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Exam 3 Flashcards

1
Q

The spinal cord has two different pathways. What are they called, what type of information do they carry and where?

A

Ascending or afferent pathway- carries sensory info. from the periphery to the brain.
Descending or efferent pathway- carries motor signals from the brain to the body.

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2
Q

What are the three main tracts in the ascending pathway? What information do each carry?

A
  1. Dorsal Column Medial Lemniscus tract- fine/localized pressure sensors from the skin touch sensitive
  2. Spinocerebellar tract- sensory information
  3. Anterolateral tract (spinothalamic) fast and slow pain signals
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3
Q

What are the two main tracts in the descending pathway? What information do each carry?

A
  1. Pyramidal (corticospinal) tract-conscious or voluntary movement
  2. Extrapyramidal tract- subconscious or involuntary movement, accessory motor
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4
Q

What are Rexed’s Laminae?

A

Laminae are how we organize grey matter in the cord. There are 10 laminae (sections) in total.

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5
Q

Lamina I: name, location and information

A

Lamina marginalis, dorsal part of the dorsal horn. Fast sharp pain via myelinated A delta fibers

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6
Q

Lamina 2, 3 and 5: name and information

A

Substantia gelatinosa. Slow pain, nonmyelinated C fibers

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7
Q

Lamina 1 through 6: type of information these receive

A

mechanoreceptors and pressure sensors

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8
Q

Lamina 7,8,9: type of information

A

large motorneurons, activated by the descending pathway in the anterior/ventral horn

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9
Q

Lamina 10: location and what’s special about it?

A

middle of the grey matter, between right and left sides, this is where crossover happens

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10
Q

Say a feather brushes your fingertip or you stub your toe and go grab it to stop the pain… what pathway is activated?

A

Dorsal Column Medial Lemniscus pathway (DCML)

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11
Q

Describe the transmission of information in the DCML from the periphery (lower extremity) to the higher processing centers in our brain…

A

Foot –> dorsal root ganglia –> dorsal column (fasciculus gracilis) –>cross over at medulla –> medial lemniscus of the pons–> ventrobasal complex in the thalamus–> the internal capsule –> somatosensory cortex in the parietal lobe

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12
Q

What type of information gets relayed in the DCML pathway?

A

Sensory information other than pain. This pathway is good at localizing the stimulus and can pick up fine pressure. This pathway uses myelinated a fibers and has very fast signal propagation.

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13
Q

What are the two parts of the dorsal column and what is unique about these parts?

A
  1. Fasciculus gracilis: carries sensory info from the legs up to the brain
  2. Fasciculus cuneatus: carries sensory info from the upper extremities up to the brain
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14
Q

How much of our somatosensory (postcentral gyrus) information gets transmitted via the DCML pathway?

A

80%

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15
Q

What are the two destinations of touch information in the DCML pathway?

A
  1. Touch sensation comes into the dorsal horn of the cord, stays in the grey matter and can participate in lateral inhibition and modulation of cord activity
  2. Info can hop over into the ascending pathways and ascend to the brain via the dorsal column
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16
Q

What are the two parts to the pyramidal tract?

A
  1. Anterior corticospinal tract
  2. Lateral corticospinal tract
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17
Q

Which corticospinal tract has the majority of motor output, how much?

A

The lateral corticospinal tract (primary pathway). 80% of motor function.

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18
Q

How much of our motor output comes from the anterior corticospinal tract?

A

17%

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19
Q

Describe the transmission of motor signals from the motor cortex (precentral gyrus) to the primary corticospinal tract.

A

motor cortex–> internal capsule–> crossover at the decussation between pyramids of the medulla –> lateral corticospinal tract

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20
Q

What is considered to be the secondary motor pathway and how much of our motor output comes from this pathway?

A

The anterior corticospinal tract. 17%.

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21
Q

What is the major difference between the anterior and lateral corticospinal tracts?

A

The location of crossover. In the lateral cs tract this occurs at the decussation of the medulla pyramids, in the anterior cs tract it happens in the spinal cord at the level of communication with the motorneuron.

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22
Q

What are the two main divisions of the anterolateral tract?

A
  1. Anterior spinothalamic tract
  2. Lateral spinothalamic tract
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23
Q

Fast pain: what pathway, which neurotransmitters, what receptors, good or bad at localization and why?

A

Fast pain is transmitted via myelinated a delta fibers in the lateral st tract.
NT: glutamate
Receptors: nociceptors/ free nerve endings
Detailed localization due to parallel processing with DCML pathway

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24
Q

What is unique about glutamate as a neurotransmitter?

A

It is always excitatory. It’s fast to release, fast to bind and fast to generate an action potential. IT’S FAST!

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25
Q

Slow pain: which pathway, what NT’s, good at localization and why?

A

Pathway: anterior ST tract via unmyelinated c fibers
NT: Substance P mostly, also glutamate and CGRP
Not good at localization because most of this pain information gets terminated before reaching the thalamus.

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26
Q

Where do the myelinated a fibers from the fast pain pathway synapse in the spinal cord? Where to the unmyelinated c fibers from the slow pain pathway synapse in the cord?

A

Fast pain: dorsal horn at Lamina 1 (Lamina marginalis)
Slow pain” dorsal horn at Lamina 2,3, and 5 (Substantia gelatinosa)

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27
Q

What are the other names for the slow pain pathway and the fast pain pathway?

A

slow pain: “paleospinothalamic tract”
fast pain: “neospinothalamic tract”

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28
Q

Where do the anterolateral/ spinothalamic tracts crossover?

A

At the anterior white commissure in the spinal cord

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29
Q

What type of sensory information does the anterolateral and spinothalamic tract carry?

A

Fast pain and slow pain. Also, temperature and irritants (such as tickle and itch sensations)

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30
Q

Where, specifically, does slow pain signals terminate before reaching the thalamus?

A

Reticular formation

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31
Q

Why does slow pain tend to “mess with our heads” more?

A

Part of the slow pain pathway gets routed to our emotional centers of the brain.

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32
Q

What are the four extrapyramidal tracts and what motor functions are relayed in each?

A
  1. Vestibulospinal: eye fixation and helps maintain balance
    Olivospinal: movement coordination from the cerebellum
    Reticulospinal: maintenance of basal muscle tone
    Rubrospinal: monitors and adjusts voluntary movement
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33
Q

What is the descending inhibitory complex (DIC)?

A

This is a system of three neurons that our body uses intrinsically to suppress pain signals.

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34
Q

What are the three neurons in the descending inhibitory complex and where do the start/synapse?

A

first order neuron is in the periaqueductal gray (near the cerebral aqueduct between the 3rd and 4th ventricle) which synapses on the second order neuron in the raphe magnus nucleus in the pons. Neuron 2 synapses on the 3rd neuron in the dorsal horn of the s.c.

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35
Q

What neurotransmitters do each of the neurons in the DIC pathway release and are they excitatory or inhibitory?

A

1: Enkephalins (endogenous opiates) excitatory
2: Serotonin, excitatory
3: Enkephalins (inhibitory in the S.C.)

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36
Q

Why might someone prescribe an SSRI or tricyclic antidepressant for chronic pain?

A

SSRI’s inhibit serotonin reuptake, therefore the more serotonin around can effect the third order neuron in the DIC pathway which inhibits the pain signals coming into the s.c. TCA’s often have drowsiness as a side effect so these can help with sleep

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37
Q

What are different signals from the body that can be registered as pain by nociceptors?

A

cellular damage (say a crush injury), H+, K+, histamines, serotonin, ACh, prostaglandins, and bradykinins.

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38
Q

What is lateral inhibition?

A

communication from an adjacent neuron (from the DCML pathway) that can help deaden pain from the nociceptor. These neurons run parallel to one another and in close proximity allowing them to have crosstalk.

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39
Q

Name three compounds that can increase pain sensitivity at the synapse between a first order neuron and second order neuron

A
  1. iNOS-
  2. COX-2
  3. prostaglandins
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40
Q

What are the three inotropic glutamate receptors? and what adjacent ion channels do they activate?

A
  1. AMPA receptors: Na+
  2. NMDA receptors: mainly Ca2+, but a little Na+ too
  3. Kanate receptors (mediates GABA)
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41
Q

What type of receptors are enkephalin receptors and what ion channel is associated with these?

A

They are GPCR’s. K+ channels.

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42
Q

What’s another GPCR that activates these K+ channels?

A

alpha 2 receptors.

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43
Q

Name three alpha 2 agonists we talked about in class

A
  1. xylazine
  2. clonidine
  3. dexmedetomidine (precedex)
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44
Q

Why are NMDA receptors “slower” to open than AMPA receptors?

A

NMDA-R need a prior depolarization to push intracellular Mg2+ out of the way.

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45
Q

Which type of receptor increases in number as we mature?

A

NMDA receptors

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46
Q

What does chronic pain do to AMPA and NMDA receptors?

A

It increases the amount of these receptors at the synapse via sensitization

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47
Q

What are some NMDA receptor antagonists we talked about in class?

A

ethanol, lead poisoning, ketamine, nitrous, tramadol

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48
Q

Name the two reflexes that use stretch receptors for input…

A
  1. stretch reflex
  2. tendon reflex
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49
Q

Name the two reflexes that use pain receptors as input…

A
  1. withdrawal reflex
  2. crossed extensor reflex
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50
Q

Stretch reflex: what is it responsible for, what muscles are engaged, and which are relaxed?

A

Goal: to keep muscles at a constant length, helps us stand upright
Quads are engaged
Hamstrings are relaxed

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51
Q

The tendon reflex: what is it responsible for, which muscles are engaged and which are antagonizing?

A

This is a protective reflex, prevents muscles from being pulled out of bones. Uses interneurons…
one excitatory (recruits antagonistic muscles for retraction from load source)
one inhibitory (ceases contraction under heavy load to prevent tears)

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52
Q

what is another name for a muscle spindle?

A

“stretch” receptor

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53
Q

The flexor reflex: what does it do, and which muscles are engaged and what are the antagonizing muscles?

A

This is the withdrawal reflex, flexor muscles are activated and they contract. Antagonistic muscles are the extensors (these relax). Goal: to withdraw from painful stimuli. Uses ascending and descending interneurons to disperse information along the cord.

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54
Q

Crossed extensor reflex: what does it do and how does it do it?

A

This reflex is also pain mediated. It occurs with dynamic movement and utilizes multiple interneurons to send information to the other side of the cord and has ascending and descending interneurons to get information to the appropriate motorneurons. Often occurs in conjunction with flexor reflex on the other side of the body.

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55
Q

Give an example of the crossed extensor reflex…

A

You stub your right toe into a coffee table while walking. The Left leg “braces itself” to hold you upright by contracting the quad and relaxing the hamstring like the stretch reflex only on the other side of the body and in response to pain. Meanwhile, the right leg can withdraw from the painful stimulus (flexor reflex).

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56
Q

Which reflex does not use any interneurons?

A

The stretch reflex. It is a direct reflex arc.

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57
Q

Which reflex is being elicited when a doctor strikes the ligament just below the Patella with a reflex hammer?

A

the stretch reflex

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58
Q

Give an example of the tendon reflex and a scenario where the body can override this reflex.

A

Fall off a two story deck and land on feet. This increase in muscle tension causes sudden complete relaxation of affected muscle to protect the muscle from tearing. The body can override this in extreme cases of fight or flight, like lifting a car off a child.

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59
Q

What are some of the differences between mature and fetal nACh receptors?

A
  1. Fetal nACh-R have a gamma subunit instead of an epsilon subunit
  2. Fetal receptors have a lower ion conductance
  3. Fetal receptor pores can stay open longer due to their higher affinity for ACh
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60
Q

In the case of muscle paralysis how does the body respond? Which receptor types can it make more of and where does it put these?

A

With muscle paralysis the body makes more immature nACh-R to try to help ACh bind and contract the muscle. It places these immature nACh receptors all along the muscle fibers (not just at the end plate).

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61
Q

Why is it so dangerous to give Succinylcholine to paralyzed patients or patients with neuromuscular disorders?

A

This patient population has much more of these fetal nACh-Rs that Succ can bind to. They stay open longer and allow more K+ out and Na+ depolarizing the muscle much longer. The increased K+ that floods out is significant and can lead to life threatening hyperkalemia and v fib.

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62
Q

Which muscle are we stimulating with train of four at the ulnar nerve?

A

the adductor pollicis muscle

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63
Q

What is supramaximal stimuli?

A

the voltage used to generate a twitch contraction, and an excellent name for a heavy metal band!

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64
Q

What is the frequency and interval applied when using a nerve stimulator to elicit ToF?

A

4 twitches administered over…
a frequency of 2 Hz
and an interval of 2 sec

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65
Q

Name three other nerves we talked about as alternatives to the ulnar nerve for ToF…

A
  1. Opthalmic branch of the facial nerve
  2. Peroneal nerve
  3. Posterior tibial nerve
66
Q

What is the difference we see in single twitch stimulation between depolarizing and non-depolarizing NMB drugs?

A

Depolarizing: loss of twitches sooner (around one minute), but return of twitches at around 3 minutes) = short acting
Non-depolarizing: loss of twitches around 3 minutes that lasts 20-30 minutes and maybe even hours in certain patients!

67
Q

What is the B/A ratio?

A

Another name for this is the ToF ratio. B is the strength of the last twitch, A is the strength of the first twitch.

68
Q

As a neuromuscular blockade wears off what will the B/A ratio approach?

A

B/A = 1 (no longer paralyzed)
corresponds to 4 strong twitches, with the fourth twitch being as strong as the first

69
Q

Why do ToF twitches get progressively weaker with non-depolarizing blocks but remain the same strength with depolarizing blocks?

A

There are two types of receptors these paralytics can bind.
1. the nACh-R on the end plate
2. ACh auto-receptors on the presynaptic motorneuron. Non-depolarizing NMBD antagonize the auto-receptors, which are responsible for readying VP2 vesicles, so less ACh can come out to play at the synapse leading to weaker and weaker twitches.

70
Q

What is another name for these nACh receptors on the motorneuron, other than auto-receptors?

A

neuronal ACh receptors

71
Q

What is the role of the neuronal ACh receptors?

A

turn VP1 ACh storage vesicles into VP2 storage vesicles ready to undergo exocytosis at the NMJ

72
Q

Why do depolarizing NMBD have ToF twitches that are all equal?

A

Two reasons…
1. Succ primarily works at the end plate of the postsynaptic cell
2. Succ mimics ACh so it would act as an agonist at the auto-receptors leading to constant depolarization necessary to turn VP1 into VP2 vesicles, plenty of ACh ready to go

73
Q

If acetylcholinesterase cannot break the ester bond of Succinylcholine, what can?

A

Cholinesterases created by the liver can!

74
Q

So you have a spinal case, and the patient needs to be proned for the case. Why should you consider using an alternative paralytic to Succ?

A

Succ can increase IOP, and if your patient is in a prone position they will likely already experience more pressure in the eyes.

75
Q

Is the adductor pollicis muscle more or less sensitive to NMBD than the diaphragm? By about how much?

A

It’s much more sensitive. At the same dose of a paralytic when the adductor pollicis demonstrates no twitches, the diaphragm may only be 15-20% blocked

76
Q

Which spinal nerves are responsible for controlling the diaphragm muscle?

A

C3, C4, C5 spinal nerves make up the phrenic nerve, which keeps the diaphragm alive!

77
Q

You finished the long spinal case and you reverse the paralytic, you notice the patient has all 4 twitches, and they are lifting their head up from the table, what do you do?

A

a. Panic!
b. Re-paralyze
c. Take the damn tube out
d. Give them a bolus

78
Q

The following twitches present corresponds to how many nACh-Rs being blocked?
1. no twitches
2. 1 twitch of 4
3. 2 of 4
4. 3 of 4

A
  1. 90-95% are blocked
  2. 85-90% blocked
  3. 85% blocked
  4. 75-80% blocked
79
Q

When the patient is able to lift their head, what percent of their nACh-R are blocked?

A

70% or less.

80
Q

What are the two inhibitory neurotransmitters in the spinal cord?

A

GABA
Glycine

81
Q

Which neurotransmitters are stimulatory/ increase awareness?

A

ACh (via muscarinic ACh receptors)
Norepinephrine
Glutamate

82
Q

What effect does Dopamine have on the skeletal muscles?

A

It is a motor inhibitor

83
Q

How does Benadryl (an anti- histamine) make us drowsy?

A

It turns out that our central histamine receptors resemble mACh-R. Benadryl binds to and blocks these mACh-R which induces drowsiness.

84
Q

What neurotransmitter is responsible for the increased muscle activity characteristic to Parkinson’s disease?

A

a lack of dopamine corresponds to less motor inhibition

85
Q

How does pH affect awareness/drowsiness?

A

low pH (acidosis) can lead to CNS depression (very drowsy)
high pH (alkalosis) can lead to seizures (hyperactive CNS)

86
Q

Recall what ventilation does to pH… what leads to alkalosis and what leads to acidosis?

A

Hyperventilation can lead to alkalosis
Hypoventilation can lead to acidosis

87
Q

What ions and carrier protein links pH to CNS activity?

A

Ca++ and H+
Carrier protein: albumin

88
Q

Describe how acidosis can lead to CNS depression at the level of the ion…

A

Acidosis = more H+ ions. These bind to albumin (outcompeting Ca2+). There is now lots of free Ca2+. Rogue Ca2+ reduces neurological activity –> CNS depression

89
Q

Describe how alkalosis can lead to increased awareness at the level of the ion…

A

alkalosis = less H+. More room near albumin for Ca2+, less free Ca2+ leading to more awareness.

90
Q

what are the 3 major arteries that supply the blood to the spine? How much blood do they supply?

A

Anterior artery 75%
2 posterior arteries 25%

91
Q

Where does the anterior artery sit within the spinal canal?

A

It rests in the anterior median fissure

92
Q

List the major feed arteries to the posterior spinal arteries

A
  1. vertebral arteries (2)
  2. anterior inferior cerebellar arteries (2)
  3. posterior inferior cerebellar arteries (2)
  4. posterior radicular arteries (from 12 sets of intercostal arteries)
93
Q

List the major feed arteries to the anterior spinal artery

A
  1. anterior radicular arteries (usually 2 cervical, 2-3 thoracic, and 1-2 lumbar)
  2. great radicular artery (artery of Adamkiewicz)
94
Q

Where is the great radicular artery located? One level? in 75% of folks? absolute range?

A

T10
T9-T12 (in 75% of people)
T5-L5 (absolute range)

95
Q

If you could choose, would you rather have your GRA branching off the aorta at T10 or L2?

A

T10 my lord! It’s much safer to have a great radicular artery branching off the aorta higher up. Cross clamp below and you don’t have to worry about ischemia as much.

96
Q

Describe the pattern of radicular arteries as they enter the spinal cord arteries…

A

The radicular arteries usually come in from the left or right (staggered) and either feed the anterior or the posterior spinal arteries. (Not both at once and not branching around the cord like most images portray)

97
Q

The great radicular artery supplies blood to how much of the entire spinal circulation?

A

It supplies about 2/3 of the arterial blood to the lower spinal spinal cord

98
Q

Does the GRA usually branch off the aorta above or below the renal arteries?

A

Usually above (75% of the time T9 to T12), but can be below

99
Q

How do we calculate cerebral perfusion pressure?

A

MAP - ICP (usually around 10 mmHg in healthy humans)

100
Q

Aortic cross clamping usually increases CSF pressure in the spinal cord by how much? What can CT surgeons do about it?

A

it increases pressure by about 10 mmHg. The surgeons can place a lumbar drain before the surgery. They usually put in a confusing order set after surgery asking you to drain x amount of CSF per hour to maintain a pressure around what is physiologically “normal”

101
Q

What is likely the biggest contributing factor to ischemia reperfusion injuries?

A

Oxygen rice blood flows too quickly to vessels that weren’t receiving blood flow during surgery. Surgeons could prevent this by slowly restoring blood flow (but they aren’t going to do this). We can help by not over-oxygenating our patients post-operatively.

102
Q

Name the two spinocerebellar tracts

A
  1. posterior or dorsal spinocerebellar tract
  2. anterior or ventral spinocerebellar tract
103
Q

What information does the posterior spinocerebellar tract send that how does it get there?

A

This sends information about the tendon and muscle spindle or stretch sensors from the skeletal muscles. This tract ascends the cord and enters the cerebellum via the inferior cerebellar peduncle.

104
Q

What information does the anterior spinocerebellar tract send that how does it get there?

A

This tract sends information regarding the motor activity from the anterior/ ventral horn. This tract ascends the cord and enters the cerebellum via the superior cerebellar peduncle.

105
Q

Why are there two spinocerebellar tracts?

A

This combination helps coordinate complex muscle movements

106
Q

Give some examples of chemical stimuli that can be received as pain at our nociceptors

A

bradykinins, serotonin, histamine, K+, H+, ACh, ischemia, prostaglandins,

107
Q

What are some key differences between parietal pain and visceral pain?

A

parietal pain is usually fast pain, and highly localized. Visceral pain is usually slow achy pain and is usually reffered pain.

108
Q

Someone who experiences chronic pain may become more sensitive to pain, how?

A

It may be related to membrane potentials. The more you elicit a certain pain response, the easier it becomes to elicit again. This could be due to lowering the threshold we perceive pain at the nociceptors. our nociceptors undergo reverse adaptation.

109
Q

Give three examples of referred pain that we talked about in class…

A
  1. appendix rupture, pain at the umbilicus (visceral component)
  2. Left shoulder pain from an MI
  3. Lower back pain may be an issue with the kidneys
110
Q

List the components of the limbic system that we discussed in class

A
  1. amygdala
  2. hypothalamus
  3. cingulate gyrus
111
Q

where is the cingulate gyrus located?

A

right above the corpus callosum

112
Q

Why does slow pain tend to mess with our heads more?

A

slow pain signals usually terminate at the reticular formation, but some of these slow pain signals can get routed through the limbic system which is responsible for emotion

113
Q

Give some examples of myelinated A alpha fibers

A
  1. muscle spindle fibers
  2. muscle tendon fibers
  3. skeletal muscle motor fibers
114
Q

Give some examples of myelinated A beta fibers

A
  1. muscle spindle fibers
  2. DCML pressure sensors
  3. lateral inhibition fibers
115
Q

give some examples of unmyelinated C fibers

A
  1. crude touch/pressure
  2. cold/warmth
  3. aching pain
  4. tickle/ itch
  5. nausea
116
Q

From a muscle to a single contractile unit list the structure of a skeletal muscle cell

A

muscle, fasciculous (a group of skeletal muscle cells), muscle cell, myofibril (about 200 myofibrils in each muscle cell), sarcomere (contractile unit)

117
Q

When describing skeletal muscle cells, what is a motor unit?

A

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

118
Q

There are two types of skeletal muscles, what is different about each type?

A

Type 1: slow longer contraction, “red” muscle due to lots of myoglobin, also has more mitochondria
Type 2: white muscle, fast twitch, less myoglobin and fewer mitochondria

119
Q

Give an example of a type 1 muscle fiber

A

slow, longer depolarization. Soleus muscle (lower back calf muscle).

120
Q

Give an example of a type 2 muscle fiber

A

fast, short duration of depolarization. Ocular muscles.

121
Q

What marks the border of a sarcomere?

A

Z discs

122
Q

What is the I band made up of?

A

Actin only

123
Q

What’s in an A band?

A

actin and myosin

124
Q

the area with just myosin in a sarcomere is called what?

A

H zone

125
Q

What is the name of the stretchy elastic connective tissue holding actin and myosin together?

A

titan

126
Q

what “shrinks” with muscle contraction in a sarcomere?

A

the I bands

127
Q

Why do skeletal muscle cells have multiple nuclei?

A

They don’t have room (all the myofibrils) for the same transport system neurons do so they are multinucleated in order to make their own proteins.

128
Q

How many chains does each myosin have?

A

(6) 2 heavy chains, and 4 light chains. 2 “essential light” chains and 2 “regulatory” chains.

129
Q

How do actin active sites get revealed to myosin heads?

A

via the troponin complex. There are 3 components to the troponin complex. I, T and C. C binds 4 Ca2+ and unravels I bound actin from the T bound tropomyosin revealing the active site on actin.

130
Q

After the active site on actin gets revealed how does cross bridge cycling work?

A

Myosin has lots of stored tension and when myosin binds the active site on the actin it can pull the actin filament shortening the sarcomere. This releases an ADP.

131
Q

How does the myosin unbind the actin and get into its tensed state again?

A

ATP!!!

132
Q

The load/contraction velocity relationship, what is it and why do we care?

A

The greater the load the slower the contraction. This is important for the heart, the “load” it has to overcome is the afterload. Increased afterload slows down contraction of the heart and takes longer to eject the blood and may not have enough time to fill with the next contraction.

133
Q

What is the difference between temporal summation and quantal summation?

A

Summation of muscle contractions occurs when lifting heavy weights, and occurs in two ways: quantal summation is more motor units contracting and temporal summation is an increase in frequency of contraction of individual muscle fibers.

133
Q

Finish this statement: Contraction velocity is directly proportional to muscle_____. The larger the diameter of the muscle the greater the ____.

A

Length. Force.

134
Q

weightlifting can increase skeletal muscle mass primarily by_______.

A

Causing hypertrophy of myofibrils (muscle fibers).

135
Q

What causes atrophy with muscle disuse say in the form of a muscle not being able to move in a cast?

A

They get smaller due to less myosin and actin being synthesized. (This is reversible once the cast is off)

136
Q

In a patient who is paralyzed, and doesn’t want to experience atrophy of their lower extremity muscles, what is a way they could keep this from happening?

A

By stimulating the skeletal muscles with electrodes you can maintain their mass, but the lack of nerve communication needs to be fixed for a permanent solution.

136
Q

What are five differences between smooth muscle and skeletal muscle?

A
  1. They are more efficient, slower cross bridge cycling and Latch mechanism
  2. The neighboring cells are connected by gap junctions
  3. Actin to myosin ratio is much larger
  4. Actin anchored at dense bodies
  5. They rely more on outside calcium (SR less well developed)
137
Q

gram for gram _____muscle is stronger than _______muscle?

A

smooth muscle is stronger than skeletal muscle.

138
Q

what is the actin to myosin ratio in smooth muscle? In skeletal muscle?

A

10-20:1 and 2:1

139
Q

What is the latch mechanism smooth muscle cells use to increase efficiency in low energy states?

A

in an ultra low energy state. Super slow cross bridge cycling. Maintains force for a longer period of time using very little energy by keeping myosin head attached to the actin filaments longer.

140
Q

What are two reasons you have no blood pressure with a super low serum calcium?

A
  1. Lack of smooth muscle vascular tone (primary reason)
  2. Don’t get calcium induced calcium release for cardiac muscle contractions (secondary)
141
Q

what is one structure in our body that has both skeletal muscle and smooth muscle?

A

The esophagus

142
Q

what is the single-cell layer inner lining of endothelial cells called in a blood vessels?

A

Tunica intima

143
Q

What is the outer layer of connective tissue called in the vascular system?

A

Adventitia

144
Q

the smooth muscle layer in the middle of the blood vessel is called what?

A

Tunica media

145
Q

Which two layers of the blood vessel can communicate and what neurotransmitter can they use?

A

the tunica intima and the tunica media are right next to one another and can communicate via nitric oxide.

146
Q

in smooth muscle the myosin head is inactive and actin is always ready to go. What activates myosin and which chain is responsible for its regulation?

A

phosphorylation activates myosin. MLCKinase adds a phosphate to a regulatory light chain on the myosin.

147
Q

what role does calmodulin have in smooth muscle contraction?

A

it binds to a bunch of calcium and is able to activate MLCK.

148
Q

where does calcium come from in smooth muscle cells?

A
  1. From outside the cell via voltage gated L type Ca channels (slow Ca channels)
  2. Some from the SR via ryanodine receptors
149
Q

What are two ways to get the cardiac smooth muscle to relax, what needs to happen?

A
  1. Myosin needs to detach itself from the actin, this requires a phosphate group to come off myosin –> via MLCP
  2. Removal of Ca2+ from the inside of the cell via SERCA pumps or Na+/Ca2+ exchangers
150
Q

What are two things that protein kinase G (PKG) can phosphorylate and what does that do?

A
  1. It can phosphorylate MLCK, which inactivates it
  2. It can phosphorylate Ca2+ channels closing them up
151
Q

How does the Ca2+/calmodulin complex impact NO in endothelial to smooth muscle cell communication?

A

It increases the activity of eNOS which acts on arginine to form nitric oxide (NO). This can cross over into the smooth muscle cell and activates guanylyl cyclase which cyclates GTP into cGMP.

152
Q

What does cGMP do in the smooth muscle cell?

A

It increases the activity of PKG, which inhibits MLCK and Ca channels, limiting contraction and causing relaxation of vascular smooth muscle.

153
Q

How do phosphodiesterase inhibitors work?

A

They inhibit the inhibitor (phosphodiesterase –> shuts down cGMP). More cGMP leads to more PKG leading to vascular relaxation.

154
Q

what is the only neurotransmitter that is able to constrict brain blood vessels?

A

Serotonin. This is why SSRIs can be used for treating headaches too!

155
Q

Where does the calcium come from in the cardiac smooth muscle cells? What proportion comes from where?

A

20% comes in from the outside. 80% of the calcium comes in from the sarcoplasmic reticulum.

156
Q

What is calcium induced calcium release?

A

An action potential causes sodium to come into the cell and calcium to enter slightly after leading to an action potential. This triggers DHP voltage sensors lining the T tubule to open ryanodine receptors on the SR and calcium to release from the sarcoplasm.

157
Q

What are the different types of calcium channels and where are they?

A

voltage gated “L type” slow calcium channels: Main channel in cardiac smooth muscle, and some in NMJ
voltage gated “P type” fast calcium channels: NMJ (main Ca channel)
calcium leak channels: cardiac smooth muscle
VG “T type” fast calcium channels: cardiac smooth muscle

158
Q

What are the three main ways calcium exits the cardiac smooth muscle cell? What percent leaves where?

A
  1. SERCA: 80%
  2. Na/Ca exchanger: 15%
  3. Ca/ATPase pump: 5%
159
Q

what is calsequestrin?

A

It is a protein that binds calcium in the SR and helps store it. It helps the SERCA pump out by taking calcium out of solution decreasing the concentration gradient making it easier to pump calcium back into the SR.

160
Q

What is phospholamban?

A

It is a protein that inhibits pumping of the SERCA pump, lengthen the contraction. There are drugs we can use to inhibit the inhibitor which shorten contractions.

Advanced A & P (5 decks)

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