Lecture 12 - Muscle Development and Disorders Flashcards

1
Q

What does the paraxial mesoderm become?

A
  • Progenitor cells (mesenchymal stem cells)
  • Dermomyotome (myotomal cells - early muscle)
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2
Q

What is the earliest form of muscle fibers?

A

Embryonic myoblast

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3
Q

Which cells repair muscle cells after birth?

A

Satellite cells.

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4
Q

Satellite cells

A
  • Can regenerate themselves
  • They live between muscle cells
  • They can create new muscle cells (before birth)
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5
Q

What do progenitor cells become?

A
  • Embryonic myoblast
  • Foetal myoblast
  • Satellite cells
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6
Q

What are primary myotubes?

A

Merged myoblasts. Made from embryonic myoblast, satellite cells, and primary myotome.

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7
Q

What do primary myotubes become?

A

Primary fibers then type I fibers.

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8
Q

What do secondary myotubes become?

A

Secondary fibers and then type II fibers.

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9
Q

What are the components of secondary myotubes?

A

Foetal myoblast and satellite cells.

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10
Q

How can muscle change after birth as a result of nutrition?

A

Muscle diameter is the only effect of nutrition after birth.

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11
Q

How does nutrition impact myogenesis before birth?

A

It impacts the number of muscle fibers and muscle mass. If nutrition is decreased, there will be less myogenesis occuring which leads to less fibers and decreased muscle mass.

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12
Q

When does primary myogenesis occur?

A

Approx 0.5 to 3.5 months after conception.

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13
Q

When does secondary myogenesis occur?

A

Approx 2.5 to 7.5 months post conception.

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14
Q

When are the total number of muscle fibers fixed?

A

End of second trimester.

Around 6 months after conception - when myogenesis tapers off.

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15
Q

When does muscle hypertrophy occur?

A

Last trimester of pregnancy.

Approx 5.5 months after conception to birth.

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16
Q

How does nutrient intake impact muscle development 5.5 months after conception to birth?

A

Impacts muscle hypertrophy. If nutrition is decreased, there will be less muscle hypertrophy and a decreased birth weight.

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17
Q

How does having more sarcomeres in parallel impact force?

A

Force is doubled when number of sarcomeres in parallel is doubled.

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18
Q

How does having more sarcomeres in parallel impact velocity?

A

No change.

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19
Q

How does having more sarcomeres in parallel impact shortening capacity?

A

No change.

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20
Q

How does having more sarcomeres in series impact force?

A

No change.

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21
Q

How does having more sarcomeres in series impact velocity?

A

Doubles when length doubles.

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22
Q

How does having more sarcomeres in series impact shortening capacity.

A

Doubles when length doubles.

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23
Q

What process increases the number of sarcomeres in parallel?

A

Hypertrophy - diameter increases.

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24
Q

What process increases length of muscle?

A

Adding sarcomeres to ends of muscles.

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25
Q

What are the early muscle cells called?

A

Myotome

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26
Q

When is the embryonic stage of myogenesis?

A

1st trimester of pregnancy.

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27
Q

What occurs during the embryonic stage of myogenesis?

A

Primary myogenesis: Embryonic myoblasts proliferate, elongate, and fuse to form myotubes.

1st wave of primary fibers.

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28
Q

When is the fetal stage of myogenesis?

A

2nd trimester of pregnancy.

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29
Q

What occurs during the fetal stage of myogenesis?

A

Secondary myogenesis: Foetal myoblasts proliferate, elongate, fuse to form myotubes.

2nd wave of secondary fibers (majority of skeletal muscle fibers formed).

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30
Q

What occurs for myogenesis post-natal?

A
  • Muscle hypertrophy.
  • Satellite cells fuse to muscle fibers.
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31
Q

Define muscle spams

A

Involuntary muscle contractions that are often painful.

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32
Q

Define muscle cramps

A

Sustained muscle spasms that can last from a couple of seconds to 15 minutes or longer.

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33
Q

What is a charley horse?

A

Muscle cramp

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34
Q

What are some causes of muscle spasms/cramps?

A
  • Dehydration
  • Overuse
  • Electrolyte imbalance
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35
Q

What are some examples of spasms in vet med?

A
  • Spasms around a damaged joint.
  • Overuse due to nerve injury or overexertion.
  • Spasms following central injury to spinal cord or stroke.
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36
Q

How can spinal cord injury or stroke cause spasms?

A

Can result in hyper-excitable muscles.

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37
Q

Are muscle spasms around an injury primary or secondary?

A

They can be both primary or secondary.

38
Q

What type of spinal cord injuries result in muscle spasms?

A
  • Traumatic injury
  • Non-traumatic injury (ex. tumor)
39
Q

What is a muscle strain?

A

Tearing of the muscle.

40
Q

What can cause muscle strain?

A
  • Overexertion
  • Stretching muscle beyond its physiological range
41
Q

What is a typical target of muscle strains?

A

Musculotendinous junction

42
Q

What type of muscles are associated with muscle strain?

A

Big muscles (hamstrings, gastroc, quad, etc). Not usually in postural muscles.

43
Q

Why are big muscles more susceptible to strains?

A

Fast muscle fibers result in more force = higher risk of tearing.

44
Q

Why are muscle strains uncommon in postural muscles?

A

They are made of slow fibers (less force).

45
Q

What is the function of having a tail?

A
  • Coordination (running, swimming).
  • Thermoregulation.
  • Signaling.
46
Q

How is the tail used during running?

A

Assists in coordination. The frequency of the tail movement matches gait - has an important function in balance.

47
Q

How is the tail used in swimming?

A

Acts as a rudder - used for direction.

48
Q

Give an example of how the tail is used for thermoregulation.

A

Coyotes use their tail to warm the air by placing their fluffy tail against their nose.

49
Q

How are tails used for signalling?

A
  • Beavers smacking water.
  • Dogs will wag their tail in a specific direction for their owners and a different direction for strangers.
50
Q

What asymmetry of a dog’s tail is used in the presence of their owner?

A

Right-left asymmetry.

51
Q

What asymmetry of a dog’s tail is used in the presence of a stranger?

A

Left-right asymmetry.

52
Q

What is “dead tail”?

A

A strain injury of the muscles at the base of the tail due to overuse.

53
Q

Describe the muscle disorder related to hypertrophy.

A

Double muscling
- Myostatin usually inhibits muscle cell hypertrophy and hyperplasia
- Double muscling is a result of a mutation in myostatin

54
Q

Which cattle breeds are associated with double muscling?

A
  • Belgian blue
  • Piedmontese
55
Q

Which superfamily does myostatin belong to?

A

TGF-beta

56
Q

What is a consequence of double muscling in cows?

A

Calving difficulties due to increased calf birth weight.

57
Q

What dog breed is associated with myostatin deletion?

A

Whippets.

58
Q

What is muscle atrophy?

A

A decrease in muscle fiber diameter which results in a decrease in muscle size.

59
Q

What are the types of muscle atrophy?

A
  • Neurogenic
  • Myogenic
60
Q

What is neurogenic muscle atrophy?

A

Muscle atrophy that results from nerve damage - results in less or no action potentials.

Denervation causes lysosomal protein degradation, leading to a 50% decrease in muscle mass and EMG abnormalities.

61
Q

What is myogenic muscle atrophy?

A

Atrophy due to issue within muscle. Caused by malnutrition, cachexia, excess corticosteroid.

More common in type 2 fibers, EMG remains normal.

62
Q

What is “Sweeney” and what animal does it occur in?

A

Sweeney is a condition in horses due to neurogenic muscle atrophy. It is caused by damage to the suprascapular nerve which impacts the supraspinatus and infraspinatus muscles.

63
Q

What type of muscle atrophy has slow progression?

A

Myogenic

64
Q

Why is EMG normal in myogenic muscle atrophy?

A

Nerve is still connected to the muscle and there are still impulses travelling through muscle.

65
Q

What type of disorder is tying up/monday morning sickness?

A

Muscle necrosis

66
Q

What is muscle necrosis / Rhabdomyolysis?

A

Breakdown of muscles.

67
Q

What is tying up/monday morning sickness/azoturia?

A

Muscle necrosis in horses (rhabdomyolysis). Occurs in horses that are exercised daily during the week but are not exercised over the weekend - still fed same diet without exercise.

Causes a reduction in sarcomeres (loss of striations)

68
Q

What are the clinical features of rhabdomyolysis in horses?

A
  • Muscle pain
  • Contracture
  • Increased respiratory rate
  • Sweating
  • Myoglobinuria
69
Q

What is increased in serum due to rhabdomyolysis?

A
  • Creatinine kinase
  • Aspartate transaminase
70
Q

What are the causes of rhabdomyolysis?

A
  1. Nutrition
  2. Infectious
  3. Immune mediated
  4. Metabolic
71
Q

What are the nutritional causes of rhabdomyolysis?

A
  • Deficiency of vitamin E and selenium (anti-oxidants)
  • Hypokalemia (low potassium)
  • Toxins (ionophores)
72
Q

What are the infectious causes of rhabdomyolysis?

A
  • Clostridial
  • Viral
  • Toxoplasmosis
  • Sarcocysts
73
Q

What are the metabolic causes of rhabdomyolysis?

A
  • Glycogenoses
  • Lipid storage disorders
74
Q

What are the immune mediated causes of rhabdomyolysis?

A

Masticatory muscle myositis in dogs

75
Q

What is muscular dystrophy?

A

Inherited, progressive degeneration of skeletal muscle in small animals.

76
Q

What is muscular dystrophy called in humans?

A

Duchenne’s muscular dystrophy

77
Q

How does muscular dystrophy manifest in golden retriever puppies?

A
  • Stunted growth
  • Elbow abduction
  • Bunny-hop gait
78
Q

How is muscular dystrophy presented in adult dogs?

A

A plantigrade stance - the surface of the whole foot touches the ground during locomotion.

79
Q

Which dog breeds commonly experience muscle dystrophy?

A
  • German short hair pointers
  • Golden retrievers
80
Q

A deficiency in what protein causes muscular dystrophy?

A

Dystrophin - a protein that normally anchors the sarcolemma to the actin of cytoskeleton. The deficiency causes sarcolemma leakage and fiber damage.

81
Q

Is muscular dystrophy curable?

A

It was previously incurable but there is new research on the disease using genetic tools.

82
Q

What is white muscle disease?

A

Deficiency of selenium causes degeneration of muscle - giving the muscle a white appearance.

83
Q

Why does myoglobinuria occur during muscle necrosis?

A

Breakdown of muscle releases myoglobin.

84
Q

What are the types of altered electrical conduction in muscles?

A
  1. Altered motor neuron firing
  2. Altered motor end plate depolarization
  3. Altered sarcolemma excitability
85
Q

What condition is an example of altered motor neuron firing?

A

Hypocalcemia (milk fever) in cattle.

Decreased ACh release leads to decreased neuronal firing causes paresis.

86
Q

What conditions are an example of altered motor end plate depolarization?

A
  • Myasthenia gravis in dogs.
  • Botulism.
87
Q

How does myasthenia gravis result in altered motor end plate depolarization?

A
  • There is a congenital deficiency of ACh receptors
  • Leads to acquired autoantibodies to the ACh receptor
  • Autoantibodies bind to Ach receptors, results in less ACh binding
  • Impacts post-synaptic side of NMJ
88
Q

How does botulism cause altered motor end plate depolarization?

A

Clostridium botulinum toxin decreases Ach release which decreases neuronal firing causing paresis

89
Q

What is an example of altered sarcolemma excitability?

A

Myotonia in dogs, horses, goats. Muscle hypertrophy, stiffness, rigidity, prolonged muscle contraction.

90
Q

What is the mechanism that causes fainting goats?

A

Autosomal dominant mutation in Cl- channel leads to decreased Cl- channel conductance. This causes increased K+ in T tubules, increasing contraction.

The stiffness caused by contraction leads to stiffness, causing the goats to fall over.

91
Q

Hyperplasia in muscles

A

Formation of new myocytes.

92
Q

Somatic growth during prenatal period involves ____, ____ and ____.

A

Somatic growth during prenatal period involves MYOGENESIS, ADIPOGENESIS and FIBROGENESIS.