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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
Which pepper is the hottest?
habanero
26
How do pain & temp info get into the CNS? This applies only to the body & back of neck.
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
Where are the TVP info & P&T info on the same side?
in the medulla & after | NOT in the spinal cord
28
A lesion of the spinal cord on one side will cause TVP & P&T loss on which sides?
TVP loss on the ipsilateral (same) side | Pain & Temp loss on contralateral side
29
How does pain & temp info from the face get into the CNS?
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
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.
True
31
What are the 2 aspects of pain sensation?
sensory-discriminative pathway that mediates location, intensity, & quality of noxious stimuli affective-motivation pathway mediates unpleasantness, anxiety etc.
32
Which part of the brain is involved in the sensory aspect of pain sensation?
somatosensory cortex
33
Which part of the brain is involved in the affective aspect of pain sensation?
Amygdala, Hypothalamus, Periaqueductal gray | Reticular formation, Cingulate cortex, Insula
34
Give an overview of the central pain pathways.
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
Generally, which parts of the central pain pathways are a part of the sensory part of pain?
The ventral posterior nucleus & on part
36
Generally, which parts of the central pain pathways are a part of the motivational/affective part of pain?
Random stuff + Midline Thalamic Nucleus
37
Which parts of the central pain pathway are important in descending control?
``` anterior cingulate cortex insular cortex amygdala hypothalamus periaqueductal grey reticular formation ```
38
Describe the affective motivational pathway of pain.
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
Where is the superior cerebellar peduncle located?
mid-pons
40
Describe--what's the deal w/ referred pain according to Kenyon?
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
What is an extreme procedure that can alleviate visceral cancer pain?
* *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
By both peripheral & central mechanisms hyperalgesia & allodynia may result. What are these?
Hyperalgesia – increased sensitivity to a painful stimulus. | Allodynia – previously nonpainful stimuli now cause pain
43
What is peripheral sensitization?
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
What is the PAN's reaction to the sensitization of its ending?
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
Aside from Substance P & CGRP...what are the things that can be a part of the inflammatory soup? A part of peripheral sensitization?
Protons, arachidonic acid, bradykinin, histamine, serotonin, *prostaglandins, ATP, adenosine, nerve growth factor
46
Why can COX inhibitors help with peripheral sensitization?
b/c they block the formation of prostaglandins
47
What is central sensitization?
Changes in Spinal cord and higher centers can increase pain sensation. this is what causes allodynia
48
What are 2 mechanisms that are transcription-independent for central sensitization?
* *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
What is a transcription dependent form of central sensitization?
cytokines promote the transcription of COX-2 that makes prostaglandins
50
Aside from working on DRG neurons...how else do NSAIDs work?
centrally on the spinal cord neurons
51
What is neuropathic pain?
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
What's the deal with descending control of pain perception?
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
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?
parabrachial nucleus, dorsal raphe nucleus, locus coeruleus, and medulary reticular formation.
54
What are the 2 main NTs involved in the descending control of pain perception?
serotonin & enkephalins
55
What is the mechanism for the descending control of pain perception at a teeny tiny level?
GPCR activation Inhibition of Voltage-Gated Ca++ channels **no calcium--no bad NT release
56
T/F Activation of low-threshold mechanoreceptors can also inhibit nociceptive activity.
True.
57
T/F The periaqueductal grey can only be activated by endogenous opioids.
FALSE | it can also be activated by exogenous opioids-how convenient!
58
What is the general idea that ppl have right now as to the mechanism of the placebo effect?
involves the release of endorphins | can be blocked by the competitive antagonist of opiate receptors, naloxene
59
What are the possible future approaches to pain management?
New NT & receptors Gene Silencing siRNA Identification & killing of nociceptors.
60
T/F It is NOT important to take extra efforts to reduce pain in patients that can't communicate.
FALSE. It is very important, esp babies. otherwise they will experience hyperalgesia
61
T/F By the opening of chloride channels, hyper polarization can become depolarization in microglia.
True. No idea why that's important.

Block 5; Week 2 (8 decks)

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