Pathophysiology Of Skeletal Muscle Flashcards
Endurance exercise responds to?
Total contractile activity
Resistance training responds to?
Loading and stretch
Biceps brachii have how many fibres?
200,000
Hypertrophy is what?
Synthesis of myofilaments
Addition of sarcomeres
satellite cell activation
Angiogenesis and vascularisation
Muscles can enlarge between?
15-50%
Effect of endurance exercise?
Increased fibre diameter Increased blood supply Mitochondrial content increase Increase in oxidative enzymes Fibres become slower
Transformation from type IIX to IIA or type I
Resistance training transformation happens from?
Type IIA to IIX
To get greater muscle force and strength
Increase in sarcomeres and myofilaments
Results in larger muscles bulk
After a sports injury what should you use?
Ice and aspirin
Mechanism of aspirin?
Inhibit COX, REDUCING SYNTHESIS OF PROSTAGLANDINS
High levels of aspirin can cause?
Gastrointestinal adverse effects, stomach bleeding and ulcers
Steroid abuse can cause?
Testes atrophy, baldness, sterility, breast and uterus atrophy, menstrual changes, facial hair
What is the effect of spacefight?
Reduction in weight bearing muscles, transition from type 1 to type 2 x/2a fibres
All muscles undergo atrophy
Effect of bed rest?
Type 1 to type 2a, decrease in protein synthesis, myofibrillar breakdown, loss of strength
What happens in contracture?
Immobilisation cause removal of sarcomeres, so shorter muscle
Skeletal muscle cells appear?
Multinucleate, start as myoblasts which are mono nucleate and then fuse, moving nuclei to periphery, multinucleate cells can’t divide
Muscle regeneration happens?
Quiescent myogenic satellite cells are activated by HGF by proliferating differentiating and fuse onto extant fibres onto muscle cell. They reform elements of muscle (multinucleate myofibres)
Myalgia can be associated with?
Rhamdomyolsis
Dystrophies?
Incorrect muscle growth, familial and progressive
Muscle stuck in degeneration and regeneration cycle, regenerative ability is lost
Paresis?
Weakness of voluntary movement or partial loss
Fasciculations?
Involuntary twitches in single motor units, common in lower motor neuron disease seen in ALS/ polio, look like ripples
Fibrillations?
Involuntary spontaneous contraction of individual muscle fibres , myogenic, invisible to eye
Rhabdomyolysis?
Rapid breakdown of skeletal muscle, risk of kidney failure, myoglobin can clog glomeruli
Urine looks tea coloured, no urine produced after 12 hours
Causes hyperkalaemia, high K
Rhabdomyolysis treatment?
IV fluid
Haemodialysis
Causes of rhambdomyolysis?
Trauma crush injury
Hyperthermia
Ischaemia to local skeletal muscle (compartment syndrome, thrombosis)
Drugs, statins or fibrates
Symptoms and signs of rhambdo?
Muscle pains,
Vomiting and confusion
Dark urine
Diagnostic for muscular dystrophies and rhambdomyolysis?
Skeletal isoform. CK MM elevated
Cardiac muscle CPK form CK MB
Test would be for total CK
What is an indicator rhambdomyolysis and MI?
Myoglobin
Another diagnostic for rhabdomyolysis?
Muscle cells lyse, release K, increase in serum
Rigor mortis?
ATP depleted after death, muscle cannot resequester Ca in SR, Ca allows cross ridge cycle contraction
Without ATO, myosin will stop after power stroke, myosin still bound to actin
Rigor mortis ends when tissue degrades, about 3 days
Myasthenia gravis is?
Progressive muscle weakness and fatigability often start with eye muscles,
Cause of myasthenia gravis?
Depletion of nAchR because autoantibodies attack them
Which cause less depolarisation of muscle fibres and repeated stimulation will lead to neuromuscular fatigue
Symptoms of myasthenia gravis?
Ptosis - one eyelid droopy
Diplopia- double vision
Proximal muscle weakness
Treatments for myasthenia gravis?
AchE inhibitors
Pyridostigmine- increases ACh activity
Edrophonium- short lived AchE inhibitor
Thymectomy- for immune system- reduces symptoms in 70% of patients
Immunosuppressive Drugs- corticosteroids
Plasmapheresis- remove antibodies
Spinal muscular atrophy cause?
Death of lower motor neurons in anterior horn of spine, causing muscular atrophy, hypotonia and muscle weakness causes fibre type grouping
Autosomal recessive
Malignant hyperthermia?
Genetic susceptibility to gas anaesthetics
Mutation in RyR, causes release of calcium,
Autosomal dominant, SERCA works too hard ca back into SR
Increase O2 and CO2, acidosis tachypnea, body overheats, rhabdomyolysis
What happens in malignant hyperthermia?
Muscle cells open and leak contents
Increase in CK MM
How to treat malignant hyperthermia?
Dantrolene sodium can stop calcium release, inhibits ryanodine receptor
Muscular dystrophies present with?
Muscles weakness, waddling gate, contracture and cardio respiratory muscle involvement
Duchenne muscular dystrophy?
X linked, 1 in 3500 males
Loss of muscle tissue replaced by fibre fatty connective tissue
Dystrophin protein mutation
What is gowers sign?
To weak to pick themselves up
Sign of muscular duchenne dystrophy?
Testosterone effects?
Increase protein synthesis
Decrease catabolism, by opposing cortisol and glucocorticoids
Reduces fat, increases BMR, differentiation to muscle
Myosatellite cells are what kind of cells?
Progenitor cells
Fibre type grouping?
Surviving axons innervate surrounding fibres, determine which type of muscle fibre it will be
How to test for myasthenia gravis?
Give short acting inhibitor endophonium, see if ptosis stops
Drug for myasthenia gravis?
Pyridostigmine
How can you treat malignant hyperthermia?
Inhibit the Ry receptor, with dantrolene sodium
