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Anatomy > NMP Duke final > Flashcards

NMP Duke final Flashcards

1
Q

Types of Sleep

A

normal sleep + REM sleep

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2
Q

Normal sleep

Stage 1

A

β-waves

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3
Q

Normal sleep

Stage 2

A

α-waves

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4
Q

Normal sleep

Stage 3

A

θ-waves; considered; light sleep; broken into stages I and II

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5
Q

Normal sleep
Stage 3
part 1

A

α with θ; the θ waves characteristic of light sleep are taking over the awake brain

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6
Q

Normal sleep
Stage 3
part 2

A

θ with spindles (spindles are alpha bursts; its like the awake doesn’t want to let go)

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7
Q

Normal sleep

Stage 4

A

δ-waves; considered deep sleep; broken into stages III and IV

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8
Q

Normal sleep
Stage 4
part 3

A

δ with spindles; deeper sleep is setting in but

α still tries to burst in

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9
Q

Normal sleep
Stage 4
part 4

A

δ

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10
Q

A person gets more out of sleep if they go through these stages _____________

A

in order

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11
Q

Physiologic Properties of Deep Sleep

Stage 4

A

↓ respiratory rate (10-8 bpm)
↓ muscle tone
↓ sympathetic tone (can drop by 10 -30%)
↓ metabolic rate (MR)

↑parasympathetic tone (↓HR, ↑ GI motility/secretions, relaxed sphincters, sexual arousal)

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12
Q

REM sleep

AKA

A

paradoxical sleep, or

β-wave sleep

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13
Q

REM sleep

occurs every

A

90 mins

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14
Q

REM sleep

duration

A

2-3 minutes, up to 30 mins (rarely longer than 10 mins)

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15
Q

REM sleep

β-waves come heavily from

A

striate cortex

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16
Q

During REM sleep what tract is activated by the PPN?

A

lateral reticulospinal tract

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17
Q

During activation of the reticulospinal tract by the PPN, what is happening?

A

inhibiting extensors, so you’re paralyzed during REM

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18
Q

How does the PPN regulate REM?

A

first sending to the LG; PPN→LG→Striate cortex

area 17

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19
Q

Regulation of Wakefulness vs. Sleep Centers

AKA

A

flip-flop circuit

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20
Q

Narcolepsy

A

a sudden loss of muscle tone

that is often accompanied by the onset of sleep

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21
Q

Orexin / hypocretin

A

produced primarily in lateral and tuberal (medial) hypothalamus; it is responsible for
wakefulness

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22
Q

narcoleptic people often show decreased

A

levels of orexin

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23
Q 
If both (ascending chemical pathways
(wakefulness), and PPN (REM))are stimulated, why don't we have wakefulness and REM and the same time?
A

The asecnding pathways actually inhibit the PPN
so if orexin is firing, the net result is wakefulness because orexin’s stimulative effect on the PPN
is negated

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24
Q

pre-optic nucleus
(anterior medial hypothalamus)
induces

A

non-REM sleep

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25
Q

pre-optic nucleus

action

A

It sends GABA-ergic axons to inhibit both the

lateral/tuberal hypothalamus and the ascending chemical pathways.

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26
Q

third major sleep center

A

PAG

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27
Q

PAG

action

A

sends GABA-ergic axons to the ascending pathway, but not to the orexin-producing hypothalamus

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28
Q

PAG

result

A

it induces REM sleep, like the PPN

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29
Q

What happens when the PAG is on?

A

he ascending chemical pathways are shut down

the PAG shuts off wakefulness centers, prevents them from turning off the PPN, and it leaves the production of orexin on, so PPN is stimulated even more = REM sleep

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30
Q

The PPN is the beginning of what pathway?

A

pontogeniculocalcarine pathway

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31
Q

the PPn activates what cells in the medulla?

A

n. gigantocellularis

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32
Q

n. gigantocellularis

messages what?

A

the lateral reticulospinal tract which inhibits extensors mm. = paralysis during REM sleep

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33
Q

skeletal muscle Ach receptors? AKA

A

nicotinic

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34
Q

Skeletal muscle AP—–>generic description

A

The AP comes down, releases ACh, & new AP is initiated in the skeletal muscle. This means we have fired the sarcolemma.

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35
Q

The AP comes down, releases ACh, & new AP is initiated in the skeletal muscle. The AP runs along the membrane until it hits an invagination. What invagination?

A

T-tubules with sodium channels and DHP receptors

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36
Q

What is DHP?

A

voltage-sensitive, integral membrane protein w/ cytosolic domain that contacts a ryanodine
recetpor on the SR(sarcoplasmic reticiulum)

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37
Q

Ryanodine Receptor is?

A

protein embedded in SR membrane. A true Ca2+

channel: comes in tetrads too

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38
Q

What happens when the AP hits the DHP?

A

It changes conformation.
The cytosolic loop causes the ryanodine to change conformation too, causing an opening of Ca2+ channels of the SR = Ca2+ release into the cell!

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39
Q

What are the steps of AP—>skeletal muscle contraction?

A
  1. AP enters skeletal muscle
  2. AP enters T-tubule & reaches DHP receptor
  3. DHP changes conformation
  4. DHP cytosolic domain causes a Ryanodine conformation change too
  5. Ryanodine opens
  6. Ca2+ pours out of SR into cell
  7. Ca2+ binds to Troponin at TnC
  8. Troponin changes conformation
  9. Tropomyosin is moved out of the way
  10. Myosin can bind to actin
  11. Skeletal muscle contraction
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40
Q

What must be pumped back into the SR?

A

Ca2+

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41
Q

As Ca2+ levels decrease, what can change conformation?

A

troponin

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42
Q

What sits in the groove in troponin blocking myosin from binding?

A

tropomyosin

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43
Q

What happens when myosin isn’t binding to troponin?

A

muscle relaxation

44
Q

How long is the delay from Ca2+ peak to muscle contraction?

A

200ms

45
Q

how do we turn “all-or-none:” AP’s into graded contractions?

A

1) Temporal Summation
2) Organization of Skeletal Muscle
3) Length/tension Relationships

46
Q

What is temporal summation?

A

stair-step effect called treppe, allows stronger contraction

One (1) AP only results in a muscle twitch,
but now those elastic fibers have all the slack
out of them.

47
Q

What leads to tetany?

A

Extremely high level of APs.

48
Q

All the myofibrils that are fired by the same motor neuron =

A

motor unit

49
Q

T or F

All motor units are the same size.

A

F

50
Q

The heavier the weight (force) against the muscle _____

A

the slower the velocity of contraction

51
Q

not many myosin heads can get a hold of the actin filaments =

A

weak contraction

52
Q

White muscle AKA

A

Fast-Twitch Glyoclytic

53
Q

Red muscle AKA

A

Slow-Twitch Oxidative

54
Q

Which type of muscle runs glycolysis for main source of energy?

A

White

55
Q

Which type of muscle is highly vascular?

A

Red

56
Q

Which type of muscle is for endurance?

A

Red

57
Q

Which type of muscle has lots of myoglobin?

A

Red

58
Q

Which type of muscle produces lots of lactic acid?

A

White

59
Q

Where does energy come from when you start exercising quickly?

A

1) Existing ATP
2) High Energy Phosphates
3) As creatine decreases, glycolysis increases
4) Red muscle (aerobic)

60
Q

What is a powerful phosphorus storing molecule important in skeletal muscle?

A

creatine

61
Q

Smooth Muscle has no ______ (part of the sarcomere)

A

Z-lines

62
Q

What does smooth muscle have instead of Z-lines?

A

dense bodies

63
Q

What is smooth muscle’s normal state?

A

contracted

64
Q

What does Ca2+ bind to in smooth muscle?

A

calmodulin (instead of troponin)

65
Q

Active calmodulin turns on what in smooth muscle?

A

myosin light chain kinase

66
Q

What is the purpose of myosin light chain (MLC) Kinase?

A

1) phyosphorylating and activating a myosin chain

2) increasing the myosin’s ATPase activity

67
Q

MLC phosphatase function

A

removing ATP from the myosin

68
Q

What ways allow increased Ca2+, which

increases calmodulin binding?

A

1) AP turns on voltage-sensitive Ca2+ channels
2) Second messengers (IP3) release Ca2+
3) Phospholipase C
4) Ryanodine Channels

69
Q

how does Phospholipase C work?

A

cleaves phospholipid to DAG & IP3

; IP3 diffuses to SR, turns on a receptor at SR, allowing Ca2+ release

70
Q

Three Ways to get rid of Ca2+

A

1) Pump it back across the SR for storage
2) Pump it out of the cell using Ca2+-ATPase
3) Pump it out of cell using cotransport
mechanism; Na+ gradient to couple Ca2+
movement across membrane; but it takes 3 Na+ for each 1 Ca2+. This produces slight depolarization

71
Q

T or F
Repeated stimulus generates the same temporal
summation in Smooth that we saw in Skeletal muscle.

A

T

72
Q

Muscle fibers

definition

A

refers to an entire muscle cell; in neurons, the
axon is elongated, but the whole cell is in skeletal mm.; cells are multinucleated ≈ 35/mm; up to 40mm long; each muscle fibercontains many myofibrils

73
Q

Myofibril

def

A

myofibrils are bundles of myofilaments

74
Q

Sarcoplasmic Reticulum

def

A

smooth ER surrounding myofibril

75
Q

Myofilaments

def

A

make up the myofibril of a muscle fiber/cell; there are 2 kinds and they are always in a 2:1ratio (actin:myosin)

76
Q

Actin

units/stains

A

up to 3000 units per myofibril; stains lightl

77
Q

Myosin

units/stains

A

up to 1500/myofibril; contains crossbridges; stains dark

78
Q

T-tubules

A

invaginations of the cell membrane; important in upcoming pathways (AP travels to here)

79
Q

Sarcomere

A

basic contractile unit of muscle; extends from Z-disc to Z-disc; resting length = 3.2-3.5μm

80
Q

Z-disc

A

the boundaries of a sarcomere; they used to be called “Z-line” but because the myofibril is 3D in
nature, like a long slender cylinder, it wraps around, making a disc; it is the anchor for actin filaments

81
Q

Actin

A

arranged in pairs; filaments are anchored to Z-disc via titin; actin filaments of adjacent sarcomeres
extend toward each other, but do not meet (assuming the muscle is at rest);stains light

82
Q

The light stain creates

A

the I-band

83
Q

the I-band =

A

actin that is not overlayed by myosin = straddles 2 sarcomeres

84
Q

Myosin

A

overlays adjacent actin filaments; contains crossbridges, that hang down and span the gap between actin and myosin; the crossbridge is golf
- club shaped and contains an arm and a head; stains dark

85
Q

The dark stain creates

A

the A-band

86
Q

the A-band =

A

all of myosin + the part of actin overlayed by myosin

87
Q

H-band =

A

portion of myosin not overlaying actin; this band shortens during contraction

88
Q

Alternating sequence of actin/myosin creates

A

a light-dark-light-dark pattern = striped or “striated”

mm.

89
Q

one actin filament =

A

2 F-actins + 2 tropomyosins, and many

troponin triplets

90
Q

F-actin contains

A

myosin binding sites

91
Q

Tropomyosin

A

two of these filaments run along grooves in the F-actin; they cover the myosin binding sites

92
Q

What covers the myosin binding sites?

A

tropomyosin

93
Q

Troponin

A

a triplet of proteins that sit on top of tropomyosin

94
Q

What are the three subunits of troponin?

A
  1. TnCa
  2. TnT
  3. TnI
95
Q

TnCa

has affinity for

A

Ca2+

96
Q

TnT=

A

sits on tropomyosin

97
Q

TnI =

A

intermediate/intercalated sits between troponin triplets and the myosin head

98
Q

Myosin
(thick filament)
contains

A

2 heavy + 2 light chains;

99
Q

Myosin forms crossbridges with the capability of

A

latching onto actin

100
Q

during excitation of the muscle, the myosin heads do what?

A

binds to sites on F-actin because (tropomyosin is moved out of the way) and pull inward, bringing actin molecules closer together; hence, the shortening of the H-band

101
Q

What causes shortening of the H-band?

A

myosin heads pulling the actin closer together

102
Q

The sarcomere contracts to what length during max contraction?

A

3.2-3.5μm down to 2.0-2.2μm

103
Q

The pulling in of actin by the myosin heads is a process known as….

A

ratcheting

104
Q

When a skeletal muscle is excited Ca2+ binds

A

TnCa, causing it to reconfigure

105
Q

When TnCa reconfigures it causes what?

A

tropomyosin to be moved out of the way, exposing the myosin binding sites on the F-actin

Anatomy (22 decks)

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