Musculoskeletal - Muscle Flashcards
clinical signs of skeletal muscle injury
weakness
muscle spasm
abnormal gait
muscle atrophy
muscle hypertrophy
dysfunction
muscle swelling
skeletal muscle fibre types
type 1 - oxidative enzymes, repetitive slow movements
type 2 - glycogen, short bursts of activity
causes of muscle atrophy
denervation e.g. laryngeal hemiplegia
disuse e.g. while fracture is healing
malnutrition / cachexia / starvation (dietary, GIT disease)
endocrine disturbance - hypothyroidism and hypoadrenocorticism
congenital myopathies
how does regeneration occur?
Regeneration requires the presence of the basal lamina and satellite cells. Myocytes,
themselves cannot replicate and become new myocytes, the satellite cells that are along the
periphery must be stimulated by external factors such as: autocrine, vasculature, immune responses
from inflammatory cells, neurotransmitters from the motor neuron. Together these allow for
myofibril renewal.
how does fibrosis occur?
when the basal lamina has been destroyed
may follow any non-fatal injury
often associated with atrophy
necrosis
ossification - rare for of metaplasia
mineralisation - chalky white areas grossly, often associated with necrosis, primary myopathies, vitamin D toxicity
malignant hyperthermia pathogenesis
stress/halothane/depolarising muscle relaxants -> defective ryanodine receptor -> calcium channels remain open -> prolonged myofiber contraction and muscle rigidity -> hyperthermia, acute myonecrosis
pigs and horses
myofibrillar hypoplasia (splay leg)
decreased quantity and quality of myofibrils
occurs in all countries where there is well-developed intensive piggeries
cannot adduct legs and may not be able to suckle
unknown cause, transient
equine polysaccharide storage myopathy
quarterhorses, drafts and warmbloods
Accumulation of glycogen or complex polysaccharide within muscle myofiber resulting in loss of normal function
genetic defect GSY1 gene
muscular hypertrophy/hyperplasia (congenital)
double muscling
defective myostatin gene
myostatin functions to limit skeletal muscle growth
X-linked muscular dystrophy
homologous to Duchene’s muscular dystrophy in human males (degenerative myopathy)
due to a mutation in the dystrophin gene
Esophageal dysfunction can lead to aspiration
pneumonia in these cases, in addition lesions in the diaphragm and heart can elicit cardiovascular
arrest.
compartment syndrome
increased intramuscular pressure (exercise, oedema) leads to swelling and collapse of venous outflow -> eventual arterial collapse -> ischaemia
Skeletal muscle is highly vascularised with an exceptional system of anastomosing blood
vessels, therefore it is not easy to induce myofiber necrosis by occluding intermuscular arteries.
muscle crush syndrome / downer syndrome
ischaemic syndrome associated with increased external pressure created by objects or oneself
vascular occlusive syndrome
major vascular occlusion of a limb vessel
commonly seen as a saddle thrombus in cats
postanaesthetic myopathy in horses
occlusion of vessels from positioning under anaesthetic
selenium deficiency
test for selenium with glutathione peroxidase test -> a Se-dependent enzyme
pathogenesis: Vit E/Selenium deficiency = Deficiency in vitamin E and/or selenium → peroxidation of
membrane lipids (sometimes exacerbated by stress) → Ca2+ enters cytoplasm and mitochondria,
damaging respiratory mechanisms → cell death → symmetrical necrosis of the most active skeletal
muscle (like postural muscles)
toxic myopathies
ionophores e.g. monensin
- common coccidiostats used in poultry, and as growth promoters in cattle, sheep and other ruminants
- Ionophores alter membrane permeability to electrolytes by influencing transmembrane transport
leading to monophasic necrosis, unlike nutritional myopathies where there is polyphasic necrosis.
- mainly issue in dogs and horses - clinical signs include lethargy, stiffness, muscular weakness and recumbency
snake envenomation - myonecrosis
degenerative - necrotising myopathies
exertional myopathies - myofiber damage as a result of primary exercise stress
equine exertional rhabdomyolysis - tying up, gluteals lumbar and femoral muscles
capture rhabdomyolysis - wild animals stressed during capture
canine exertional rhabdomyolysis - racing greyhounds, sled dogs
myopathies associated with endocrine/metabolic diseases
hypothyroidism - altered carb metabolism, muscle atrophy of type 2 fibres (weight gain, lethargy)
hyperthyroidism - associated with increased catabolic state (weight loss, increased appetite, PU/PD)
hyperadrenocorticism - increased catabolism and inherited synthesis of muscle proteins (PU/PD, weight gain, non-pruritic alopecia)
primary canine masticatory myositis
immune-mediated
antibodies against myofibres of the masticatory muscles
early on = swelling of the muscles, difficulty opening the jaw
chronic = anorexia, weight loss, muscle atrophy, difficulty opening the jaw
microscopic inflammation with B cells, dendritic cells, macrophages
serology for 2M antibody blood test
polymyositis
immune-mediated
dogs - adults, GSDs most common
no type 2M antibodies
diagnosis involves extensive work up ruling out other diseases/conditions
muscle biopsy of affected muscles
suppurative myositis
myositis resulting from infection
often from inoculation via penetrating wound, contamination of injection site, laceration or extension
variably sized abscess
extraoccular polymyositis
immune-mediated
6-18 months of age, golden retrievers
bilateral extraocular swelling (protrusion of eyes)
visual, normotensive, not in pain
may resemble MMM
no type 2M antibodies
clostridial myositis
common and important in livestock
clostridial species = septicum, chauvoei, novyi, sordelli, perfirngens
moderate increase CK and AST
depression, fever, tachypnoea, toxemia
muscle necrosis is characteristic and often oedematous, haemorrhagic with variable gas production
