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Physiology Block 5 > Muscle (smooth/cardiac) > Flashcards

Muscle (smooth/cardiac) Flashcards

1
Q

What two ways can a muscle contract

A
  • isotonically

- isometrically

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2
Q

Force generated is sufficient to move load

A

Isotonic (same strength)

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3
Q

What can determine the force-velocity relationship?

A

Isotonic contract

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4
Q

Force generated is insufficient to move weight placed on muscle (afterload)

A

Isometric contraction (same length)

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5
Q

What can determine the length-tension relationship?

A

Isometric contraction (same length)

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6
Q

Example of isometric contraction

A

Pressing in door frame

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7
Q

Afterload is above maximal force and preload is changed

A

Length-tension relationship

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8
Q

What is measured in the length tension relationship?

A

Active force

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9
Q

What does the length tension relationship show

A

That stretching a muscle (to a point) can increase force generated

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10
Q

Why does stretching a muscle increase force generated?

A

Stretching of a muscle allows cross bridges to form more easily because of betters alignment of actin and myosin fibers

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11
Q

How is skeletal muscle already set in terms of preload

A

It is set close to the optimal preload (length)

-bc fixed at both ends mostly

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12
Q

What happens when you overstretch a muscle?

A

Lose force generation

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13
Q

Preload is set, afterload is changed

A

Isotonic and force-velocity relationship

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14
Q

Muscles and afterload

A

Muscle will develop as much force as is needed to lift specific load

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15
Q

What does the isotonic and force velocity relationship determine

A

As load increases, the speed at which you lift decreases

  • more cross bridges need to form
  • slower contraction gives more cross bridges more time to form
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16
Q

Given Jame’s diagnosis of Duchenne muscular dystrophy, what would you except if someone experimentally excited the motor neuron to his bicep

A

Normal AP propagation, because the dystrophy is in the muscle, not the nerve

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17
Q

What is smooth muscle controlled by

A

Endocrine and ANS

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18
Q

Smooth muscle

A
  • no conscious control
  • can operate effectively when greatly stretched
  • fatigue resistant
  • generate resting tone-stay partially contracted
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19
Q

What are the two types of smooth muscle units

A

Single unit

Multi unit

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20
Q

Single unit smooth muscle cells

A
  • GI, bladder, uterus
  • cells linked by gap junctions
  • littler innervation
  • some can generate own AP
  • all contract together to form own rhythm to expel things
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21
Q

Multi unit smooth muscle

A
  • Iris, vas deferens
  • each cell has its own innervation
  • function as distinct muscle cells (like skeletal)
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22
Q

Smooth muscle appearance compared to skeletal muscle

A

Smaller than skeletal muscle and spindle shaped, no sarcomeres

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23
Q

How are actin and myosin held in place in smooth muscle

A

With dense bodies, intermediate filaments

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24
Q

Does smooth muscle have troponin

A

No

Has calponin and caldesmon which are similar

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25
Q

What kind of connections do smooth muscle have

A

Mechanical, can have gap junctions

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26
Q

Do smooth muscle have T tubules

A

No, by they have caveolae whihc function similarly

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27
Q

Does smooth muscle have SERCA or SR

A

Yes, but they don’t have a triad configuration

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28
Q

E-C coupling in smooth muscle

A
  • extracellular calcium enters cytoplasm
  • this releases Ca2+ from SR, whihc binds to calmodulin
  • calmodulin activates myosin-light chain kinase (MLCK), which controls cross bridge cycling
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29
Q

`how does calcium enter the cytoplasm of the smooth muscle

A

-depolarization, ligand gated channels, or 2nd messenger gated channels

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30
Q

What kind of calcium release is involved in smooth muscle

A

Calcium induced calcium release

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31
Q

What does myosin-light chan kinase (MLCK) do

A

Phosphorylates myosin light chain

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32
Q

Where does the calcium come from for smooth muscle

A

Some in the SR

Some from outside

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33
Q

Where does the calcium come from for skeletal muscle

A

ALL Ca2+ from SR

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34
Q

Calcium entry through the 2nd messenger gated channels

A
  • hormones of NT activate Gq receptors, which make IP3
  • directly open IP3 gate channels on SR
  • IP3 dependent Ca2+ opens other Ca2+ channels
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35
Q

Calcium enters into smooth muscle via depolarization

A
  • spread through gap junctions, opens VGCC on cell surface

- this calcium can open RyR channels on the SR to increase calcium more

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36
Q

Calcium enters into smooth muscle via ligand gated channels

A
  • hormones and NT open channels and let calcium in

- this calcium can open RyR channels on SR, can also open VGCCs

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37
Q

Cross bridge cycling in smooth muscle

A
  • calcium binds/activates calmodulin
  • calmoduling activates MLCK
  • MLCK will phosphorylate myosin whihc increases ATPase activity
  • cross bridge cycling proceeded as in skeletal muscle as long as myosin is phosphorylated
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38
Q

What is myosin de phosphorylates by in smooth muscle

A

Myosin phosphatase

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39
Q

Cross bridging in smooth muscle simplified

A

Ca2+-calmodulin-MLCK-myosin phosphorylated

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40
Q

How does smooth muscle relax?

A

Dephosphorylation of myosin by myosin phosphatase

  • occurs when MLCK is no longer active, requires low ICF Ca2+
  • reduces ATPase activity and actin affinity
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41
Q

How does smooth muscle contract?

A

Either physically or tonically

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42
Q

Phasic contractions in smooth muscle

A

Are like skeletal muscle

-single spike of Ca2+, single contraction, and relaxation

43
Q

Tonic contractions in smooth muscle

A
  • signed Ca2+ spike but maintinaed force
  • possible because of the ‘latch state” of smooth muscle myosin
  • low metabolic demand
44
Q

What is latch state in smooth muscle

A
  • for myosin to let go it has to bind ATP
  • unphosphorylatd mysoin has low affinity for ATP
  • if it dephosphorylates while still attached to actin, it is slow to release because it is unlikely to bind ATP
45
Q

What does latch state of smooth muscle allow for

A

Retina muscle tone to be generated at a much lower metabolic cost

46
Q

Why is smooth muscle not striated

A

No sarcomere

47
Q

Is the cycling of cross bridges slower or faster in smooth muscle compared to striated?

A

MUCH slower

48
Q

Length of contractions in smooth compared to striated

A

Longer

49
Q

What type of muscle can “latch”

A

Smooth

50
Q

What is the metabolic demand on smooth muscle compared to striated

A

Lower

51
Q

What causes the release of ca2+ in smooth muscle

A

Extracellular calcium

52
Q

What kind of junctions do smooth muscle have

A

Gap

53
Q

What is smooth muscle activated by

A

Circulating hormones or NT

54
Q

Can you overstretched smooth muscle?

A

Not really because they don’t have sarcomeres

55
Q

Length tension relationship of smooth muscle

A

Given time to accommodate, it will generate maximum force at any length
-same maximal force at all lengths because always have myosin/actin lineup

56
Q

Force velocity relationship of smooth muscle

A

Increased load increases Ca2+ flux, increases MLCK activation, so it occurs stronger and faster

  • velocity of contraction increases with % of myosin phosphorylated
  • % phosphorylated increases with load
57
Q

What does force velocity relationship of smooth muscle depend on

A

Phosphorylation of calcium

58
Q

Muscles that need ECF Ca2+

A
  • cardiac (always) and smooth (depends)
  • hypercalcemia (stronger)
  • hypocalcemia (weaker)
59
Q

How does ECF calcium alter cell excitability (AP)

A

By changing threshold of Na(v)

-this is one instance where presence of Na will affect depolarization

60
Q

Hypercalcemia in smooth muscle and cardiac muscle

A

Threshold more negative

  • less excitable
  • Ca2+ likes to keep Na+ channels closed
  • contractions strong, but harder to have one
61
Q

Hypocalcemia in smooth and cardiac muscle

A

Threshold less negative

  • more excitable
  • easy for muscle to contract but it is a weaker contraction
  • test for it by flicking face and seeing if the muscles twitch
62
Q

What would you expect to occur to strength of skeletal muscle contraction in the setting of hypercalcemia

A

Nothing

63
Q

What would you expect to occur to strength of smooth muscle contraction in the setting of hypercalcemia

A

Stronger

64
Q

Shape of cardiac muscle cells

A

Short, Y-shaped, chunky cell

65
Q

What is responsible for the fact that the cardiac muscle contracts as one muscle?

A

Gap junctions at intercalated disks

-intrinsic muscle

66
Q

Are APs longer or shorter in cardiac muscle

A

Longer

67
Q

T-tubules in cardiac muscle

A

Fewer, but larger

68
Q

Metabolism of cardiac cells

A

Fatigue resistance, more mitochondria, highly metabolic

69
Q

Proximity of DHPR and RyR in cardiac muscle

A

Not close, must have extracellular calcium

70
Q

Sarcolemmal calcium pumps in cardiac muscle

A

There are more of them (NCX and SERCA)

71
Q

Resting membrane potential of cardiac muscle cells

A

Slightly lower

-there’s more K+ channels here, that’s why

72
Q

How many phases are in a cardiac muscle action potential

A

4

73
Q

Phase 4 of cardiac AP

A

RMP same as other excitable cells

-K+ leak channels (iK1)

74
Q

Phase 0 of cardiac muscle AP

A 
Upstroke
Na(v) channels open
75
Q

Phase 1 of cardiac muscle AP

A

Early repolarization

K+ channels i(t0)

76
Q

Phase 2 of cardiac muscle AP

***

A

Plateau

  • L-type Ca2+ channels and SR dump
  • really long because of all of the calcium that moves
  • reduces arrhythmia and tetanus
  • needs to fully contract, and fully relax, not go into tetanus, this is why is needs to be this long
77
Q

Phase 3 of cardiac muscle AP

A

Late repolarization

-K+ channels i(K)

78
Q

Absolute refractory period of cardiac muscle (ARP)

A

Much longer

  • this prevents tetany
  • calcium open for a very long time
  • ECF ca2+ is required to open RyR channels on SR, occurs during phase 1 and 2
79
Q

Effective refractory period of cardiac muscle AP

A
  • no conducted potential can generate AP (AP will fire nut not go anywhere)
  • can get AP but not from normal source (such as electrodes)
80
Q

Why do doctors want to lengthen the cardiac effective refractory period?

A

If you lengthen it, it treats arrhythmia. Do it by using K+ channel blockers

81
Q

Relative refractory period (RRP) in cardiac AP

A

AP can fire if a greater than normal stimulus is provided

-will have shortened plateau

82
Q

Supra normal period (SNP) in cardiac AP

A

Cell is more excitable than normal. Has yet to reach full RMP

83
Q

Cardiac muscle mechanical

A

-contains sarcomeres and cross bridge cycling occurs as in skeletal muscle

84
Q

Force generation in cardiac muscle compared to skeletal

A

Very slow

  • different mysoin isoform, lower ATPase activity
  • cardiac muscle needs to fully contract every time (100%), skeletal muscle has to be repeatedly stimulated
85
Q

How do you increase force generation in cardiac muscle

A

Increasing calcium flow and sensitivity

86
Q

What relationship is muy importante in cardiac muscle

A

Length tension relationship

87
Q

Length tension relationship in cardiac muscle

A

Resting length is much shorter than optical length

  • heart can generate more force when preload is increased
  • it can stretch more than normal which causes much more force
88
Q

What is the length-tension relationship in cardia muscle called

A

Frank starling law

89
Q

Frank starling law

A

Length tension relationship in cardiac muscle

-heart can generate more force when preload is increased

90
Q

What are cardiac pacemakers

A

Specialized cells in heart

  • electrical conduction system
  • SA node is primary
  • no SR
91
Q

RMP in cardiac pacemakers

A

Have an unstable RMP, the line is slanted, not straight

92
Q

How do cardiac pacemakers depolarize

A

At a set rate

93
Q

What is the basis of heart rate

A

Cardiac pacemakers

94
Q

What phases of cardiac AP does the pacemakers have

A

4,0,3

95
Q

Phase 4 AP in cardiac pacemakers

A
  • unstable RMP
  • i(K) channels slowly close, depolarization
  • I(h) (funny channels, i(f)) channels open, Na+ channel, depolarize
  • I(ca)T opens, more depolarization
96
Q

What is the funny channel

A

A Na+ channel on the cardiac pacemaker that opens during phase 4 AP. Unstable RMP because this channel opens up

97
Q

What is the funny channel activated by

A

Repolarization

98
Q

Phase 0 cardiac pacemakers AP

A

Firing of AP

  • I(ca)L opens
  • depolarize
99
Q

Phase 3 of AP in cardiac pacemakers

A

Repolarization

-i(K) channels open

100
Q

PNS synapses of SA node

A
  • M2 receptors (Gi)
  • increase i(K) flow (hyperpolarize)
  • decrease I(h) flow (funny) reduce slope, takes longer to depolarize
  • decrease Ca2+ flow (harder to depolarize)
101
Q

What is the total effect of PNS synapses of SA node

A

Make slow of phase 4 flatter

102
Q

SNS synapses of SA node

A

Opposite PNS

  • B1 receptors (Gs)
  • increase I(h) flow (steeper slope) funny
  • increase Ca2+ flow
103
Q

What would you expect to happen to SA node depolarization rate (Phase 4) during hypernatremia?

A

Faster
-funny current open, allows Na+ in

Everywhere, Na+ doesn’t effect RMP

Physiology Block 5 (8 decks)

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