MSK Flashcards
chrondrodysplasia
cattle and sheep
bulldog calves
spider lamb syndrome
scottish fold and american curl cats
bulldog calves
dexters and other miniature cattle breeds
mutations in ACAN gene
usually aborted between month 7 gestation
mutations not compatible with life
rotated short limbs
domed head
cleft palate
abdominal hernia
protruding mouth
lack of growth plates - tightly packed chondrocytes with no orderly arrangement
spider lamb syndrome
sheep
autosomal recessive
long limbs and neck
scoliosis
concave sternum
valgus deformity of forelimbs - knock knees
abnormal ossification centres in bone
scottish fold and american curl cats
autosomal dominant fold ears gene
irregular tarsal, carpal, metatarsal and metacarpal bones, phalanges and caudal vertebraw
defective endochondrial ossification
physeal dysplasia
cats - mostly overweight, male, large breeds
physeal dysplasia seen in all grown plates
femoral physeal fracture
head of femur avulsed
clusters of chondrocytes surrounded by abundant matrix
osteogenesis imperfecta
gene mutation
marked hypermobility of joints - unable to stand
brittle bones
calcified cartilage spindles
little osteoclast resorption
nutritional osteodystrophies
rickets
fibrous osteodystophy
osteoporosis
osteopenia - increased bone radiolucency
first lactation dairy cows, horses on bran based diet, copper deficient farm animals, rapidly growing animals with deficient diets, malabsorption syndrom
rickets
vitamin d and phosphorus deficiency (in carnivores - too much phosphorus –> secondary hyperparthyroidism –> rickets)
defective endochondrial ossification
most prominent at sites of rapid growth
and costochrondral junctions of large middle ribs - firm raised nodules
persistance of hypertrophic chondrocytes
rachitic rosary - typical in humans -
in adult animals - osteomalacia - softening of bones, growth plates not involved
common in alpacas because not enough sun –> vitamin D deficiency
fibrous oestodystrophy
metabolic/nutritional
persistent elevation of parathyroid hormone
primary hyperparathyroidism - will show high calcium and high phosphorous
secondary hyperparathyroidism - calcium and phosphorus will be normal
secondary more common cause
key features -
renal disease or dietary imbalance
osteoclastic bone resorption
bone replaced by fibrosis
deposition of new woven bone
bilateral enlargement of bones in face
vitamin A toxicity
in cats fed liver
inhibited chondrocyte proliferation and reduced RNA and protein synthesis
destabilisation of lysosomal membrane
physeal lesions
osteoporosis
lead toxicity
impaired osteoclastic resorption
lead line - band of sclerosis on xray
bacterial osteomyelitis
hematogenous, local extension of implantation
hematogenous common - joint ill
staph aureus - can invade osteoblasts
trueperella pyogenes - vertebral osteomyelitis
e coli, salmonella
lumpy jaw
atrophic rhinitis
lumpy jaw
cow
mandibular osteomyelitits
honeycomb appearance, pockets of inflammatory tissue
actinomyces bovis
atrophic rhinitis
pigs
bacterial toxins - pasteurella multocida and bortedella bronchiseptica - work together to inhibit bone cell differentiation and activity - wonky nose
viral bone infection
canine distemper and BVD - infect osteoclasts
impaired osteoclastic resorption
growth retardation lattice - dense band at metaphysis (similar to lead toxicity) - band of firm sclerotic bone instead of being nice and spongy looking
avascular necrosis of femoral head
legg-calves-perthes disease
westies
genetic - autosomal recessive
ischemia to femoral head- delayed incorporation of vessels supplying femoral head, blood doesn’t get there
subchondral epiphyseal osteonecrosis
types of fracture
transverse
linear
oblique non displaced - diagonal but pieces not separated
sprial
greenstick - just one side
comminuted - messy, smashed up
salter harris fractures - through growth plate
avulsion fracture - trauma at sites where ligaments attach, get pulled away and tear off a fragment of bone
salter harris fracture types
1 - straight through
2 - through and part up metaphysis
3 - through and though epiphysis
4 - cross - through growth plate, metaphysis and epiphysis
5 - crush injury
if break through growth plate while still growing then that part of the leg can no longer grow properly
fracture healing process
inflammation
soft callus formation
hard callus formation
remodelling
primary skeletal tumours
benign - osteoma, chondroma, fibroma
malignant - osteosarcoma, chrondrosarcoma, fibrosarcoma
osteosarcoma
most common bone tumout in dogs and cats
usually long bones
aggressive, painful and quick to metastasise
grey-white appearance
large pale areas surrounded by haemorrhage
doesn’t invade joint space
sunburst on xray
fibrosarcoma
appendicular skeleton or soft tissue
less common than osteosarcome but 3rd most common tumour of cats
can be injection site associated
relatively common in mouth
hypertrophic osteopathy (maries disease)
secondary to thoracic pathology, bladder tumours and hyperadrenocorticism
progressive bilateral ner bone formation in distal limbs
bone growth on outside of long bones
if seen look for underlying disease
can be secondary to bladder tumours in dogs and stomach tumours in horses
don’t know why
bone cysts
common in horse
just cysts in bones, may have some blood in
lung digit syndrome
cats
mammary, liver, lung and prostatic tumours metastasise to bone
third phalanx - nail bed destruction
stains used to investigate muscle disease
massons trichrome - differentiates collagen from other tissues (blue)
reticulin - stains reticular fibres - outlines individual muscle fibres
PTAH - stains cross striations
von kossa - stains carbohydrates and phosphates with calcium in mineralised fibres
alizarin red - strains calcium in necrotic and mineralised fibres
PAS - identifies glycogen and proteoglycans as well as protozoal cysts
process of muscle repair
destructive phase - satellite cells and macrophages migrate to site of injury - initial inflammation
regeneration phase - satellite cells generate new muscle fibres
remodelling phase - myoblasts mature new fibres
monophasic and polyphasic degeneration
monophasic - resulting from a single event
polyphasic - different stages of repair present at the same time, ongoing injury
muscle atrophy pathogenesis
various -
denervation
disuse
endocrine
malnutrition
congenital
sweeny
atrophy of supraspinatus or infraspinatus due to damage to suprascapular nerve
horses
immune mediated myositis
dogs
masticatory muscles - unique muscle type, bacterial infection can lead to misdirected antibodies against this type of fibre
bilaterla wasting
polyphasic muscle degeneration and necrosis
usually underlying systemic disease - lupus, lymphoma, thymoma
cats - FIV
wooden tongue
bacterial muscle disease - tongue
cattle
actinobacillus lignieresii
blackleg
bacterial muscle disease - legs
sheep
clostridium chauvoei
necrosis and gas formation
white muscle disease
vitamin e/selenium deficiency
porcine stress syndrome
stress –> defective calcium channels –> pale soft exudative pork
capture myopathy
stress from capture causing muscular disease
exertional rhabdomyolysis
mild - increased CK/AST/LDH, myoglobin release, myoglobinuria
severe - myoglobin toxic to renal cells –> renal failure
double muscling
congenital
myostatin defect
hyperplastic, hypertrophic muscles
congenital muscular dystrophy
defect in dystrophin
X linked
splay leg
congenital muscle disease
hyperkalemic periodic paralysis
congential defect in sodium channel
muscles
horses
polysaccharide storage myopathy
defect in glycogen handling
muscles
rhabdomyosarcomas
dog -
rhabdomyoma - larync
rhabdomyosarcoma - bladder
pig and guinea pig - rhabdomyoma - heart
horse osteoarthritis
age related
loss of articular cartilage
abnormal bone proliferation
synovial membrane dysfunction
subchondral sclerosis
commonly affecting hock, pastern, coffin, fetlock, knee and stifle joints
accounts for up to 60% of equine lamness
cause - either abnormal loading of normal cartilage or normal loading of abnormal cartilage or both
cartilage homeostasis
should be homeostasis between cartilage synthesis and degradation
synthesis - dependent on growth factors, hyaluronic acid, tissue inhibitors of MMPs
degradation - by cytokines, aggrecanases, MMPs (collagenases)
biomarkers of equine osteoarthritis
loss of articular cartilage (primary change)
subchondral bone remodelling
osteophytes
bone marrow lesions
changes in synovium
changes in joint capsule
changes in ligament
changes in peri articular muscles
meniscal tears and extrusion
pathogenesis of equine osteoarthritis
molecular changes to organisation of chondrocytes –> changes to ECM
proliferative response - chondrocytes make more ECM rapidly (unusual for chondrocytes)
catabolic factors released - break down of ECM - cartilage integrity lost
chondrocyte apoptosis - lose cartilage
OA signs
grading of equine OA
wear lines - vertical, deeper and further over worse
erosions of cartilage - horizontal, thicker worse
palmar arthroses - scored by deepness
equine osteoarthritis histo
chondrocyte necrosis - more orangey nuclei
chondrocyte formation - more groups of chondrocytes clumped together
fissuring or articular surface
focal cell loss - less chondrocytes
equine OA biological factors
Wnt signalling - altered in OA, leads to stopping production of ECM
complement - increased complement –> increased TNF and IL-B –> chondrocyte death and increase MMP production
circadian rhythm - chronic disturbances associated with elevated risk/acceleration of OA
roarer’s/laryngeal hemiplagia
horses
denervation atrophy in the larynx
right side normal - rounded, red-brown
left - atrophied, smaller, pale
due to unilateral nerve damage
(denervation atrophy usually only one side)
common in draught horses with the big collar on - damages laryngeal nerve
