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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
what happens to the muscles during spaceflight?
- due to decrease weight bearing-->all muscle undergo some atrophy- - weight bearing muscle show greatest atrophy
26
what is the effect of bed rest on muscle fibre types?
From Type I----->type IIA
27
what is the effect of bed rest on the weight bearing muscles?
- 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
What are the possible treatment options for muscle atrophy?
- Resume minor activity early | - physiotherapy
29
what is a contracture?
-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
Describe the nucleation process for the skeletal cells?
-Multinucleate develop as myoblasts which are mononucleate these then fuse -Nuclei are peripheral
31
Why does multinucleate cells do not dividie?
mitosis cells do not divide
32
How are the skeletal muscles enlarged?
- fibre enlargement | - increased vascularisation
33
What causes muscle degeneration?
inflammation
34
How is this damage repaired?
- Satellite cell- activated by inflammation 1. proliferate, differentiate and fuse onto extant fibres 2. contribute to forming multinucleate myofibers
35
what is the role of myosatellite (satellite cell)?
- Progenitor cells in muscle | - essential for regeneration and growth
36
What activates the satellite cell?
mechanical strain
37
what is myalgia and what are the possible causes?
-muscle pain causes: injury, overuse, infection and autoimmune Can be associated with rhabdomyolysis
38
What is myopathy?
muscular weakness due to muscular fibre dysfunction
39
What is muscle dystrophy and what are the causes?
dystrophy- stuck in degeneration and regeneration cycle- until regenerative ability is lost Causes- familial/progressive
40
What is paresis?
weakness of the voluntary movement- partial loss of voluntary movement or impaired movement
41
What are fasciculations?
- 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
what are fibrillations?
Involuntary spontaneous contractions of individual muscle fibres invisible to the eye
43
what is rhabdomyolysis?
rapid breakdown of skeletal muscle
44
what are the signs and symptoms of rhabdomyolysis?
- 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
what are the treatment options for rhabdomyolysis?
- IV fluids- to treat shock | - haemodialysis
46
what are the possible causes of Rhabdomyolysis?
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
what are the diagnostics of rhabdomyolysis?
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
what is the cardiac form of CK?
CK-MB
49
What is rigor mortis?
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
What is myasthenia gravis and its causes?
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
How is the myasthenia gravis caused?
- Due to less depolarisation of muscle fibres- many fibres do not reach the threshold - Repeat stimulation causes neuromuscular fatigue
52
what are the symptoms of Myasthenia gravis?
ptosis and diplopia- weakness in the eyelid and extraocular muscles - proximal muscle weakness - fatigue
53
what are the main treatment options for Myasthenia gravis?
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
What are the other treatment options for Myasthenia gravis?
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
what is spinal muscular atrophy(SMA) and who does it affect?
SMA is degeneration of lower motor neurons- | Most common cause of genetic infant death
56
what is the cause of SMA?
genetic defect- | autosomal recessive
57
what does the death of lower motor neuron in the anterior horn of the spine cause?
1. Muscle atrophy: hypotonia and muscle weakness | 2. Fibre type grouping
58
Why is the sensory system spared?
due to anterior horn is not affected
59
What is fibre type grouping?
During spinal muscular atrophy Cycles of denervation are followed by collateral reinnervation surviving axons innervate surrounding fibres resulting in fibre type grouping
60
what is malignant hyperthermia?
Genetic (rare) susceptibility to gas anaesthetics | Eg sevoflurane
61
what is the cause of malignant hyperthermia?
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
What are the signs and symptoms of MH?
Increased O2 consumption, Increased CO2, acidosis, tachypnea, muscles overheat, the body overheats, muscles are damaged (rhabdomyolysis), hyperkalaemia, muscles become rigid
63
Explain malignant hyperthermia in simple term?
Muscle cells open and leak their contents Plasma CK-MM increases Kidney failure possible: urine red from myoglobin
64
what are the treatment options for Malignanat hyperthermia?
dantrolene sodium can stop the abnormal calcium release- | Inhibits ryanodine receptor
65
what are muscular dystrophies?
- Group of inherited disorders - Severe and progressive - muscle weakness due to myopathy - Waddling gate - Contractures - Cardio-respiratory muscle involvement
66
what is Duchenne muscular dystrophy?
- x-linked disease-gene for dystrophin protein - affects 1:3500 live male births - progressive loss of muscle tissue - replaced by fibrofatty connective tissue
67
what is Gower's sign?
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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