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A&P Test 3 > 10/11 > Flashcards

10/11 Flashcards

1
Q

what is the length tension relationship?

A

a graph that shows how well a muscle stretches out

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2
Q

What is active force/tension?

A

the amount of force the muscle is generating when we shock the muscle and an AP goes through the muscle

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3
Q

how do you stretch out the muscle without an action potential?
what kind of tension is this?

A

pull on the two ends of the muscle
passive tension

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4
Q

what is active tension shown by on the graph?

A

the upside down V graph

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5
Q

as the overlap section in a sarcomere decrease in size we have

A

an overstretched muscle

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6
Q

what creates more tension? length tension or relaxing tension plus action potential?

A

action potential plus relaxing potential

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7
Q

describe length tension relationship:

A

if you have a muscle stretched to it’s optimal stretch using a metal weight and measure the tension, it should be the same as the metal weight.
If you shock this muscle with an action potential it should contract.

However, if you have a muscle being overstretched using too heavy of a weight and try to shock it with an AP, you probably wouldn’t have much if any contraction because the myosin heads aren’t talking to the actin filaments.

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8
Q

describe load contraction velocity diagram:

A

The velocity of our skeletal muscles shortening is directly and inversely related to the load on our muscles.

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9
Q

if the muscle if lifting a really heavy load, then the velocity of shortening/contraction is

A

slower

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10
Q

increased load = ________ muscle contraction speed

A

decreased

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11
Q

where is load/contraction velocity important?

A

in the heart

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12
Q

what is an example of the heart being effected by the load/contraction velocity

A

if the heart is pumping against a high afterload (BP) it takes the heart longer to eject the blood. This can cause problems in the cardiac cycle. If it’s taking longer to eject blood then it may not have as long to refill.

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13
Q

how can the body control how much force is being produced by the skeletal muscle?

A

recruiting more and more motor units when we need more and more force. (quantal regulations/ summation)

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14
Q

what is quantal summation?

A

The number of motor units activated.
Recruiting larger and larger motor units and portions of the muscle to recruit more and more force

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15
Q

what is temporal summation?

A

force generation in comparison to rate of stimulation in Hz (number of stimuli/second)

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16
Q

At a stimulation frequency of less than 10 or 12hz, we have

A

individual contractions with the muscle being able to relax between stimuli

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17
Q

after a frequency of 10 or 12 hz, what happens?

A

the contractions become additive. We don’t have complete relaxation before the next action

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18
Q

why is a frequency of 10 or 12 hz additive?

A

because calcium is coming out of the SR faster than it can be put into the SR.

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19
Q

we can increase the force of contraction of our muscle until we reach what frequency?

A

40hz

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20
Q

define tetany:

A

when Ca++ receptors are saturated and the muscle is at the peak amount of force that it can generate.

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21
Q

what happens at 40 hz that makes us loose any of the little twitches seen in the measurment?

A

so much calcium inside the cell (outside the SR) that we begin to loose any of the individual twitches. At this point the calcium receptors are saturated and this is the peak of the amount of force that the skeletal muscle can generate.

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22
Q

what do you get when you stimulate the muscle at supramaximal stimulation at a really high rate? (tetany)

A

you get 3 times the force.

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23
Q

define atrophy:

A

skeletal muscle cells get smaller because they lose myofibrils. If this happens for a very long time, skeletal muscle cells can disappear too.

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24
Q

define hypertrophy:

A

having more myofibrils in the skeletal muscle cells. The cells get bigger

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25
Q

what percent of body mass is smooth muscle?

A

10%

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25
Q

if you have really healthy muscles that get a bunch of use all the time, the vascular bed will

A

increase and grow. This adds to you muscle mass.

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25
Q

the downside of anything that increases cell division is that it

A

increases the chance of cancer

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25
Q

what are the first thing that disappears in an atrophy person

A

the internal cylinders (myofibrils)

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25
Q

define hyperplasia:

A

Exercising an awful lot for a very long period of time. (generating new muscle cells)
this happens really slow.

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25
Q

is the heart cell capable of regenerating heart cells?

A

yes but it happens at such a super slow rate that it isn’t much help when you have a massive MI

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26
Q

why is smooth muscle more efficient?

A

cross bridge cycling is slower than in skeletal muscle

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26
Q

people with hope for a future cure after a spinal cord injury that paralyzes them can do what?

A

pay people to come in and stimulate their muscles with electrodes so their muscles don’t atrophy.

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27
Q

smooth muscles is usually _____ to perform a specific task

A

specialized

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28
Q

on a gram to gram basis, smooth muscle is ____ than skeletal muscle

A

stronger

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29
Q

what is the ultra low cycling rate in smooth muscle called?
what is the benefit?

A

latch mechanism

the smooth muscle can maintain a contraction for a long period of time using very minimal amounts of energy

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30
Q

boa constrictor analogy?

A

boa constrictors grab and hold on like smooth muscle?
boa constrictors use skeletal muscle though

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31
Q

what is the ratio of actin and myosin in the sarcomere in the skeletal muscle?

A

actin 2: myosin 1

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31
Q

how does smooth muscle look different than skeletal?

A

the cells are much smaller
they attach to one another via some type of fascia or connective tissue, or sometimes neighboring cells can share walls like in a gap junction
*actin and myosin arrangements are different than in skeletal muscle
*the places where the actin is anchored
*calcium internal stores

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32
Q

what is the ratio of actin to myosin in the sarcomere in the smooth muscle?

A

10-20 actin: 1myosin

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33
Q

the structure that actin is anchored to is called

A

dense bodies

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34
Q

How is the SR in the smooth muscle?

A

not well developed

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34
Q

which has more calcium: smooth or skeletal muscle?

A

skeletal

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35
Q

how does Smooth muscle cells get calcium?

A

leaky channels
VG calcium channels
Ligand gated ion channels

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36
Q

smooth muscle is dependent on _______ calcium

A

outside

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37
Q

if you have a patient with a blood calcium of 0 you aren’t going to have ________

A

the calcium induced calcium release that it does every time the heart beats

probably the more important reason is that: tone in your vessels to create blood pressure

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38
Q

how are smooth muscle cells aranged?

A

cells are functionally linked to one another via gap junctions.

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39
Q

what is another term for visceral smooth muscle?

A

unitary smooth muscle (act as one unit)

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40
Q

where is visceral/unitary muscle founds?

A

in the internal lining of our hollow organs

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41
Q

what goes through gap junctions in the smooth muscle?

A

Na+ and Ca++

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42
Q

what is a multiunit smooth muscle?

A

a smooth muscle without any gap junctions. this allows for much more delicate control of how much the smooth muscle is squeezing.

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43
Q

If a smooth muscle isn’t connected via gap junctions, what are they dependent on to produce an action potential?

A

neurotransmitters

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44
Q

what are examples of multiunit Smooth Muscle?

A

ciliary muscles in the eye
iris muscles in the eye

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45
Q

most the body has what type of smooth muscle?

A

visceral

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46
Q

What is the only hybrid muscle in the body?

A

esophagus

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47
Q

esophagus is a hybrid of what 2 muscles?

A

skeletal muscle and visceral smooth muscle

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48
Q

what are the 3 types of muscles in the body?

A

skeletal
smooth
cardiac

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49
Q

what are the shape of the smooth muscles cells around the blood vessel?

A

diamond or triangular

50
Q

what is layer of connective tissue next to smooth muscle cells that are there for structural support?

A

adventitia

51
Q

what type of cells are 1 layer thick that layer the inside of the circulatory system?

A

endothelial cells

52
Q

the only Blood vessels that are exclusively endothelial cells and does not have smooth muscle is the

A

capillaries

53
Q

what are the 3 layers of the smooth muscle?

A

inner: tunica intima
middle: tunica media
outer: tunica adventitia/externa

54
Q

the smooth muscle layer and endothelial layers talk to each other with

A

gasses
neurotransmitters

55
Q

how is myosin set up in skeletal muscle?

A

in the middle there is a gap because all of the myosin heads are orientated at an angle spreading out from the middle of the molecule
the left and right side are differentiated by the gap and heads pointing in different directions.

56
Q

because of the way that the myosin and actin are oriented in the smooth muscle, smooth muscle can contract__________ shorter

A

a lot

57
Q

if you have a 2 micrometer smooth muscle and you contract it strongly, it can shorten to

vs a big skeletal muscle will only shorten about

A

half it’s length

a couple of centimeters.

58
Q

in a smooth muscle the neurotransmitter is always_____ however depending on where it is it may have a different action

A

ACh

59
Q

the ACh receptors that are expressed in vascular beds typically

A

mediate vascular relaxation

60
Q

what do we need on the inside of the cell to get a contraction?

A

actin
regulatory light chain of the myosin head

61
Q

how is actin different in the smooth muscle than the skeletal muscle?

A

the active sites are always exposed in the smooth muscle

62
Q

in smooth muscle the regulatory light chain is not always _____ it requires

A

turned on
phorphorylization

63
Q

what regulates the activity of the smooth muscle?

A

myosin light chain kinase

64
Q

what is a kinase?

A

an enzyme that phosphorolyates

65
Q

when MLCK is really active, you should have a lot of

A

activity

66
Q

what plays a role in the activity of MLCK?

A

Ca++

67
Q

what does calmodulin do?

A

wraps itself around the MLCK which activates it.

68
Q

what does calmodulin require to change shape?

A

Ca++

69
Q

where does Ca++ come from in the smooth muscle?

A

ECF
Some in the SR

70
Q

What is a really important Ca++ channels in the smooth muscle?

A

VG L type calcium channels (slow)

71
Q

If we want a smooth muscle to relax what has to happen?

A

myosin head ATPase activity has to decrease to do this we have to remove phosphate from the myosin heads.
They can fall off but it takes a long time so we use the enzyme MLCP to speed up this process.

AND/OR

get rid of Ca++ (3 ways)

72
Q

what is one of the signal transduction pathways that can affect the activity level of MLCK?

A

nitrates hitting tissue and increasing cGMP.
cGMP changes the level of kinases.

72
Q

A&P: what is the process to get a contraction of the smooth muscle

A
  • Ca++ comes into cell via leak or L type channels
  • Ca++ binds with calmodulin
  • Calmodulin phosphorylates MLCK.
  • MLCK increases the cycling rate of the myosin head
    = contraction
73
Q

what is myosin light chain phosphatase?

A

the enzyme that dephosphorolates MLCK

73
Q

where can Ca++ exit the smooth muscle sarcoplasm?

A

SR via SERCA pump
plasma membrane Ca++ ATPase pump PMCA
main way: NCX 3 Na+ in 1 Ca++ out
Na+/K+ pump cleans up the extra Na+

74
Q

after protein kinase g is activated by cGMP in the smooth muscle, what does protein kinase G do?

A

it sticks phosphates on things.
More cGMP=more activity of protein kinase G=more MLCK being phosphorylated=reduce the amount of activity=relax

75
Q

A target other than MLCK for protein kinase G is the

A

calcium entry pathways:

phosphorylates calcium channels which closes them = relax

76
Q

where do nitrates come from in the smooth muscle of a healthy person?

A

endothelial cells

77
Q

what is the result of L-arginine being converted by endothelial nitric oxide synthase (eNOS)

A

Nitric Oxide

78
Q

what is a stimulator for endothelial cells to use eNOS to convert L-arginine into NO?

A

signaling compounds/ Neurotransmitters
ACh
bradykinin

78
Q

what happens when ACh binds to the mACh receptor in the endothelial cells?

A

this causes Ca++ release from the endothelial cell’s endoplasmic reticulum.
When Ca++ comes out it talks to calmodulin. Calmodulin changes shape and this increases activity of eNOS. eNOS acts on L-arginine to form NO.

NO freely diffuses outside of the endothelial cell and interacts with targets(soluble guanylyl cyclase) on the vascular smooth muscle cell.

Soluble guanylyl cyclase turns GTP into cGMP.

cGMP can upregulate protein kinase G which phosphorylates targets that inhibit contraction including MLCK and the Ca++ entry channels

79
Q

what is eNOS?

A

endothelial nitric oxide synthase

80
Q

cGMP is kind of unstable and will fall apart on its own, but if it doesn’t fall apart fast enough, what enzyme speeds up this process?

A

phosphodiesterase

80
Q

what is a phosphodiesterase inhibitor example?

A

sildenafil

81
Q

what does a inhibitor of phosphodiesterase do? inhibitor of the inhibitor.

A

prolonging the life of cGMP. increased activity of protein kinase G= relaxed vascular smooth muscle

82
Q

what was sildenafil intended for?

A

pulmonary htn

83
Q

why is pulmonary htn so bad?

A

most people don’t realize they have it until they’ve had it for 30-40 years and by then it is end stage

84
Q

a couple months in the the sildenafil trial, they didn’t like the results so they halted the experiment and asked for the drugs back, but no one gave any of the drugs back. Why?

A

the drug was really good for “other stuff”

85
Q

alpha 1 receptor activation on vascular smooth muscle causes what?

A

contraction of the smooth muscle

86
Q

what is the pathway of an agonist binding to an alpha 1 receptor in the vascular smooth muscle?

A

IP3 mediated vascular smooth muscle constriction

  • Phospholipase C cleaves PIP2 into IP3(inositol triphosphate) and DAG (diacylglycerol)
  • IP3 releases Ca++ from the SR
  • Ca++ binds with calmodulin
  • Calmodulin phosphorylates MLCK.
  • MLCK increases the cycling rate of the myosin head
    = contriction
87
Q

phospholipase 3 cleaves PIP2 into

A

DAG and
IP3

88
Q

IP3 does what in the vascular smooth muscle?

A

increase ca++ in the cell which binds to calmodulin and phosphorylates MLKC which increases the cycling rate of the myosin head.

89
Q

what does DAG do in the vascular smooth muscle?

A

It increases the activity of protein kinase C which (skip a few steps) increases the vascular constriction of the vascular smooth muscle.

90
Q

serotonin is also something that can constrict smooth muscle vasculature via the same pathway as

A

alpha one agonist in the smooth muscular vasculature

91
Q

what is weird about serotonin?

A

only neurotransmitter than can constrict brain blood vessels

92
Q

Why would you not want Norepinephrine and epi to be released and constrict blood Vessels in the brain?

A

if you’re trying to run from a tiger and the Sympathetic nervous system is stimulated, you wouldn’t want your vessels to be constricted or you wouldn’t be able to run very well.

93
Q

why are SSRI good for headaches in some people?

A

increases the vascular tone which decreases the amount of pressure in the head that creates a headache

94
Q

Smooth muscle doesn’t require an action potential because there is

A

enough leaky Ca++ channels that the amount of Ca++ coming into the cell can cause the muscles to start tensing up but it isn’t enough to cause an action potential so they are independent of an action potential.

95
Q

Ca++ isn’t necessarily required for contraction of smooth muscle, there are some oddball instances where we can have some

A

intercellular signaling machinery working with the phosphorylation levels of the myosin head to generate a contraction

96
Q

Action potentials in smooth muscle is sometimes appear

A

periodic
as a single short lived spike
as a long drawn out action potential

97
Q

the long action potential is probably d/t

A

L-Type Ca++ channels

98
Q

what is the oscillation of smooth muscle?

A

pacemaker activity. when the membrane potential is just changing all on its own, going up and down in a rhythm.

99
Q

smooth muscle in our small intestine function in what way?

A

oscillating, generating pacemaker activity that generates an action potential every 10-20 seconds. This helps to mix the food in our small intestine as well as pushing it forward through the system.

100
Q

How is the cardiac muscle set up?

A

similar sarcomere to skeletal muscle

100
Q

stomach cramps come and go, why?

A

pacemaker activity

101
Q

how does Ca++ get into the heart cell?

A

L-type ca++ channels (slow)
T-type Ca++ channels (faster)

102
Q

what is the ratio of calcium coming into the heart cells from the SR and the ECF?

A

1:4 ratio
80% from SR
20% from ECF

102
Q

majority of the Ca++ that comes into the heart cells is from the

A

internal stores of the heart cell
SR

103
Q

what do you need to release Ca++ from the sr in the heart?

A

ECF ca++ (trigger ca++)
calcium induced calcium release

104
Q

what is the trigger for L and T type ca++ to open?

A

Action Potential dependent on Na+ flooding in through VG Na+ channels

“Na+ induced Action Potential” starts off the Action potential in the heart. it then turns into a Ca++ dependent action potential by T type and then L type Ca++ channels opening

105
Q

in the heart we have very _____ t-tubules

A

large

106
Q

a lot of the Ca++ that comes into the heart is parked near the

A

t-tubules
this is where most of the ECF Ca++ comes into the cell

107
Q

How is Ca++ removed from the Heart cell?

A

SERCA pump (80%)
NCX 3Na+ in 1 Ca++ out
Plasma Membrane Ca++ ATPase PMCA

108
Q

what does PMCA stand for?

A

Plasma Membrane calcium ATPase

109
Q

what is calsequestrin?

A

found in the SR of all muscle cell.

sequestering protein that takes Ca++ out of the circulation and binds to it in the SR

110
Q

what helps the SERCA pump?

A

Calsequestrin.
It concentrates a lot of calcium in the SR. It helps us hold a lot more Ca++ in the SR

111
Q

what is phospholamban

why is it used?

A

inhibitor of the SERCA pump only found in cardiac muscle

it allows Ca++ to stick around in the sarcoplasm for longer period of time = longer contraction of the heart

111
Q

SR in the heart vs smooth muscle and skeletal muscle

A

heart has a modulator of the SERCA called the phospholamban- inhibitor of the SERCA pump

112
Q

what does a phospholamban inhibitor do?

A

inhibits the inhibitor and increases activity of the SERCA pump

Ca++ tucked back into the SR faster=shorter length of contraction

opportunity to reset the cell faster

this is what speeds up the heart rate. Drug target.

113
Q

what type of signaling compounds do heart cells respond to?

A

ACh
adrenergic receptors

114
Q

the more catecholamine activity the heart

A

faster the HR and strong the contractions

115
Q

the more cholinergic the heart

A

slower the HR and weaker the contraction

116
Q

cAMP dependent relationship beta activity

A

stimulation of adenylyl cyclase (similar to guanylyl cyclase)

ATP to cAMP
in the heart cAMP has effects on the activity of protein kinases
when PKA activity increases you have stronger strength of contraction

117
Q

higher beta activity

A

higher PKA activity

118
Q

mACh activation in the heart does what?

A

adenylyl cyclase slows down
decreases cAMP
reduces PKA
relaxes

119
Q

most heart cells are programed to talk to both

A

ACh and beta agonists

120
Q

Where in the heart does mACh agonist open potassium channels and slow the HR?

A

nodal conduction tissue where the heart pacemakers are

121
Q

what produces a strong force, quantal or temporal summation?

A

temporal (3X)

122
Q

What do motor neurons do to increase force of contraction?

A

sending waves of action potentials down the motor neuron in a way that it can’t reset between the different the contractions

123
Q

dense bodies can be shared between neighboring muscle cells. This acts as an

A

anchor to provide force

124
Q

how are the myosin set up in the smooth muscle sarcomere?

A

there is no middle gap, and the myosin heads are arranged in an alternating pattern

125
Q

when stimulated, ACh receptors in the small intestine

A

contract

A&P Test 3 (8 decks)

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