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204: The Musculoskeletal System > Pathophysiology of skeletal muscle > Flashcards

Pathophysiology of skeletal muscle Flashcards

1
Q

Muscle plasticity: adaptations

A

Structural
- e.g. size, capillarisation

Contractile properties
- e.g. fibre type transitions

Adaptability occurs from embryogenesis into maturity

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2
Q

Capillarisation

A

The formation and development of a network of capillaries to a part of the body

Often occurs in muscle in response to long term exercise

Also occurs in cancerous tissue

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3
Q

Structural adaptation

A

Total number of muscle fibres fixed at birth
- e.g. 200,000 biceps brachii

Muscle growth: hypertrophy

  • synthesis of myofilaments
  • addition of sarcomeres
  • satellite cell activation
  • angiogenesis and vascularisation

Some muscles enlarge by between 15-50%

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4
Q

Effect of endurance exercise

A

Increased

  • fibre diameter
  • blood supply
  • mitochondrial content

Will express increase in oxidative enzymes

Fibres become slower

Gradual transformation from type IIX to type IIA

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5
Q

Non-endurance exercise

A

Conversion to type IIX

  • from type IIA
  • greater muscle force and strength

Increase in type IIX fibre size due to increase in number of sarcomeres and myofilaments

Results in much larger muscles

Increase in power

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6
Q

Ice

A

Reduces swelling
- by reducing perfusion

After an acute injury
- sprain

After exercise in overuse injury

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7
Q

Heat

A

To relax and loosen tissues

Use before activities that irritate chronic injuries
- strain

Increases blood flow

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8
Q

Sprain

A

Injury to a ligament

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9
Q

Strain

A

Injury to muscle or a tendon

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10
Q

Aspirin

A

NSAID, reduces pain, reduces inflammation

Used for

  • chronic diseases (osteoarthritis)
  • sports injuries

Mechanism

  • inhibits COX
  • reduces synthesis of prostaglandins
  • part of arachidonic acid pathway

Side effects

  • stomach bleeding
  • ulcers
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11
Q

Anabolic effects of testosterone

A

Increases protein synthesis

Decreases catabolism by opposing cortisol and glucocorticoids

Reduces fat: increases BMR, increases differentiation to muscle

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12
Q

Anabolic steroid abuse

A

Used to increase muscle size and strength

Large doses required- leads to damaging side effects (kidney, liver, heart, mood changes)

Male- testes atrophy, sterility, baldness

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

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13
Q

Effect of spaceflight

A

Humans- transition of type I fibres to type IIA/X fibres

Decrease relative muscle mass- all muscles undergo some atrophy, but predominantly weight bearing muscles

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14
Q

Effect of bed rest

A

Transition of type I fibres to type IIA

Weight bearing muscle atrophy

  • decrease muscle protein synthesis
  • myofibrillar breakdown
  • decrease strength
  • loss of type I fibres

Treat by resuming minor activity early

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15
Q

Contracture

A

If limb immobilised for long periods

  • process of growth is reversed
  • sarcomeres are removed in series from myofibrils
  • resulting in shortening of muscle called a contracture

Patients with paralysed limbs must have physical therapy to prevent contractures occurring

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16
Q

Skeletal muscle cells are multinucleate

A

They develop as myoblasts

  • which are mononucleate
  • then the myoblasts fuse

The nuclei are peripheral

The multinucleate cells do not divide
- mitosis with multiple nuclei is usually impossible

Skeletal fibres are enlarged by

  • fibre enlargement
  • increased vascularisation
17
Q

Muscle regeneration

A

During inflammation and degeneration of damaged muscle tissue

Previous quiscent myogenic cells, called satellite cells, are activated

  • they proliferate, differentiate and fuse onto extant fibres
  • they contribute to forming multinucleate myofibres
18
Q

Myosatellite cells

A

Progenitor cells in muscle
- also called satellite cells

Essential for regeneration and growth

Most are quiescent
- activated by mechanical strain

Activation -> proliferation and differentiation

19
Q

Myalgia

A

Muscle pain

Causes: injury, overuse, infections, auto-immune

Can be associated with rhabdomyolysis

20
Q

Myopathy

A

Muscular weakness due to muscular muscle fibre dysfunction

  • cf. meuropathy and neurogenic disorders
  • failure to contract cause possibly muscle or nerve

Systemic vs familial

Dystrophies: familial, progressive

  • stuck in degeneration- regeneration cycle
  • eventually regenerative ability is lost
21
Q

Paresis

A

Weakness of voluntary movement, or partial loss of voluntary movement or impaired movement

Usually referring to a limb

From greek ‘to let fall’

22
Q

Fasciculations

A

Involuntary visible twitches in single motor units

Commonly occur in lower motor neuron diseases such as damage to anterior horn cell bodies characteristic of ALS or polio

Clinically appear as brief ripples under the skin

23
Q

Fibrillations

A

Involuntary spontaneous contractions of individual muscle fibres invisible to the eye

Identifiable by electromyography

24
Q

Rhabdomyolysis

A

Rapid breakdown of skeletal muscle
- not cardiac muscle, not myocardial infarct

Risk of kidney failure

  • cellular proteins released into blood can clog renal glomeruli
  • urine is tea coloured, no urine produced 12 hours after injury
  • leads to electrolyte changes: hyperkalaemia
25
Q

Treatment of rhabdomyolysis

A

Intravenous fluids

Possibly haemodialysis

26
Q

Causes of rhabdomyolysis

A

Trauma: crush injury

Drugs
- adverse effects of statins or fibrates

Hyperthermia

Ischaemia to the skeletal muscle

  • compartment syndrome
  • thrombosis
27
Q

Symptoms and signs of rhabdomyolysis

A

Muscle pains

Vomiting and confusion

Dark urine

28
Q

Serum levels CPK: diagnostic

A

Creatine phosphokinase

  • CK or CPK abbreviations used interchangeably
  • the enzyme, not creatine phosphate

Distinct forms of CPK not found in different tissues

Skeletal muscle CPK isoform is CK-MM

Cardiac muscle CPK isoform is CK-MB

When tissue damage and cells lyse there is a relase of tissue specific CK from cells into blood

Elevations in CK-MM occur after skeletal muscle trauma or necrosis

29
Q

Myoglobin: diagnostic

A

Buffers O2

Protein and haem group

Tea coloured

In plasma indicated rhabdomyolysis or MI

  • can lead to renal failure
  • urine tested for myoglobin

Diagnostic: hyperkalaemia

  • when muscle cells lyse
  • they release K+
  • this increases serum K+
30
Q

Myasthenia gravis

A

Progressive muscle weakness and fatiguability
- often starts with eye muscle

Caused by depletion of nAChR

Arises as the immune system inappropriately produces auto-antibodies against nAChR

Less depolarisation of muscle fibres
- many fibres do not reach threshold

Repeated stimulation -> neuromuscular fatigue

Symptoms include ptosis, diplopia

Proximal muscle weakness

31
Q

Myasthenia gravis: treatment and diagnostics

A

AChE inhibitors

  • neostigmine: increases ACh activity at NMJ
  • endrophonium: short lived AChE inhibitor for diagnosis

Other category of treatment is directed at immune system

32
Q

Spinal muscular atrophy

A

Floppy baby syndrome

  • one of the most common genetic causes of infant death
  • severity ant time of onset can vary greatly

Death of lower motor neurone in anterior horn of spine

  • muscle atrophy -> hypotonia and muscle weakness
  • fibre type grouping
  • sensory system is spared
33
Q

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

In healthy muscles, motor units are intermingled

During reinnervation, nearby surviving neurons re-innervate the denervated fibres, resulting in clusters

34
Q

Malignant hyperthermia

A

Genetic (rare) susceptibility to gas anaesthetics
- e.g. sevoflurane

Mutation in RyR means gas anaesthetic -> Ca2+ release

  • autosomal dominant
  • channel is suceptible if any of subunits are

Results: SERCA works too hard

Increase O2 consumption, increase CO2, acidosis, tachypnoea, muscles overheat, the body overheats, muscles are damaged, hyperkalaemia, muscle become rigid

35
Q

Muscular dystrophies

A

Group of inherited disorders

Severe and progressive wasting of muscle

  • muscle weakness
  • due to myopathy, not neuropathy

Waddling gait

Contracture

Cardiorespiratory muscle involvement - leads to death

36
Q

Duchenne muscular dystrophy

A

X linked disease

Affects 1:3500 live male births
- 1/3 cases arise spontaneously

Progressive loss of muscle tissue

Replaced by fibrofatty connective tissue

Mutation: gene for dystrophin protein

37
Q

Causes of spinal muscular atrophy

A

Caused by genetic defect

  • SMN1 gene (required for survival of anterior horn neurones)
  • autosomal recessive
  • other genes cause similar syndromes
38
Q

Dantrolene sodium

A

Can stop abnormal calcium release in malignant hyperthermia

Inhibits ryanodine receptor

204: The Musculoskeletal System (23 decks)

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