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A&P Test 2 > 09/23 > Flashcards

09/23 Flashcards

1
Q

What is one reason that skeletal muscle is important (big picture)

A

regulate body temperature

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2
Q

What is the largest container within the body?

A

skeletal muscle

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3
Q

Does every skeletal muscle have 1 motor neuron?

A

yes, but some can have more than 1

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4
Q

what is an example of a skeletal muscles that has multiple motor neurons?

A

ocular muscle in the eye socket

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5
Q

what can excite a motor neuron cell body?

A

descending spinal pathways sent from the brain
or
reflex arc from the horizontal spinal sensory neurons in the posterior horn

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6
Q

If we have a strong pain signal coming into the spinal cord what can get involved?

A

reflex arc

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7
Q

what is a group of muscle cells called?

A

a muscle fiber

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8
Q

some motor neurons can control 1 cell, or

A

multiple called a muscle fiber

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9
Q

What are the contractile elements of skeletal muscle?

A

actin and myosin

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10
Q

How are actin and myosin typically arranged?

A

in a tube-like structure

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11
Q

What is the endoplasmic reticulum in a skeletal muscle called?

A

sarcoplasmic reticulum
SR

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12
Q

What is stored in the sarcoplasmic reticulum?

A

Ca++ storage

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13
Q

What is a transverse tubule?

A

a perpendicular in-folding “tube” where action potentials can move lengthwise and deep into the skeletal muscle

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14
Q

How long can a skeletal muscle cell be?

A

over a foot long

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15
Q

Where do action potentials start?

A

at the NMJ

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16
Q

We are going to assume for now that there is a process that basically allows Ca++ to be freed from it’s storage locations in the SR then we’ll assume that the Ca++ is able to

A

drive actin and myosin cross bridge cycling which causes a contraction

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17
Q

in a contraction the muscle

A

shortens

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18
Q

What is the zebra pattern on a skeletal muscle?

A

the alignment of actin and myosin

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19
Q

Ca++ entry into the neuron is the result of what?

A

an action potential that passes through the neuron

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20
Q

Where is mitochondria typically found?

A

in the specialty areas of the NMJ

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21
Q

What is situation next to an AChr in the skeletal muscle?

A

a lot of fast sodium channels

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22
Q

What is a primary and secondary cleft in the skeletal muscle?

A

a single in-folding in the skeletal muscle near the NMJ

more than one in-folding in the skeletal muscle near the NMJ

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23
Q

Where is AChE created and found?

A

expressed by the skeletal muscle and bound to the skeletal muscle at the NMJ

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24
Q

What does AChE use to break ACh down?

A

Hydrolysis

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25
Q

What is ACh broken down into?

A

Acetate OR Acetyl OR Acetic acid? (pharm)
choline

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26
Q

What happens to Acetyle and choline after it is broken down by AChE?

A

It gets reabsorbed into the neuron to be used again

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27
Q

Where are schwann cell bodies found?

A

on the nerve terminal (synaptic bouton)

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28
Q

How many ACh receptors do we have in a typical NMJ?

A

5 million

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29
Q

How many ACh receptors are activated in a typical synaptic response?

A

500,000 or 10%

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30
Q

What is the bare minimum ACh that has to be released to create an AP? How much is actually released?

A

1 million
2 million

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31
Q

where was curare first discovered?

A

in the rainforest used to paralyze prey. its a natural paralytic

32
Q

What is involved in exocytosis?

A

SNAP-25
SNARE proteins

33
Q

How do skeletal muscles sense a fast sodium channel-mediated action potential?

A

through voltage sensors in the cell wall or T-tubule called Dihydropyridine

34
Q

What does the DHP receptor do to contribute to a contraction?

A

they open the Ca++ release channels and let Ca++ flood out

35
Q

Some calcium channel blockers are called

A

dihydropyridine ca++ channel blockers

36
Q

What is the tubule called that follows the primary infolding?

A

a t-tubule

37
Q

Where does most of the Ca++ come into the skeletal muscle cell and what accounts for a smaller portion of Ca++ coming into the cell?

A

the SR
the DHP sensors

38
Q

What is another name of the calcium release channel on the SR?

A

Ryanodine receptor RyR
Odd because it just happens to open to a chemical called ryanodine, but the DHP sensor is physically attached to it which isn’t receptor like

39
Q

How does Ca++ get put back into the SR?

A

through the SERCA pump
Sarcoendoplasmic reticular ATPase

40
Q

Skeletal muscle: Excitation Contraction Coupling steps.

A

Motor neuron depolarizes (AP from brain or reflex arc)
Ca++ influx into motor neuron through VG P-Type Ca++ channels
Ca++ makes ACh vesicles fuse to the presynaptic neural cell wall/membrane
ACh exocytosis
ACh interacts with nACh receptors
Na+ comes in, some Ca++ comes in
Positive influx generates end plate potential EPP (local depolarization)
EPP in a physiological setting ALWAYS causes an action potential in skeletal muscle
AP spreads down the muscle fibers in both directions via VG Na+ channels
Muscle depolarization sensed by DHP sensors
DHP pulls on RyR= Ca++ released from SR
Ca++ tucked back away in SR via SERCA

41
Q

What is the fluid called on the inside of a skeletal muscle cell?

A

sarcoplasm

42
Q

What does a muscle cell depend on to stop contracting?

A

Ca++ being tucked back into the SR via the SERCA pump

43
Q

Choline gets recycled by

A

ATPase pump
secondary active transporter that uses Na+ going into the cell with a choline going into the cell

44
Q

Acetyl recycling _____, but we know that acetate comes from

A

isn’t well understood
the mitochondria

45
Q

there are a lot of mitochondria found within the neuron to do what?

A

serve as a source for acetate
provides energy for the ion channels in the neuron

46
Q

Where can extra choline be stored?

A

in the cell wall- phosphatidylcholine

47
Q

Leak channels are found in the cell wall of any

A

excitable tissue

48
Q

Potassium leaks out of the cell during repolarization, and therefore has to be pumped back into the cell. This isn’t a big deal because it is only pumped out

A

for a short amount of time. Comes in through Na+/K+ pump

49
Q

Where are actin and myosin located?

A

near the sarcoplasmic reticulum. Ca++ gets released from the SR and then causes a cross-bridge cycling and muscle contraction

50
Q

Do we need vg k+ channels to help reset the cell?

A

Not really because there are so many K+ leak channels. The VG K+ channels do speed up this process though

51
Q

What is myasthenia Gravis?

A

An autoimmune response where the body makes antibodies against the nicotinic acetylcholine receptors

52
Q

How do antibodies play a role in MG?

A

The antibodies park themselves on the nAChr and call the immune system to come in and destroy the receptors. It then scars over the clefts, taking away the surface area that would normally hold nAChr as well as fast Na+ channels

53
Q

What causes MG

A

a confused thymus gland

54
Q

MG gets worse or better over the course of the day?

A

worse

55
Q

What are the treatments for MG?

A

removing of the thymus
plasmapheresis(very non-specific)
AChE inhibitors

56
Q

What is an example of an AChE inhibitor?

A

-stigmine drug

57
Q

Lamburt Edom or ELMS is a condition usually caused by

A

paraneoplastic
like lung cancer

58
Q

ELMS is pretty specific for what type of neuron?

A

motor neuron

59
Q

How does ELMS work?

A

Antibodies park themselves on the opening’s of P-type Ca++ channels causing a decrease in Ca++ that’s allowed to influx into the cell. No Ca++ = no contraction

60
Q

Why won’t AChE work for LEMS or ELMS?

A

There’s no ACh to break down because Ca++ is not allowed into the cell

61
Q

What are the treatment options for ELMS or LEMS?

A

plasmapheresis
removal of lung tumor
block K+ channels, Leak<VG

62
Q

Why are K+ channel blockers dangerous?

A

they are not specific for Motor neurons, they work pretty much everywhere, like in the heart

63
Q

How does K+ channel blockers work?

A

They keep the VG K+ channels closed which makes the cell depolarized longer, (because P-Type Ca++ channels open with depolarization and close with repolarization) which allows ACh to work at the NMJ longer

64
Q

What are K+ channel blocking drugs?

A

TEA Tetraethylammionium
4-5 diaminopurine

65
Q

curare is a

A

nAChr blocker
non-depolarizing muscle relaxant

66
Q

Succs is made of

A

2 acetylcholines stuck together

67
Q

Succs binds to nAChr, and causes

A

prolonged receptor opening

68
Q

Succs initially causes a

A

depolariztion- twitching

69
Q

why can’t AChE break down succs?

A

It is very specific for regular ACh

70
Q

Because succs binds to the nAChr and keeps them open, Na+ keeps coming in. This makes it very difficult for what

A

the VG Na+ channels to reset

71
Q

Where are the inactivation gates on Na+ channels?

A

the bottom

72
Q

If all of our fast Na+ channels are stuck in the inactive state then they are essentially

A

paralyzed

73
Q

Why does the rest of the cell reset when the NMJ is paralyzed in the open position?

A

That allows a constant large leak of sodium in. The farter away from the NMJ you go, the more normal the cell looks. The Na+/K+ pumps can keep up farther aware from the NMJ where Na+ is flooding in

74
Q

If sodium is leaking in at the NMJ for a long period of time, you would expect the cell membrane to be

A

more positive.

75
Q

Why do you have a loss of a lot of potassium when you give succs?

A

The cell becomes very positive d/t prolonged open nAChr allowing sodium into the cell. More positive the cell more K+ wants to leave

76
Q

How much more is potassium in the plasma when you give succs in a healthy person?

A

0.5mOsm/L

77
Q

In a person who has had a stroke or has been paralyzed for a while, you would expect them to have

A

increased nAChr, found at other places than just the NMJ

A&P Test 2 (7 decks)

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