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LS1 Histology > L16 - Alterations in skeletal muscle function > Flashcards

L16 - Alterations in skeletal muscle function Flashcards

1
Q

What are the functions of skeletal muscle?

A

Posture
Movement
Stability of joints
Heat generation

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2
Q

In the remodelling of muscles, which of the following statements are true?

(i) You can increase the number but not size of the muscle fibres
(ii) You can increase the size but not number of muscle fibres

A

(ii) you can increase the size but not numbers of muscle fibres

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3
Q

How often does muscle remodel?

A

Continuously

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4
Q

How long does it take to replace to contractile proteins (actin and myosin) present in muscle fibres?

A

2 weeks

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5
Q

What is the name for when destruction of contractile proteins is greater than replacement?

A

Atrophy - especially present in the upper limbs of elderly

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6
Q

What is the name for when the replacement of contractile proteins is greater than their destruction?

A

Hypertrophy - muscle increases in (cell) size

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7
Q

What effect on muscles due to exercise is there little evidence for?

A

hyperplasia

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8
Q

What are the affects on skeletal muscle of exercise?

A 
metabolic adaption
Increased volume of mitochondria
Increased ATPase
SR swells
Increased density of T tubule systems
Increased Z band width
Increase in number of contractile proteins
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9
Q

What is the purpose of the Z line?

A

Serves as an anchoring point for actin, at either end of the sarcomere

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10
Q

What is an example of high resistance exercise?

A

Weightlifting at high intensity e.g. 70-90% intensity (of 1 repetition max), short duration (3 sets of 8-12 reps), modest frequency (2-3 days per week)

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11
Q

What is the effect on muscle of high resistance exercise?

A
  1. Larger muscle - stimulates contractile protein synthesis -> fatter muscle fibres
  2. Increased number of cross-link between C proteins

Increased muscle mass and strength may lead to HYPERTROPHY (myosatelite cells)

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12
Q

What is an example of an endurance exercise?

A

Jogging e.g. low intensity for longer duration (30-60 mins) for 5 days a week

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13
Q

What is the effect of endurance exercise on skeletal muscle?

A

Increases its metabolic activity without increasing its size:

  1. Stimulates synthesis of mitochondrial proteins
  2. Vascular changes -> greater oxygen utilisation
  3. Shift to oxidative metabolism (lipids) - therefore reducing the concentration of lipids in blood
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14
Q

Give examples of disuse atrophy

A

Bed rest
Limb immobilisation
Sedentary behaviour

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15
Q

What happens in disuse atrophy to the skeletal muscles?

A

Loss of contractile proteins -> reduced muscle fibre diameter -> loss of power

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16
Q

Define sarcopenia

A

the loss of skeletal muscle mass and strength as a result of ageing

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17
Q

When do muscle begin to atrophy?

A

30+ (slowly at first)

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18
Q

Approximately how much muscle mass is lost by age 80?

A

50%

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19
Q

What problems can loss of muscle mass have in the elderly?

A
  1. Problems with mobility - e.g. getting out of chairs, due to weaker muscles
  2. Temperature regulation - less heat produced from shivering
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20
Q

What is denervation atrophy (neurogenic muscular atrophy)?

A

Atrophy caused by inhibition of a motor nerve

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21
Q

What are signs of motor neuron lesions?

A

Weakness
Flaccidity (part of body soft and hanging limply/loosely)
Muscle atrophy

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22
Q

How long does it take for re-innervation of skeletal muscle?

A

Re-innervation within 3 months for recovery

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23
Q

How does atrophied muscle compare to the look of normal muscle?

A

Atrophic fibres are small, angulated and brightly eosinophilic. Looks like an apparent increase in the number of nuclei.

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24
Q

How can you increase muscle length?

A

Stretching

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25
Q

Why can the length of muscle be reduced?

A

Immobility

26
Q

How can the length of muscle be changed?

A

Addition of sarcomeres (?)
Changes in neurology (pain, stretch receptors and stretch reflex)
Viscoelastic properties ( connective tissue alignment)

27
Q

How many fibres can a motor neurone innervate?

28
Q

What is the name of the ACh receptor located on the folded end-plate region of the motor neurone synaptic cleft?

A

nicotinic receptor

29
Q

What is the affect of ACh binding to nicotinic receptors on the motor end plate?

A

Binding of ACh opens the sodium channels. Sodium enters the sarcolemma causing local depolarisation that spread along the sarcolemma and down T tubules into the muscle fibres.

30
Q

What causes ACh release at the presynaptic terminal?

A

Opening of pre-synaptic voltage-dependent calcium channels

31
Q

In what direction does the myosin heads pull the actin?

A

Towards the center of the sarcomere

32
Q

How is the affect of ACh, at motor end plates, removed?

A

By acetylcholinesterase - breaks down very quickly

33
Q

What happens to ACh release at high motor neuron firing rates?

A

ACh release decreases

34
Q

What percentage of ACh receptors need to be fully occupied to get full muscle contraction?

35
Q

What is the name of a type of neuromuscular junction disorder?

A

Myasthenia Gravis

36
Q

What causes Myasthenia gravis?

A

Autoimmune destruction of the end-pate ACh receptors IgG antibodies to ACHRs)

37
Q

What is the result of the autoimmune destruction of ACHRs in Myasthenia gravis?

A

Loss of junctional folds at end plate and widening of synaptic cleft

38
Q

What are the primary signs of Myasthenia gravis?

A 
Drooping upper eyelids (ptosis)
Double vision (eyes not moving at the same time)
39
Q

How can you do a basic test for Myasthenis gravis?

A

Ask an individual to hold their arm out: at first they have enough ACh released to maintain there arm out and then suddenly the arm drops - not from fatigue but from lack of ACh.

40
Q

Why do symptoms of Myasthenia Gravis fluctuate?

A

It is effected by general state of health, fatigue and emotion

41
Q

How can Myasthenis gravis be treated?

A
  1. Acetylcholinesterase inhibitors (stop ACh breaking down so fast)
  2. Immune supressants
  3. Plasmapheresis: removal of harmful antibodies from patients serum
  4. Thymectomy - linked to thymus (T-lymphocytes)
    Though eventually individual will have to use a wheelchair
42
Q

Describe some ways that toxins can affect the neuromuscular junction

A 
They could affect:
neuronal Na+ channel
Ca2+ channel
muscle Na+ channel
AChR channel
acetylcholinesterase
ACh release
43
Q

What are muscular dystrophies?

A

Genetic disorders causing progressive muscle weakness and wasting

44
Q

What is the most common type of muscular dystrophy?

A

Duchenne-type and Becker-type

45
Q

Where does Duchenne and Becker muscular dystrophy affect?

A

Proximal limbs

46
Q

What in general is the cause of muscular dystrophy?

A

Protein deficiency

47
Q

What is the cause of Duchenne MD?

A

Complete absence of the protein dystorphin which normally connects the sarcolemma to actin

48
Q

What is the cause of Becker MD?

A

Altered truncated form of dystrophin

49
Q

What histological changes do you seen in Duchenne muscular dystrophy?

A

Absence of dystrophin if stained for
Muscle fibres different sizes
Damaged and dying muscle fibres
Replacement of muscle fibres with fibrous connective tissue and fat

50
Q

Why does the lack of dystrohin in DMD cause damage to muscle fibres?

A

Dystrophin pulls the sarcolemma alongwith the actin as the muscle fibre contract. If this is missing or damaged muscle fibre contraction can cause tearing

51
Q

What are the consequences of protein abnormality in DMD?

A
  1. Muscle fibres tear themselves apart on contraction
  2. Enzyme creatine (phosph)kinase liberated into the serum
  3. Calcium eneters cell causing cell death (necrosis)
  4. Pseudohypertrophy (swelling) before fat and connective tissue replaces muscle fibres
52
Q

What are is the sign of DMD, which involves an individual using their arms to help extend their legs?

A

Gower’s sign

53
Q

What is the age of onset of DMD?

A

Early onset - child falls down often, crawls more than others at playgroup

54
Q

Define contracture

A

a condition of shortening and hardening of muscles, tendons, or other tissue, often leading to deformity and rigidity of joints

55
Q

Why do individuals with DMD experience contractures?

A

They have an imbalance between agonist and anatgonist muscles

56
Q

What treatment is used for DMD?

A

Prednisolone - an anti-inflammatory seems to work even though it is not an inflammatory disease (and anabolic steroids don’t work)

57
Q

What is the current genetic research for MDM treatments?

A

gene therapy and stem cell therapy to get cells to produce dystrophin

58
Q

What are the two categories of skeletal muscle disorders?

A
  1. Myopathies (primary muscle disease)

2. Denervation (loss of nerve supply to muscle)

59
Q

List three types of myopathies

A

Muscular dystrophies
Inflammatory myopathies
Myopathies secondary to systemic disease

60
Q

List 5 origins of skeletal muscle problems

A 
Neurological
Metabolic
Immunological
Neuromuscular junction
Muscle tissues itself (proteins, ion channels, inflammation)

LS1 Histology (13 decks)

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