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Block 5; Week 2 > Kenyon-Pain > Flashcards

Kenyon-Pain Flashcards

1
Q

T/F Effective analgesic therapy improves quality of life.

A

TRUE!! Chronic/neuropathic pain particularly difficult to understand, though.

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2
Q

What are some examples of analgesic therapy?

A

Opiod analgesics
COX-2 Inhibitors
Adjuvant Analgesics

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3
Q

What percentage of patients receive adequate pain relief from neuropathic pain?

A

only 1/3

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4
Q

T/F Pain is in your head.

A

true.

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5
Q

Most studies of pain have been done in rodents. However, rodents lack certain structures. Which structures are they?

A

insular cortex

midline thalamic nuclei

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6
Q

lesion of the ventromedial nucleus of the thalamus or insula can cause what?

A

complete and permanent loss of contralateral pain and temperature sensation

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7
Q

Aside from verbal pain scales…what is some promising research that will help scale a patient’s level of pain?

A

fMRI

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8
Q

What are nociceptors?

A 
A special class of primary afferent neurons with their cell bodies in the dorsal root ganglia
these are the pain guys!
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9
Q

Which fibers make up nociceptors? Are they large or small?

A

They are small in diameter.
C & Adelta fibers make up nociceptors.
**therapeutic target to kill these fibers.

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10
Q

Capsaicin triggers which receptors?

A

TRPV1–noxious heat sensors

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11
Q

What is TRPM8 a receptor for?

A

cold sensors

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12
Q

What is TRPA1 a receptor for?

A

a subset of nociceptors

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13
Q

Explain what weird pathological thing can cause there to be a synapse in the DRG.

A

This can happen w/ an injured postganglionic sympathetic neuron. It will synapse in the DRG of a sensory neuron instead! This preganglionic sympathetic activity will cause pain.

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14
Q

Which has a lower threshold:

Nociceptors or Thermoreceptors?

A

Temp has a lower threshold.

Takes a pretty high temp before it becomes painful & nociceptors get involved.

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15
Q

When you hit your thumb with a hammer you feel a first pain & then a second pain a little while later…what is responsible for each pain wave?

A

First Pain: Adelta

Second Pain: C fibers

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16
Q

How fast do A delta fibers conduct? Which type of stimuli does it respond to?

A

pretty slow…def slower than TVP but faster than C fibers

**these are mainly mechanothermal sensitive

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17
Q

How fast do C fibers conduct? What are some of its characteristics? Which type of stimuli does it respond to?

A

slowly
they are unmyelinated
they are polymodal–respond to different kinds of painful stimuli

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18
Q

What is one of the main ion channel families under research that respond to nociceptors?

A

TRP

  • *transient receptor potential
  • *involved in temp & pain sensation among other things
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19
Q

What are the important characteristics of TRPV1?

A

These are capsaicin receptors. They also respond to a low pH & heat.
They are considered nonselective cation channels.
help with sensitivity to noxious stimuli

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20
Q

What are some things that regulate TRPV1?

A

intracellular calcium
kinases lipids
AND MORE
It is VERY regulated.

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21
Q

TRPV1 receptors are activated by capsaicin…but what is another weird response they have to capsaicin?

A

they can also be inactivated by it.

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22
Q

What is the mechanism by which capsaicin activates TRPV1?

A

capsaicin is lipid soluble so it goes across the membrane & binds the channel from the inside.

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23
Q

T/F Itch & pain are the same sensations.

A

False. They are different.

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24
Q

What is the basic way that itch works?

A

specific pruritic ligands carrying itch & pain info are selectively recognized by different GPCRs

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25
Q

Which pepper is the hottest?

A

habanero

26
Q

How do pain & temp info get into the CNS? This applies only to the body & back of neck.

A

they entire the cord & synapse in the dorsal horn

axons from secondary neurons cross & form the anterolateral tract aka spinothalamic tract to the thalamus

27
Q

Where are the TVP info & P&T info on the same side?

A

in the medulla & after

NOT in the spinal cord

28
Q

A lesion of the spinal cord on one side will cause TVP & P&T loss on which sides?

A

TVP loss on the ipsilateral (same) side

Pain & Temp loss on contralateral side

29
Q

How does pain & temp info from the face get into the CNS?

A

this info from the face returns via the trigeminal nerve

axons descend in the spinal cord before they synapse & cross over to form the trigeminothalamic tract

30
Q

T/F Between the mid-pons and middle medulla pain and temperature from both sides of the face are on both sides of the brainstem.

A

True

31
Q

What are the 2 aspects of pain sensation?

A

sensory-discriminative pathway that mediates location, intensity, & quality of noxious stimuli
affective-motivation pathway mediates unpleasantness, anxiety etc.

32
Q

Which part of the brain is involved in the sensory aspect of pain sensation?

A

somatosensory cortex

33
Q

Which part of the brain is involved in the affective aspect of pain sensation?

A

Amygdala, Hypothalamus, Periaqueductal gray

Reticular formation, Cingulate cortex, Insula

34
Q

Give an overview of the central pain pathways.

A

Anterolateral System–>Ventral Posterior Nucleus + Random + Midline Thalamic Nucleus
Ventral posterior nucleus–>somatosensory cortex
Midline Thalamic Nucleus–>Anterior Cingulate Cortex + Insular Cortex
Random–>Reticular formation + Superior Colliculus + Periaqueductal grey + hypothalamus + amygdala

35
Q

Generally, which parts of the central pain pathways are a part of the sensory part of pain?

A

The ventral posterior nucleus & on part

36
Q

Generally, which parts of the central pain pathways are a part of the motivational/affective part of pain?

A

Random stuff + Midline Thalamic Nucleus

37
Q

Which parts of the central pain pathway are important in descending control?

A 
anterior cingulate cortex
insular cortex
amygdala
hypothalamus
periaqueductal grey
reticular formation
38
Q

Describe the affective motivational pathway of pain.

A

Signal gets into the brainstem.
part branches off to the reticular formation in the middle medulla
a part continues up to the mid-pons
Here, a part synapses at the parabrachial nucleus. It the hops off to the amygdala & hypothalamus
Another part continues up to synapse @ the intralaminar nuclei of the thalamus
There you get another 2 branches: 1 goes to the cingulate cortex & 1 goes to the insula

39
Q

Where is the superior cerebellar peduncle located?

A

mid-pons

40
Q

Describe–what’s the deal w/ referred pain according to Kenyon?

A

referred pain is visceral pain & is felt @ another part of the body
this is b/c some dorsal horn neurons receive input from visceral & cutaneous nociceptors.

41
Q

What is an extreme procedure that can alleviate visceral cancer pain?

A
  • *you could theoretically cut the dorsal column b/c some second order nociceptive neurons travel this way & end up not in the primary sensory cortex but in the insula.
  • *then you would reduce visceral pain of abdominal & pelvic cancers
  • *but you would also sacrifice TVP from your feet etc.
42
Q

By both peripheral & central mechanisms hyperalgesia & allodynia may result. What are these?

A

Hyperalgesia – increased sensitivity to a painful stimulus.

Allodynia – previously nonpainful stimuli now cause pain

43
Q

What is peripheral sensitization?

A

increased sensitivity of nociceptors adjusted @ the periphery b/c of the inflammatory soup released following injury. the substances respond to the ends of nociceptors & make them more sensitive.

44
Q

What is the PAN’s reaction to the sensitization of its ending?

A

it releases things too & gets in on the fun!

releases Substance P & CGRP–>these make his neighbors sensitive too! Spreads the love. Positive feedback.

45
Q

Aside from Substance P & CGRP…what are the things that can be a part of the inflammatory soup? A part of peripheral sensitization?

A

Protons, arachidonic acid, bradykinin, histamine, serotonin, *prostaglandins, ATP, adenosine, nerve growth factor

46
Q

Why can COX inhibitors help with peripheral sensitization?

A

b/c they block the formation of prostaglandins

47
Q

What is central sensitization?

A

Changes in Spinal cord and higher centers can increase pain sensation.
this is what causes allodynia

48
Q

What are 2 mechanisms that are transcription-independent for central sensitization?

A
  • *Windup: progressive increase in response by a dorsal horn neuron to repetitive stimulation. makes the second order neuron more sensitive to PAN
  • *Ca2+ influx via NMDAR and Ca2+ channels.
49
Q

What is a transcription dependent form of central sensitization?

A

cytokines promote the transcription of COX-2 that makes prostaglandins

50
Q

Aside from working on DRG neurons…how else do NSAIDs work?

A

centrally on the spinal cord neurons

51
Q

What is neuropathic pain?

A

Damage to the pain pathways can result in the sensation of pain after the injury has healed
**most difficult type of pain to treat

52
Q

What’s the deal with descending control of pain perception?

A

There is an affective motivational pathway that is descending that dampens the neurotransmission of pain & cuts it off right @ the dorsal horn of the spinal cord. Endogenous opiates are released by certain structures.
The structures involved include: amygdala & hypothalamus & Midbrain Periaqueductal Grey (big one) & Medullary Reticular Formation.

53
Q

The neurons in the periaqueductal grey project to 4 things that inhibit the pain @ the dorsal horn of the spinal cord. What are these 4 things?

A

parabrachial nucleus, dorsal raphe nucleus, locus coeruleus, and medulary reticular formation.

54
Q

What are the 2 main NTs involved in the descending control of pain perception?

A

serotonin & enkephalins

55
Q

What is the mechanism for the descending control of pain perception at a teeny tiny level?

A

GPCR activation
Inhibition of Voltage-Gated Ca++ channels
**no calcium–no bad NT release

56
Q

T/F Activation of low-threshold mechanoreceptors can also inhibit nociceptive activity.

A

True.

57
Q

T/F The periaqueductal grey can only be activated by endogenous opioids.

A

FALSE

it can also be activated by exogenous opioids-how convenient!

58
Q

What is the general idea that ppl have right now as to the mechanism of the placebo effect?

A

involves the release of endorphins

can be blocked by the competitive antagonist of opiate receptors, naloxene

59
Q

What are the possible future approaches to pain management?

A

New NT & receptors
Gene Silencing siRNA
Identification & killing of nociceptors.

60
Q

T/F It is NOT important to take extra efforts to reduce pain in patients that can’t communicate.

A

FALSE. It is very important, esp babies. otherwise they will experience hyperalgesia

61
Q

T/F By the opening of chloride channels, hyper polarization can become depolarization in microglia.

A

True. No idea why that’s important.

Block 5; Week 2 (8 decks)

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