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BSMS 204- Theme 3 > Lecture 2- Pathophysiology of skeletal muscle > Flashcards

Lecture 2- Pathophysiology of skeletal muscle Flashcards

1
Q

what is known as the plasticity of the skeletal muscles?

A

exercise

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2
Q

what does muscle plasticity mean?

A

adapting of changes in functional demand

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3
Q

what does the endurance exercise respond to ?

A

total contractile activtivty

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4
Q

What does resistance exercise respond to?

A

loading and stretching

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5
Q

what are the muscles adaptations that allow plasticity?

A

structural- eg size and capillarisation

contractile properties- e.g. fibre type transitions-

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6
Q

when does adaptability occur?

A

from embryogenesis into maturity

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7
Q

what is the total number of muscle fibres of bicep brachii at birth?

A

200,000

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8
Q

what does muscle growth mean?

A

hypertrophy- (growth due to enlargement without cell division)
synthesis of myofilaments
satelite cell activation
angiogenesis and vascularisation

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9
Q

what are the effects of endurance exercise on the muscles?

A
  • Slight increase in Fibre diameter
  • blood supply-increased oxidative capacity
  • mitochondrial content
  • will express Increased in oxidative enzymes
  • Fibres become slower
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10
Q

what happens to the fibre types during endurance exercise>

A

gradual transformation of type :

IIX —–> IIA

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11
Q

what happens to the muscle fibres types during non-endurance exercise?

A

conversion to:
IIA—-> IIX
Greater muscle force and strength

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12
Q

what causes increase in power in type IIX fibre?

A
  • Increase in IIX fibre size due to increased numbers of sacromeres and myofilaments
  • results in LARGER muscles (BULK)
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13
Q

what is the role of ice in acute muscle injury?

A

-reduce swelling- reduces perfusion

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14
Q

what is the role of heat in muscle injury?

A
  • to relax and loosen tissue
  • to use before activities that irritate chronic injury
  • INCREASES blood flow
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15
Q

why is aspirin/NSAIDs use in MSK pain?

A

-Reduces pain/inflammation

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16
Q

Describe the mechanism of action of NSAIDS?

A
  • Inhibits COX
  • Reduces the synthesis of prostaglandins
  • Part of the archidonic pathway
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17
Q

Name a chronic disease which NSAIDs are used?

A

Osteoarthritis

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18
Q

what are the possible SEs of using NSAIDS (inc aspirin)?

A

-STomach bleeding
-ulcers
amongst others

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19
Q

what effects does the testosterone have?

A

anabolic and androgenic

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20
Q

Describe the anabolic effects of testosterone?

A
  • Increased protein synthesis
  • decrease catabolism- opposes cortisol and glucocorticoids
  • reduces fat- increases basal metabolic rate
  • Increases differentiation to muscle rather than fat
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21
Q

what is the purpose of anabolic steriod use?

A

increase muscle size and strength

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22
Q

why do the anabolic steroids lead to damaging SE’s?

A

-Large doses required

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23
Q

what are the some of the SE’s of using anabolic steriods?

A

Male- testes atrophy, sterility and baldness

Female- breast/uterus atrophy, menstrual changes, facial hair and deepening of voice

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24
Q

what is the effect of spaceflight on muscle fibre transition?

A

From type I—->IIA/X

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25
Q

what happens to the muscles during spaceflight?

A
  • due to decrease weight bearing–>all muscle undergo some atrophy-
  • weight bearing muscle show greatest atrophy
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26
Q

what is the effect of bed rest on muscle fibre types?

A

From Type I—–>type IIA

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27
Q

what is the effect of bed rest on the weight bearing muscles?

A
  • Atrophy due to:
    1. decreased muscle protein synthesis
    2. myofibrillar breakdown
    3. decreased strength due to decreased size
    4. Loss of type I fibres
28
Q

What are the possible treatment options for muscle atrophy?

A
  • Resume minor activity early

- physiotherapy

29
Q

what is a contracture?

A

-If a limb is immobilised for long periods then:
-process of growth is reversed
(sacromeres are removed in series from myofibrils)
-results in shortening of the muscle

30
Q

Describe the nucleation process for the skeletal cells?

A

-Multinucleate
develop as myoblasts which are mononucleate
these then fuse
-Nuclei are peripheral

31
Q

Why does multinucleate cells do not dividie?

A

mitosis cells do not divide

32
Q

How are the skeletal muscles enlarged?

A
  • fibre enlargement

- increased vascularisation

33
Q

What causes muscle degeneration?

A

inflammation

34
Q

How is this damage repaired?

A
  • Satellite cell- activated by inflammation
    1. proliferate, differentiate and fuse onto extant fibres
    2. contribute to forming multinucleate myofibers
35
Q

what is the role of myosatellite (satellite cell)?

A
  • Progenitor cells in muscle

- essential for regeneration and growth

36
Q

What activates the satellite cell?

A

mechanical strain

37
Q

what is myalgia and what are the possible causes?

A

-muscle pain
causes:
injury, overuse, infection and autoimmune
Can be associated with rhabdomyolysis

38
Q

What is myopathy?

A

muscular weakness due to muscular fibre dysfunction

39
Q

What is muscle dystrophy and what are the causes?

A

dystrophy- stuck in degeneration and regeneration cycle- until regenerative ability is lost
Causes- familial/progressive

40
Q

What is paresis?

A

weakness of the voluntary movement- partial loss of voluntary movement or impaired movement

41
Q

What are fasciculations?

A
  • Involuntary visible twitches in a single motor unit
  • commonly occur in lower motor neuron disease such as ALS
  • clinically appear as brief ripples under the skin
42
Q

what are fibrillations?

A

Involuntary spontaneous contractions of individual muscle fibres invisible to the eye

43
Q

what is rhabdomyolysis?

A

rapid breakdown of skeletal muscle

44
Q

what are the signs and symptoms of rhabdomyolysis?

A
  • Risk of renal failure due to:
    1. cellular proteins (esp myoglobin) release into the blood- clog renal glomeruli
    2. Dark urine- usually no urine produced after 12 hours after injury
    3. leads to electrolyte changes- Hyperkalemia
    4. muscle pain
    5. vomiting&confusion
45
Q

what are the treatment options for rhabdomyolysis?

A
  • IV fluids- to treat shock

- haemodialysis

46
Q

what are the possible causes of Rhabdomyolysis?

A

occurs when cell membrane loses integrity due to:

  1. Trauma
  2. Drugs- statins/fibrates
  3. hyperthermia
  4. Ischaemia to skeletal muscle- thrombosis and compartment syndrome
47
Q

what are the diagnostics of rhabdomyolysis?

A
  1. Total serum level creatine phosphokinase (CK)
    - When tissue damaged- release CK into blood
    -CK increases after skeletal muscle trauma/necrosis
  2. Myoglobin in plasma indicative of Rhab or MI- can lead to renal failure
  3. Hyperkalaemia-
    when muscle cell lyse they release K+=increase in in serum K+
48
Q

what is the cardiac form of CK?

A

CK-MB

49
Q

What is rigor mortis?

A

ATP depleted after death.
muscle cells does not requester Ca2+ into SR thus Increase cytosolic Ca
Ca2+ allows crossbridge cycle contraction
Until ATP & creatine-P run out
W/o ATP —-> myosin stops just after power stroke
With myosin still bound to actin.
Rigor mortis ends when muscle tissue degrades after 3 days

50
Q

What is myasthenia gravis and its causes?

A

progressive muscle weakness and fatigability- often starts with eye muscle
caused by:
depletion of nAChR- due to the immune systme inappropriately producing antibodies against nAChR

51
Q

How is the myasthenia gravis caused?

A
  • Due to less depolarisation of muscle fibres- many fibres do not reach the threshold
  • Repeat stimulation causes neuromuscular fatigue
52
Q

what are the symptoms of Myasthenia gravis?

A

ptosis and diplopia- weakness in the eyelid and extraocular muscles

  • proximal muscle weakness
  • fatigue
53
Q

what are the main treatment options for Myasthenia gravis?

A
  1. AChE inihibitors: pyrodostigmine: increases ACh activity at NMJ- prevents breakdown of Ach in the synapse
  2. Edrophonium- short acting AchE- inhibitor- used mainly for diagnosis-
54
Q

What are the other treatment options for Myasthenia gravis?

A

Treatment directed at Immune system:

  1. Thymectomy- reduces symptoms in 70% of the patients
  2. Corticosteriods- immunosuppresive effects
  3. Plasmapheresis: removal an anti AChR antibodies from the blood
55
Q

what is spinal muscular atrophy(SMA) and who does it affect?

A

SMA is degeneration of lower motor neurons-

Most common cause of genetic infant death

56
Q

what is the cause of SMA?

A

genetic defect-

autosomal recessive

57
Q

what does the death of lower motor neuron in the anterior horn of the spine cause?

A
  1. Muscle atrophy: hypotonia and muscle weakness

2. Fibre type grouping

58
Q

Why is the sensory system spared?

A

due to anterior horn is not affected

59
Q

What is fibre type grouping?

A

During spinal muscular atrophy
Cycles of denervation are followed by collateral reinnervation
surviving axons innervate surrounding fibres
resulting in fibre type grouping

60
Q

what is malignant hyperthermia?

A

Genetic (rare) susceptibility to gas anaesthetics

Eg sevoflurane

61
Q

what is the cause of malignant hyperthermia?

A

Mutation in RyR means gas anaesthetic —-> Ca2+ release
Autosomal Dominant:
Channel is susceptible if any of sub-units are

Result: SERCA works too hard (to pump Ca back into SR)

62
Q

What are the signs and symptoms of MH?

A

Increased O2 consumption, Increased CO2, acidosis, tachypnea, muscles overheat, the body overheats, muscles are damaged (rhabdomyolysis), hyperkalaemia, muscles become rigid

63
Q

Explain malignant hyperthermia in simple term?

A

Muscle cells open and leak their contents

Plasma CK-MM increases

Kidney failure possible: urine red from myoglobin

64
Q

what are the treatment options for Malignanat hyperthermia?

A

dantrolene sodium can stop the abnormal calcium release-

Inhibits ryanodine receptor

65
Q

what are muscular dystrophies?

A
  • Group of inherited disorders
  • Severe and progressive
  • muscle weakness due to myopathy
  • Waddling gate
  • Contractures
  • Cardio-respiratory muscle involvement
66
Q

what is Duchenne muscular dystrophy?

A
  • x-linked disease-gene for dystrophin protein
  • affects 1:3500 live male births
  • progressive loss of muscle tissue
  • replaced by fibrofatty connective tissue
67
Q

what is Gower’s sign?

A

indicates weakness of hip and thigh muscles associated with muscular dystrophy. The patient has to use hands and arms to “walk” up his own body from a squatting position

BSMS 204- Theme 3 (5 decks)

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