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| + | <big><center>[[Musculoskeletal System - Anatomy & Physiology|'''BACK TO MUSCULOSKELETAL ANATOMY AND PHYSIOLOGY''']]</center></big> |
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| + | ===Introduction=== |
| + | |
| + | *Skeletal muscle includes muscles of: |
| + | **Posture |
| + | **Movement |
| + | **Respiration |
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| + | |
| + | *Two basic types of skeletal myofibre: |
| + | **<u>'''Type I'''</u> |
| + | ***Grossly '''red''' |
| + | ***'''High''' myoglobin level |
| + | ***'''Slow''' rate of contraction |
| + | ***High '''oxidative''' activity |
| + | ***Function - postural |
| + | **<u>'''Type II'''</u> |
| + | ***Grossly '''white''' |
| + | ***'''Low''' myoglobin level |
| + | ***'''Fast''' rate of contraction |
| + | ***High '''glycolytic''' activity |
| + | ***Function - exercise |
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| + | |
| + | *Each muscle is composed of multiple '''fascicles''' |
| + | **Each fascicle is composed of multiple polygonal '''myofibres''' |
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| + | |
| + | ===Response to injury=== |
| + | |
| + | *Limited array of ways in which to respond to injury |
| + | **[[Muscles - degenerative#Degeneration|Degeneration]] |
| + | **[[Muscles - degenerative#Necrosis|Necrosis]] |
| + | **[[Muscles - normal#Regeneration|Regeneration]] |
| + | **[[Muscles - degenerative#Atrophy|Atrophy]] |
| + | **[[Muscles - hyperplastic and neoplastic#Hypertrophy|Hypertrophy]] |
| + | |
| + | *Large number of factors indicing the changes above, e.g.: |
| + | **Trauma |
| + | **Toxins |
| + | **Infectious agents |
| + | **Nutritional deficiencies |
| + | **Ichaemia |
| + | **[[Muscles - developmental|Hereditary diseases]] |
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| + | |
| + | |
| + | *Specific diagnosis is often not possible based on morphological or histological features alone |
| + | *Additional tests, clinical information and history are often required |
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| + | |
| + | |
| + | ===Regeneration=== |
| + | [[Image:Muscle regeneration.jpg|right|thumb|100px|<small><center>Muscle regeneration (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] |
| + | |
| + | *Skeletal muscle myofibres have substantial regenerative ability |
| + | *Success depends on: |
| + | **An intact '''sarcolemmal tube''' - to act as a support and guide |
| + | **Availability of '''satellite cells''' - to act as progenitor cells for new sarcoplasm production |
| + | **Macrophages to clear up cell debris |
| + | **If these conditions are not met (e.g. severe thermal damage) '''fibrosis''' will occur |
| + | *Stages: |
| + | #Nuclei in [[Muscles - degenerative#Necrosis|necrotic segement]] disappear, hyalinased sarcoplasm due to loss of normal myofibrillar structure, may separate from adjacent normal myofibrils and/or [[Muscles - degenerative#Calcification|mineralise]] |
| + | #Monocytes from capillaries -> macrophages in necrotic portion, satellite cells swell -> vesicular with prominent nucleoli -> mitosis (within 1-4 days after initial injury) |
| + | #Satellite cells move to centre |
| + | #Macrophages clear the sacrolemmal tube, plasmalemma disappears, shape maintained by basal lamina |
| + | #Satellite cells -> myoblasts (contain myosin) -> fuse forming myotubes with row of central nuclei; cytoplasmic processes fusing |
| + | #Growing and differentiating fibre, striations appear - formation of sarcomeres |
| + | #Nuclei move to peripheral position (2-3 weeks after initial injury) |
| + | *Regeneration by '''budding''' |
| + | **When conditions are not optimal, disrupted sacrolemma |
| + | **E.g. injection of irritating substance, trauma, [[Muscles - degenerative#Ischaemia|infarction]] |
| + | **Myoblasts proliferate -> sacrolamma bulges from cut part -> club-shaped with numerous central nuclei = muscle giant cells |
| + | *Monophasic lesions - all at same phase above |
| + | **Damage occured at one time, e.g. trauma or one toxin exposure |
| + | *Multiphasic lesions - different stages as described above |
| + | **Ongoing damage, e.g. vitamin E - selenium deficiency, continuous exposure to toxin |
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| + | |
| + | ===Rigor Mortis=== |
| + | |
| + | *Muscles remain biochemically active after the death of an animal |
| + | *Following a period of relaxation, contraction and stiffening occurs |
| + | *Due to deficiency of ATP releasing myosin heads from their binding sites at end of power stroke |
| + | *Onset faster in ATP deprived animals (starvation, hunting, tetanus...) |
| + | *May be absent in cachetic animals |
| + | *Disappears due to autolysis or putrefaction |
| + | *See [[General Pathology - Post-Mortem Change#Rigor Mortis|general pathology]] |
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| <big><center>[[Musculoskeletal System - Anatomy & Physiology|'''BACK TO MUSCULOSKELETAL ANATOMY AND PHYSIOLOGY''']]</center></big> | | <big><center>[[Musculoskeletal System - Anatomy & Physiology|'''BACK TO MUSCULOSKELETAL ANATOMY AND PHYSIOLOGY''']]</center></big> |