09/30 Flashcards

1
Q

Which pathway is the pain pathway?

A

the anterolateral spinothalamic pathway

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2
Q

What are the three paths that information can take in the corticospinal pathways?

A
  1. Decending motor-internal capule- brainstem in medulla:crossover-decend in laterocortical corticopinal tract. 80%
  2. anterior corticopspinal tract. Crossover in the spinal cord 17%
  3. doesn’t cros over at all 3%
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3
Q

Fast pain is transmitted through which fibers?

A

A delta- heavily myelinated

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4
Q

nociceptors are the same thing as

A

free nerve endings

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5
Q

Fast pain gets routed through which portion of the anterolateral tract?

A

lateral

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6
Q

which neurotransmitter is used for fast pain?

A

glutamate

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7
Q

where does fast pain information get sent to in the brain?

A

Parietal lobe

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8
Q

Fast pain fibers are parallel to which fibers?

A

DCML

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9
Q

Which part of the parietal lobe takes care of the lower extremities?

A

top portion

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10
Q

Which part of the parietal lobe post central gyrus takes care of the trunk?

A

second to the top

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11
Q

Which part of the parietal lobe post central gyrus takes care of the upper extremities?

A

the second from the bottom

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12
Q

Which part of the parietal lobe post central gyrus takes care of the face?

A

the bottom portion

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13
Q

why are we able to localize fast pain?

A

because fast pain is routed to the same areas that DCML signals are sent

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14
Q

Where does cross over happen for fast pain?

A

in the anterior white commisur

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15
Q

What does neo mean?

A

new

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16
Q

what is another name for the fast pain tract besides spinothalamic?

A

neospinothalamic

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17
Q

what is another name for the slow pain tract?

A

paleospinothalamic

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18
Q

why is the fast pain called the neospinothalamic tract?

A

it is a new pathway that has branched off the slow pathway recently, making it more sophisticated.

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19
Q

what does Smidt think of with the word paleo?

A

dinosaurs

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20
Q

Slow pain uses what kind of fibers?

A

C fibers nonmyelinated

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21
Q

what type of neurotransmitters are used in slow pain?

A
  1. substance P(main one)
  2. CGRP(calcitonin gene related peptide)
  3. Glutamate (works slower here)
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22
Q

What makes the slow pain pathway slow?

A

c fibers
the slow release, binding and effect of neurotransmitters

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23
Q

a lot of slow pain pathways terminate at the

A

top of the brainstem

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24
Q

Why does slow pain have poor localization?

A

because the information doesn’t make it all the way up to the parietal lobe where information like this is sorted

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25
Q

Thermoreceptors and vibration sensors are associated with which pain pathway?

A

slow pain pathway

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26
Q

Where does slow pain have synapses in the spinal cord?

A

substantia gelatinosa
lamina 5

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27
Q

After lamina 5, slow pain crosses over at the _____ and goes into the _______ part of the anterolateral pathway

A

anterior white commisur
anterior

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28
Q

If you have fire on your finger, what is the pathway the pain will take

A

dorsal rootlets
synapses in the dorsal gray horn
cross over in the spinal cord
-slow: ascends in the anterior anterolateral pathway
-fast: ascends in the lateral anterolateral pathway

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29
Q

slow pain engages what part of the brain that fast pain doesn’t?

A

emotional. It messes with your head

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30
Q

Where are the emotional centers of the brain found?

A

very close to the middle of the brain
where the brainstem connects with the diencephalon

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31
Q

What is the ventrobasal complex?

A

a place where the dcml pathway runs through

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32
Q

what is the reticular formation?

A

a swath of tissue that is located in the top of the brainstem where a lot of the slow pain signals terminate

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33
Q

What is the vestibulospinal extrapyramidal tract?

A

a descending motor pathway.
eye fixation and muscle orientation during acceleration i.e. balance

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34
Q

Olivospinal tracts are what type of tract?

A

extrapyramidal tract

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35
Q

The reticulospinal tract maintains

A

baseline muscle tone

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36
Q

the rubrospinal tract is very similar to the tracts that the cerebellum uses and is in charge of

A

modulating voluntary movement

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37
Q

What are the extrapyramidal tract descending motor pathways?

A

vestibulospinal
olivospinal
reticulospinal
rubrospinal

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38
Q

What is the descending pain suppression system?

A

inhibitory in nature and activated by pain.

It is something that operates in the background and helps the body deal with pain

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39
Q

What does DIC stand for?

A

descending inhibitory complex

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40
Q

The DIC has how many neurons?

A

3

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41
Q

Where is the primary or initial neuron found in the dic tract?

A

periventricular nucleus or periaqueductal gray

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42
Q

Where is the periaqueductal gray found?

A

in the midbrain of the brainstem

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43
Q

Where is the periventricular nuclei found?

A

right in front of the third ventricle

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44
Q

When the first neuron is excited in the DIC pathway, what does it release, and where?

A

Enkephalin in the pons

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45
Q

What is situated right in the middle of the pons?

A

the cell body of our second-order descending neuron

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46
Q

In the pons are enkephalins excitatory or inhibitory?

A

excitatory

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47
Q

What does the second neuron in our DIC pathway release?

A

Serotonin

48
Q

What is the abbreviation for serotonin?

A

5-HT

49
Q

Where does serotonin get released by the second neuron in the DIC pathway?

A

in the spinal cord at the area of the dorsal horn

50
Q

What does serotonin act on in the DIC pathway?

A

the third neuron

51
Q

Is the third order neuron in the DIC pathway big or small?

A

very small

52
Q

What does the third order neuron in the DIC pathway secrete?

A

enkephalin

53
Q

In the spinal cord are enkephalins excitatory or inhibitory?

A

inhibitory

54
Q

What kind of receptors are found on nociceptors in the spinal cord?

A

enkephalin receptors -these are our pain sensing neurons

55
Q

Our pain sensing neurons have dendrites where?

A

in the periphery

56
Q

What happens when enkephalin binds to our nociceptors in the spinal cord?

A

it shuts down activity in the pain sensor

57
Q

After the second neuron in the DIC pathway, where is enkephalin receptors found?

A

in the next neuron in the ascending pain pathway. There are synapses on lamina 1,2,3 or 5 and from there the transmission would hop over to the other side of the cord and then ascend in the anterolateral pathway.

58
Q

There are synapses in lamina 1,2 or 3 and from there the transmission in the pain pathway would

A

would hop over to the other side of the cord and then ascend in the anterolateral pathway.

59
Q

What is enkephalin?

A

an endogenous morphine analogue

60
Q

all of our morphine receptors are actually

A

enkephalin receptors

61
Q

What is the specific place in the middle of the pons where we have this first synapse in the Descending inhibitory complex?

A

raphe magnus nucleus
RMN

62
Q

If we were to implant electrodes and stimulate either the periventricular nucleus or the periaqueductal gray area, we would expect

A

an inhibitory pain signal that can reduce the amount of pain that we perceive

63
Q

What is deep brain stimulation?

A

activation of the descending inhibitory complex by placing electrodes in either the periventricular nucleus or the periaqueductal gray area

64
Q

What is something that people rarely hear about but gives us a target for our drugs?

A

the descending inhibitory complex

65
Q

A nociceptor out in the periphery senses pain and sends that information to

A

the spinal nerve
dorsal root
dorsal rootlet
eventually it gets to the first order neuron
this synapses in lamina i, ii, iii or V with the second order neuron
the second ascending pain transmission neuron hops over to the other side of the cord via the AWC
and then rides in the anterolateral columns
slow pain Terminates in the brainstem
fast pain goes through the thalamus to the parietal lobe

66
Q

The descending pathway first order neuron starts at either the periaqueductal gray or the peri ventricular nuclei and then synapses at the _____ and then

A

in the middle of the pons (Raphe Magnus Nucleus)
the second neuron travels to the level of the cord it needs to interact with
this releases serotonin
which excites the third order neuron
which releases enkephalin
which binds to both the nociceptor and second order neuron
which is inhibitory and suppresses pain in the pre and post synaptic synapse

67
Q

You could lift a car off a kid, or completely deaden your pain senses if you have

A

enough training, self control, and high pain tolerance

68
Q

the synapse for the second, serotonergic DCIM neuron is found

A

outside of the gray matter

69
Q

if we can get a needle close enough to the ________ receptors, you can shut down pain

A

enkephalin

70
Q

In reverse adaptation what is happening to our ascending and descending pain pathways, specifically in chronic pain?

A

Enkephalin does not work as well because there’s less of those receptors and more glutamate receptors

71
Q

What can elicit a response in a nociceptor?

A

physical damage
crush injuries
cuts

potassium
Histamines
acids H+ lactic acid
Bradykinin
5-HT/serotonin
ACh
prostaglandings

72
Q

potassium follows

A

protons

73
Q

What type of patients have higher potassium and lower pH?

A

a patient with diabetes and renal failure that hasn’t had dialysis in a while

74
Q

Prostaglandins can’t produce pain in itself but they

A

augment the pain sensation for other things

75
Q

If we could somehow increase the bioavailability of serotonin near the second order serotonergic neuron, we could potentially

A

decrease chronic pain

76
Q

What are things that increase bioavailability of serotonin in the cord?

A
  • SSRI
    -paxel
    -prozac
    *tricyclic antidepressants
77
Q

Serotonergic neurons like to reuse their serotonin and do this by

A

a serotonin reuptake system

78
Q

SSRI’s block the

A

reuptake system of serotonin

79
Q

What is an older drug class that is prescribed fairly often for the treatment of chronic pain? Why?

A

Tricyclic antidepressants
They have other side effects that is sometimes helpful, like drowsiness.

80
Q

how long have tricyclic antidepressants been around for?

A

50-60 years

81
Q

Why did tricyclic antidepressants go out of favor for a while?

A

their side effects

82
Q

Because the pressure or DCML sensors run parallel to nociceptors, they can

A

talk to each other- though it isn’t understood how, it’s probably through some neurotransmitter and receptor.

83
Q

neighboring neurons can shut down

A

their neighbor

84
Q

If you injure yourself, and then you squeeze the part of the body that hurts, you can decrease the pain. what is this called?

A

lateral inhibition

85
Q

how does acupuncture work?

A

lateral inhibition

86
Q

Where does lateral inhibition work?

A

in the dorsal horn of the cord

87
Q

how much dcml pressure sensor information make it out of the dorsal horn if it didn’t go up towards the brain?

A

not very much. Lateral inhibition stops most of it in the dorsal horn of the cord

88
Q

what is our primary neurotransmitter for the pain system?

A

glutamate

89
Q

Is glutamate ever inhibitory?

A

no, it’s excitatory

90
Q

What is drawn in the first order neurotransmitter (the nociceptor that is out in the periphery detecting pain) at the synapse in the dorsal horn between it and the second order neuron that would hop to the other side of the cord and then send information into the anterolateral column and ascend towards the brain?

A

VG Ca++ channel that opens in response to an AP and allows calcium into the cell
which drives the VP holding glutamate to exocytosis

91
Q

after glutamate is released into the synapse between first and second order neuron, what does it do?

A

binds to either AMPA or NMDA receptors

92
Q

What is an AMPA receptor?

A

a ligand gated receptor next to an ion channel that opens in response to glutamate and lets Na+ into the cell

93
Q

What is the primary receptor on the second order neuron in the dorsal horn after the nociceptor?

A

AMPA

94
Q

What is the secondary receptor on the second order neuron in the dorsal horn after the nociceptor?

A

NMDA receptor

95
Q

What is a NMDA receptor?

A

a slow ligand gated receptor next to an ion channel that opens in response to glutamate and lets a lot of Ca+ and a little Na+ into the cell

96
Q

Why are NMDA’s slow?

A

because Mg++ blocks the opening intracellularly and the receptor has to wait for the AMPA receptor to produce an EPP to depolarize the inside of the cell and repel Mg++ from the NMDA’s opening

97
Q

If we depolarization via an AMPA receptor, and want to send more or a second type of information using the same synapse, what do we use?

A

NMDA receptor

98
Q

The more NMDA receptors that we have, the

A

more information that we can send

99
Q

NMDA receptors are placed in our CNS as a result of

A

development

100
Q

What is the tertiary receptor on the second order neuron in the dorsal horn after the nociceptor?

A

Kainate

101
Q

What blocks the NMDA receptors?

A

Ketamine
Lead
Ethanol
Nitrous
Tramadol

102
Q

People who are wasted don’t feel much pain, why?

A

their NMDA receptors are blocked

103
Q

If we live in an old house and eat paint chips, it will

A

block our NMDA receptors

104
Q

Ketamine is what kind of drug?

A

a dissociative. It shuts off part of the CNS but doesn’t put people to sleep

105
Q

Ketamine effects the _______ of pain

A

perception

106
Q

Ketamine ONLY works on which receptors?

A

NMDA. You can still have some pain through the AMPA and other receptors

107
Q

Tramadol is a terrible drug, why?

A

tramadol doesn’t do a ton with enkephalin receptors (morphine receptors)

108
Q

What does tramadol do to help with pain?

A

Serotonin reuptake inhibitor
inhibits NMDA but not AMPA

109
Q

Who is a good candidate for tramadol?

A

elderly
people super sensitive to opiates.

110
Q

Tramadol should not be used as a pain med after

A

surgery

111
Q

What do Kainate receptors mediate?

A

GABA activity in the brain

112
Q

Chronic pain inserts more ______ receptors

A

AMPA and NDMA

113
Q

What are the ionotropic glutamate receptors?

A

Kainate
AMPA
NDMA

These mediate changes to the cell wall permeability to ions

114
Q

What is the second, broad category of glutamate receptors?

A

metabotropic

GPCR’s that are involved in signal transduction

115
Q

What is the first class of glutamate receptors?

A

ionotropic

116
Q

If you remove the source of pain, do the excess NMDA receptors go away?

A

Yes, but it will take a long time, like months

117
Q

Where does ketamine work in kids that makes it useful?

A

in the brain