Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

A&P 1 > Exam 3 - Lecture 2 > Flashcards

Exam 3 - Lecture 2 Flashcards

1
Q

Where do pain signals cross over?

A

AWC; At the level of the cord immediately, before ascending up anterolateral/spinothalamic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Characteristics of fast pain

A

Detailed localization, lateral pathway, Glutamate NT’s, “fast”, through A-delta fibers, nociceptors/free nerve endings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Connects pain sensor to next order ascending neuron

A

Glutamate NT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Glutamate is very _____ to be released, bind, and _________.

A

Fast; fire an action potential.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Everything about glutamate is

A

Fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Fast pain gets transmitted to _________ as regular sensor signals

A

the same part of the brain in parietal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Characteristics of slow pain

A

Anterior spinothalamic tract, not all of it makes it to past thalamus, poor localization, C-fibers, thermoreceptors/heat, also uses glutamate NT’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Paleospinothalamic tract

A

anterior spinothalamic/slow pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Neospinothalamic tract

A

Fast pain/lateral spinothalamic tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Neo means

A

new

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Fast pain passes through _______ with __________

A

Ventrobasal complex; DCML sensory information

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

NT also used by slow pain pathways

A

CGRP: Calcitonin G-related peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Main NT for slow pain pathway

A

Substance P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does glutamate act different in the slow pain pathway?

A

Its slower for some reason.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why does slow pain have poor localization?

A

Less dense receptors and because not much of the pain signal actually makes it to the parietal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Slow pain ascends up which pathway?

A

Anterior spinothalamic tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Somatosensory areas

A

part of the brain that allows us to localize where pain is coming from.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where do slow pain signals often terminate?

A

Brain stem or thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Slow pain can impact ________ areas of brain.

A

Emotional.

Chronic pain can mess with your head and make you more emotional.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Emotional centers of brain are typically near diencephalon so thats why slow pain being terminated there can affect ______

A

Emotion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ventrobasal complex

A

DCML and fast pain run through here in thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Reticular formation

A

swath of tissue in top of brain stem where slow pain signals end up terminating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Extrapyramidal tracts

A

Vestibulospinal

Olivospinal: just know it exists lol

Reticulospinal

Rubrospinal

-All are CNS outputs to spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Vestibulospinal

A

eye fixation, muscle formation, maintain balance, descending motor pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Reticulospinal

A

maintenance of muscle tone, we have a small amount of tone at all times in our muscles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Rubrospinal

A

Used by cerebellum; modulation of voluntary movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Descending pain suppression system

A

Inhibitory in nature, usually activated in response to pain. Helps take the edge off for pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

DIC

A

Descending inhibitory complex (pain suppression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Primary/initial neuron of DIC

A

Periventricular nuclei (near 3rd ventricle) or periaqueductal gray (near cerebral aqueduct)

-Send APs towards targets further down brainstem/spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What do periventricular or periaqueductal gray neurons release when excited?

A

Enkephalins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

2nd order neuron

A

Serotonergic neuron: releases serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Name for serotonin

A

5-HT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where is enkephalin released by 3rd order neuron?

A

In the dorsal horn of cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Serotonin acts on ______

A

3rd neuron in DIC.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

3rd order neuron is (size?)__________. What does it secrete?

A

Very small; enkephalin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

In the cord, enkephalin is a _________ NT.

A

Inhibitory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Enkephalin receptors are located

A

on the pain sensing neuron/nociceptor, binds to it and shuts down pain sensor outside and in spinal cord.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

1st order ascending pain neuron

A

pain receptor neuron outside spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

2nd order ascending pain neuron

A

pain receptor relaying signal in spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Enkephalin is a ________ analog.

A

Morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Opiate receptors are actually _______.

A

Enkephalin receptors

42
Q

Enkephalin receptors could also be thought of our bodies __________.

A

Endogenous opiates receptors.

43
Q

Specific place in middle of pons with first synapse in DIC

A

Raphe magnus nucleus, aka RMN

44
Q

If we were to implant electrodes into periventricular nuclei or periaqueductal gray areas, it would

A

Generate an inhibitory pain signal that could reduce perceived pain.

45
Q

DIC is a system that could be a target for

A

stimulating this pathway with drugs to inhibit pain and dull perception of brain.

46
Q

Enkephalin is released by enkephalin neuron on both _____________ and ___________.

A

Pre and post synaptic of nociceptor

47
Q

Meditation/inner wellness can control

A

Pain and develop a high pain tolerance, by utilizing the DIC.

48
Q

What are you injecting into patients in spinal cord

A

enkephalin receptors essentially.

49
Q

DIC can affect both:

A

slow and fast pain

50
Q

Chronic pain can _______ glutamate NTs

A

upregulate

51
Q

Chronic pain is a mix of an increase in _________ and a decrease in _________.

A

Glutamate NTs; enkephalin receptors

52
Q

Physical damage such as crush/cuts/acid to a nociceptor will cause it to

A

depolarize and feed that information into cord as painful

53
Q

Lactic acid can be _________

A

painful

54
Q

What ions with a high concentration can cause increased pain signals?

A

Potassium/Protons

55
Q

Elevated K+ are going to do what more than normal healthy people?

A

Complain about pain more because they are truly more sensitive to pain than a normal person.

56
Q

Serotonins nature in the cord vs in the periphery

A

It is painful when outside the cord in the periphery but it is inhibitory for pain inside the cord.

57
Q

Prostaglandins role in pain in the periphery

A

Not directly painful, but they augment the pain sensation for anything thats painful. Increase pain without activating action potentials.

58
Q

7 examples of things in the periphery that can increase interpretation of pain

A

K+, H+, 5-HT, Ach, bradykinins, prostaglandins, and histamines.

59
Q

In DIC, increased serotonin results in

A

More pain inhibition, can treat chronic pain.

60
Q

SSRI’s role in chronic pain management

A

Increases serotonin in spinal cord by inhibiting reuptake of serotonin, resulting in less perceived pain.

drugs examples: paxil and prozac.

61
Q

Tricyclic antidepressants

A

Also known as TCA’s: help treat chronic pain with increased serotonin, tend to cause drowsiness and helps people with chronic pain go to sleep.

62
Q

2nd order neuron in DIC

A

Serotonin

63
Q

3rd order neuron in DIC

A

Enkephalin

64
Q

Old antidepressant drugs that went out of favor, but are now useful for chronic pain

A

TCA’s due to crappy/problematic side effects like drowsiness, but the drowsiness is beneficial for sleep in chronic pain patients.

65
Q

why can’t people with chronic pain sleep well?

A

Overactive brain from receiving pain signals.

66
Q

Sensory receptors that run parallel to nociceptors to the spinal cord

A

Pressure receptors

67
Q

Lateral inhibition

A

Pain signals run parallel to pressure signals to spinal cord, and activating those pressure sensors can inhibit the pain signals. Thats why we grab the body part that hurts, and why acupuncture works.

68
Q

neurons next to each other can _____________ but its not fully understood how

A

Talk to eachother and shut down their neighbors, such with lateral inhibition.

69
Q

Where does the pain get inhibited by lateral inhibition?

A

In the dorsal horn of the cord

70
Q

Glutamate

A

Primary neurotransmitters with fast pain, excitatory in nature.

71
Q

Nociceptor uses ______ as the neurotransmitter to excite the second order neuron in the ascending pathway

A

Glutamate

72
Q

1st order neuron in pain sensor

A

actually sensing the pain in the periphery

73
Q

Neurotransmitter in 1st order neuron that gets released to excite 2nd order neuron

A

Glutamate

74
Q

How does glutamate get released from nociceptor?

A

Ca++ influx into cell, vesicles fuse to cell wall and dump glutamate into synapse

75
Q

Primary glutamate receptor of fast pain system

A

AMPA-r

76
Q

What type of channel are AMPA-r?

A

Ligand gated Ion channels

77
Q

How does the AMPA-r open?

A

Glutamate binds to AMPA-r on second order neuron, which opens up a sodium channel for sodium to flood into and excite the second order neuron to generate an action potential.

78
Q

NDMA-r - what’s the neurotransmitter for it and is it faster or slower than AMPA-r?

A

Glutamate receptor attached to ion channel, but takes longer than AMPA-r to work.

79
Q

Whats the ion current in NDMA-r?

A

Calcium channels, thats why its slower.

80
Q

Which of the second order neuron receptors have larger channels?

A

NDMA-r because its calcium

81
Q

In order to actually open NDMA-r, they need 2 things:

A

Glutamate binding, and the neuron needs to be depolarized.

82
Q

Why does NDMA-r require depolarization before the channels actually open?

A

Intracellular Mg++ is bound to inside of receptor channel, clogging the channel.

Once the inside of the cell becomes positive, the magnesium moves out of the way and allows calcium to flood in.

83
Q

What causes the depolarization of this second order neuron?

A

AMPA-r allowing sodium in, or “anything” that would depolarize the neuron.

84
Q

AMPA-r and NDMA-r receptors being on the same synapse allows for

A

more information to go through the neurons

85
Q

At birth, do we have NDMA-r?

A

Not alot, but as we grow and mature, they get plugged into the cell walls of the nervous system.

86
Q

What is the main receptor of pain transmission?

A

AMPA-r

87
Q

What can block NDMA-r?

A

Ethanol, lead poisoning, ketamine, nitrous, tramadol

88
Q

Why dont drunk people feel alot of pain?

A

Inhibition of NDMA-r

89
Q

What happens if you eat paint chips off the wall in a old house?

A

Lead intoxication, leads to inhibition of NDMA-r

90
Q

Ketamine

A

A dissociative, makes people unaware of what’s going on but doesn’t put them to sleep. It works by inhibiting NDMA-r through taking out calcium portion of the pathway, thus affecting perception of pain. Does not affect AMPA-r.

91
Q

What drug is a terrible drug mentioned during NDMA-r? What is it classified as? But how is it supposed to help with pain?

A

Tramadol. It inhibits NDMA-r but not very well. It’s classified as a narcotic.

Decent SSRI, and inhibits NDMA-r. Still does not inhibit AMPA-r.

92
Q

What gas inhibits NDMA-r

A

Nitrous

93
Q

Who is tramadol best for?

A

Elderly patients, who are super sensitive to opiates.

94
Q

What drug should not be used for after surgery but it is?

A

Tramadol

95
Q

What can increase the amount of AMPA and NDMA-r?

A

Chronic pain, leading to increased sensitivity.

96
Q

Other glutamate receptors not much discussed and how does it work? The ionotropic one!

A

Kanate, it inhibits GABA activity in the brain.

97
Q

Three types of ionotropic glutamate receptors

A

Kanate, NDMA, AMPA

98
Q

Separate category of glutamate receptors we are not discussing

A

Metabotropic (GPCRs), involved in signal transduction pathways in nervous system. Just be aware thats the second class of glutamate receptors.

99
Q

Main class of glutamate receptors

A

Ionotropic

100
Q

Is the calcium channel in first order nociceptor also a p-type channel?

A

No, but it is voltage gated.

A&P 1 (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions