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Path EOY - Diseases > MSK > Flashcards

MSK Flashcards

1
Q

chrondrodysplasia

A

cattle and sheep

bulldog calves
spider lamb syndrome
scottish fold and american curl cats

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2
Q

bulldog calves

A

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

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3
Q

spider lamb syndrome

A

sheep
autosomal recessive

long limbs and neck
scoliosis
concave sternum
valgus deformity of forelimbs - knock knees
abnormal ossification centres in bone

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4
Q

scottish fold and american curl cats

A

autosomal dominant fold ears gene

irregular tarsal, carpal, metatarsal and metacarpal bones, phalanges and caudal vertebraw
defective endochondrial ossification

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5
Q

physeal dysplasia

A

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

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6
Q

osteogenesis imperfecta

A

gene mutation
marked hypermobility of joints - unable to stand
brittle bones
calcified cartilage spindles
little osteoclast resorption

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7
Q

nutritional osteodystrophies

A

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

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8
Q

rickets

A

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

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9
Q

fibrous oestodystrophy

A

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

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10
Q

vitamin A toxicity

A

in cats fed liver

inhibited chondrocyte proliferation and reduced RNA and protein synthesis
destabilisation of lysosomal membrane
physeal lesions
osteoporosis

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11
Q

lead toxicity

A

impaired osteoclastic resorption
lead line - band of sclerosis on xray

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12
Q

bacterial osteomyelitis

A

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

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13
Q

lumpy jaw

A

cow
mandibular osteomyelitits
honeycomb appearance, pockets of inflammatory tissue

actinomyces bovis

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14
Q

atrophic rhinitis

A

pigs
bacterial toxins - pasteurella multocida and bortedella bronchiseptica - work together to inhibit bone cell differentiation and activity - wonky nose

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15
Q

viral bone infection

A

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

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16
Q

avascular necrosis of femoral head

A

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

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17
Q

types of fracture

A

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

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18
Q

salter harris fracture types

A

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

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19
Q

fracture healing process

A

inflammation
soft callus formation
hard callus formation
remodelling

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20
Q

primary skeletal tumours

A

benign - osteoma, chondroma, fibroma

malignant - osteosarcoma, chrondrosarcoma, fibrosarcoma

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21
Q

osteosarcoma

A

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

22
Q

fibrosarcoma

A

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

23
Q

hypertrophic osteopathy (maries disease)

A

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

24
Q

bone cysts

A

common in horse

just cysts in bones, may have some blood in

25
Q

lung digit syndrome

A

cats
mammary, liver, lung and prostatic tumours metastasise to bone
third phalanx - nail bed destruction

26
Q

stains used to investigate muscle disease

A

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

27
Q

process of muscle repair

A

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

28
Q

monophasic and polyphasic degeneration

A

monophasic - resulting from a single event

polyphasic - different stages of repair present at the same time, ongoing injury

29
Q

muscle atrophy pathogenesis

A

various -
denervation
disuse
endocrine
malnutrition
congenital

30
Q

sweeny

A

atrophy of supraspinatus or infraspinatus due to damage to suprascapular nerve

horses

31
Q

immune mediated myositis

A

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

32
Q

wooden tongue

A

bacterial muscle disease - tongue
cattle
actinobacillus lignieresii

33
Q

blackleg

A

bacterial muscle disease - legs
sheep
clostridium chauvoei
necrosis and gas formation

34
Q

white muscle disease

A

vitamin e/selenium deficiency

35
Q

porcine stress syndrome

A

stress –> defective calcium channels –> pale soft exudative pork

36
Q

capture myopathy

A

stress from capture causing muscular disease

37
Q

exertional rhabdomyolysis

A

mild - increased CK/AST/LDH, myoglobin release, myoglobinuria

severe - myoglobin toxic to renal cells –> renal failure

38
Q

double muscling

A

congenital
myostatin defect
hyperplastic, hypertrophic muscles

39
Q

congenital muscular dystrophy

A

defect in dystrophin
X linked

40
Q

splay leg

A

congenital muscle disease

41
Q

hyperkalemic periodic paralysis

A

congential defect in sodium channel
muscles
horses

42
Q

polysaccharide storage myopathy

A

defect in glycogen handling
muscles

43
Q

rhabdomyosarcomas

A

dog -
rhabdomyoma - larync
rhabdomyosarcoma - bladder

pig and guinea pig - rhabdomyoma - heart

44
Q

horse osteoarthritis

A

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

45
Q

cartilage homeostasis

A

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)

46
Q

biomarkers of equine osteoarthritis

A

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

47
Q

pathogenesis of equine osteoarthritis

A

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

48
Q

grading of equine OA

A

wear lines - vertical, deeper and further over worse
erosions of cartilage - horizontal, thicker worse
palmar arthroses - scored by deepness

49
Q

equine osteoarthritis histo

A

chondrocyte necrosis - more orangey nuclei
chondrocyte formation - more groups of chondrocytes clumped together
fissuring or articular surface
focal cell loss - less chondrocytes

50
Q

equine OA biological factors

A

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

51
Q

roarer’s/laryngeal hemiplagia

A

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

Path EOY - Diseases (11 decks)

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