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Schmidt’s World Of Anatomy > Exam 3 Content > Flashcards

Exam 3 Content Flashcards

1
Q

DCML

A

Dorsal Column Medial Lemniscus

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2
Q

what type of fibers does the DCML use ?

A

FAST
All the A’s
A-delta
A-Gamma
A-Beta
A-alpha

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3
Q

Where is the DCML located and what are its sub-tracts?

A

Dorsal Horn
Fasciculus Gracilis
Fasciculus Cuneatus

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4
Q

Where does the Fasciculus Gracilis originate from ?

A

Lower body afferent sensory information

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5
Q

Where does the Fasciculus Cuneatus originate from ?

A

Upper body/extremity afferent sensory information

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6
Q

Where does the DCML pass through and in what direction ?

A

Afferent information through the medial lemniscus in the brain

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7
Q

Is the Medial Lemniscus second or third order neuron of the DCML?

A

SECOND

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8
Q

What is the Ventrobasal complex?

A

A portion of the Thalamus that DCML pathway signals pass through , to the internal capsule , then parietal lobe.

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9
Q

DCML pathway relays what kind of senses?

A

Touch
Pressure
And vibrations

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10
Q

What is a Homunculus ?

A

A anatomical pictograph of the different portions of the parietal lobe that processes information from different portions of the body
Proportions are equal to amount of sensors
low density = low sensors
High density = high sensors

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11
Q

Where is the Internal Capsule and which pathway uses it?

A

Internal Capsule is situated between the thalamus and parietal lobe
DCML uses it to relay signals to the parietal lobe

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12
Q

Major Relay center for pain/pressure information in the brain ?

A

THALAMUS

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13
Q

How many categories of spinal tracts are there?

A

5

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14
Q

What is the name of the grey matter in the spinal cord ?

A

REXED’s LAMINAE

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15
Q

How many subdivisions are there in REXED’s laminae

A

9 throughout the grey matter
1 central canal (laminae 10)
10 total

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16
Q

How are REXED’s laminae numbered ?

A

From the dorsal portion of the cord to the ventral portion
(Back to front)

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17
Q

Lamina 1 is also called

A

Lamina Marginalis

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18
Q

Lamina Marginalis sends what kind of signals ?

A

FAST/Sharp pain
via A-Delta fibers
Myelinated

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19
Q

Substantial Gelatinosa is comprised of what?

A

Combination of Laminae 2 and 3 of Rexed’s laminae
these sometimes synapse with lamina 5

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20
Q

Do laminae 2 & 3 synapse with other laminae?

A

Yes, sometimes, laminae 5

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21
Q

Where is substantia gelatinosa located ?

A

Dorsal horn of the cord, just anterior to Lamina Marginalis (lamina 1) in the grey matter

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22
Q

What kind of pain does Substantia Gelatinosa relay and how ?

A

SLOW PAIN
Via C- Fibers
Non-myelinated

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23
Q

Mechanoceptors synapse where in the cord ?

A

Anywhere through lamina 1-6 in the grey matter

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24
Q

What are Rexed’s Laminae 7- 9? And where are they ?

A

Lamina 7-9 are located in the anterior horn of the grey matter
These are where motor neurons live and can be activated by descending motor pathways

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25
Q

Can laminae 7-9 send action potentials?

A

Yes. If they are stimulated enough

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26
Q

What is laminae 10 (X)

A

Central canal of the cord where cross over can happen.

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27
Q

What are the DESCENDING Pathways?

A

DESCENDING are motor pathways
ExtraPyramidal Tracts
Corticospinal/Pyramidal Tract

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28
Q

What are the ASCENDING pathways called ?

A

ASCCENDING are afferent sensory pathways comprised of
Anterolateral/Spinothalamic tract
Spinocerebellar Tract
Dorsal-Column Medial Lemniscal System (DCML

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29
Q

How many different Anterolateral/Spinothalamic tracts are there ?

A

Two
Anterior and lateral spinothalamic tracts

1 of each on each side of the cord ! (2 types, 4 tracts)

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30
Q

How many types of Spinocerebellar Tracts are there ?

A

Two
Posterior and Anterior Spinocerebellar tracts

1 of each type on each side of the cord
2 types , 4 tracts

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31
Q

How many types of DCML are there ?

A

TWO
Fasciculus Gracilis (medial dorsal portion)
Fasciculus Cuneatus (lateral dorsal portion)

2 types, 4 total

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32
Q

Are Pyramidal tracts ASCENDING or DESCENDING ?

A

DESCENDING

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33
Q

Where is the internal Capsule ?

A

Just outside the thalamus

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34
Q

What signals get sent through the internal capsule? Ascending or descending ?

A

BOTH
sensory afferent information on its way to the parietal lobe goes through the internal capsule
AND
Descending motor signals are also sent through the internal capsule.

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35
Q

what structure do all signals have to pass through ?

A

The medulla

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36
Q

Where are the pyramids ?

A

the medulla

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37
Q

What is the primary pathway of the major motor tract?

A

Corticospinal Tract
Originates at the cortex ->
Internal Capsule ->
Pyramids of Medulla ->
(Crosses over at Pyramidal Decussation) ->
Descends down the Lateral Corticospinal tract.

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38
Q

Which tract takes care of the most of our motor function and how much ?

A

Primary Pyramidal tract
80%

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39
Q

What is the name of the secondary motor pathway ?

A

Anterior Corticospinal tract

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40
Q

What percentage of motor signals are the Anterior Corticospinal tracts responsible for ?

A

17 %

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41
Q

Does any motor information not cross over at all?

A

2-3%
Schmidt doesn’t know where

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42
Q

What are pyramids ?

A

Ridges of the medulla

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43
Q

Describe the pattern of the medullary decussation

A

Cross hatch

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44
Q

Are there pyramids in the Pons?

A

NO

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45
Q

Where is the primary motor pathway?

A

Lateral to the dorsal horns

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46
Q

Where is the secondary pathway ?

A

Anterior close to the AWC

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47
Q

Where does the secondary pathway cross over ?

A

At the level of the cord where it needs to interact with a motor neuron

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48
Q

Can incoming sensory information choose its own path in the spinal cord?

A

YES.
Enters through dorsal rootlets and chooses based on which tract is a function of the tissue

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49
Q

Are pain pathways ascending or descending ?

A

Ascending

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50
Q

What are the pain pathways called?

A

SPINOTHALAMIC / ANTEROLATERAL tract

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51
Q

What are the 2 main divisions of Spinothalamic tracts?

A

FAST pain
SLOW pain

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52
Q

How is FAST pain transmitted through Spinothalamic/Anterolateral Tracts?

A

A-Delta myelinated fibers

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53
Q

What are the pain sensors of the FAST Pain Spinothalamic/Anterolateral tracts?

A

Nociceptors - free nerve endings
Via A-Delta myelinated fibers

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54
Q

What neurotransmitters do the FAST pain division of the Spinothalamic tract use ?

A

Glutamate, always.
It’s always fast in the spinothalamic/anterolateral tract

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55
Q

What connects the pain sensors to the next order neuron?

A

Neurotransmitters !
Glutamate, always in Fast tract
Glutamate, Substance P, and Calcitonin Gene Related Peptide (CGRP)

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56
Q

What is the fast pain pathway?

A

Ascends the cord via ANTEROLATERAL tract->
through the VENTROBASAL complex just outside the THALAMUS ->
And Projected to different parts of the PARIETAL lobe

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57
Q

What kind of pain is best localized ?

A

FAST / sharp pain signals
Via the parallel system in the DCML

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58
Q

FAST Pain route:

A

Lamina 1
Cross over at AWC in the cord Anterolateral/Spinothalamic tract
(Lateral portion)
Ventrobasal complex w/ DCML sensory information

Called NEOSPINOTHALAMIC tract

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59
Q

What’s the other name for Slow pain tract ?

A

Paleospinothalamic
Ex: Dinosaurs

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60
Q

What is the main neurotransmitter the slow pain tract uses ?

A

Substance P mainly used in slow pain pathways

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61
Q

Where is slow pain projected to ?

A

Top of the brain stem & not much further

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62
Q

Why is slow pain poorly localized ?

A

No parallel system with DCML

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63
Q

Where does slow pain synapse in the cord ?

A

Laminae 2 & 3
(Sometimes 5 )

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64
Q

What tract does slow pain take?

A

Anterior portion of ANTEROLATERL tract

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65
Q

What part of the brain allows us to localize pain ?

A

Somatosensory areas

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66
Q

What engages our emotions?

A

SLOW pain

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67
Q

Why does slow pain mess with our head?

A

Closer to the middle of the brain where the brain stem connects to diencephalon

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68
Q

What is the Reticular Formation ?

A

Swath of tissue on top of the brain stem where most slow pain signals terminate

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69
Q

What are the ExtraPyramidal Tracts?

A

Vestibulospinal - balance & eye fixation
Olivospinal - just know it exist
Reticulospinal - muscle tone
Rubrospinal - voluntary movement

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70
Q

Are ExtraPyramidal tracts ascending or descending?

A

DESCENDING motor tracts
Vestibulospinal
Olivospinal
Reticulospinal
Rubrospinal

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71
Q

How many overall pain signaling systems do we have and are they afferent or efferent?

A

TWO
DCML - ASCENDING - major pressure/touch/vibration
DIC (DESCENDING inhibitory Complex) - descending pain suppression system

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72
Q

What does the first neuron in the DIC release?

A

First order RELEASES Enkephalins in the middle of the pons.

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73
Q

Where do DIC pain suppression signal originate?

A

Periventricular Nucleus or
Periaqueductal Gray

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74
Q

Where is the periaqueductal Gray ?

A

Near cerebral aqueduct and third ventricle

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75
Q

Where is the periventricular nuclei located?

A

“Right in front of the third ventricle

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76
Q

How many neuron orders are there to transmit pain signals?

A

THREE orders

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77
Q

What kind of neuron is the second order neuron ?

A

SEROTONERGIC - 5-HT
Released in the spinal cord near dorsal horn

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78
Q

Where is the Serotonergic neuron ?

A

Excited by 1st order neuron in the pons stretches down to dorsal horn and releases serotonin there.

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79
Q

What are the responses to released enkephalin in the brain?

A

Excitation of second order descending neuron

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80
Q

What is the response of serotonin being released in the spinal cord?

A

Acts on third neuron in DIC.
This neuron is an enkephalin secreting neuron

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81
Q

What does the third order neuron secrete ?

A

ENKEPHALIN

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82
Q

What is ENKEPHALINS function in the spinal cord?

A

An inhibitory neurotransmitter

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83
Q

Where are enkephalin receptors?

A

On nociceptors that reach into the periphery.
And the second neuron in the ascending pain pathway

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84
Q

What is ENKEPHALIN ?

A

Endogenous morphine analog

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85
Q

All of our opiate receptors are what ?

A

ENKEPHALINS

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86
Q

Where is the first synapse in the descending pain pathway ?

A

RMN
Raphe Magnus Nucleus

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87
Q

What is 5-HT ?

A

Serotonin

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88
Q

Where is the RMN ?

A

Raphe Magnus Nucleus - middle of the pons
-first order synapse of descending pain pathway

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89
Q

Enkephalin released in the dorsal horn has what response ?

A

Released enkephalin at the synapse in the dorsal horn can shut down the pre - and post - synaptic side of synapse . Lowers activity of both neurons (Ascending and descending portions)

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90
Q

What types of pain does the DIC complex target?

A

SLOW and FAST pain

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91
Q

Descending Pain Suppression System route ?

A

1st order - originates at periaqueductal or periventricular
{Releases Enkephalin}

Excites 2nd order in Pons
2nd order descends to cord and {releases serotonin }

Serotonin excites 3rd order neuron that reaches into grey matter of dorsal horn
{releases Enkehphalin

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92
Q

Ascending Pain route ?

A

1st order - Nociceptors from free nerve endings in periphery

Synapse with 2nd order in dorsal horn (lamina 1,2,or 3)

crosses over cord at AWC and ascends anterolateral columns

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93
Q

How do some people have higher pain tolerances ?

A

Meditation , inner - wellness, long and hard training that probably modulates the DIC

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94
Q

What is pain?

A

“A survival thing
Tells us when were doing something stupid “
-Schmidt

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95
Q

What does chronic pain increase ?

A

With chronic pain we have more neurotransmitter receptors within the pain transmission system, this causes glutamate receptors to get up-regulated and the system becomes more difficult to inhibit with enkephalin analog.

  • Reductions in enkephalin receptors and increases in glutamate receptors in the pain system
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96
Q

What will nociceptors deem as pain ?

A

Damage /cuts = depolarization = PAINful
Acidosis - builds up with workouts
Potassium - dialysis pts
Histamine - swelling
5-HT - in periphery
ACh - in periphery
Bradykinins

Prostaglandins - increase sensitivity to pain !

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97
Q

what does increasing bioavailability of serotonin do ?

A

Should increase the inhibition of pain by inhibiting the re-uptake of serotonin

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98
Q

What order will SSRI’s effect?

A

Augmented effect on THIRD order inhibitory neuron

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99
Q

Examples of SSRI’s given by Schmidt ?

A

Paxil
Prozac

TCA’s - older drugs with other effects
But used for chronic pain

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100
Q

One side effect of TCA’s that can help chronic pain ?

A

Cause drowsiness
- chronic pain people have trouble sleeping, so TCA’s allow them to actually sleep due to its sides effects

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101
Q

Extra Serotonin does what?

A

Encourages increased release of Enkephalins to help suppress pain

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102
Q

What is the divergence of DCML pressure sensors?

A

DCML run parallel to pain signals, follow same route into dorsal horn, but then Ascends in dorsal columns .

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103
Q

What is the decision making apparatus of the cord?

A

grey matter

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104
Q

Lateral Inhibition works when two what run parallel?

A

A nociceptor (pain signal )
A pressure sensor (DCML)

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105
Q

Where does lateral inhibition occur?

A

Most likely in the dorsal end of the cord

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106
Q

What is acupuncture based on ?

A

LATERAL INHIBITION
- needles placed in various pressure points can deaden the pain signals running in that area

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107
Q

What is Glutamates natural state?

A

Excitatory
- main neurotransmitter for pain transmission

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108
Q

What causes Glutamate to release from 1st order neuron ?

A

Ca++ coming into 1st order neuron
-usually in reaction to some previous action potential

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109
Q

What is the Primary glutamate receptor in the pain system ?

A

AMPA-R’s

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110
Q

What ion are AMPA-R’s permeable to ?

A

Na+

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111
Q

Other Glutamate receptors ?

A

NMDA receptor

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112
Q

What is the primary current allowed in NDMA-R’s

A

Ca++ (Primary )

Some Na+

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113
Q

What do NMDA-R’s require to open ?

A
  1. Initial Depolarization to removal blockade of Mg+
  2. Glutamate binding

Allows Ca++ to come in after magnesium removal
Also adds to why NDMA-R is slower than AMPA

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114
Q

Which glutamate receptor is fastest?

A

AMPA-R

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115
Q

What sends pain information faster, AMPA-R or NDMA-R?

A

AMPA-R reacts and opens faster, this depolarization can allow NDMA-R to open and will DOUBLE the rate at which we sent the signal

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116
Q

Where do NDMA-R come from ?

A

Important part of development from birth

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117
Q

What blocks NDMA-R’s?

A

Alcohol
Lead
Ketamine - dissociative
Nitrous
tramadol

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118
Q

Does Ketamine work on NDMA and AMPA receptors?

A

No ONLY NDMA

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119
Q

Can pain signals still be sent with ketamine ?

A

YES
But perception of pain is different
Dissociated from normal

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120
Q

How does tramadol work ?

A

“Terrible drug”
Decent SSRI , and NDMA antagonist

Does nothing for narcotic or enkephalin receptors

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121
Q

What increases NDMA and AMPA receptors?

A

CHRONIC PAIN will populate more of these receptors at the synapse

Will increase action potentials or sensitivity to pain

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122
Q

Other type of glutamate receptor?

A

Kanate

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123
Q

What are the three ionotropic glutamate receptors?

A

AMPA
NDMA
Kainate

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124
Q

what are Metabotropic receptors?

A

G-protein coupled receptors involved in signal transduction of nervous system

Second broad category or glutamate receptors

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125
Q

Can NDMA-R’s be decreased in population ?

A

Over long period of time

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126
Q

what kind of ion channel do we have in first order pain neuron?

A

Voltage Gated Ca++ channel
- no class given

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127
Q

Will DIC take away all the pain ?

A

Not all the pain all the time, but gives us a good target with anesthetic drugs

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128
Q

What kind of receptors are enkephalin receptors ?

A

G-protein coupled opiate receptors (7-transmembrane)

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129
Q

What are opiate receptors usually linked too ?

A

potassium channels

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130
Q

Where are opiate receptors?

A

on both pre and post synaptic cell

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131
Q

what other receptors are also found on pain synapses ?

A

ALPHA 2 receptors

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132
Q

Alpha 2 receptor activation at the pain synapse causes what ?

A

open K+ channels
can shut down 1st and 2nd order nociceptors

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133
Q

Example of alpha 2 agonist drugs that stimulate pain synapse

A

Xylazine - not most specific
Clonidine - mid specificity
Precedex - most alpha 2 specific

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134
Q

Xylazine , Clonidine, and precedex will have what effect when stimulated ?

A

general pain suppression, slows down CNS system, less euphoric, less addiction concerns

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135
Q

Which alpha 2 agonist is usually abused ?

A

xylazine - horse tranquilizer

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136
Q

General effects produced by volatile anesthetics?

A

suppress CNS activity
can loose consciousness and decrease ability to feel

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137
Q

How do volatile anesthetics work

A

cause general increase in Potassium conductance at the synapse

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138
Q

MOA of volatile anesthetics?

A

open K+ channels and increase potassium conductance

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139
Q

Potassium is always doing what?

A

LEAVING the cell!!

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140
Q

How does COX-2 affect pain ?

A

produces prostaglandins that interact with 1st&2nd order neurons, increases SENSITIVITY to pain !

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141
Q

COX-2 can be expressed where in the pain pathways ?

A

1st and 2nd order ascending pain neurons

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142
Q

How do PGs work in pain ?

A

increase likelyhood of an action potential by increasing the expression of receptors on 2nd order neuron

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143
Q

How does Nitric Oxide work in pain pathways ?

A

increases sensitivity to painful stimuli.

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144
Q

Mg+ does what in the synapse of pain

A

blocks NDMA receptor activity.
OTC Magneisum is safe but causes GI upset

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145
Q

Do extracellular Ca levels affect pain ?

A

NO

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146
Q

does Ca suppress pain ?

A

No, ,decreases neural activity but doesn’t help with chronic pain

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147
Q

COX-2 is induced by what ?

A

can be induced by pain

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148
Q

iNOS

A

Inducible Nitric Oxide Synthase

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149
Q

What are the four reflex pathways ?

A

Stretch
Tendon
Withdrawal
Crossed Extensor

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150
Q

Which reflex pathways are stretch or tension ?

A

Stretch and tendon reflexes

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151
Q

which reflex pathways are pain ?

A

Withdrawal and Crossed Extensor

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152
Q

Basic wiring for all reflexes ?

A

Sensory Neuron
Alpha motor
Interneuron

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153
Q

What sensory things can cause a reflex ?

A

pain, tension , stretch
afferent portion

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154
Q

Where are reflex sensors located in the body?

A

sensor in periphery and springs embedded in the muscles that sense tension or pain

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155
Q

How do sensory and motor components of muscles talk to each other?

A

direct connections or interneurons (1 or many)

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156
Q

where do motor neurons hang out ?

A

ventral/anterior horn ( front.)
efferent portion

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157
Q

what are interneurons ?

A

intermediary neurons - bridge between sensor and motor neuron
and between two sides of the cord
can be excitatory or inhibitory

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158
Q

Is there a direct path from the dorsal horn to opposite side of cord ?

A

NO . need interneuron

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159
Q

Which reflex is weight bearing, helps us maintain posture, and does not need interneurons ?

A

STRETCH reflex

does not need interneurons has direct synapse on motor neurons but can use them sometimes.

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160
Q

What is the stretch reflex useful for ?

A

standing up
keep posture constant
keep muscles at a constant length

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161
Q

What receptors does the stretch reflex use ?

A

muscle spindles - springs

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162
Q

How would you clinically test to confirm intact stretch reflexes?

A

stretch reflex with tendon hammer

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163
Q

What happens with a stretch reflex test ?

A

patient position with leg dangling
hammer is tapped at patellar

the stretching induced by hammer tap stimulates stretch sensory receptor (Muscle spindle)
then exciting the sensory neuron

Sensory neuron activates motor neuron in the spinal cord.

excited motor neuron then activates effector muscle - which contracts and relieves the initial stretching.

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164
Q

Which Reflex prevents muscle from being pulled out of the bone?

A

TENDON

embedded in the collagen of our tendons

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165
Q

which reflex is the simplest ?

A

STRETCH
weight baring reflex

166
Q

Imbalance from the head would cause a stretch in which muscles?

A

Quads

167
Q

Stretch causes what ?

A

reflex activation of muscles being stretched

stretched muscle will contract then release

168
Q

What do inhibitory interneurons of the stretch reflex allow ?

A

reflex relaxation of the antagonistic muscle

relaxing would help straighten out the muscle

169
Q

Where are the sensors for the Tendon reflex?

A

Golgi Tendon sensors embedded in tendons of skeletal muscles

170
Q

Can Tendon reflexes be turned off ?

A

Yes, can be deactivated to lift a car off a kid, but not known how.

171
Q

How many interneurons do tendon reflexes connect with?

A

TWO
one excitatory
one inhibitory

172
Q

what is the job of the inhibitory interneuron in the tendon reflex pathway ?

A

inhibitory is in charge of inhibiting activity in the motor neuron attached to effector muscle group = RELAXES

173
Q

what is the job of the excitatory interneuron in the tendon reflex pathway ?

A

excitatory causes reflex activation of the antagonistic muscles = CONTRACTION

174
Q

How does reflex activation of the tendon reflex serve ?

A

to pull muscle away from the intense tension its sensing.

175
Q

tendon reflex involves which side of the body ?

A

usually unilateral ( one side )

176
Q

Stretch reflex involves which sides of the body ?

A

unilateral

177
Q

Flexor Reflex is known as ?

A

WITHDRAWAL Reflex

178
Q

Withdrawal / Flexor Reflex is stimulated by what ?

A

pain

179
Q

Withdrawal / Flexor Reflex involves which muscles ?

A

FLEXORS - to pull away from pain

180
Q

Which side of the body does flexor reflex involve ?

A

unilateral on its own

no interneurons crossing over

181
Q

Can Flexor reflex engage antagonistic muscles ?

A

yes, will cause relaxation to help speed up withdrawal from painful stimuli

182
Q

What happens with flexor/withdrawal refelx when we encounter pain ?

A

activation of flexor muscle = flex of muscle to pull away

183
Q

Does flexor/withdrawal reflex only involve one level of the spinal cord ?

A

NO. usually unilateral
but engages a couple spinal vertebrae levels up and a couple down (2 up/2 down)

184
Q

How does flexor/withdrawal reflexes recruit other levels of the spinal cord ?

A

interneurons that ascend and descend the cord

CELL BODY IN WHITE MATTER

185
Q

Where does the ascending and descending interneuron live ?

A

tract of Lissaur

186
Q

Where is the tract of Lissaur

A

dorsal border of the dorsal horn
CELL BODY IN WHITE MATTER

187
Q

What is the flexor/withdrawal reflex useful for ?

A

pain and pressure to detect potentially life-threatening stimuli , usually when body is not in motion

188
Q

Most complicated reflex ? and why ?

A

Crossed Reflex/ Crossed Extensor Reflex

involves both sides of the cord
more useful with bodies in motion

189
Q

why does the crossed extensor reflex involve both sides of the cord ?

A

helps us maintain out balance/ support our bodies as we pull away from source of pain

190
Q

How many levels of the cord does the crossed Extensor involve?

A

multiple levels and both sides of the cord

191
Q

What happens in effector muscle group with crossed Extensor Reflex?

A

contraction of flexors in effector muscle and antagonistic relaxation of extensor muscles in effector leg

192
Q

What happens in the muscle groups of non stimulated muscles with crossed extensor reflex?

A

activation of extensor in non-effected leg , and relaxation of flexor group of this leg

193
Q

Which reflex uses most interneurons?

A

Crossed Extensor Reflex

194
Q

ALL reflexes are

A

Protective in nature

195
Q

What receptors are at the NMJ ?

A

MATURE nACh-R

196
Q

Where should we find mature nACh-Recptors?

A

AT THE NMJ should not be anywhere else

197
Q

How many subunits make up the nACh-R ?

A

5 subunits
2 Alpha binding sites
1 Epsilon - in between alphas
1 Delta
1 Gamma

198
Q

Mature nACh- R have what kind of flow ?

A

HIGH conductance channels
high current , high permeability , high speed of ions moving through

199
Q

What are Immature nACh-R?

A

Fetal nACH-R
populated by our CNS when our body detects something wrong or no feedback form muscles
usually in strokes

200
Q

Describe the domain of a immature nACh-R

A

2 alpha sites, 2 GAMMA , 1 delta

201
Q

Placement of fetal nACH-R ?

A

Can be expressed on other parts of the muscle - outside the NMJ

202
Q

Fetal nACH-R conductance ?

A

SLOW , less current , LOW conductance - but open longer

203
Q

Concern with low conductance fetal nACH-R?

A

extended response to NTs = longer reaction - especially to succ’s

204
Q

what is the third type of nACh-R?

A

alpha 7 -in CNS
7 alpha binding sites

205
Q

What sends information back to the brain to confirm or deny muscle contraction ?

A

muscle spindles

206
Q

What kind of nACH-R does the CNS populate ?

A

only fetal nACh-Rs. not mature ones. they mature throughout our development

207
Q

What else do fetal nACh-R ‘s allow for ions ?

A

a place for K+ to hemorrhage through
Can cause VFib

208
Q

Post junctional area

A

furthest from NMJ
nACh-r should NOT be here

should not be effected by activity in NMJ

209
Q

Peri-Junctional Areas

A

In between post and junctional area

may be effected by junctional area activity

210
Q

Junctional area

A

where motor neuron talks to skeletal muscle
where nACh-r should be , where ACh binds to receptors to send action potentials etc

211
Q

Supramaximal Stimuli

A

a stimulus trong enough to recruit all muscles in contraction

212
Q

what clinical testing do we use to test nervous systems talking to motor neurons?

A

Neuromuscular Monitoring

213
Q

Neuromuscular responses mean what ?

A

large contraction - minimal block if any
small contraction - block is transitioning out or deeper
no contraction - very deep block

214
Q

Train of Four

A

repetative stimulation at 2hz over 2 secs each (4 twitches

215
Q

How do electrode work with neuromuscular stimulants ?

A

takes away the natural polarity difference from the inside and outside

removing this with electrode stimulants is DEPOLARIZING

216
Q

Train of four ratio ?

A

B/A
b= fourth twitch (if any )
a= first twitch
as drug approaches 1 drug is wearing off

217
Q

non-depolarizing twitch assessment

A

staggered - as drug wears off TOF increases

218
Q

depolarizing twitch assessment

A

even - first and last contraction are similar

219
Q

incomplete block with depolarizing twitch assessment

A

height will all be the same

220
Q

tetanic

A

muscle contraction that occurs when a muscle is stimulated at high speed and frequency

221
Q

post -tetanic count

A

counting the number of impulses a muscle generates after a tetanic contraction

222
Q

Double burst stimulation

A

multiple tetanic contractions in a series
two short burst of three pulses each at 50 hz (high frequency)

223
Q

where do we apply electrodes for neuromuscular monitoring ?

A

Adductor Pollicis - thumb & pinky
opthalamic branch - eye brow
perineal nerve - butt
posterior tibial nerve - lower leg extension

224
Q

Non-depolarizing onset and offset ?

A

few minutes onset , offset hours

225
Q

depolarizing onset and offset?

A

fast onset - offset three minutes

SUCC’s is cheap and fast

226
Q

why is succs popular ?

A

fast onset, fast offset, cheap, and can be given IM

227
Q

how many twitches do you need to determine a TOF ratio?

A

FOUR

228
Q

non-depolarizing blocks effect what part of the synapse?

A

inhibit both sides of synapse

229
Q

depolarizing agents effect what part of the synapse ?

A

more effect on skeletal muscles (but also both with different effects)

230
Q

What are autoreceptors ?

A

Alpha-3 , Beta-2 - second type of ACh recepotors on motor neuron

231
Q

where are autoreceptors found ?

A

motor neuron

232
Q

What do autoreceptors do ?

A

bind to dumped ACh from same neuron, allows Na+ influx (some Ca+) , causes long term NT stores (VP-1) to merge into VP-2 form

233
Q

What breaks down Succinylcholine ?

A

Plasma cholinesterase - function out of the liver

234
Q

are L-type Calcium Channels required for normal motor function ?

A

NO.
P-Type is required

235
Q

will CCB paralyze a patient through P-type or L-type Ca+ Channels ?

A

P- Type channels.

L-type are not required for normal motor function

236
Q

P-Type Ca+ Channels have what effect on CNS ?

A

depression of CNS

237
Q

Phrenic nerve originates where ?

A

C-3, 4, and 5

238
Q

Phrenic nerve connects what ?

A

DIAPHRAGM to C-3,4,&5

239
Q

know what forever ?

A

PHRENIC NERVE CONNECTIONS
C-3,4,& 5 to diaphragm

240
Q

Adductor Pollicis inhibition starts at what dosages?

A

20mcg/ kg
40mcg/kg is total inhibition

241
Q

Total inhibition of Adductor Pollicis is seen at what dosages?

A

40mcg/kg

242
Q

What order do muscles recover after paralysis ?

A

in order of importance
DIaphragm will recover first.

243
Q

Diaphragm inhibition starts at what dosages?

A

40 mcg/kg
total inhibition 90-100

244
Q

Total inhibition of Diaphragm is seen at what dosages?

A

90-100 mcg/kg

245
Q

What controls the diaphragm ?

A

PHRENIC NERVE
(C-3,4,&5)

246
Q

What kind of muscle is the diaphragm ?

A

SKELETAL muscle

247
Q

which muscles are harder to block ?

A

more important muscles, they have lots of receptors , requires more medication at these muscles to block

248
Q

How high can a neck injury occur and maintain oxygenation ?

A

C-5 - you can breathe

C-4 - depends

C-3 - you will suffocate

249
Q

How many twitches will you see with 70-80% blockade?

A

3

fourth twitch should disappear at this percentage of blockade

250
Q

How many twitches will you see with 85% blockade?

A

2

third twitch disappears at this blockade

251
Q

How many twitches will you see with 85-90% blockade?

A

1

second twitch disappears with this blockade

252
Q

How many twitches will you see with 90-95% blockade?

A

0

all twitches should disappear at this blockade

253
Q

Neuromuscular monitor settings?

A

50-80 mA

254
Q

Is a NM blockade a supramaximal stimuli ?

A

YES

255
Q

how many skeletal muscle cells does a motor neuron control ?

A

ONE

exception - ocular muscles

256
Q

How can succinylcholine increase IOP?

A

causes leakage of Ca+ at NMJ which can cause the eye socket to contract just enough to increase IOP

chances increased with head down

257
Q

What would a reduction in GABA neurotransmitters cause ?

A

uncontrolled overactivity of the CNS (seizures )

258
Q

What do GABA neurotransmitters cause ?

A

increased chloride permeability

259
Q

Where does K+ leave from with succs ?

A
  1. primarily through leak channels
  2. VG K+ channels
  3. loss through ACh-R’s
260
Q

Which Neurotransmitters are inhibitory ?

A

GABA and GLYCINE

261
Q

what is the MOA of Glycine ?

A

unknown
but inhibitory in nature and very important in the spinal cord

262
Q

Which Neurotransmitters are most inhibitory in the spinal cord ?

A

GABA and GLYCINE

263
Q

ACh, MOA and effects ?

A

allows nervous system to talk skeletal muscles

increases alertness/awareness

264
Q

how do anticholinergics cause drowsiness ?

A

they block ACh which usually increases alertness/awareness

265
Q

What does GABA do in the brain ?

A

limits neuronal activity

266
Q

Treatment for Alzheimers ?

A

Centrally acting ACh-ase inhibitors (-stigmine)

-can cross BBB and enhance ACh activity at m-ACh-R

267
Q

where does ACh awareness come from ?

A

MUSCARINC ACh-R

268
Q

what OTC drug is good at blocking mACh-R’s?

A

BENADRYL

cross reactivity with histamine

large dose can increase HR

269
Q

inhibition of ACh-ase causes what?

A

increases awareness / activity

270
Q

Side effects of ACh-ases ?

A

waking patient up too early
decrease HR - through reduce mACh-R at heart
increased gland secretions/ mucus

271
Q

Histamine has what effect ?

A

increases awareness

reduce histamine will make you drowsy

272
Q

Glutamate facts

A

stimulatory in nature
increases neuronal activity - can burn out CNS

273
Q

Dopamine is associated with what ?

A

pleasure and reward
and motor inhibitor

more we reward- more released

274
Q

what neurotransmitter are Parkinsons patients missing ?

A

DOPAMINE

shakey from lack of dopamine which naturally inhibits motor

275
Q

Norepinephrine has what effects ?

A

increases awareness

276
Q

which NT’s increase awareness ?

A

ACh
Histamine
Glutamate
Norepinephrine

277
Q

GABA , GLYCINE, and DOPAMINE all have what similar effect ?

A

prevent CNS overactivity

278
Q

ACIDOSIS causes what centrally ?

A

CNS activity is reduced

279
Q

ALKOLOSIS causes what centrally ?

A

CNS activity is increased

280
Q

what are acid- base imbalances related to ?

A

Ca levels

281
Q

Causes of acid - base imbalances ?

A

Direct increase or decrease in protons
and CO2 levels

282
Q

how does the body manage acid-base imbalances ?

A

chemical reactions

283
Q

ACIDOSIS reduces CNS activity how ?

A

causes more protons to bind to Albumin - which means less Ca+ is bound to albumin and increased in the ECF = reduced CNS activity

284
Q

ALKALOSIS increases CNS activity how ?

A

causes less protons to be bound to albumin, so Ca would bind to it- decreasing the free Ca+ and increasing CNS activity

285
Q

With hypoventilation what would increase?

A

increase in protons - which would bind to albumin- leaving increased free Ca - reducing/inhibiting CNS activity

286
Q

Which circulations are good at autoregulation ?

A

Cerebral and spinal (within reasonable blood pressure range)

287
Q

How many spinal arteries do we have ?

A

3
1 in the front in the anterior median fissure
and 2 posterior on each lateral side

288
Q

Whats the different in the blood supply of the three different spinal arteries ?

A

anterior artery - 75%
posterior arteries collectively = 25%

289
Q

whats the source for the spinal arteries ?

A

posterior - combination of vertebral arteries (neck) , and cerebellar artery (anterior inferior and posterior inferior Cerebellar arteries.)

Lower in the cord source of blood is from intercostal arteries that branch into the radicular arteries then feed into main spinal area

290
Q

What are radicular arteries ?

A

Branches of intercostal arteries

can feed into front or bakc of cord

291
Q

Intercostal arteries are combined of what ?

A

form to make radicular artery and feeds into the front OR back of spinal artery.

NOT front and back on the same level of the cord

292
Q

Are feed vessel patterns the same for everyone ?

A

feed vessel is irregular

293
Q

explain feed vessel pattern for the spinal arteries

A

every 5/6 levels artery will come in from either side of the body and feed anterior OR posterior spinal cord

294
Q

What else are radicular arteries called ?

A

segmental
medullary
or both
segmental medullary arteries

295
Q

where are coronal arteries found ?

A

outer surfaces of the cord

coronal means crown - they do not wrap all the way around the spinal cord

296
Q

whats one big difference between Cerebral circulation and spinal circulation ?

A

spinal cord doesn’t have circle of willis which means circulation cannot continue with collateral circulation.

297
Q

what vessel do we have at every level of spinal cord ?

A

Spinal branch

298
Q

Does the Aorta connect to the spinal cord on every level ?

A

NO

299
Q

What is the posterior radicular artery ?

A

a feed vessel that branches from the posterior spinal artery into the dorsal portion of the cord

300
Q

What are some arteries attached to the aorta ?

A

Intercostal arteries, thoracic arteries, renal arteries, mesenteric arteries

300
Q

what is the anterior radicular artery ?

A

feed vessel that branches from anterior spinal artery

301
Q

Is cross clamping above the GRA okay for aneurysm repair?

A

NO, above the GRA increases risk and concern for paralysis of lower extremities

302
Q

Where is it okay to cross clamp on the GRA ?

A

Below, this may cause sensory loss, but lower risk of paralysis

303
Q

What can cross clamping cause and how ?

A

cross clamping of the aorta or GRA can cause neuron death due to decreased perfusion and can lead to paralysis

304
Q

What can help in decreasing risk of paralysis due to decreased perfusion from cross clamping ?

A

imaging to locate where GRA and aorta are

anything that reduces inflammation in the cord
and drugs can be given to slow metabolic rate

305
Q

Clamping below the GRA also increases possibility of what ?

A

less ischemia to lower extremities
and normal blood pressure

306
Q

What determines how dangerous aneurysm repairs are ?

A

the branch point

307
Q

normal CSF pressure ?

A

10 mmhg

308
Q

How much can cross clamping increase CSF ?

A

10 mmHg

309
Q

normal ICP

A

10mmHg

310
Q

perfusion pressure for cerebrum equation ?

A

MAP - ICP

311
Q

How can un-clamping artery be bad ?

A

rapid re-perfusion can cause damage from rapid influx of oxygen to vessels that have been deprived for a period of time.

312
Q

What worse, loosing perfusion in a posterior or anterior spinal artery ?

A

Anterior spinal artery - we only have one

313
Q

how many feed vessels go into the neck from the anterior spinal artery?

A

two feed arteries.

314
Q

How many feed vessels are in the throax from the anterior spinal artery?

A

2-3

315
Q

how many feed vessels are in the lumbar portion from the anterior spinal artery ?

A

1-2

316
Q

What feed vessel takes care of 2/3rd arterial blood supply to lower extremities

A

GRA Great Radicular Artery

317
Q

Whats another name for the GRA ?

A

Adamkiewicz

318
Q

who is Adamkiewicz?

A

the GRA

319
Q

Where does the GRA come from in most patients ?

A

LEFT - closest to the aorta

320
Q

What spinal level is most associated with the GRA (Adamkiwicz) ?

A

T10 - “pick this”

T9-T12 = 75% - vast majority

absolute ranges T5-L5

321
Q

Adamkiwica branches off of what ?

A

the aorta !!!!

322
Q

Low MAP makes it hard to perfuse what ?

A

EVERYTHING

323
Q

What can help lower CSF pressure?

A

drain

324
Q

What are the Spinocerebellar tracts ?

A

ascending feedback tracts

Anterior and Dorsal spinocerebellar

325
Q

which ascending spinal tract delivers information about activity in the anterior horn ?

A

Anterior spinocerebellar

sends information back to anterior lobe of cerebellum through the Superior Cerebellar Peduncle

326
Q

which ascending spinal tract delivers information about tendons and muscle spindles ?

A

Dorsal Spinocerebellar

sends information back to posterior cerebellum through Inferior Cerebellar Peduncle

327
Q

What are the spinocerebellar tracts help with ?

A

sensors in periphery collect and send this information to help the cerebllum coordination of complicated movements

328
Q

How much of our total body mass is skeletal muscle?

A

40%

329
Q

What is skeletal muscle used for ?

A

communicate, regulate body temperature, defending ourselves, energy storage

330
Q

where is glycogen stored?

A

skelettal muscles and liver

331
Q

Ligaments connect what?

A

bone to bone

patellar/ACL/MCL

332
Q

Tendons connect what ?

A

MOSTLY muscle to bone

333
Q

What is a intermediary tendon ?

A

muscle to muscle connection
“tendon bridge”

334
Q

Muscle Fibers are what ?

A

individual muscle cells

335
Q

Fasciculous

A

grouping of multiple skeletal muscle cells seperated by connective tissue - functions as a unit

336
Q

Muscle definition

A

group of many Fasciculi

337
Q

Sarcomere definition

A

basic functional unit of skeletal muscle

338
Q

Myofibrils

A

internal cylinders within muscle cells with contractile proteins (actin and myosin)

339
Q

how many myofibrils are there per skeletal muscle cell ?

A

200 myofibrils per muscle cell

large muscle cells have more

340
Q

the stronger the muscle the more myofibrils ?

A

YES /TRUE

341
Q

are weaker muscle cells okay ?

A

yes having SOME weak muscle cells give up precise control

342
Q

myofibril contractile unit is called what?

A

Sarcomere

343
Q

Thick filament

A

MYOSIN

344
Q

thin FIlament

A

ACTIN

345
Q

what happens at the overlap of actin and myosin?

A

ability to produce force

346
Q

What is a motor unit ?

A

collection of one or more skeletal muscle cells/fibers controlled by a single motor neuron

347
Q

fewer skeletal muscle cells

A

make up small motor neurons
these are delicate and dont contract super fast

348
Q

small motor neurons are used for ?

A

fine motor tasks and control
easy to exicte but do not contract fast

349
Q

Are Large Motor Neurons easy to excite ?

A

NO , they require larger stimuli

350
Q

whats the order of activation for motor neurons ?

A

small motor neurons activate first then larger motor neurons become activated

351
Q

Can we selectively recruit large motor neurons?

A

no, not with out recruiting smaller ones as well

352
Q

Type 1 Classification of muscles

A

red in color - dark meat
slow contractions that can be sustained
lots of mitochondria - run through ATP
lots of myoglobin iron containing protein to help O2 unload from blood into the muscles

353
Q

Type 2 Classification of Skeletal Muscle

A

white muscle - fast twitch
produce strong force but unsustained
less mitochondria, less myoglobin

354
Q

What is organ pain

A

Visceral and Parietal

355
Q

What is Visceral Pain ?

A

Internal organ pain poorly localized and transmitted via CNS

356
Q

What os Parietal pain ?

A

tissue pain localized fairly close to where the pain is

357
Q

What kind of pain is Parietal Pain?

A

FAST pain via A delta fibers

358
Q

What kind of pain fibers would Visceral pain use ?

A

slow C-fibers

359
Q

What is pain threshold?

A

ease or difficulty of eliciting a painful feeling
high degree of variabilty

360
Q

What organs do not have pain sensors?

A

Soft tissue in the lungs
and the liver itself

361
Q

Where does kidney pain get referred to ?

A

lower back

362
Q

what is decompression pain ?

A

pressure place on pain of lower right quadrant - usually helps pain until pressure is removed

363
Q

Can visceral pain be relieved with pressure?

A

no - due to lack of lateral inhibition

364
Q

Where does heart pain radiate and why ?

A

Left shoulder or arm

R heart is less prone to ischemia - lower pressures on right side

365
Q

Soleus Muscle

A

calf muscle - weight bearing , sustained force

366
Q

Ocular muscle contractions

A

fast and short contractions - less myoglobin, and mitochondria

367
Q

Gastrocnemius is where

A

next to soleus muscles
- sustains contraction longer than ocular but not as long as soleus , due to weight

368
Q

Sarcolemna

A

cell wall of skeletal muscle

369
Q

Sarcoplasm

A

fluid inside skeletal muscleS

370
Q

SR

A

Sarcoplasmic reticulum specialized endoplasmic reticulum for muscles

371
Q

Myosin Filament tail contain what ?

A

two long strings of myosin molecules wrapped together at the tail

372
Q

Myosin head contains what ?

A

1 set of Essential Lite Chains (2)
1 set of Regulatory Lite Chains (2)

373
Q

Myosin filaments are made of how many chains total

A

6 chains total , 2 tails wrapped and 2 sets of head

374
Q

What determines the shape change of Myosin heads in smooth muscle ?

A

Regualtory lite changes determine shape change after phosphorylation

375
Q

F-actin is responsible for ?

A

binding sites for myosin head

376
Q

Tropomyosin functions as what ?

A

a shield - hides active sites on actin from myosin - musy be moved to induce contraction

377
Q

What is the troponin complex comprised of ?

A

Troponin I
Troponin T
Troponin C

378
Q

Troponin I binds to what ?

A

Binds to actin strand

379
Q

Troponin C binds to what ?

A

binds to Calcium
-4 binding sites for Ca++

380
Q

Troponin C binds to what ?

A

Ca++

381
Q

Troponin complex is used for what ?

A

causes configuration changes on actin to loosen and expose binding sites.

382
Q

“Cocked” State of myosin head in cross bridge cycle

A

heavy chain tail of Myosin is perpindicular to Actin and attached to Phosphate and ADP in its ready to bind state.

383
Q

Weak cross bridge state of cross bridge cycle

A

Ca binds to troponin C or troponin complex, causes conformational change and exposes the binding sites of on actin

384
Q

Strong (power stroke) cross bridge state

A

Myosin head binds to troponin I and the head bends pulling the actin over the myosin with strong force toward the center of the sarcomere. Phosphate is released.

385
Q

Post Power stroke stage of cross bridge cycle

A

ADP remains on myosin head which sustains contraction

386
Q

Attached state

A

ADP falls off eventually but head remains in place until another ATP comes to detach the head

387
Q

Released State of Cross Bridge cycle

A

ATP releases tension of myosin head and is metabolized into ADP. then the cycle repeats.

388
Q

Problems with cross bridge cycle

A

run out of ATP = no force = stiff muscles

389
Q

Sequestrin Protein

A

Stores Ca to remove from SR

390
Q

What connect bone to bone?

A

LIGAMENTS

391
Q

What connects muscle to bone?

A

TENDON

392
Q

Over lap of thin and thick filaments is called what ?

A

A BAND

393
Q

How many classifications of skeletal muscle are there ?

A

two - Type1 and Type 2

394
Q

How many skeletal muscle motor units can a motor neuron control ?

A

1 OR MANY

395
Q

What are the 5 layers that make up the cell ?

A

Sarcomere - Stretch
Myofibril
Muscle Fiber Cell -NMJ
Fasciculous
Muscle (Fasiculi)

396
Q

What part of the muscle is the NMJ ?

A

Muscle fiber cell

397
Q

What layer of the muscle is responsible for the stretch ?

A

Sacrcomere

398
Q

Is there a axon terminal on every single muscle fiber cell?

A

YES

without it the muscle would be useless

399
Q

This is found at each end of each sarcomere

A

Z-Disc

400
Q

Whats wrapped around the Z-Disc

A

Actin is wrapped around ends

401
Q

Place where we have only thin filaments

A

I BAND - actin only - light in color

402
Q

Darker colored area where there is only thick filaments

A

H ZONE/BAND

403
Q

this connective tissue holds our thick and thin filaments together

A

titin

404
Q

How many myosin molecules make up each myosin filament ?

A

200

404
Q

Contracted Sarcomere

A

z - disc are pulled closer together
I band shrinks
A stays the same

405
Q

Is the force of contraction directly related on stretch of heart muscle ?

A

YES . Frank Starling law.
Heart is usually slightly under-stretched at rest

406
Q

Passive tension is what ?

A

Outside tension/force to stretch muscle from tendon

407
Q

Active tension is what?

A

force produced in the skeletal muscle as a result of the AP

408
Q

Passive tension + Active tension is what ?

A

TOTAL Tension

409
Q

stretch happens where that increases performance ?

A

stretch at the tendons - lengthens muscle tissue

410
Q
A

Schmidt’s World Of Anatomy (3 decks)

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