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A/P > Lecture 14: 9/30 - Pain > Flashcards

Lecture 14: 9/30 - Pain Flashcards

Test 2

1
Q

What pathway does fast pain go up?

A

Lateral spinothalamic tract

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2
Q

What pathway does slow pain go up?

A

Anterior spinothalamic tract

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3
Q

Where are the fast pain synapse?

A

Laminae I

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4
Q

What type of fibers do fast pain travel on?

A

Heavily mylinated A-Delta fibers

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5
Q

What is a pain neuron called?

A

Nociceptor

Free nerve ending

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6
Q

What are the neurotransmitters on for fast pain?

A

Glutamate

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7
Q

Where is fast pain sent to?

A

Parietal Lobe (post central gyrus)

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8
Q

What pathway slightly mimics the fast pain pathway?

A

DCML

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9
Q

Describe Glutamate in fast pain

A

Fast to release and bind to receptor
Fast to generate AP

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10
Q

If there is fast pain on your LE, what part of the parietal lobe is that sent to?

A

Midline/Top

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11
Q

If there is fast pain on your face, what part of the parietal lobe is that sent to?

A

Lateral

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12
Q

Why can you localize fast pain better than slow pain?

A

Fast pain mimic the DCML and terminates in the parietal lobe vs slow pain that does always reach that far. The parietal lobe controls your senses

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13
Q

What are the neurotrasmitters in slow pain?
What is the main one?

A

Glutamate
Substance P
Calcitonin Gene-related peptide (CGRP)

Substance P

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13
Q

Where are the synapse for slow pain?

A

Laminae II, III, and V

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14
Q

Describe Glutamate in slow pain vs fast

A

Glutamate acts slower in slow pain

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15
Q

What is a Neospinothalamic tract?

A

New pain pathway that has branched off of slow pain pathway. More sophitocated

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16
Q

What is a paleospinothalamic tract?

A

older tract that hasnt been developed much

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17
Q

T/F: Slow pain transmitters are slow to release and bind to receptor and generate an AP

A

T

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18
Q

Where does crossover happen in pain?

A

Anterior White Commisure (AWC)

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19
Q

T/F: Pain goes up the spinal cord on the same side the pain went into the spinal cord

A

F

Pain crosses over at the AWC before going up

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20
Q

Describe the pathway of fast pain

A

Dorsal root/rootlets -> Dorsal horn -> Laminae 1 (Laminae marginalis) -> Crossover at AWC -> Lateral spinothalamic tract -> ascends through the spinomesencephalic tract -> thalamus -> ventrobasal and intralaminar nuclei of the thalamus -> internal capsule -> Parietal lobe / cortex

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21
Q

Where are the somatosensory areas?

A

Parietal lobe

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22
Q

What areas do the DCML and fast pain have in common?

A

Ventrobasal complex in the thalamus and the internal capsule

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23
Q

Where do slow pain signals normally terminate?
Where is this?

A

Reticular formation

Tissue at the top of the brainstem

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24
Q

If slow pain does go pass the reticular formation, where does the signaling usually go?

A

Limbic system

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25
Q

Describe extrapyramidal tract: Olivospinal

A

Descending motor pathway

only needs to know it exists

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25
Q

Describe extrapyramidal tract: Vestibulospinal

A

Descending motor pathway

Balance; focuses eyes when body is moving

26
Q

Describe extrapyramidal tract: Reticulospinal

A

Maintains muscle tone

27
Q

Describe extrapyramidal tract: Rubrospinal

A

Monitors involuntary movements from the brain

28
Q

DIC =

A

Descending Inhibitory Complex

29
Q

T/F: DIC can completely suppress pain

A

T

DOES NOT USUALLY DO THIS but it can

30
Q

What activates the DIC pain suppression system?

A

Pain

31
Q

What receptors do opiods act on?

A

Enkephalin receptors

32
Q

In the DIC: where are the initial neurons located?

A

The periaqueductal gray (superior to the 4th ventricle)

or

The periventricular nuclei (anterior to 3rd ventricle)

33
Q

In the DIC: what does the 1st order neuron release?
Where is this released?

A

Enkephalin

On the 2nd order cell body (Serotenergic neuron) locate at the Nucleus raphe

34
Q

In the DIC: where is the synapse for the 1st and 2nd order neuron?

A

Nucleus raphe in the center of the pons

35
Q

In the DIC: what is the 2nd order neuron?

A

Serotonin neuron

36
Q

What is Serotonin called?

A

5-HT

37
Q

In the DIC: what is the 3rd order neuron?
Is it excitatory or inhibitory?
What does it do?

A

Enkephalin neuron

Inhibitory

Releases enkephalin on the synapse/laminae in the grey matter where pain is before crossover

38
Q

Deep brain stimulation of the periventicular nuclei and periaqueductal gray does what?

A

activate DIC pathway
decrease pain…

39
Q

What are things that can be perceived as pain?

A

Damage to the receptor
Increase in H+
Increase in lactic acid (ex. exercise)
Increase in K+ (think about dialysis pts)
Histamine (ex. mosquito bites)
5-HT in periphery
Ach in periphery
PGs in periphery
Bradykinin

40
Q

T/F: taking antidepressants will increase pain

A

F

They help pain by increase the bioavailability of serotonin in the cord

41
Q

What are antidepressants that can help with chronic pain?

A

SSRIs
Tricyclic antidepressants

42
Q

What neuron runs parallel to pain neuron?

A

pressure neurons

43
Q

What is lateral inhibition?

A

Pressure sesnor inhibiting pain senses

44
Q

What is a negative SE associated with tricyclic antidepressants?

A

Drowsy

But will give them if depressed, with chronic pain, and cant sleep…

negative side effects are not helping

45
Q

How does accupuncture works?

A

Lateral inhibition

46
Q

What type of receptor is an opiate receptor?
What type of ion channel is it linked to?

A

GPCR

K+ ion channel

47
Q

Volatile anesthetics increase ____ conductance

A

K+

48
Q

T/F: Cox 2 decreases pain

A

F

COX2 increases PG which increase pain sensitivity

49
Q

What is an AMPA receptor linked to?

A

Na+ ion channel

50
Q

What is an NDMA receptor linked to?

A

Primarily Ca++ ion channel

Na+ gets through here as well

51
Q

What are the differences between the AMPA and the NDMA receptors?

A

NDMA receptor is much slower to open/react after AP

NDMA receptor also needs to be depolarized FIRST

52
Q

What ion blocks the NDMA receptor?
How do we unblock it?

A

Magnesium

Depolarizing the cell and Glutamate binding to the receptor

53
Q

What happens to our NDMA receptors after we are born?

A

We develop more

54
Q

What happens when we block the NDMA receptors? What can block them?

A

Decrease pain

Ethanol
Lead
Ketamine
Magnesium
Nitrous
Tramodol

55
Q

What happens to the AMPA and NDMA receptors when we have chronic pain?

A

More AMPA and NDMA receptors appear at the synapse

56
Q

What are the 3 glutamate receptors?
What type of receptors are these?

A

AMPA
NDMA
Kanate

Ionotropic

57
Q

Where are metabotropic glutamate receptors found?

A

In the brain

58
Q

What is a SE of taking alot of magnesium for pain?

A

GI disturbances - pooping

59
Q

Which is better for pain; Ca++ or Mg++?

A

Mg++

60
Q

What type of fiber for slow pain travel on?

A

Non-myelinated C-fibers

61
Q

T/F: None of the slow pain signals make it to the parietal lobe

A

F

Some do; but most dont. Most terminate in the reticular formation. some make it to the limbiic system. some make it to the parietal lobe

62
Q

How does COX2 contribute to pain?

A

Increased pain activates the release of COX2

COX2 increases PG which increase pain sensitivity

63
Q

What is iNOS? What does it do?

A

Induceable form of NOS (nitric oxide synthase)

Increases pain signaling/sensitivity

64
Q

What does Alpha 2 agonist do in the CNS?

A

Suppress pain and increase relaxation

help increase K+ permeability

65
Q

What are some examples of Alpha-2 agonists?

A

Xylazen (horse tranquilizer)
Precedex (most specific)
Clonidine

A/P (33 decks)

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