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22 Cards in this Set
- Front
- Back
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Describe the contents of a skeletal muscle
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- Each muscle contains bundles of muscle fibres (cells)
- Also found in a skeletal muscle is: • connective tissue • blood vessels • lymphatics • nerves |
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Describe the arrangement of connective tissue within muscle
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- regular arrangement of collagen around the individual fibres /, & bundles of fibres( fascicles) , & whole muscle
- endomysium, perimysium and epimysium blend together to form tendons which are attached to bone and transmits the forces generated by contracting myocytes |
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Describe the structure of a muscle fibre
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- Sarcolemma
- Sarcoplasm - Sarcoplasmic Reticulum - Organelles - Nucleus on the periphery of cell - Series of parallel subunits known as Myofibrils which are very fine fibres |
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Describe the structure of myofibrils
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- 80% of a muscle cell is occupied by myofibrils which in turn are made up of finer myofilaments
- Appear by light & electron microscopy as a cross banded light (I bands) & dark (A bands) pattern - Arranged as repeated units known as sarcomeres = the basic contractile unit (Z-Z line) - A & I bands are formed by an orderly array of thick & thin myofilaments - Myofilaments overlap each other = the thin myofilaments interdigitated between adjacent thick myofilaments and are attached to Z lines |
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What are myofilaments?
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- Consist of numerous proteins including:
• Thin filaments –actin, tropomyosin & troponin • Thick filaments mostly myosin |
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List some of the proteins found in muscle cells
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- Actin = alpha helical polymer
- Tropomyosin = two helices coiled around actin - Troponin complex = three parts: troponin T which binds to tropomyosin , troponin C binds with calcium & troponin I binds to actin and inhibits contraction - Myosin - Myostatin = inhibitory factor - Alpha actinin = anchor actin filaments to Z line - Nebulin = regulates thin filament length during sarcomere assembly and runs parallel to actin - Desmin = attches Z-disk to sarcolemma - Myomesin = attaches myosin filaments to M-line - Dystrophin = connects the cytoskeleton of a muscle fiber to the surrounding extracellular matrix through the cell membrane - Titin = contains binding sites for muscle associated proteins so it serves as an adhesion template for the assembly of contractile machinery in muscle cells |
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What are transverse tubules?
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- Unique to muscle cell inward
- Extension of sarcolemma - Allows electric impulse to move deeper into cell |
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Describe the mechanism of muscle contraction
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- Excitation by motor nerve at motor end plate
- Impulse is conducted over sacrolemma and inwards by T tubules to the sarcoplasmic sacs - This triggers the release of calcium from sarcoplasmic reticulum - Calcium binds to troponin C - This results in a shift in tropomyosin which uncovers active sites on the actin G - Myosin binds to the active sites on the actin = ADP & Pi are released - Release of energy results in bending of the myosin heads pulling the actin along towards H zone - Sliding Filament Theory - with small temporal delay in adjacent sarcomeres - Myosin remains bound to actin until ATP binds with the myosin & pulls the head back to the resting position - Cycle repeats as long as ATP & calcium are available |
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Describe how muscles relax
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- After the impulse is over SR actively pumps calcium back into sacs
- Calcium stripped off the troponin - Tropomyosin blocks the active sites on actin - Myosin cross bridges are prevented from binding with actin - Fibre returns to its resting length |
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What is a motor unit?
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- One muscle fibre is innervated by one nerve ending
- However a given motor neuron may innervate numerous muscle fibres e.g. eye muscles one neuron to three muscle fibres, postural muscles hundreds of fibres - Lower motor neuron & the fibres it innervates referred to as the motor unit - Depolarisation of the motor unit leads to “all or none “ phenomenon |
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Describe the characteristics of the sub-types of skeletal muscle
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How would you type a skeletal muscle fibre?
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- Histochemical analysis:
1. Biopsy 20mg tissue frozen in liquid nitrogen 2. Section stained to reveal oxidative and glycolytic enzymes 3. Examined by microscopy 4. Type I, IIa or IIb - Muscles types are naturally variable and therefore will have varying amounts of these fibres |
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Describe muscular hypertrophy
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- Increase in muscle size
- Type II fibres only = type I hypertrophies little - Increase by: • Weight training can cause if you have more Type II fibres than type I • Anabolic steroids • Knock out the gene for myostatin |
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What are anabolic steroids and what are their effects?
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- Synthetic derivatives of testosterone
- Testosterone secreted by Leydig cells of testes & adrenal cortex - Anabolic : increases skeletal muscle mass stimulating the process of myofilament formation - Androgenic : masculinising - Side effects: • Minor = Acne = Alopecia = Oedema • Major = Gynaecomastia = Testicular tissue shrinkage = Tendon rupture → tendons don't keep up with muscle size and force • Most serious = Atherosclerosis = Heart disease = Stroke = Liver cancer • Women = Mascalinisation = Causes permanent deep voice = Facial hair = Male pattern baldness = Menstral cessation = Clitoral enlargement |
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What is atrophy and what are its causes?
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- Decrease in cell size type II
- May be due to disuse but also seen as part of a complex pathology in many diseases - Cachexia - Weight loss and wasting - Seen in: • cancer • heart failure • diabetes • AIDS - Causes of atrophy • reduced activity • loss of innervation • reduced blood supply • diminished nutrition • loss of hormones • loss of growth factors • cytokines |
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What is myostatin?
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- Inhibitory growth factor – limits the size of muscle growth
- Knock out mice = used to study myostatin - Monoclonal antibody to myostatin - When gene expression or protein inhibited – hypertrophy results - Atrophy - myostatin protein expressed ++ |
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Describe the features of a neuromuscular junction
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- Motor nerve meets myofibre
- Acetylcholine is liberated from the nerve ending - Synaptic cleft - Binds with the sarcolemma = membrane depolarization - Intracellular calcium released - muscle contraction - Acetylcholine removed by acetycholinesterase |
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Define:
1. Myopathy 2. Myositis 3. Myasthenia 4. Myotonia 5. Muscular dystrophy |
1. Myopathy – disease of voluntary muscle
2. Myositis –inflammation 3. Myasthenia –weakness 4. Myotonia –sustained contraction 5. Muscular dystrophy – inherited disorders Weakness is the predominant features |
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What is polymyositis and dermatomyositis?
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Polymyositis:
- Most common age 40-60 years - 3:1 female to male - Insidious onset with exacerbations & remissions - Muscle weakness “difficulty rising from chair “ - Muscles usually painful but may not be - Symmetrical large proximal muscles - Systemic features: malaise weight loss, fever - Pulmonary → altered lung function test and interstitial disease, gastrointestinal involvement → dysphagia Dermatomyositis - Involves the skin as well as muscle –eyelids, knuckles - Note the distinctive heliotrope (purplish) rash and oedema periorbital Investigations: - Bloods – normocytic anaemia & creatine kinase - Electromyography –abnormal fibrillation at rest - Muscle biopsy- inflammation Screen for malignancy –occult may not become apparent for 2-3 years CXR, mammography, tumour markers Treatment: - Corticosteroids & azathioprine or cyclophosphamide |
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What is Myasthenia Gravis and how is it investigated and treated?
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Aetiology
- Unknown - Autoimmune Anti-AChR antibodies - Twice as common in women - Peak age 30 Pathology - IgGs block binding of AChR & Complement mediated damage to membrane - Larger than normal synaptic gap - Simplified folding pattern on muscle membrane - Inefficient neuromuscular transmission - Thymic hyperplasia 70% , thymic tumour 10% History: - Patient complains of SPECIFIC muscle weakness which fluctuates, pronounced with activity improves with rest - Exacerbations & remissions. Triggers include bright sunlight, viral illness, surgery & stress - Most initially complain of ptosis & diplopia - 50% progress to generalised disease involving oropharyngeal muscles, limb & trunk muscles, respiratory muscles- crisis can present Investigations: - Bloods for antibodies - Single fibre electromyography - Tesilon (edrophonium ) test = immediate improvement (but can cause anaphylaxis - Ice-cube test = put ice cube on eyelid and it will improve - Chest X ray for thymoma Treatment: - Life style advice - Anticholinesterase medication = prolongs action of Ach - Corticosteroids & azathioprine - Thymectomy |
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Describe muscular dystrophy and how it can be investigated and treated
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Pathology:
- Genetically determined disorders - Duchenne Muscular Dystrophy - X linked recessive - 1:3000 male infants - Absence of the protein dystrophin essential for membrane stability - Obvious by the age of 4 and death by 20 - Child will have difficulty rising from floor = Gower’s sign, proximal limb weakness, pseudo-hypertrophy of calves, severely disabled Investigations: - Bloods – creatine kinase grossly raised - Muscle biopsy – replacement of muscle with fat - EMG- abnormal Treatment: - No cure - Physiotherapy - Respiratory support |
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What is botulism and how can it be investigated?
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- Clostridia botulinum produce neurotoxins
- Contaminated food, wounds & infantile botulism (hence never give babies <1 year honey) - Food preformed → soluble neural toxins ingested - Blocks the release of Ach permanently - Paralysis of cranial & peripheral nerves - Untreated respiratory failure - Diagnosis usually clinical : • CT brain scan • EMG • LP • Tensilon test • Take stool or blood inject into peritoneal cavity of mice and death rapidly occurs |
