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A&P Fall '24 > Test 3 - 9/30 Lecture > Flashcards

Test 3 - 9/30 Lecture Flashcards

1
Q

True/False: Spinothalamic and Anterolateral Tracts are used as interchangable terminology

A

True

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2
Q

True/False: Spinethalamic goes up to spine and to thalamus

A

True

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3
Q

Fast pain ascends to brain via what portion of the anterolateral tract

A

Lateral pathway

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4
Q

What neurotransmitter is used for fast pain?

A

Glutamate

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5
Q

What kind of fibers relay fast pain signals

A

A delta fibers

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6
Q

Fast pain is first sensed by what?

A

Nociceptors (free nerve endings)

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7
Q

Where does the cross over happen for fast pain? and at what level?

A

AWC at the level that the pain enters

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8
Q

Why does fast pain have a detailed localization?

A

It is sent to the parietal lobe from the thalamus and there it is in the same region as the DCML pathway so the pain can be interpreted in the portion of the parietal lobe that the pain is happening.

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9
Q

What lamina does fast pain interact with?

A

Lamina I (lamina marginalis)

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10
Q

Does Neospinothalamic tract correspond to fast or slow pain?

A

Fast

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11
Q

True/False: Neospinothalamic is described by Schmidt as a “newer pathway” that could have branched off of slow pain pathway.

A

True

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12
Q

What portion of the Anterolateral tract does slow pain get sent up?

A

Anterior pathway

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13
Q

What is the main neurotransmitter for slow pain

A

Substance P

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14
Q

What are the three neurotransmitters for slow pain as mentioned in lecture

A

Glutamate, Substance P, CGRP

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15
Q

What fibers transmit slow pain signals

A

C fibers

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16
Q

How does Glutamate work in fast pain vs slow pain?

A

In fast pain it releases, binds and generates AP fast.
In slow pain it does everything slower.

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17
Q

Why is there poor localization of slow pain?

A

It doesn’t make it to the parietal lobe where it can be localized, a lot of the info makes it to the top of brain stem and then stops.

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17
Q

What lamina are associated with slow pain?

A

Lamina II & III and then V

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18
Q

True/False: Paleospinothalamic Tract corresponds with slow pain

A

True

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19
Q

How many paths can the Pyramidal tract take?

A

3.

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20
Q

True/False. Slow pain can elicit more emotional responses

A

True

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21
Q

Where is the emotional center located?

A

Toward the middle of the brain where the brain stem meets the diencephalon.

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22
Q

True/False. Slow pain typically goes past the thalamus to the parietal lobe

A

False. It rarely goes past the thalamus.

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23
Q

What passes through the ventrobasal complex?

A

DCML and fast pain signals

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24
Q

What is the tissue at the top of the brain stem where slow pain signals terminate?

A

Reticular Formation

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25
Q

What are the four extrapyramidal tracts? What kind of pathway are these?

A
  1. vestibulospinal
  2. olivospinal
  3. reticulospinal
  4. rubrospinal
    They are descending motor accessory pathways
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26
Q

What is the vestibulospinal tract used for?

A

Used for maintaining balance and focus eyes while body is in motion

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27
Q

What is the reticulospinal tract used for?

A

maintaining muscle tone (always have some baseline muscle tone)

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28
Q

what is the rubrospinal tract used for?

A

modulation of voluntary movements.
(similar to cerebellum tracts)

29
Q

True/False. The descending pain system is inhibitory in nature

A

True

30
Q

Why does the descending pain system get activated?

A

It is activated in response to pain.

31
Q

True/False. The descending pain pathway will take the edge off of pain

A

True

32
Q

How many neurons make up the DIC pathway?

A

3

33
Q

What is the first order neuron in DIC?

A

Enkephalin

34
Q

Where does the body for the first order neuron reside?

A

Originates in the periventricular nuclei or the periaqueductal grey

35
Q

Enkephalin neurons release _____ neurotransmitters in the _____ which is located in the middle of the _____

A

Enkephalins.
Raphe magnus nucleus (RMN)
Pons

36
Q

Are the neurotransmitters from the first order neuron (Enkephalin) excitatory or inhibitory?

A

Excitatory

37
Q

Where is the periaqueductal gray located?

A

Near the cerebral aqueduct in the midbrain

38
Q

Where is the periventricular nuclei located?

A

It sits in front of the 3rd ventricle

39
Q

What is the 2nd order neuron in DIC?

A

Serotonergic neuron

40
Q

The serotonergic neuron releases _____ in the _____.

A

Serotonin.
Dorsal horn

41
Q

What is the 3rd order neuron in DIC?

A

Enkephalin neuron

42
Q

Is the 3rd order neuron inhibitory or excitatory?

A

Inhibitory

43
Q

How is the 3rd order neuron enkephalin inhibitory? How does it work on pain?

A

There is a pain receptor neuron (nociceptor) that enters via the dorsal horn, there are enkephalin receptors on the nociceptors and when the neurotransmitter is released it shuts down pain

44
Q

What is the abbreviation for serotonin?

A

5-HT

45
Q

Enkephalin is _____(endogenous/exogenous).

A

Endogenous

46
Q

True/False. Enkephalin is a morphine analog. All of our opioid receptors are actually enkephalin receptors

A

True

47
Q

If we implant electrodes into _____ or ______ and stimulate, that would generate an _____ pain signal that could _____ the amount of pain we perceive.

A

Periventricular nuclei
Periaqueductal grey
inhibitory
Reduce

48
Q

Where does the first synapse occur in the DIC pathway?

A

Raphe magnus nucleus, located in the middle of the pons

49
Q

What are things that can be perceived as pain in the periphery according to the lecture. (8)

A
  1. Physical damage
  2. Acid build up (lactic acid)
  3. Increase in ECF K
  4. Histamine
  5. Serotonin
  6. Ach
  7. PG’s
  8. Bradykinin
50
Q

Why could a dialysis patient have more pain?

A

Their K could be messed up and the increase in K can depolarize cells and be interpreted as pain

51
Q

Excess of protons usually means excess of _____

A

K

52
Q

How can we decrease chronic pain via the serotonin neuron in the DIC?

A

Typically serotonin neurons have a natural reuptake system. If we inhibit this reuptake we will have more serotonin at the synapse and can augment the effects of the 3rd order inhibitory neuron.

53
Q

Why are TCA’s not used as much now as an serotonin reuptake inhibitor?

A

The side effects. Caused drowsiness but people with chronic pain would probs benefit from that.

54
Q

What is lateral inhibition? How does it work?

A

Pressure sensor and nociceptor run parallel to each other..they can talk to each other and the nearby pressure sensor can shut down pain.

55
Q

If we hit our hand with a hammer and grab our hand and apply pressure we are doing what to the pain?

A

lateral inhibition

56
Q

Where does lateral inhibition take place?

A

in the dorsal horn of grey matter

57
Q

Acupuncture is an example of what?

A

lateral inhibition

58
Q

What is the main glutamate receptor for pain synapse?

A

AMPA-r

59
Q

How does the AMPA-r work?

A

Glutamate binds to receptor and opens a Na ion channel. Enough Na comes in and generates an AP to send info to brain

60
Q

NMDA is a _____ receptor

A

Glutamate

61
Q

How does the NMDA-r work?

A

Have to have depolarization and glutamate binding to receptor to activate. Once activated ion channel opens and allows primarily Ca through (some Na too)

62
Q

Why do the NMDA-r need depolarization to be activated?

A

Bc Mg sits at the cell wall and blocks it. If we make the inside more + it will move away from the cell wall and it can open.

63
Q

True/False. NMDA-r work faster than AMPA-r.

A

False. AMPA-r are faster

64
Q

How is glutamate released from the nociceptor?

A

Voltage gated Ca+ channels open and move the glutamate to the outside of the nociceptor.

65
Q

True/False. When we are born we dont have many NMDA-r, they are placed in nervous system as we grow

A

True

66
Q

What are some examples of things that can block NMDA-r as mentioned in lecture? (5)

A
  1. Ethanol
  2. Lead poisoning
  3. Ketamine
  4. Nitrous
  5. Tramadol
67
Q

Does ketamine work on both AMPA and NMDA?

A

No, only NMDA

68
Q

What happens with the AMPA and NMDA receptors with chronic pain?

A

The more often the are activated, the more receptors get populated and are able to send more action potentials making us more sensitive to pain

69
Q

What are the 3 ionitropic glutamate receptors mentioned in class?

A
  1. AMPA
  2. NMDA
  3. Kanate
70
Q

How do the Ionitropic receptors work?

A

They increase cell wall permeability to ions

71
Q

What is the one metabotropic glutamate receptor mentioned in class?

A

GCPR

A&P Fall '24 (11 decks)

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