Musculoskeletal - Muscle

Question 1

clinical signs of skeletal muscle injury

Answer 1

weakness
muscle spasm
abnormal gait
muscle atrophy
muscle hypertrophy
dysfunction
muscle swelling

Question 2

skeletal muscle fibre types

Answer 2

type 1 - oxidative enzymes, repetitive slow movements
type 2 - glycogen, short bursts of activity

Question 3

causes of muscle atrophy

Answer 3

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

Question 4

how does regeneration occur?

Answer 4

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.

Question 5

how does fibrosis occur?

Answer 5

when the basal lamina has been destroyed
may follow any non-fatal injury
often associated with atrophy

Question 6

necrosis

Answer 6

ossification - rare for of metaplasia
mineralisation - chalky white areas grossly, often associated with necrosis, primary myopathies, vitamin D toxicity

Question 7

malignant hyperthermia pathogenesis

Answer 7

stress/halothane/depolarising muscle relaxants -> defective ryanodine receptor -> calcium channels remain open -> prolonged myofiber contraction and muscle rigidity -> hyperthermia, acute myonecrosis

pigs and horses

Question 8

myofibrillar hypoplasia (splay leg)

Answer 8

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

Question 9

equine polysaccharide storage myopathy

Answer 9

quarterhorses, drafts and warmbloods
Accumulation of glycogen or complex polysaccharide within muscle myofiber resulting in loss of normal function
genetic defect GSY1 gene

Question 10

muscular hypertrophy/hyperplasia (congenital)

Answer 10

double muscling
defective myostatin gene
myostatin functions to limit skeletal muscle growth

Question 11

X-linked muscular dystrophy

Answer 11

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.

Question 12

compartment syndrome

Answer 12

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.

Question 13

muscle crush syndrome / downer syndrome

Answer 13

ischaemic syndrome associated with increased external pressure created by objects or oneself

Question 14

vascular occlusive syndrome

Answer 14

major vascular occlusion of a limb vessel
commonly seen as a saddle thrombus in cats

Question 15

postanaesthetic myopathy in horses

Answer 15

occlusion of vessels from positioning under anaesthetic

Question 16

selenium deficiency

Answer 16

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)

Question 17

toxic myopathies

Answer 17

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

Question 18

degenerative - necrotising myopathies

Answer 18

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

Question 19

myopathies associated with endocrine/metabolic diseases

Answer 19

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)

Question 20

primary canine masticatory myositis

Answer 20

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

Question 21

polymyositis

Answer 21

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

Question 22

suppurative myositis

Answer 22

myositis resulting from infection
often from inoculation via penetrating wound, contamination of injection site, laceration or extension
variably sized abscess

Question 23

extraoccular polymyositis

Answer 23

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

Question 24

clostridial myositis

Answer 24

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

Question 25

granulomatous myositis

Answer 25

more common in the tongue
e.g. actinobacillosis - wooden tongue

Question 26

myasthenia gravis

Answer 26

a chronic autoimmune, neuromuscular disease that causes weakness in the skeletal muscles that worsens after periods of activity and improves after periods of rest.

acquired form = may be associated with neoplasia or hypothyroidism, production of antibodies against the acetylcholine receptor, common in great dane, golden, lab, clinical signs include voice changes, oxercise-related weakness, inability to close eyes even when sleeping, excessive drooling, difficulty breathing

congenital form = JRT, smooth fix terrier, springer spaniel, exercise-induced weakness and collapse

diagnosis - detection of circulating anti-acetylcholine receptor antibodies
treatment - pyridostigmine bromide for entire life of patient

Question 27

repair process of tendons

Answer 27

tendons have the ability to repair, however, the type 1 collagen is replaced by type 3 collagen - less elastic and decreased ability to withstand forces

tendons can naturally undergo cartilaginous metaplasia - however osseous metaplsia is pathologic