Pathophysiology of skeletal muscle Flashcards

1
Q

Changes in the muscle after prolonged endurance exercise

A

Increase in capillarisation
- Increases blood supply

Fibres become more slow twitch

Increase in mitochondria

Increase in oxidative enzymes

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2
Q

Changes in the muscle after prolonged non-endurance exercise

A

Increase in muscle size (but not number)= hypertrophy

  • increase in microfilaments, sarcomeres= increase in power
  • Satellite cell activation
  • Angiogenesis and vascularisation
Fibres become more 
fast twitch (IIX)
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3
Q

ICE therapy

A

Used AFTER exercise
- Reduces perfusion in soft tissue= reduces oedema

Best after acute injury

  • Sprain
  • Overuse injury
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4
Q

HEAT therapy

A

Used BEFORE exercise
- Increases perfusion into tissue= relaxes and loosens

Best for strains (muscle/tendon)

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5
Q

Aspirin

  • Mechanism
  • Indication
  • Adverse effects
A

NSAID- COX 1/2 inhibitor

Indication: Pain/inflammation

  • Osteoarthritis
  • Sports injuries

Adverse effects: chronic use= affects arachidonic acid and less prostaglandins produced
- GI ulcers, stomach bleeds

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6
Q

Effects of space flight/ bed rest on muscles

A

Flight:
Decreases mass of weight bearing muscles

Transition from Type 1 to Type 2A/X fibres

Bed rest: Similar to flight

  • Transition to Type 2A fibres
  • Reduced protein synthesis= less myofibrils
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7
Q

Testosterone and androgens effects on muscles

A

Anabolic effect= increase in protein synthesis

Opposites cortisol and glucocorticoids= decreased catabolism

Reduces fat

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8
Q

Anabolic steroid abuse

A

Large doses damage to:

  • Kidney
  • Liver
  • Heart

Mood changes

Testes atrophy
Sterility
Baldness

Breast/uterus atrophy
Menstrual changes
Hirsuitism
Deepening of voice

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9
Q

Contractures

  • Definition
  • Causes
A

Shortening of muscle due to sarcomeres removed in series with myofibrils.

Cause
- Immobilisation of limbs for very long period of time: bed bound, paralysis of limb

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10
Q

Myosatellite cells

A

Quiescent progenitor myogenic cells
- Regeneration and growth

Are activated when there is tissue damage/ inflammation

When activated= proliferate and differentiate into myofibres
- Fuse damaged fibres together.

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11
Q

Myalgia

A

Muscle pain

Causes:

  • Injury
  • Overuse
  • Infection
  • Autoimmunity
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12
Q

Myopathy

  • Definition
  • Signs and symptoms
A

Muscle weakness due to muscle fibre dysfunction.

Can be systemic of familial.

Signs and symptoms:

  • Myalgia
  • Muscle weakness
  • Cramps
  • Stifness
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13
Q

Muscle dystrophies

  • Description
  • Signs/symptoms
A

Type of myopathy that is famililal

  • Characterised by constant degradation and regeneration of muscle
  • Eventually muscles are not able to regenerate

Signs/ symptoms:

  • Waddling gait
  • Contractures
  • Cardioresp. problems
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14
Q

Paresis

A

Weakness/ partial loss of voluntary movement

or General impairment of movement of a limb

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15
Q

Fasciculations

A

Involuntary movements of a single motor unit that is visible to the eye
- neurogenic cause= spontaneous depolarisation of lower motor neurones.

Causes= motor neurone diseases

  • ALS
  • Polio
  • Spinal muscular atrophy
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16
Q

Fibrillations

A

Involuntary twitches of the muscle that are not visible o the eye and are of a myogenic cause

  • Unsynchronised contraction of muscle fibres
  • Can be detected by electromyography.

Causes:

  • Peripheral nerve disease
  • Myopathies
17
Q

Rhabdomyolysis

  • Mechanism
  • Signs
  • Symptoms
  • Treament
A

Rapid breakdown of skeletal muscle
- Cellular contents of myocytes rapidly released into plasma and EC space

Signs:

  • Tea coloured urine
  • Anouria (12 hours)
  • Hyperkalaemia (due to cell lysis release K+)
  • Elevated CK

Symptoms

  • Myalgia
  • Vomitting
  • Confusion

Shock:

  • IV fluids
  • Haemodialysis
18
Q

Rhabdomyolysis causes

A

Crush injuries

Drugs: statins, fibrates

Hyperthermia, malignant hyperthermia

Ischaemia

  • Thrombosis
  • Compartment syndrome

Hypokalemia

19
Q

Compartment syndrome

  • Description
  • Causes
  • Signs/ symptoms
  • Treatment
A

Increase pressure in a fascial compartment of the body
- Leads to Obstructured blood supply and nerve supply

Causes:

  • Fracture
  • Crush injury

Signs/ Symptoms

  • Disproportional pain
  • Poor pulses,
  • Decreased ability to move
  • Numbness, or a pale color of the affected limb

Treatment
- Fasciotomy

20
Q

CK-MM, Total CK

A

CK-MM

  • Creatine phosphokinase specific to skeletal muscle
  • Cannot be measured

So Total CK is measured instead

Elevated in:

  • Muscular dystrophy
  • Polymyositis
  • Rhabdomyolysis
21
Q

Myoglobin

A

Protein in myocytes that buffers oxygen

- elevated levels is a marker for rhabdomyolysis

22
Q

Myasthenia Gravis

  • Pathology
  • Signs/ symptoms
A

Autoimmune condition that produces auto-antibodies against nicotinic acetylcholine receptors (nAchR)
= Less depolarisation of muscle fibres

Signs/ symptoms:
Progressive, proximal muscle weakness (often starting form eye muscles)
-	Increasing fatigability
-	Ptosis
-	Diplopia
23
Q

Myasthenia Gravis treatment [5]

A

Neostigmine

  • Ach-esterase inhibitor
  • Prevents breakdown of Ach at neuromuscular junction (NMJ), longer acting time of Ach at NMJ.

Edrophonium
- Short-lived AchE inhibitor used for diagnosis. Symptoms will rapidly improve when administered.

Thymectomy
- removal of thymus reduces symptoms in majority of patients.

Immunosuppresants
- corticosteroids

Plasmapheresis
- removes anti- AChR autoantibodies from plasma

24
Q

Spinal muscular atrophy

A

Death of lower motor neurone of anterior horn of spine (motor fibres).

Cause= SMN1 gene defect
- autosomal recessive

Signs and symptoms:

  • Muscular atrophy
  • Hypotonia
  • Paresis/ muscle weakness
  • Fibre type grouping
25
Q

Fibre type group

A

Occurs after deinnervation of muscle fibres.

The surviving muscle fibres re-innervate deinnervated muscle fibres and form clusters of fibre types.

Seen in spinal muscular atrophy

26
Q

Malignant hyperthermia

  • Description
  • Cause
  • Pathology
  • Signs and symptoms
  • Treatment
A

Increased susceptibility to gas anaesthetics (I,e sevoflurane)

Cause

  • Mutation in ryanodine receptor= excess efflux of Ca.
  • Autosomal dominant

Pathology

  • SERCA is overwhelmed with excess Ca2+= uses up too much ATP.
  • More O2 consumption = more Co2= acidosis
  • Leads to hyperthermia

Signs and symptoms

  • Rhabdomyolysis
  • Elevated total CK
  • Tea coloured urine

Dantrolene sodium
- Inhibits RyR receptor

27
Q

Duchenne muscular dystrophy

  • Genetics
  • epidemiology
  • Pathology
A

X-linked
- Most common muscular dystrophy (1:3500 live births)

Genetics
- Mutation of dystrophin

Pathology
- Muscle tissue is lost progressively and replaced with fibrofatty connective tissue

Signs and symptoms

  • Gower’s sign
  • Toe walking
  • Skeletal deformities: lumbar hyperlordosis
  • Fatigue
  • Paralysis