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Block 5 Week 2 Meg > Kenyon: Pain > Flashcards

Kenyon: Pain Flashcards

1
Q

Do monkeys or rodents experience pain in the same way that humans do?

A

No

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2
Q

A special class of primary afferent neurons with their cell bodies in the dorsal root ganglia

A

nociceptors

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3
Q

Which nociceptive fibers conduct relatively slowly? Why?

A

C and A-gamma fibers; small diameter axons, small diameter cell bodies

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4
Q

Normally there are no synapses in the DRG. What can happen when there is injury to post-ganglionic sympathetics?

A

these neurons will synapse with sensory neurons and cause pain :(

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5
Q

Which has a higher threshold, thermoreceptors or nociceptors?

A

nociceptors!

Ex: something feels hot, then too hot, then OUCH pain!

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6
Q 
Stimulation of (blank) mechanoreceptors, thermoreceptors, etc. results in a non-painful sensation. It might be intense but not painful.
Stimulation of (blank) nociceptors results in pain
A

low threshold; high threshold

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7
Q

What’s this?

Conduct APs faster than C fibers but slower than TVP neurons

A

A-delta fibers

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8
Q

A-delta fibers are involved in which type of pain?

A

first pain

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9
Q

What’s this?

Slow unmyelinated fibers

A

C fibers

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10
Q

C fibers are involved in which type of pain?

A

second pain, polymodal (several kinds of painful stimuli)

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11
Q

What’s this?

Relatively fast A-delta fibers mediate a sharp pain

A

first pain

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12
Q

What’s this?

Relatively slow C fibers mediate a delayed, longer lasting pain

A

second pain

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13
Q

What is the capsaicin receptor?

A

TRPV1

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14
Q

What’s this?

A family of ion channels that have a variety of functions including temp and pain sensation

A

TRP channels

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15
Q

nonselective cation channels opened by heat, low pH, and capsaicin (the hot in hot peppers).

A

capsaicin receptors

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16
Q

What happens to mice without TRPV1?

A

they have reduced sensitivity to noxious stimuli

**TRPV1 channels are a target for pain therapy

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17
Q

TRP channels are tightly (blank)

A

regulated

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18
Q

Where do pain and temperature afferents synapse?

A

dorsal horn neurons

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19
Q

Axons from the secondary neurons cross and form the (blank) to the thalamus

A

anterolateral tract

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20
Q

TVP and pain/temperature are on opposite sides (blank) the medulla, and are on the same side (blank) the medulla

A

below; above

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21
Q

A lesion in one side of the spinal cord will result in reduced TVP on the (blank) side and reduced pain and temperature sensation on the (blank) side.

A

same side; opposite side

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22
Q

How to pain and temperature from the face enter the brainstem?

A

from the trigeminal nerve

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23
Q

What happens to the axons of the face before they cross over to form the trigeminothalamic tract?

A

they descend

24
Q

Between the mid-pons and the middle medulla, pain and temperature from (blank) sides of the face are on (blank) sides of the brainstem

A

both; both

25
Q

In the brain, we separate two aspects of pain sensation. What are they?

A
  1. sensory-discriminative pathway, which mediates location, intensity, and quality of the noxious stimulation
  2. affective-motivational pathway which mediates unpleasantness, anxiety, fear associated with pain
26
Q

Which part of the brain is associated with the sensory-discriminative pathway?

A

somatosensory cortex

27
Q

What part of the brain is associated with the affective-motivational pathway?

A

amygdala, hypothal, periaqueductal gray
anterior cingulate cortex
insular cortex
reticular formation

28
Q

What’s this?

mediates location, intensity, and quality of noxious stimulation

A

sensory-discriminative pathway

29
Q

What’s this?

mediates unpleasantness, anxiety, fear associated with pain

A

affective-motivational pathway

30
Q

Areas important in the affective-motivational pathway?

A 
anterior cingulate cortex
insular cortex
reticular formation
amygdala
hypothalamus
periaqueductal gray
31
Q

Is the affective-motivational pathway associated with the primary sensory cortex?

A

No!

32
Q

Some dorsal horn neurons receive input from visceral and cutaneous nociceptors. What can this cause?

A

referred pain

33
Q

In which pathway are there projections to the insula?

A

affective-motivational pathway

34
Q

Ablation of the dorsal column pathway for visceral pain can reduce pain associated with (blank)

A

visceral cancers of abdomen and pelvis

35
Q

increased sensitivity to a painful stimulus.

A

hyperalgesia

36
Q

previously nonpainful stimuli now cause pain

A

allodynia

37
Q

Hyperalgesia and allodynia can arise by (blank) and by (blank) mechanisms

A

peripheral; central

38
Q

What’s this?
The sensitivity of nociceptors can be adjusted in the periphery.

An “inflammatory soup” of substances is released following injury. The endings of nociceptors respond by becoming more sensitive.

A

peripheral sensitization

39
Q

What are sensitizing compounds involved in peripheral sensitization?

A 
protons
arachidonic acid
bradykinin
histamine
seratonin
prostaglandins
ATP
adenosine
nerve growth factor
CGRP
substance P
40
Q

T/F: Nociceptive neurons themselves can release sensitizing compounds

A

True…Yipes!

41
Q

Prostaglandins are potent sensitizers. What can inhibit them?

A

COX inhibitors ex: aspirin

42
Q

What’s this?
Changes in Spinal cord and higher centers can increase pain sensation.
For example, following injury light touch will activate dorsal horn neurons that receive nociceptive input (allodynia).

A

central sensitization

43
Q

What are two transcription independent mechanisms of central sensitization?

A

“Windup”

Ca2+ influx via NMDAR and Ca2+ channels.

44
Q

Progressive increase in response by a dorsal horn neuron to repetitive stimulation.

A

windup

45
Q

What’s this?

Cytokines promote transcription of COX-2 that makes prostaglandins that increase neuronal activity.

A

trx dependent mechanism of central sensitization

46
Q

Damage to the pain pathways can result in the sensation of pain after the injury has healed.
What kind of pain is this?

A

neuropathic pain

47
Q

Where is pain sensation regulated?

A

several locations, including the brainstem and spinal cord

48
Q

Discuss the descending control of pain perception starting at the somatic sensory cortex and going to the dorsal horn of the spinal cord.

A

somatic sensory cortex –> amygdala and hypothalamus –> midbrain periaqueductal gray –> parabrachial nucleus, medullary reticular formation, locus coeruleus, raphe nuclei –> dorsal horm of spinal cord

49
Q

What happens when pain signals finally reach the dorsal horn of the spinal cord?

A

activity in the descending pathways inhibits nociceptive activity

50
Q

In the dorsal horn of the spinal cord, several neurotransmitters are important in inhibiting nociceptive activity. How do they do this? What neurotransmitters can you think of?

A

they activate GPCRs coupled to the inhibition of voltage-gated Ca++ channels; this will decrease the release of neurotransmitter from the C fibers

51
Q

What can Raphe nuclei do?

A

essentially, they can shut down the generation of the pain signal

52
Q

Activation of (blank) can also inhibit nociceptive activity.

A

low-threshold mechanoreceptors **esp if mom activates them

53
Q

Activation of (blank) receptors in the periaqueductal gray and in the spinal cord can reduce pain. How are these activated?

A

opioid; exogenous or endogenous opioids

54
Q

Note that reduction of pain by a placebo can be blocked by (blank), a competitive antagonist of opiate receptors. The implication is that the placebo causes the release of (blank).

A

naloxone; endorphins

55
Q

What are these?
New neurotransmitters and receptors
Gene silencing (siRNA)
Identification and killing of nociceptors

A

new approaches to the management of pain

Block 5 Week 2 Meg (10 decks)

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