Pathophysiology of skeletal muscle Flashcards
Changes in the muscle after prolonged endurance exercise
Increase in capillarisation
- Increases blood supply
Fibres become more slow twitch
Increase in mitochondria
Increase in oxidative enzymes
Changes in the muscle after prolonged non-endurance exercise
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)
ICE therapy
Used AFTER exercise
- Reduces perfusion in soft tissue= reduces oedema
Best after acute injury
- Sprain
- Overuse injury
HEAT therapy
Used BEFORE exercise
- Increases perfusion into tissue= relaxes and loosens
Best for strains (muscle/tendon)
Aspirin
- Mechanism
- Indication
- Adverse effects
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
Effects of space flight/ bed rest on muscles
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
Testosterone and androgens effects on muscles
Anabolic effect= increase in protein synthesis
Opposites cortisol and glucocorticoids= decreased catabolism
Reduces fat
Anabolic steroid abuse
Large doses damage to:
- Kidney
- Liver
- Heart
Mood changes
Testes atrophy
Sterility
Baldness
Breast/uterus atrophy
Menstrual changes
Hirsuitism
Deepening of voice
Contractures
- Definition
- Causes
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
Myosatellite cells
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.
Myalgia
Muscle pain
Causes:
- Injury
- Overuse
- Infection
- Autoimmunity
Myopathy
- Definition
- Signs and symptoms
Muscle weakness due to muscle fibre dysfunction.
Can be systemic of familial.
Signs and symptoms:
- Myalgia
- Muscle weakness
- Cramps
- Stifness
Muscle dystrophies
- Description
- Signs/symptoms
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
Paresis
Weakness/ partial loss of voluntary movement
or General impairment of movement of a limb
Fasciculations
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
Fibrillations
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
Rhabdomyolysis
- Mechanism
- Signs
- Symptoms
- Treament
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
Rhabdomyolysis causes
Crush injuries
Drugs: statins, fibrates
Hyperthermia, malignant hyperthermia
Ischaemia
- Thrombosis
- Compartment syndrome
Hypokalemia
Compartment syndrome
- Description
- Causes
- Signs/ symptoms
- Treatment
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
CK-MM, Total CK
CK-MM
- Creatine phosphokinase specific to skeletal muscle
- Cannot be measured
So Total CK is measured instead
Elevated in:
- Muscular dystrophy
- Polymyositis
- Rhabdomyolysis
Myoglobin
Protein in myocytes that buffers oxygen
- elevated levels is a marker for rhabdomyolysis
Myasthenia Gravis
- Pathology
- Signs/ symptoms
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
Myasthenia Gravis treatment [5]
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
Spinal muscular atrophy
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
Fibre type group
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
Malignant hyperthermia
- Description
- Cause
- Pathology
- Signs and symptoms
- Treatment
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
Duchenne muscular dystrophy
- Genetics
- epidemiology
- Pathology
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
