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Physiology 2 > KIN 406 > Flashcards

KIN 406 Flashcards

1
Q

4 functions of muscle?

A

Generate force, fuel storage, temperature regulation, force absorber

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2
Q

3 fuels in muscle

A

Glycogen, fat (lipid droplets), and protein

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3
Q

Why is it important to study mechanisms?

A

Better outcomes because specific things can be treated and less negative effects because specific things are treated

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4
Q

Is muscle a homogenous tissue?

A

NO. It is heterogeneous. No 2 fibres are the same because they all differ in neural input, MHC form, enzymes, proteins, etc.

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5
Q

Contractile proteins?

A

Actin and myosin

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6
Q

Regulatory proteins?

A

Troponin and Tropomyosin

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7
Q

Role of SR?

A

storage, release (RyR receptors), and uptake (SERCA) of Ca2+

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8
Q

Responsible for weak to strong binding?

A

Release of Pi

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9
Q

Responsible for power stroke?

A

Release of ADP

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10
Q

Responsible for detachment of myosin from actin?

A

ATP binding

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11
Q

Why are muscle cells multi-nucleated?

A

Ability to regenerate and ability to adapt and be eliminated to physciological and environmental stimuli

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12
Q

Muscle cell = ?

A

Muscle fibre or myocyte

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13
Q

Cell membrane = plasma membrane = ?

A

Sarcolemma

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14
Q

Cytoplasm = ?

A

Sarcoplasm

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15
Q

What does the sarcoplasm contain?

A

All portions of the cell that are not membrane or nucleus

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16
Q

What does the cytosol contain?

A

The fluid portion of the cell (does NOT contain cell membrane, organelles, or nucleus)

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17
Q

Endoplasmic reticulum = ?

A

Sarcoplasmic reticulum

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18
Q

Organization of a skeletal muscle?

A

Muscle > fasicles > fibres > myofibrils > thick/thin filaments > sarcomeres

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19
Q

Triad of the reticulum?

A

2 terminal cisternae and 1 transverse tubule

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20
Q

Cytoskeleton proteins?

A

Titin (elastic and helps arrange thick filaments) and Nebulim (not elastic, helps arrange thin filaments)

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21
Q

Components of myosin molecule?

A

2 heads each with 1 heavy chain and 2 light chains (alkali and phosphorylable)

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22
Q

Why does muscle damage cause a significant loss in force?

A

Shape of sarcomere is alters = less cross bridges can form = less force production

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23
Q

What causes the contraction and relaxation of a muscle?

A

Changing the voltage across the membrane via sodium and potassium

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24
Q

What is the role of the Na+/K+ ATPase?

A

Controls cell volume and maintains the Na+ /K+ gradient across the cell membrane

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25
Q

What is the main cause of relaxation in muscle?

A

The neural signal stops, so the DHPR are no longer tripping of the Ry receptors on the SR, so calcium release ceases, and SERCA uptakes calcium, causing it do dissociate from TN-C, allowing TM to slide back into its blocking position, thus stopping muscle contraction

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26
Q

Two parts of the SR?

A

Terminal cisternae and the longitudincal SR

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27
Q

Role of the terminal cisternae?

A

Forms junction with T-tubule called triad membrane, contains Ca2+ release channel, most Ca2+ is bound to calsequestrin, major function is Ca2+ release

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28
Q

What is the role of the longitudinal SR?

A

Contain the CA2+ ATPase pumps (SERCA), major function is Ca2+ uptake

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29
Q

Primary factor that differentiates muscle or muscle fibre types?

A

The rate/speed of contraction

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30
Q

What determines Vmax, and therefore fibre type?

A

Myosin heavy chain

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31
Q

Myosin heavy chain forms from slowest to fastest?

A

Type I < Type IIa < Type IIx(d) < Type IIB

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32
Q

Do humans have Type IIb fibres?

A

NOOOO, only rodents

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33
Q

Why does a Type II fibre have a shorter twitch than a Type I fibre?

A

It has much faster calcium release (RyR-1 Fast), and much faster Ca2+ uptake due to more SERCA and a faster isoform of SERCA (SERCA 1)

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34
Q

Do humans have just one kind of muscle fibre?

A

NO, need the 50-50 split so we can perform a variety of activities

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35
Q

Why is the epxression of fibre type different throughout a muscle?

A

Because it is multinucleated, so there is different expression of myosin heavy chains throughout the muscle

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36
Q

Other factors, aside from MHC, that can differentiate muscles?

A

Fatigue characteristics, metabolic characteristics, and morphological characteristics

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37
Q

Fibres that fatigue the fastest? The slowest?

A

Type II is fastest. Type I is slowest.

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38
Q

How are the metabolic characteristics of a muscle measured?

A

Measure enzyme activities of representative pathways

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39
Q

Fast-glycolytic fibres? Fast oxidative-glycolytic_ Slow-oxidative?

A

Type IIx/b, Typpe IIa, Type I

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40
Q

Fibre type with a bigger diameter?

A

Type II

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41
Q

Fibre type with more SR?

A

Type II

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42
Q

Fibre type with more mitochondria?

A

Type I

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43
Q

Smallest amount of a muscle that can be activated?

A

Motor unit

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44
Q

Ways to increase force in a muscle?

A

recruit more motor units and increase the frequency of firing to the motor units to have summation

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45
Q

What is a motor unit?

A

The motor neuron and the muscle fibres it innervates

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46
Q

Why is the loss of MNs in a diseased state a problem?

A

Fibres are re-innervated by other MN, causing an increase in the size of the motor unit, which decreases the control of force

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47
Q

The fewer the number of fibres per motor unit, the…?

A

Finer the control of force because there are more steps involved until summation is reached

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48
Q

What type of motor units are recruited first?

A

Type I motor units are recruited first because they won’t fatigue as fast

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49
Q

What are the differences in force in a motor unit attributed to?

A

The differences in the number of fibres per motor unit

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50
Q

What type of motor unit produces the most force?

A

Type IIB FF

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51
Q

Fibre type transformation sequence?

A

IIb IIbx IIx IIa IIc Ic I

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52
Q

Most oxidative fibre in rats? In humans?

A

IIa in rats, and I in humans

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53
Q

3 energy delivry systems in muscle?

A

HEPT, glycolysis, and oxidative phosphorylation

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54
Q

HEPT?

A

Transfer of a phosphate group to ADP to make ATP, doesn’t involve O2, VERY fast (high power), but can only last approx. 10 s (low capacity)

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55
Q

Glycolysis?

A

Degradation of glucose or glycogen (glycogenolysis), does not involve O2, 11-12 reactions in cytosol

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56
Q

Power of anaerobic glycolysis?

A

Medium/high power because the large amount of ATP that be generated per unit time, due to hte high activity of enzymes in this pathway

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57
Q

Why can’t you rely heavily on glycolysis for a long time?

A
  1. availability of substrates (i/e/ muscle glycogen) 2. Build up of lactic acid (H+ causes acidosis)
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58
Q

Capacity of glycolysis for producing ATP?

A

Moderate capacity

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59
Q

Enzyme that converts glyocgen to G-1-P?

A

phosphorylase

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60
Q

Enzyme that takes glucose to G-1-P?

A

hexokinase

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61
Q

Energy investment for glycogen? Glucose?

A

1 ATP, 2 ATP

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62
Q

Capacity of aerobic metabolism?

A

Larage capacity because of large fa and glycogen stores (liver and muscle)

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63
Q

Power of aerobic metabolism?

A

Low-moderate power because the rate of ATP regeneration is fairly low and is limited by O2

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64
Q

Oxidative phosphorylation?

A

The formation of ATP from ADP and Pi in association with electron transfer from fuel substrates to coenzymes to oxygen

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65
Q

Krebs cycle?

A

completes the oxidation of substrates and produces NADH and FADH2 to enter the ETC

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66
Q

ETC?

A

oxidative phosphorylation, electrons removed from NADH and FADH2 are passed along a series of carriers to produce ATP, H+ from NADH and FADH2 are accepted by O2 to form water.

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67
Q

3 stages of oxidative phosphorylation?

A
  1. formation of acetyl-CoA from CHO (pyruvate), fats (fatty acids), or amino acids (proteins) 2. oxidation of acetly groups in Krebs cycle to form NADH and FADH2 3. Oxidation of NADH and FADH2 in ETC to form ATP from ADP and Pi
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68
Q

Skeletal muscle is derived from what type of cells, and where are they found?

A

Derived from myogenic stem cells found in the embryonic mesoderm

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69
Q

At what point in gestation do mesodermal stem cells migrate to their appropriate site and differentiate into myoblasts?

A

At 6 weeks gestation

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70
Q

What do the large majority of myoblasts become?

A

They aggregate and fuse to form multinucleated myotubes (primary myotube) The myoblast plasma membranes fuse, and form a central chain of nuclei.

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71
Q

What does some myoblasts remain as?

A

2-5% remain as a single cell with mitotic potential…aka satellite cells found in fully differentiated muscles

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72
Q

At what point in muscle development do cells lose their mitotic potential?

A

After myoblasts are formed

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73
Q

Why does it make sense that muscle cells cannot undergo mitotsis once myoblasts are formed?

A

Muscle fibres are very long, making it difficult from an engineering standpoint to allow for replication. Also, if the cells were actively dividing, it would decreae force production because the hexagonal shape of the sarcomeres needed for contraction would be altered.

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74
Q

What type of myotubes can independently form a muscle fibre?

A

Primary

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75
Q

How do secondary myotubes become their own fibres?

A

The additional myoblasts aggregate on the primary myotube and form a secondary myotube.These secondary myotubes will also become independent fibres with their own basement membrane. Early during development, though, both the primary and secondary myotubes are contained within the same basement membrane.

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76
Q

Primary myotubes are suggested to form what type of muscle?

A

Slow muscle (soleus)

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77
Q

Secondary myotubes are suggested to form what type of muscle>

A

Fast (EDL)

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78
Q

In what week of gestation in humans are most muscle groups well defined?

A

7-9th week

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79
Q

At what time of gestation does the synthesis of contractile protein (actin and myosin) begin and the first signs of cross-striation appear?

A

7th-9th week. Up until then there was no contractile proteins because there was no contraction or innervation…myogenic stem cells and myoblasts have no actin or myosin.

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80
Q

How does the transition from myoblast to myotube occur>

A

Upregulation in the epressions of important muscle specific transcription facots (Myf genes,,,Myf-5, MyoD, myogenin)

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81
Q

What are the Myf genes, what do they do?

A

Myogenic factor 5 (Myf-5), myogenic determination (myoD), and myogenin. Promote myoblast proliferation and differentiation.

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82
Q

If Myf genes are overexpressed in non-myogenic cells (e.g. fibroblasts) whay happens?

A

The cells will form muscle

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83
Q

Once myotubes are formed, proliferation and differentiation are blocked by?

A

Myostatin and inhibitor of differentiation proteins (Id)

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84
Q

How does myostatin and Id protein primarily work?

A

Through the inhibition of MyoD

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85
Q

What doe MyoD/Myf-5 mice lack, but what do they have?

A

They lack skeletal muscle development (no actin, myosin, desmin, etc), but they do still develop smooth muscle.

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86
Q

From what week of gestation on do myofibrils proliferate leading to hypertrophy of the muscle fibre?

A

11 weeks onward. At his stage, there are increases in girth, but also increases in length by the addition of sarcomeres at each end

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87
Q

At what week of gesetation are all myotubes enclosed in the basement membrane?

A

16 weeks

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88
Q

At what weeks of gestation do all the nuclei of hte myotubes (primary and secondary) move to the periphery of the fiber?

A

18-23 weeks

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89
Q

At what week of gestation are muscle fibres in each human set?

A

24 weeks

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90
Q

What form of myosin to embryonic and fetuses express?

A

Type IIC

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91
Q

What type of MHC do Type IIC fibres express>

A

Both Type I and Type IIa, which will allow the fibres to develop into Type I or Type II muscle

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92
Q

WHen is the fetal form of myosin replaced by the adult myosin?

A

Once the muscle starts contracting, following innervation

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93
Q

Approximate number of nuclei per mm of muscle length?

A

100-200 nuclei

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94
Q

The number of nuclei is positively correlated to what?

A

Fiber size…larger fibres have more nuclei and smaller fibres have less nuclei

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95
Q

The greater the number of nuclei, the greater the…

A

protein production

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96
Q

Change in nuclei number affects…

A

fibre size. Lose nuclei = becomes smaller. Gain nuclei = become bigger.

97
Q

Where do satellite cells lie?

A

Between the plasma and basement membrane

98
Q

What does each satellite cell contain?

A

A single nucleus with a thin layer of cytoplasm

99
Q

What do satellite cells provide?

A

A source of new genetic material (nucleus) that is required fro muscle growth, hypertrophy, and repair

100
Q

When activated, what do satellite cells do?

A

Divide and fuse to replace or add nuclei to the muscle fibre in response to damage or adaptation

101
Q

Where do muscle fibre nuclei reside?

A

Just below the plasma membrane

102
Q

At what weeks of gestation do motor neurons start innervating the fiber?

A

10-11 weeks

103
Q

Prior to innervation, Ach receptors are distributed across the muscle fibre, what happens after the nerve makes contact and electrical activity is generated?

A

Ach receptors aggregate to the region of the NMJ. As the muscle matures, extrajunctional Ach receptors decrease while junctional receptors increase

104
Q

When does the majority of muscle growth occur?

A

During childhood and adolescence

105
Q

By how much does the cross-sectional area of each fiber increase from newborn to adult?

A

10-fold….HYPERTROPHY, not hyperplasia

106
Q

In general, when is max adult muscle CSA reached?

A

Shortly after puberty, but this can be affected by training. At this point in life, muscle makes up 40-50% of body weight (slightly lower in females). Males have a greater CSA than females.

107
Q

What is often used as a functional measure of muscle development?

A

Strength…sometimes difficult given that during development there are large improvements in both strength and coordination/skill

108
Q

Why is there a more rapid increase in muscle strength at the onset of puberty?

A

Testosterone!! Very anabolic.

109
Q

Prior to puberty, muscles of the lower limb grow in proportion to…

A

lower limb growth…this makes sense because lower limbs bear the weight of the body. Muscle growth of the upper body grows less rapidly.

110
Q

At puberty, skeletal muscle grows faster than…

A

the change in body weight

111
Q

In biology, what is aging referred to as?

A

An accumulation of deleterious changes in cells/tissues that occur which increase the risk of disease and health

112
Q

What does aging ultimately result in?

A

An alteration in the optimal structure and function of various tissues and systems. Eventually, negative changes to the system will result in death.

113
Q

At what point in gestation are no new fibres added?

A

24 weeks…only new myofibrils WITHIN each fibre are added

114
Q

An important transcription factor involved in promoting myoblast differentiation?

A

MyoD

115
Q

How much muscle wasting occurs in healthy adults between 25-40? How much occurs in healthy adults age 40-90?

A

<10% and up to 50% (approx. a 1-2% loss per year at age 50)

116
Q

What two factors accelerate skeletal muscle aging and loss in young adults?

A

Disease and inactivity

117
Q

At what age does sarcopenia start?

A

Age 30

118
Q

What is sarcopenia, and what does it mean?

A

It is the age related loss of muscle mass, and comes from Greek meaning “poverty of flesh”

119
Q

What are some of the consequences brought on by the morphological changes associated with aging/sarcopenia?

A

Loss of strength, coordination, mobility, which ultimately leads to a loss of independence and health, social, and economic burdens

120
Q

Conservative estimates state that what percentage of the US population over the age of 65 have some degree of sarcopenia?

A

About 45% (this doesn’t include the people from 40-65 that are also experiencing sarcopenia, just to a lesser degree)

121
Q

What happens to the metabolic rate due to loss of muscle mass, and what are the implications of this?

A

It causes a decrease in metabolic rate, which increases the risk of obesity and its associtated diseases, including Type II diabetes, hypertension, and heart failure.

122
Q

Is there muscle atrophy in animals, and why is this important?

A

Yes. Important because it suggests it’s a biologically conserved process, so although the environment contributes to the problem, sarcopenia is a part of normal, healthy aging.

123
Q

3 general aspects of sarcopenia from a muscle level

A
  1. Muscle fibre atrophy in both fibre types 2. Loss of muscle fibres 3. Slowing of contractile properties of the muscle
124
Q

Muscle fibre atrophy is greater in what type of fibre?

A

Type II

125
Q

Why is muscle fibre atrophy initially difficult to see?

A

Because CSA doesn’t change due to an increase in connective tissue and fat…but the contractile CSA decreases

126
Q

What type of muscle fibre is lost more?

A

Greater loss of Type II fibres compared to Type I

127
Q

What are the factors that cause the slowing of contractile properties of muscle?

A
  1. Decreased number of Type II fibres 2. Some fibre type switching (Type II –> Type I) 3. Loss of alpha-1 MN that supply the Type II fibres 4. Excitation-contraction coupling is slower for a give myosin isoform
128
Q

3 reasons why it is advantageous to lose Type II fibres versus Type I?

A
  1. We would fatigue really fast and not be able to go about out daily functions 2. We would lose our ability to gradiate force because Type II motor units have more fibres per unit, so can’t control increase in force as well. 3. Type II fibres need a lot of neural input to be activated, and some of them we have to be trained to activate. Type I fibres, though, are already easy to activate because we use them everyday.
129
Q

What is the major consequence of skeletal muscle atrophy and fibre loss with aging?

A

Increased proportion of Type I compared to Type II

130
Q

What are some of the functional consequences that are brought on by the increased proportion of Type I to Type II fibre?

A
  1. Increase in fatigability (muscle atrophy and fibre loss) 2. Loss of strength (atrophy, fibre loss, fibre type changes) 3. Loss of power/speed (loss of Type II fibres and switching) 4. Complex tasks can become more difficult (less endurance) 5. Reaction time (balance, etc) is slower (loss of Type II)
131
Q

Why does muscle loss occur at a faster rate in males versus females?

A

Thestosterone decreases in men as they age, this reduces their muscle more so because females didn’t rely on T during puberty to gain all that muscle mass.

132
Q

Aging is generally associated with…

A
  1. an increase in overall proportion of Type I fibres 2. more atrophy in Type II than Type I 3. greater loss of Type II than Type I
133
Q

What happens to the synthesis rate of MHC II during aging?

A

It decreases

134
Q

What happens to the production of MHCII mRNA during aging?

A

It decreases

135
Q

What happens to the amount of nerve axons at T8 and T9 with age?

A

Decreases

136
Q

What happens to the number of motor units with aging?

A

It decreases

137
Q

Due to the loss of motor units with age, why does force production decrease?

A

If there is degradation of the MNs innervating a fibre, even if it is stimulated less force will be produced because there are less fibres, so less CSA to produce force

138
Q

What happens with the mitochondria during aging?

A
  1. Synthesis rate of muscle mitochondrial proteins decreases with age 2. Activity of oxidative enzymes is also reduced
139
Q

Why does endurance decrease in endurance during aging even though there is an increased proportion of Type I fibres?

A

Endurance will still decrease strictly because there is a decrease in mtichondrial properties, so less ATP can be made aerobically

140
Q

Influence of Skeletal Muscle Aging on Disease?

A
  1. Aging increases fatiguability, muscle weakness, decreases endurance capacity, and increased muscle wasting 2. This all leads to decreased physical activity 3. Decreased physical activity leeads to decreased expenditure, increased obesity, increased insulin resistance 4. These all lead to hypertension, type 2 diabetes, dyslipidemia 5. All of which lead to CVD
141
Q

2 types of muscle disease?

A
  1. Myopathies 2. Neuropathies
142
Q

What are myopathies?

A

Muscle dysfunction is due to changes that occur directly at the muscle or muscle fibre

143
Q

What are neuropathies?

A

Muscle dysfunction is due to changes that initially occur at the nerves innervating the muscle

144
Q

How are myopathies classified?

A

Loss of muscle mass myopathies and normal mass myopathies

145
Q

2 types of loss of mass myopathies?

A
  1. Atrophic myopathies 2. Destructive myopathies
146
Q

2 types of normal mass myopathies?

A
  1. Channelopathies 2. Metabolic myopathies
147
Q

2 subclasses of atrophic myopathies?

A
  1. Secondary 2. Inactivity
148
Q

Examples of secondary atrophic myopathies?

A

Glucocorticoid treatment, Cushing’s disease, hypothyroidism, malnutrition, alcohol abuse, cachexia

149
Q

Examples of inactivity atrophic myopathies?

A

Immobilzation, injury, disuse

150
Q

2 subclasses of destructive myopathies?

A
  1. Idiopathic 2. Familial
151
Q

Examples of iodiopathic destructive myopathies?

A
  1. Polymyositis 2. Dermamyositis
152
Q

Examples of familial destructive myopathies?

A

The muscular dystrophies…Duchenne, Becker, Limb Girdle

153
Q

What are atrophoc myopathies?

A

Reduced size of indifvidual fibers with number remaining relatively constant…some fibers are lost over longer periods of time

154
Q

What are destructive myopathies?

A

Fibres are destroyed, damaged, or die; therefore, the number of fibers in the muscle is drastically reduced

155
Q

What usually causes the loss of muscle mass in secondary atrophic myopathies?

A

Usually a secondary feature of an underlying disease or state of metabolic stress such as starvation, malignant disease/cancer, hyopthyroid disease, HIV, diseases associated with raised circulating cortisol levells or a consequence of glucocorticoid treatment (anti-flammatory treatment)

156
Q

Why is the breakdown of muscle during starvation a good adaptation?

A

Because a muscle can’t work if all the other systems are failing…

157
Q

Secondary atrophic myopathies usually result in the loss of what fibres?

A

Type II

158
Q

Why is there more atrophy of Type II fibres in secondary atrophic myopathies?

A

Thought that is is due to a need for protein as a fuel source for other vital organs and tissues that Type II responds to

159
Q

Are fibers lost in secondary atrophic myopathies?

A

No, just become very small

160
Q

What is the atrophy in atrophic myopathies due ti inactivity usually from?

A

Immobilization or injury

161
Q

How can atrophy due to inactivty be exacerbated by disease?

A

Not only a result of biochemical alterations that occur during the disease, but also because of 1. the inactivity associated with a diseased state and 2. treatment strategy used

162
Q

How is inactivity atrophy usually investigated?

A

Bed rest (due to chronic condition), limb immmobilization (casting), and restricted movement (animal studies of hindlimb suspension)

163
Q

Why does inactivity cause atrophy?

A

Not due to injury to muscle or bone itself but to the lack of activity/contraction (although, disease states can contribute)

164
Q

Inactivty atrophic myopathies usually cause preferential atrophy and loss of what fibre type?

A

Type I fibres

165
Q

Why do you lose more Type I fibres from inactivity atrophic myopathies than Type II Fibres?

A

Type I fibres are used to being stimulated all the time, so when they aren’t they will show a greater loss. Whereas, Type II fibres aren’t stimulated as much, so inactivty doesn’t reallychange the neural input to them, so they don’t have as much atrophy.

166
Q

What are the changes in metabolic enzymes due to inactivity?

A

Oxidative enzymes (succinate dehydrogenase) activity decreases and glycolytic enzyme activity increases (glycerol phosphate dehydrogenase)

167
Q

What are the metabolic changes in skeletal muscles form inactivity due to?

A

More Type II fibres, so increased glycolytic capacity

168
Q

What happens to fibre size and force production, and Vmax in a slow fibre following disuse?

A

Fibre size and force production decrease, and Vmax increases due to changes in MHC and MLC

169
Q

What are the consequences of inactivity for atrophic myopathies?

A
  1. Loss of strength (due to atrophy in all fibres) 2. Fatigue (due to atrophy in all fibres, particularly Type I and some loss of slow fibres, through fibre type switching) 3. Metabolic alterations (decreased ability to maintain aerobic metabolism due to less slow fibres) 4. Need for higher and more frequeny simulation to maintain force (due to increaed proportion of fast fibres)
170
Q

What are the familial destructive myopathies?

A

The Muscular Dystrophies: Dechenne, Becker, and Limb Girdle

171
Q

What do the muscular dystrophies cause?

A

Progressive disorders that lead to fibre destruction

172
Q

What happen during muscular dystrophies?

A

Continuous and extensice replacement of lost fibres withnew muscle, fat, and connective tissue

173
Q

Most serious MD?

A

Dechenne

174
Q

What chromosome is the Duchenne MD found on?

A

The X

175
Q

What usually causes the diagnosis of DuchenneMD?

A

Motor milestones aren’t being reached, so usually diagnosed at about 4 years of age

176
Q

Which of the following would likely result in a significant loss of muscle mass? a) channelopathy b) metabolic myopathy c) Becker MD d) b and c only e) a,b,c

A

c) Becker MD

177
Q

What of the following do NOT usually occur during inactivity induced atrophy? a) a faster rate of contraction b) greater atrophy of Type II c) decreased overall muscle force d) need for higher frequency of stimulation to reach max force e) both a and b

A

b) greater atrophy of Type II

178
Q

When does Duchenne MD usually kill?

A

teens to early 20s

179
Q

What does biopsies of Fuchenne MD patients show?

A

Differences in fibre size with numerous internal (centralized) nuclei–indicative of muscle regeneration and areas lacking fibers are also present

180
Q

Morphology of a normal muscle slide?

A

A few nuclei in the periphery, very little extra cellular space, uniform fibre size

181
Q

Morphology of a DMD-early slide?

A

More extracellular space, lots of extracellular nuclei and satellite cells, lots of immune cells, atrophy in some fibres and hypertrophy in others, centralized nuclei

182
Q

Morphology of DMD-Mid Stage slide?

A

Lots of extracellular space, decrease in satellite cells because the pool has become exhausted due to too much cell division, not as much regeneration in fibres, fibres that aren’t destroyed show hypertrophy because the same demand is placed on the muscle, but there are less fibres, so more work in done from the fibres that are still there

183
Q

Morphology of a DMD-late slide?

A

Fibres are getting smaller due to inactivity (wheelchair), areas with essentially nothing because damages fibres aren’t being replaced anymore, which leads to a huge increase in immune cells, brought in to clean up the mess.

184
Q

Individuals with DMD lack what?

A

Don’t express the dystrophin protein in their muscle fibres

185
Q

Is there a complete deletion of the dystrophin in Becker MD?

A

In the less severe form of the dystrophy (i.e., Becker) there is a deletion in the gene but an incomplete protein with some function is expressed

186
Q

What is the role of dystrophin?

A
  1. Maintains cellular integrity and structure (attaches outermost myofibrils to the sarcolemma and allows the distribution of force along the fibre) 2. Supports signaling processes within the myoplasm, across the sarcolemma, and into the extracellular matrix
187
Q

What is the problem associated with the lack of dystrophin?

A

Continuous damage/repair cycles (eventually damage predominates)

188
Q

Why type if mouse model is used to study DMD?

A

MDX mouse because it lacks dystrophin…regeneration outweighs repair

189
Q

Limb girdle MD?

A

Problems with sarcoglycans…not as bad as DMD or BMD

190
Q

Congenital MD?

A

Problems within laminin…not as bad as DMD or BMD

191
Q

Do all MDa affect the same muscle groups?

A

No, these dystrophies are also characterized by affecting different muscle groups and having different onsets

192
Q

2 most common idiopathic (inflammatory) destructive myopathies?

A

Polymyositis and dermatomyositits…2 conditions are likely variants of the same disorder

193
Q

Who does idiopathic myopathies effect the most?

A

Women

194
Q

What is the cause of idiopathic destructive myopathies?

A

Autoimmune process

195
Q

What happens in diopathic destructive myopathies?

A

Massive destruction of the muscle fibre (rhabdomyolysis)

196
Q

What is the treatment of idiopathis destrcutive myopathies?

A

Immunosuppressive drugs often used (glucocorticoids) because they downregulate immune response by inducing apoptosis of the immune cells…these drugs may also lead to atrophy/apoptosis of muscle, which is better to have some atrophy versus immune cells destroying everything

197
Q

What are some other problems, besides, muscle destruction that idiopathic destructive myopathies cause?

A

Destruction of fibers not only decreases muscle mass, strength and function but releases many soluble proteins into circulation (can lead to systemic problems)…CK levels with be high and can used to monitor the disease…There’s a threat of myoglobin precipitating and blocking renal tubules ultimately leading to renal failure…Urine is often dark brown in color

198
Q

What are the only cases that cause new fibres to be made?

A

MD and most severe inflammatory myopathies

199
Q

What happens in iodioapathic (inflammatory) destructive myopathies?

A

Immune cells will slowly infiltrate the muscle, cause damage, and start removing the fibre. Eventually, there will be immune cell accumulation and large scale inflammtion

200
Q

Where do neuropathies occur?

A
  1. Brain stem and spinal cord (spinal muscular atrophy) 2. Peripheral nerves (multiple scelorsis) 3. Neuromuscular junction (myasthenia gravis)
201
Q

What is denervation?

A

Nerve to muscle is severed or blocked. FIbre atrophy occurs within 2 days; in some cases, fiber may be almost completely depleted within 2 months

202
Q

If a fiber is denervated and reinnervated, what happens?

A

There will be some fiber transition (slow –> fast) due to decreased activity

203
Q

What happens to the myonuclei due to denervation?

A

They lose their elongated shape and become rounded and centrazlied in the muscle fiber where they line up and form chains. Over time, the number of myonuclei and satellite cells decrease.

204
Q

What happens to mitochondria form denervation?

A

Become smaller

205
Q

What is small group atrohpy?

A

Only some fibers are affected, and those not affected hypertrophy

206
Q

What is large group atrophy?

A

Many motor units are affected!

207
Q

Loss of neural activity in denervation leads to what in rspect to the Ach receptor density?

A

Reversal of the devlopmental process, so there is an increase in the number of Ach receptors

208
Q

What is NCAM and what does it do?

A

Neural cell adhesion molecule…it is upregulated during denervation and represents a signal fro new NMJ to develop. Axons will sprout form nearby, undamaged MN and branch to form new contacts with the denervated fiber. Since this process is slow, loss of function and atrophy occurs until reinnervation is established. In disease states, the old and new nerves can continue to die.

209
Q

The inflammatory response during idiopathic myopathies is associated with infiltration of?

A

Immune cells

210
Q

The MD associated with defects in the sarcoglycan structure?

A

Limb Girdle

211
Q

Why is the fibre type grouping that is caused by reinnervation a problem?

A

There is no longer a random distribution of fibres because the fibres have re-adapted to being reinnervated by a new MN. When the number of fibres per MU increases, there is no longer as much control over the force gradation. Also, there is a loss of diversity of fibres, so smaller range of properties/contraction styles.

212
Q

What are the general symptoms for conditions with normal muscle mass?

A

Rapid onset of fatigue, abnormally long contractions, episodes of brief paralysis

213
Q

What are the two groups of conditions with normal muscle mass?

A

Channelopathies and metabolic myopathies

214
Q

Channelopathies that affect Ca2+ release?

A

Malignant hyperthermia and hypokalaemic periodic paralysis

215
Q

Channelopathies that affect Cl- channel?

A

Myotonia

216
Q

Channelopathies that affect Na+ channels?

A

Kyperkalaemic periodic paralysis

217
Q

Glycogenoses metabolic myopathies?

A

Phosphorylase (McArdle) and Phosphofructokinase (Tauri)

218
Q

Mitochondrial metabolic myopathies?

A

Pyruvate dehydrongenase, cytochrome deficiency, carntitine palmitoyl transferase

219
Q

What are channelopathies?

A

Diseases that effect the structure and/or function of the ion channels found in the muscle. These diseases have a major impact on muscle function

220
Q

2 most common channelopathies?

A

malignant hyperthermia, myotonia, periodic paralysis

221
Q

What causes malignant hyperthermia?

A

Caused by a group of 20 mutations to the ryanodine receptor

222
Q

What are individuals with malignant hyperthermia sensitive to?

A

The anesthetic halothane and some stressful situations

223
Q

What does anesthetic or stress result in in malignant hyperthermia?

A

Prolonged release of Ca2+ from ryanodine receptors, which results in prolonged contraction, metabolic substrate depletion, and muscle damage

224
Q

What are the complications of malignant hyperthermia?

A

Deplete ATP, means other cell processes don’t have ATP. Switch to making ATP glycolytically - acidosis = muscle damage = renal failure due to myoglobin release. Also increased heat production because so much ATP is being made/broken down.

225
Q

What is myotonia?

A

A disorder caused by a defect in the gene coding for the muscle Cl- channel. Cl- channels have the effect of reducing membrane excitability (controlling ion gradient between muscle membrane and extracellular fluid. In myotonia, the CL- channels do not respond appropriately, so the membrane remains in an excitable state for an extended period of time. Leads to contractions that continue for up to 30 seconds.

226
Q

What is periodic paralysis caused by hyperkalaemia?

A

There is a defect in the Na+ channel. Channels stop functioning during excitation and remain open. There is a continued Na+ influx and the muscle remains depolarized. Results in an abnormal refractory state (not ready for subsequent excitation) Leads to associated high blood K+, because the fibre tries to compensate for the change in MP by pumping out positive charges/K+, which can leak into the blood.

227
Q

What is periodic paralysis caused by hypokalaemic?

A

A defect in DHPR. DHPR become inactive in the presence of low K+. Muscle cannot link electrical activity with Ca2+ release.

228
Q

What do both hyper and hypokaleamic PP cause?

A

Abnormal contractions that result in periodic paralysis

229
Q

When do metabolic myopathies become most apparent?

A

During exercise when there is a huge increase in the need for ATP. In general, individuals with these myopathies have normal strength and muscle function during rest.

230
Q

What are two types of metabolic myopathies?

A

Include glycogenoses and mitochondria myopathies

231
Q

What are glycogenoses?

A

Diseases in which there are defects (or deficiencies) in the enzymes of the glycolytic patheay

232
Q

What do glycogenoses usually result in?

A

Abnormal accumulation of glycogen in the muscle. This high glycogen can become toxic and damage muscle proteins and membranes and also disrupt myofibril architecture which can affect force

233
Q

Why do people with glycogenoses have problems with exercise?

A

They lack key enzymes in the glycolytic pathway, so ATP production is decreased

234
Q

Most studies glycogenoses disorder?

A

McArdle’s disease

235
Q

What is deficient in McArdle’s disease?

A

Myophosphorylase deficiency

236
Q

What is the problem caused by McArdle’s disease?

A

Cannot metabolize muscle glycogen…severe exercise limitation in the absence of lactic acid accumulation

237
Q

What is deficient in Tauri’s disease?

A

PFK

238
Q

What is the problem caused by Tauri’s disease?

A

Enzyme missing is muscle and RBCs. Similar to McArdle’s, but more severe problems with exercise. Haemolytic anaemia may occur

Physiology 2 (16 decks)

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