do they do?

A

C fibers

Polynodal nociceptors are activated by high intensity mechanical, chemical, or thermal stimuli.

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14
Q

Capsaicin activates nociceptors, how is it used as an analgesic?

A

Intense activation of capsaicin → massive secretion/depletion of Sub P

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15
Q

Stimuli that activates VR-1 receptor

A

VR-1 (capsaicin rcptr) strongly activated by capsaicin and weakly activated by acids and moderate heat (43 C)

  • the VR-1 rcptr is part of an ion channel complex: Rcptr is activated → NSC channel opens → depolarization
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16
Q

Where is the VR-1 receptor located?

A

Expressed on Polymodal nociceptors (that have C fibers as their afferents)

17
Q

Order of pain for Aδ fibers and C fibers

A

First pain: Aδ fiber

  • tolerable, localized, prickling pain
  • smaller receptive fields allows for more localization

Second pain: C fiber

  • slower, burning, intolerable pain
  • larger receptive fields: poorly localized pain
18
Q

Out of all of the fibers, which one would get activated first with high pressure? higher pressure than that?

A

The most metabolically active ones
- so if you rub your arm w/ high P → activate larger Aα and Aβ fibers ( non nociceptive afferent pathways, which leads to activation of dorsal horn interneurons that inhibit synapses activated by nociceptive fibers.

  • at higher P than that, C fibers also activated
19
Q

Out of all of the fibers, which are the ones to become activated first?
- which ones get activated with small shock? larger shock than that?

A

larger Aα and Aβ fibers
(these ones activated first are also the first ones to be blocked with P first - (not drugs))

  • this results in sensations of touch, vibration, joint movement - all without pain
  • larger shock → prickling pain → even larger shock → BURNING pain (C fibers)
20
Q

Out of all of the fibers, which are the ones to become nonconductive first with low dose anesthetics? Med dose? High dose?

A

anesthetics preferentially block small diameter fibers (C fibers - burning pain)

higher dose: block prickling pain

Higher dose than that: touch, afferents, motor axons (paralysis)

(Note: The order that they are blocked are opposite from that of how they get activated with shock)

21
Q

Activators of nociceptors

A

BK
K+
Acid
5-HT

= pain producing agents

22
Q

Sensitizers of niceptors

A
ATP
ACh
PG
Sub P
5-HT

-Sensitizer in that it lowers threshold for nociceptor activation = more pain = hyperalgesia

23
Q

How does aspirin help with pain?

A

Inhibits COX → prevents synth of PG → prevents nociceptor SENSITIZATION

24
Q

Allodynia

A

Extreme sensitization

lowered threshold

25
Triple response
Red: BK → potent vasodilator → hot and red Wheal: BK → increase cap permeability → fluid accum → swelling Flare: Sub P @ periph terminal (BK activates C fiber nociceptors → depol → AP)
26
Where do C fiber afferents terminate?
Rexed Laminae (substantia gelatinosa) in dorsal horn of sc.
27
Referred pain is due to?
Convergence of visceral and somatic pain inputs | - Typically cutaneous input dominates and this is where pain is "recognized"
28
Wind up
form of central sensitization - Stimulation dependent enhancement of post syn response of pain Stim C fibers → Activ. AMPA R → more intense/persistent stimulation → AMPA and NMDA R activated
29
What happens when sub P is released and binds to NK-1?
Closure of the K channels and depolarization | - but really it leads to enhancement / prolongation of the actions of glutamate which was also released with it.
30
PAG descending analgesic pathway
PAG → nucleus raphe magnus (medulla) → dorsal lateral funiculus secretes 5-HT → excites inhibitory interneuron → secretes enkaphalin → inhibits second order dorsal horn neuron (via 2 methods) → treat pain (This is why sometimes SSRIs can be used to treat pain!)
31
How does enkephalin secretion by inhibitory interneurons block second order dorsal horn neurons?
1. Presynaptically - block VGCC | 2. Postsynaptically - open K channels
32
Does naloxone block analgesia produced by PAG stim or by central opiate admin?
Both they involve activation of the same descending pathway
33
Stress induced analgesia
Stress + Emotions → Increased activity in Limbic system (hypothalamus, amygdala) → Activates PAG
34
Placebo effect
Placebo effect (Cognitive factors) → Frontal cortex/Insular cortex → activates PAG
35
Damage to which, peripheral or central NS can lead to neuropathic pain?
Either one.
36
Under normal conditions, the substantia gelatinosa receives inputs exclusively from which fibers? What happens with injury to these fibers?
C fibers - if they get injured, Aβ afferents will sprout and invade the normally forbidden territory of the substantia gelatinosa. - The 2nd order neurons in the SG that are NORMALLY activated by only pain are now also activated by non-noxious stimuli → PAIN PATHWAY IS INAPPROPRIATELY ACTIVATED (ALLODYNIA)
37
How does microglia contribute to hyperalgesia?
In the dorsal horn, ATP activates microglial cells → secrete BDNF → changes Cl- reversal potential and makes GABA excitatory instead of inhibitory → decreasing inhibition @ dorsal horn → hyperalgesia