Difference between revisions of "Muscles Degenerative - Pathology"

From WikiVet English
Jump to navigation Jump to search
 
(18 intermediate revisions by the same user not shown)
Line 1: Line 1:
==Degeneration==
+
#redirect[[:Category:Muscles - Degenerative Pathology]]
[[Image:Degenerate muscle fibres.jpg|right|thumb|100px|<small><center>Degenerate muscle fibres (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
 
 
*Different types of degeneration
 
*May, or may not, be reversible
 
*Cloudy swelling, hydropic, vacuolar, granular and fatty change
 
*Occur following many different types of insult and are usually '''segmental'''
 
*If regeneration does not occur after formation of small vacuoles, [[Muscles Degenerative - Pathology#Necrosis|necrosis]] follows
 
**Vacuolation -> floccular degeneration -> granular degeneration -> [[Hyaline Degeneration|hyaline]] and [[Zenker Degeneration - Pathology|Zenker’s degeneration]]
 
*[[Hydropic Degeneration#Vacuolar Degeneration|'''Vacuolar degeneration''']]:
 
**Due to swelling of organelles or due to glycogen or fat accumulation
 
**May be caused by hypokalaemia, hyperkalaemia or necrosis
 
*Histologically:
 
**Swollen
 
**Hypereosinophilic
 
**Lost cross striations
 
 
 
 
 
===Calcification===
 
 
 
*Due to:
 
**Old age - myofibres
 
**Following necrosis - [[Mineralisation - Pathology#Dystrophic|dystrophic calcification]]
 
***May be visible grossly as white foci
 
 
 
 
 
===Ossification===
 
 
 
*Metaplasia of muscle to bone
 
*'''Localised'''
 
**Only in single muscle or a single group of muscles
 
**May be associated with trauma
 
**Seen in horses and dogs
 
**Histologically:
 
***Central zone - proliferating undifferentiated cells and [[Chronic Inflammation - Introduction#Fibroblasts|fibroblasts]]
 
***Middle zone - [[Bones - Anatomy & Physiology|osteoblasts]] depositing osteoid and bone
 
***Outer zone - [[Bones - Anatomy & Physiology|trabecular bone]] remodelled by [[Bones - Anatomy & Physiology|osteoclasts]]
 
*'''Progressive''' (fibrodysplasia ossificans progressiva)
 
**In connective tissue associated with skeletal muscle
 
**Secondary involvement of muscle tissue
 
**In pigs and cats
 
**Histologically:
 
***Bundles of dense fibrous connective tissue
 
***May contain accumulations of cartilage, bone or calcium
 
**Hyperplastic connective tissue -> compression of adjacent skeletal muscle -> [[Muscles Degenerative - Pathology#Atrophy|atrophy]]
 
 
 
 
 
===Pigmentation===
 
 
 
*[[Pigmentation - Pathology#Lipofuscin|'''Lipofuscin''']]
 
**Wear and tear pigment accumulating in secondary lisosomes -> converted into compact residual bodies
 
**Due to old age, past or recent cachexia or starvation
 
**Mostly stored in skeletal muscle of old high producing dairy cattle
 
**Masseters and diaphragm mainly involved
 
**No clinical importance
 
**Histologically:
 
***Rounded yellow to brown granules at both poles of nucleus of the skeletal myofiber
 
*[[Pigmentation - Pathology#Melanin|'''Melanin''']]
 
**As part of congenital melanosis of calves in fascial sheaths and epimysium
 
**Grossly - black foci
 
*'''Myoglobin'''
 
**After extensive muscle necrosis - '''rhabdomyolysis'''
 
**Leaks to adjacent tissue after sudden injury
 
*May also be present after some types of intramuscular injections e.g. iron dextran or tetracycline
 
 
 
 
 
==Necrosis==
 
 
 
*Necrosis of an entire myofibre is uncommon
 
*Segmental necrosis is more typical
 
*Muscle cell contents may leak into the blood if the cell membrane is damaged
 
*Creatine kinase (CK) is an enzyme which leaks following injury
 
**Used to measure the extent of muscle damage
 
*Often is followed by [[Muscle Regeneration - Anatomy & Physiology|regeneration]]
 
*Histologically:
 
**Hyaline hypercontracted fiber rounded at cross-section and increased diameter and eosin staining
 
***May also be an artifact due to hypercontraction of normal fibres at fixation
 
**Fragmenting portions of fibre -> floccular or granular
 
**Normal portion of fibre may detach from necrotic part -> retraction caps
 
**Infarction may cause '''discoid degeneration''' - necrotic fibres detach at '''Z lines'''
 
**May [[Muscles Degenerative - Pathology#Calcification|mineralise]]
 
*[[Zenker Degeneration - Pathology|'''Zenker's degeneration''']] - secondary to systemic disease
 
**Scattered small segments of necrosis and fast regeneration
 
**Sacrolemmal tubes are intact
 
 
 
==Atrophy==
 
[[Image:Atrophic muscle fibres.jpg|right|thumb|100px|<small><center>Atrophic muscle fibres (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
 
 
*Decreased myofibre or whole muscle diameter
 
*Myofibrils removed by disintegration -> sacrolemma too large -> forms folds
 
*Caused by:
 
**<u>'''Disuse'''</u> (e.g. fracture, failure to use limb, recumbency)
 
***Slower than denervation atrophy
 
***Reversible unless too prolonger or severe to cause loss of myofibres
 
**<u>'''Denervation'''</u>
 
***Any interference or damage to its nerve supply results in muscle atrophy
 
****Can be rapid - over 50% of muscle mass may be lost in a few weeks e.g. roarer horses with [[Laryngeal Hemiplegia|laryngeal hemiplegia]]
 
***May be reversible if innervation re-established
 
***Histologically:
 
****Fibres become rounded in cross section unless compressed by normal fibres
 
****Increased concentration of nuclei as they take much longer to disintegrate
 
****Fibrous stroma of epimysium and endomysium condenses -> more prominent
 
****End result in muscle consisting of almost only fibrous tissue
 
***Sometimes replaced by fat tissue -> increased size of muscle = ''pseudohypertrophy''
 
***Muscle may have a mixture of atrophied and [[Muscles Hyperplastic and Neoplastic - Pathology#Hypertrophy|hypertrophied]] (due to increased work load) fibres if some motor units are not damaged
 
**<u>'''Metabolisation of muscle protein'''</u> for nutrients during:
 
***Malnutrition, cachexia, senility
 
***Gradual onset except for some febrile diseases causing cachexia
 
***Postural muscles are not affected, sometimes even [[Muscles Hyperplastic and Neoplastic - Pathology#Hypertrophy|hypertrophy]]
 
***Histologically:
 
****Some nuclei disappear as myofibre volume is decreased
 
***Grossly:
 
****Smaller, darker, thinner muscles
 
 
 
 
 
==Toxic myopathy==
 
 
 
*'''Plants'''
 
**E.g. ''Cassia occidentalis'' (coffee senna), ''Karwinskia humboldtiana'' (coyotillo), ''Eupatorium rugosum'' (white snakeroot), cotton seed
 
**Lesion an skeletal and cardiac muscle
 
**Grossly:
 
***Pale areas with ill-defined borders
 
***May involve very extensive [[Muscles Degenerative - Pathology#Necrosis|necrosis]]
 
**Histologically:
 
***Segmental necrosis, no calcification
 
***[[Muscle Regeneration - Anatomy & Physiology|Regeneration]] may occur in surviving animals
 
*'''Drugs'''
 
**E.g. corticosteroids, cholinesterase inhibitors, vincristine, dimethyl sulfoxide (DMSO)
 
**'''Monensin''' is a coccidiostat toxic to horses, donkeys, zebras, cattle, sheep, dogs and birds
 
***Causes muscle necrosis in heart and skeletal muscle
 
***Grossly:
 
****Pale streaks, mostly in hind limbs
 
***Histologically:
 
****[[Muscles Degenerative - Pathology#Necrosis|Segmental necrosis]]
 
****Possibly [[Muscle Regeneration - Anatomy & Physiology|regeneration]] in surviving animals
 
***Can cause rapid onset recumbency and potentially death
 
***Usually due to mixing errors in feed
 
**Also from intramuscular injections, e.g. oxytetracycline, lidocaine, chloramphenicol, produce local necrosis
 
***As satellite cells are destroyes, repair is via fibrosis with some budding
 
*'''Chemicals'''
 
**Iron injections can cause local myonecrosis
 
*'''Mycotoxins'''
 
**Metabolites cause persistent tremors
 
**Lesions in skeletal muscle only, possibly secondary to sustained contractions (similar to [[Muscles Degenerative - Pathology#Exertional myopathies|exertional myopathy]])
 
**Histologically:
 
***Tiny foci of [[Muscles Degenerative - Pathology#Necrosis|segmental necrosis]]
 
 
 
 
 
==Endocrine myopathy==
 
 
 
*[[Hyperadrenocorticism|Hyperadrenocorticism]]
 
**Muscle weakness is a clinical sign
 
**-> [[Muscles Degenerative - Pathology#Atrophy|muscle atrophy]]
 
***Type II myofibre atrophy is non-specific
 
***Type IIB myofibre atrophy is preferential in hyperadrenocorticism
 
*[[Hypothyroidism|Hypothyroidism]] can cause muscle atrophy
 
 
 
 
 
==Nutritional myopathy==
 
[[Image:White muscle disease.jpg|right|thumb|100px|<small><center>White muscle disease (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
[[Image:White muscle disease histo.jpg|right|thumb|100px|<small><center>White muscle disease (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
===[[White Muscle Disease - Pathology|White muscle disease]]===
 
*Very important economic disease of sheep, cattle and pig
 
*Caused by:
 
**Deficiency of selenium, vitamin E or both
 
**Exacerbated by rapid growth, unaccustomed exercise or other dietary factor
 
*Pathogenesis:
 
**Oxygen free radicals (OFR) can damage cell membranes
 
**Vitamin E usually mops up OFRs
 
**Selenium as part of glutathione peroxidase neutralises effects of OFRs
 
**If Vit E or Se are deficient -> the balance shifts to membrane damage, calcium entry and mitochondrial damage -> cell swells and dies -> segmental muscle [[Muscles Degenerative - Pathology#Necrosis|necrosis]]
 
*Grossly:
 
**Lesions are bilaterally symmetrical in hard working muscles (vary with species)
 
**Early lesions are pale areas and streaks
 
***Difficult to see especially in pale muscles
 
**Later becoming calcified necrotic areas
 
***More obvious
 
**Pigs also have lesions in their [[Hyaline Degeneration|heart]] and [[Liver Fibrosis#Hepatosis dietica|liver]]
 
*Histologically:
 
**[[Muscles Degenerative - Pathology#Necrosis|Segmental necrosis]] +/- [[Muscles Degenerative - Pathology#Calcification|calcification]] and [[Muscle Regeneration - Anatomy & Physiology|regeneration]]
 
**Multifocal and multiphasic lesions
 
 
 
==Exertional myopathies==
 
 
 
*Caused by intensive and exhaustive activity of major muscle masses
 
*Glycogen used up -> local heat and lactic acid -> muscle degeneration
 
*Other forms include '''capture myopathy''', racing greyhounds, sheep chased by dogs
 
 
 
 
 
===Equine rhabdomyolysis===
 
 
 
*'''Azoturia''' (Monday morning disease)
 
**Acute
 
**Due to exercise following a prolonged period of rest
 
**Clincal signs:
 
***Unable to move
 
***Sweating
 
***Tremors
 
***Swollen and hard lumbar, gluteal and femoral muscles
 
**Myoglobin leaks from muscle cells -> leaks into urine -> urine is dark red/brown (myoglobinuria) -> damages renal tubules
 
**Grossly:
 
***Salmon pink muscles -> dark, moist, swollen +/- pale streaks
 
**Histologically:
 
***Segmental myofibre [[Muscles Degenerative - Pathology#Necrosis|necrosis]]
 
****Multifocal and monophasic, but may be multiphasic if repeated bouts
 
***Both, type IIA and IIB fibres affected; type IIB preferentially affected in acute disease
 
***Minor inflammatory reaction and calcification
 
 
 
*'''Tying-up'''
 
**Similar to azoturia but much milder
 
**Grossly - normal muscle
 
**Histologically - same as azoturia
 
 
 
 
 
===[[Porcine Stress Syndrome]]===
 
 
 
 
 
==Neuromuscular junction diseases==
 
 
 
===Aquired myasthenia gravis===
 
 
 
*See [[Muscles Developmental - Pathology#Myasthenia gravis (MG)|congenital MG]]
 
 
 
 
 
===Botulism===
 
 
 
*Caused by:
 
**Ingestion of ''[[Clostridium botulinum]]'' toxin which inhibits acetyl choline release
 
*Diagnosis by demonstration of toxin in faeces, ingested material or serum
 
 
 
 
 
==Circulatory disturbances==
 
 
 
===Congestion===
 
 
 
*Localised or generalised stasis -> dark red muscle
 
*E.g. in ruminal tympany ([[Bloat|bloat]]) - congestion of muscles cranial to thoracic inlet
 
*May resemble haemorhage grossly
 
 
 
 
 
===Ischaemia===
 
 
 
*Firstly [[Muscles Degenerative - Pathology#Necrosis|segmental necrosis]]
 
*-> death of satellite cells
 
**Causes [[Muscle Regeneration|regeneration]] but myoblast precursors have to be recruited from viable fibres
 
*-> death of all cells
 
*Mostly healed by fibrosis and scar formation
 
*May attempt regeneration by [[Muscle Regeneration|budding]]
 
Main causes:
 
*'''Vascular occlusion'''
 
**Infarction from embolism is rare due to collateral circulation
 
**Extension of infarcts depends on size of vessels occluded
 
***Small capillaries -> segmental [[Muscles Degenerative - Pathology#Necrosis|necrosis]]
 
***Large arteries -> whole muscle areas, including sattelite cells, are killed
 
**Healed by fibrosis
 
**May be due to:
 
***Blockage of iliac arteries by aortic-iliac thrombosis in horses
 
***Blockage of aortic bifurcation in cats
 
***[[Dirofilaria immitis|''Dirofilaria immitis'']] arteritis in dogs
 
***Vasculitis due to [[Reoviridae#Bluetongue Virus|bluetongue virus]] in sheep
 
***[[Haemorrhage#Purpura haemorrhagica|'''Equine purpura haemorrhagica''']]
 
****Non-contagious, sporadic
 
****Grossly:
 
*****Subcutaneous oedema
 
*****Scattered haemorrhagic foci throughout skin and muscles
 
*****Vasculitis -> infarcts of muscles
 
****May cause myoglobinuria if extensive
 
****Possibly immune mediated
 
****In horses post [[:Category:Streptococcus species|streptococal]] infection, especially [[Respiratory Bacterial Infections - Pathology#Strangles|strangles]]
 
*'''External pressure'''
 
**During prolonged recumbency, e.g. anaesthesia, inability to rise, or due to too tightly fitting bandages or casts
 
**Post anaesthesia myopathy especially in horses
 
***Dorsal recumbancy -> gluteals and longissimus ischaemia
 
***Lateral recumbancy -> triceps brachii, pectoralis, deltoideus and brachiocephalicus ischaemia
 
**Caused by pressure on muscle > perfusion pressure of capillaries
 
**Downer cows - vetral recumbency -> ischaemia of pectoral muscles and muscles of limbs tucked under the animal
 
**Pregnant ewes with twins or triplets -> internal abdominal oblique muscle ischaemic necrosis -> potential rupture
 
*'''Muscle swelling''' where it cannot expand
 
**E.g. supracoracoid muscle infarction in some breeds of turkeys after flapping their wings
 
***Surrounded by inelastic fascial sheath and bone
 
 
 
==Trauma==
 
 
 
*Due to:
 
**Direct transection of myofibres
 
**Compression of myofibres
 
**Secondary from haemorrhage (bruising)
 
***May increase muscle pressure -> [[Muscles Degenerative - Pathology#Ischaemia|ischaemia]] -> [[Muscles Degenerative - Pathology#Necrosis|necrosis]]
 
**Partial rupture - ''e.g.'' of diaphragm in road traffic accident
 
**Complete rupture - ''e.g.'' quadriceps of racing greyhounds
 
**Myorrhexis (tearing) - ''e.g.'' slippery floor causing 'splits' in cattle -> adductor muscle tear
 
*Healing is by [[Muscle Regeneration|regeneration]]
 
*Fibrosis (scarring) will compromise function
 
*During [[Bones Fractures - Pathology|fractures]], fragments may cause further trauma if moved
 
 
 
 
 
[[Category:Musculoskeletal System - Pathology]]
 

Latest revision as of 18:20, 3 March 2011