Skeletal Muscle Flashcards
Changes in bloodwork with muscle damage
Elevations in:
Creatinine kinase (CK)
Lactate dehydrogenase (LDH)
Aspartate aminotransferase (AST)
Alanine aminotransferase (ALT)
Changes in urine with muscle damage
Myoglobinuria (myoglobin released into bloodstream + filtered by kidney into urine)
Muscle atrophy
Loss of myofilaments (actin + myosin) —> decrease in myofiber size
Causes of muscle atrophy
Denervation
Disuse
Malnutrition
Histology of denervation atrophy
Patchwork myofiber atrophy (due to motor unit organization)
Causes of denervation atrophy
Wallerian degeneration (most common) - secondary to trauma to peripheral nerve
(Rarely) Axonal degeneration or demyelination
Example of denervation muscle atrophy
Laryngeal hemiplegia
Reinnervation
Schwann cells proliferate at motor end plate of denervated fiber
Reinnervatioin by collateral sprouting or axon regrowth —> hypertrophy (regeneration of muscle)
Histology of disuse muscle atrophy
Diffuse myofiber atrophy
Cells uniformly decreased in size (due to low mechanical load)
Causes of hypertrophy
Exercise conditioning
Compensatory hypertrophy (compensation for loss of other myofibers)
Histology of hypertrophy
Diffuse enlargement of muscle cells
Histology of muscle degeneration
Multifocal (or regional) random pattern
Hydropic swelling, fatty change
Causes of muscle degeneration
Peracute/acute nutritional/toxic causes (i.e. selenium deficiency)
Histology of muscle necrosis (myonecrosis, rhabdomyolysis)
Segmental (portion of myfiber)
Loss of striations + hyper eosinophilic cytoplasm
Within 24-48 h —> macrophages/neutrophils infiltrate
Sequelae of necrosis
Regeneration (if basal lamina intact)
Fibrosis (if basal lamina destroyed)
Process of muscle regeneration
Removal of debris by macrophages —> sealing off injured areas —> satellite cell proliferation in basal lamina —> fusion of satellite cells into myofiber
Histo/gross appearance of muscle mineralization
Chalky white areas of gross specimen
Blue-purple granular material on histo
Types of mineralization
Dystrophic (necrosis, primary myopathy)
Metastatic (hypercalcemia)
Myositis
Inflammation of muscle
Follows necrosis
Associated with trauma, infection, infarction, immune-mediated
Inflammatory infiltrate gives clues to cause
X-linked muscular dystrophy
Mutation of dystrophin gene in young male dogs/cats
Dystrophin helps anchor muscle cell membranes to ECM —> integrity of muscle cell membrane affected
Polyphasic muscle necrosis —> macrophage infiltration / mineralization —> fibrosis
**Golden retrievers, Rottweilers
Clinical presentation of muscular dystrophy
Diffuse muscle atrophy
Splaying of limbs
Weakness
Equine Exertional Rhabdomyolysis
Aka: chronic intermittent rhabdomyolysis, exertional myopathy, Monday morning disease, tying up
Acute myofiber necrosis triggered by exercise
Potential cause: metabolic abnormality leading to oxidative damage
Monophonic or polyphasic
Clinical pathology of exertional rhabdomyolysis
Elevation of CK / AST
Myoglobinuria
(May lead to acute renal failure)
Clinical signs of exertional rhabdomyolysis
Sudden onset of stiff gait/reluctance to move/pain
+/- swelling of affected muscles (gluteal, femoral, lumbar groups)
Equine polysaccharide storage myopathy
Carbohydrate metabolism defect
Abnormal aggregates of polysaccharide, variable degress of myofiber necrosis
Related to equine exertional rhabdomyolysis
Masticatory myositis
Loss of any of muscles of mastication (Masseter, temporal, Pterygoids)
Multifocal, polyphasic necrosis with inflammation (eosinophilic, + lymphocytic)
AUTO-IMMUNE —> autoantibodies to Type 2M myosin isotope and myositigen (myosin-binding protein)
Young large breed dogs predisposed (G. Shepard, Rott)
Polymyositis
AUTO-IMMUNE - but don’t know protein target of antibodies
Multifocal, polyphasic necrosis with inflammation
Lymphocytic inflammation
Variable clinical signs by muscle affected (weakness, stiff gate, muscle atrophy, regurgitation, etc)
Adult dogs - Boxers, Newfies
Extraocular muscle myositis
Myositis of extraocular rectus and oblique muscles
RARE, not painful
Multifocal polyphasic necrosis with lymphocytic inflammation
Young female dogs (Goldens)
Immune mediated
Immune mediated myositis of horses
Associated with Strep equi —> immune complexes of antibodies to strep M protein
Hemorrhagic necrosis of muscle due to vascular injury
Increase in CK/AST, muscle weakness, pain
Vasculitis + fibrinoid necrosis of vascular walls, hemorrhage/infarcts in muscle; inflamm infiltration not seen in muscle
Infectious causes of muscle disease
Clostridium myositis —> black leg, pseudo-black leg
Leishmania
Nutritional myopathies
Selenium / Vit E deficiency
Toxic myopathies
Ionophores
Plants
Vascular myopathies
Vascular occlusive syndrome
Postanesthetic myopathy in horses
Downer syndrome (LA)
Compartment syndrome
Neoplasias
Rhabdomyoma/rhabdomyosarcoma
Infiltrative lipoma
Metastatic neoplasms (lymphosarcoma, hemangiosarcoma, malignant melanoma, carcinomas, sarcomas)
Rhabdomyoma
Benign tumor
Most common in larynx of young dogs —> respiratory distress (difficult to remove, need wide margins)
Rhabdomyosarcoma
Malignant, locally invasive; Rare
Histologic subtypes:
Embryonal, botryoid, alveolar (young dogs)
Pleomorphic (adult dogs)
Common sites of rhabdomyosarcoma
Urinary bladder, face skill, tongue
Infiltrative lipoma
Benign (doesn’t metastasize), but infiltrates muscle
Wide excision is curative but difficult
