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111 Cards in this Set

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osteochondrosis: signalment
dogs, pigs, horses, turkey, broilers, cattle

young animals, growing rapidly, M > F, esp. of large size
osteochondrosis: etiology
hereditary factors
high plane of nutrition
pushed for rapid growth
trauma
weight bearing
Cu deficiency (horses)
osteochondrosis: pathogenesis
local ischemia (vessels in AE complex die prematurely) --> necrotic cartilage --> failure of mineralization of necrotic cartilage --> failure of endochondral ossification --> plug of dead cartilage + trauma to weight bearing region --> fx in dead plug --> leakage of synovial fluid into cartilage --> inflammation --> synovial hyperplasia --> joint mice --> chronic DJD --> ossification of cartilaginous flaps, synovial metaplasia, bone marrow fibrosis, remodeling of trabeculae, sclerosis of subchondral bone
most common sites of osteochondrosis
a. dog
b. pig
c. horse
d. poultry
a. shoulder
b. stifle, elbow
c. stifle, shoulder
d. tibia (tibial dyschondroplasia)
main defect in osteochondrosis
failure of endochondral ossification
2 major types of dwarfs
- non-pituitary dependent: disproportionate dwarfs

- pituitary dependent: proportionate dwarfs
main defect in non-pituitary dependent dwarfs
failure of endochondral ossification
chondrodysplasia (dwarfism) in cattle, dogs: main lesions
defective longitudinal growth but normal width growth --> short, stubby bones w/ wide, mushroom shaped epiphyses

ossification centers don’t form in epiphyses --> epiphysis is a solid cap of cartilage
primary lesion in pituitary dependent dwarfs
failure of adenohypophysis to develop --> panhypopituitarism --> secondary hypofunction of multiple endocrine organs
osteopetrosis: major defect in mammals
malfunctioning osteoclasts that fail to resorb bone (excess ENDOSTEAL bone)
osteopetrosis: lesions
excess mineralized bone & mineralized cartilage in bones --> solid but fragile bones that contain lacking medullary cavity
osteopetrosis: prevalence & px
rare

lethal
osteogenesis imperfecta: major defect
defect in quantity &/or quality of type I collagen --> grossly normal but extremely fragile bones & hypermobility of joints
osteogenesis imperfecta

a. lesions
b. prevalence
c. px
a. blue sclera, fx bones, fx teeth, fx ribs in utero, translucent pink/gray teeth
b. rare
c. terrible
malformation abnormalities:

a. amelia
b. syndactyly
c. micromelia
d. brachygnathia inferior
e. polydactyly
f. brachygnathia superior
g. adactyly
a. absence of a limb
b. fused digits
c. abnormally small limb
d. undershot of jaw
e. extra digits
f. overshot of jaw
g. no digits
angular limb deformities: pathogenesis
usually d/t abnormality in a part of 1 physis (focal closure of physis) --> 1 side of bone continues to grow & becomes longer than other side
parathyroid hormone (PTH)

a. secreted d/t:
b. effects
a. secreted d/t low calcium

b. effects:
- osteoclastic osteolysis (PTH receptors on OSTEOBLASTS)
- ↑ reabsorption of Ca, ↑ excretion of P (hyperphosphaturia) by kidneys
- ↑ vitamin D production/activation by kidney
- ↑ GI absorption of Ca & P d/t ↑ vitamin D
calcitonin

a. secreted d/t:
b. effects
a. secreted d/t high calcium

b. effects:
- inhibits osteoclasts
- ↑ excretion of Ca & P by kidneys
vitamin D

a. secreted d/t:
b. effects
a. secreted d/t PTH, low phosphorous

b. effects
-increases serum Ca & P (esp. Ca) by increasing GI absorption of both
-required for mineralization of bone
rickets: signalment
young, growing animals
rickets: etiology
vitamin D deficiency: dietary, no sunlight, renal dz, etc.

OR

phosphorous deficiency
rickets: main defect
failure of endochondral ossification
rickets: lesions
- wide, irregular epiphyseal plates w/ long tongues of cartilage projecting into metaphysis
- growth plate: irregular contour, thickened
- “rachitic rosary”: swollen costochondral junction
- numerous thick unmineralized & weak trabeculae b/c no osteoclastic resorption (only mineralized bone resorbed) --> osteomalacia
osteomalacia

a. etiology
b. signalment
c. lesions
a. impaired mineralization in osteoid (newly formed bone) d/t vitamin D or P deficiency
b. adult animals
c. excess osteoid on bone spicules accumulates --> thick, weak, soft bone
fibrous osteodystrophy (FOD): pathogenesis
increased PTH --> increased osteoclastic osteolysis --> extensive bone resorption & replacement w/ fibrous tissue & woven bone --> weak (but mineralized) bone
FOD: etiology
hyperparathyroidism

primary: parathyroid adenoma (rare)
secondary: renal failure or nutritional imbalance
FOD secondary to renal failure: pathogenesis
hypocalcemia, hyperphosphatemia d/t renal failure --> 2° hyperparathyroidism & ↑ in PTH secretion

uncommon to have clinical signs related to bone lesions
FOD secondary to nutritional imbalance: pathogenesis
- low Ca diet
- high P diet (ex. bran  “Big Head dz”, liver, nuts)
FOD: how to dx
quantitate Ca/P in urine (fractional excretion study): esp. P; analyze feed (Ca:P ratio should be ~ 1:1)
FOD: lesions
- excessive fibrous tissue
- marked ↓ in bone density
- bilateral swelling of maxillae &/or mandibles: “big head”
FOD: species affected
-horses, pigs, goats: usually secondary nutritional

-dogs, cats: usually secondary renal

-rare in cattle & sheep
osteoperosis: major defect
↓ amt. of normally mineralized bone d/t ↓ bone production w/ normal or mildly ↑ resorption
osteoperosis: etiology
- nutritional: available protein used for energy production, not synthesis of bone, muscle, etc. (serous atrophy of fat)

- disuse: immobilization, casts (need wt. bearing to stimulate bone production)

- other: IBD, parasitism, corticosteroids
osteoperosis: lesions
- serous atrophy of fat

- growth arrest lines in metaphysis: intermittent periods of premature physeal closure followed by reactivation of growth (often d/t alternating periods of starvation &/or parasitism)

-thin cortices (if severe)

- depletion of trabecular bone in metaphysis (holes in bone)
vitamin D toxicity

a. pathogenesis
b. etiology
a. excessive vitamin D effects GI, kidney --> hypercalcemia, hyperphosphatemia --> mineralization of soft tissue thru out body

progressive renal & cardiac mineralization --> death, often before bone lesions develop

b. plants (Solanum), rodenticides
vitamin A deficiency

a. pathogenesis
b. prevalence
a. failure of bone resorption along endosteal surface --> thick bones w/ ↓ central cavity

b. rare
vitamin A toxicity

a. lesions
b. etiology
c. prevalence
a. exostoses: hip, stifle, shoulder, elbow, cervical vertebrae; fused cervical vertebrae

b. primarily cats fed raw beef liver for several months

c. rare
copper deficiency

a. pathogenesis
b. prevalence
a. abnormal collagen (Cu required for cross linkage) --> increased bone fragility
b. rare
lead toxicity

a. pathogenesis
b. lesions
a. impaired osteoclastic & chondroclastic resorption --> persistence of mineralized cartilage in metaphysis

b. lead line: double line in metaphysis; metaphyseal sclerosis
ddx for hyperostoses
- vitamin A toxicity
- fluorine toxicity
- HOD
- HO
- craniomandibular osteopathy - eosinophilic panosteitis
- hepatozoonosis
- Coccidiodes Immitis
canine hypertrophic osteodystrophy (HOD): signalment
young, rapidly growing dogs (3-6 mos.), large breeds
HOD: etiology
probably infectious (bacterial, canine distemper)
HOD: clinical signs
intermittent fever, lameness, swollen metaphyses (esp. distal tibia, radius, ulna)
HOD: lesions
PNB
microfractures or osteomyelitis subadjacent to physis
multiple bones involved
HOD: px
good if dz is mild: ↓ plane of nutrition, cage rest --> lesions resolve (excess bone resorbed)
hypertrophic osteopathy (HO): pathogenesis
likely neurogenic or vascular

pulmonary or abdominal lesion (ore some other space occupying mass) stimulates production of periosteal new bone
HO: lesions
markedly thickened distal limbs d/t excessive PNB formation along diaphysis & metaphyses

usually long bones (appendicular skeleton), not axial (vertebrae)
HO: px
bone lesions resolve if mass removed
craniomandibular osteopathy: signalment
usually young dogs (~8 mo.), Westies, Scotties, Cairn Terriers, Labs, Dobermans
craniomandibular osteopathy

a. etiology
b. lesions
c. px
d. ddx for lesion
a. unknown

b. excess PNB along mandibles, occ. occipital & temporal bones

c. good, lesions may regress by 11-15 mo.

d. osteomyelitis, tooth abscess, trauma, CMO
eosinophilic panosteitis: lesion
increased ENDOSTEAL new bone --> ↑ radiodensity in DIAPHYSIS of long bones (usually forelimbs only)
eosinophilic panosteitis: signalment
usually young (6-18 mo.), large breed dogs, esp. GSD; M > F
Hepatozoonosis

a. signalment
b. lesion
a. dogs in Texas (rare)

b. subperiosteal new bone along vertebral column & rarely along limbs
Coccidiodes immitis

a. signalment
b. lesion
a. dogs in southwest US

b. fungal osteomyelitis that produces excess PNB, often on vertebrae (lumbar most common)
top 2 causes of necrosis of bone
1. infection
2. ischemia
What factors affect healing of necrotic bone?
-volume of dead bone
-status of blood supply
-presence of infection
Define sequestrum & involucrum
sequestrum: necrotic pieces of bone isolated in middle of lesion

involucrum: surrounding granulation tissue & sclerotic bone
Legg-Perthes' dz: signalment
small breed dogs 4-11 mos. of age; poodles, terriers, F > M
Legg-Perthes' dz: pathogenesis
aseptic necrosis of femoral head

blood vessels supplying femoral head run along femoral neck (prone to injury)

susceptible breeds have delayed incorporation of vessels into fibro-osseous canals, which protect vessels from injury

continued wt. bearing --> fragmentation or fx of necrotic bone --> deformed & malfunctioning femoral head
Legg-Perthes' dz: px
removal of femoral head: good px

else, dog will develop DJD
2 routes of infectious osteomyelitis

Which is more common?
How many bones involved in each?
direct extension: 1 bone
hematogenous: multiple bones

direct extension more common
Examples of osteomyelitis caused by direct extension
-foot rot: sheep, cattle
-atrophic rhinitis (Bordatella + Pateurella): pigs
- endotoxin --> ↑ osteoclastic osteolysis via cytokines released from inflammatory cells, ↓ osteoblast production --> marked ↓ of turbinates & bone
-middle ear: any species
-chronic periodontal dz: common
-bite wound: culture for ANAEROBES
osteomyelitis caused by hematogenous spread

a. signalment
b. site of infection in bone
c. causes
a. young animals

b. usually lodges in metaphysis: (or epiphysis): caps patent at their endpoint in metaphyses --> bacteria exit soft tissue there

c. compromised immune system ↑ likelihood of dz (ex. failure of passive transfer of colostrum), umbilicus, sx
common etiologic agents for osteomyelitis caused by hematogenous spread

a. foals
b. cattle
c. dogs
d. poultry
a. E. coli, Strep, Salmonella, Klebsiella
b. Actinomyces bovis (lumpy jaw)
c. Coccididoes immitis, Hepatozoon canis, Brucella
d. Staph aureus (green livers)
non-infectous osteomyelitis

a. cause
b. sequelae
a. often d/t localized periosteal trauma (single or repeated)
b. often leads to formation of exostoses or osteophytes (ex. splint bones in horses)
osteosarcoma: signalment in dogs
large breeds, males 2x more frequent than females, avg. age: 7.5 yrs
osteosarcoma: most common sites in dogs
originates in medullary cavity of METAPHYSIS of long bones

most common sites: proximal humerus, distal radius, distal femur, proximal tibia

if found in diaphysis, highly probable that there was a previous fx of that bone & OSA is arising in that fx site d/t poor healing of fx: ↑ bone turnover for a prolonged period --> neoplastic transformation
osteosarcoma: most common site in cats
flat bones most common site (skull: #1 site)
osteosarcoma: radiographic signs in dogs
rads: lysis + sclerosis

elevated periosteum by tumor + considerable amt. of reactive new bone formation forms a triangle of new growth (“Codman’s triangle”)

“sunburst” appearance: array of radiating bone spicules that project from neoplasm into adj. soft tissue

pulmonary mets
osteosarcoma: radiographic signs in cats
rads: lysis of metaphysis --> “moth eaten” appearance

NO PNB formation
osteosarcoma: px

a. cats
b. dogs
a. cats: good w/ amputation in appendicular OSA, poor in axial OSA

b. dogs: poor
osteosarcoma: keys for biopsy
3 sites in metaphysis

choose lytic regions

must enter medullary cavity
chondrosarcoma

a. signalment in dogs
b. common sites
a. medium to large breeds, middle aged (10% of bone tumors in dogs)
b. flat bones in ribs, sternum, pelvis, turbinates
fibrosarcoma: common sites in dogs
periosteal surface of facial bones is most common site (nasal, oral fibrosarcomas are relatively common)
mutilobular osteoma & chondroma
head of dogs

locally aggressive

may become malignant
multiple cartilaginous exostoses (osteochondromatosis)

a. prevalence
b. signalment
c. lesions
a. rare

b. young animals

c. multiple firm nodules near costochondral junctions & metaphyses
synovial sarcoma

a. prevalence
b. site
a. rare

b. in JOINT, yet may extend into bones on both sides of joint space
histiocytic sarcoma

1. prevalence
2. px
3. behavior
1. relatively common in Rotties, Mastiffs, Retrievers
2. poor
3. rapidly growing, locally aggressive tumor often occurring in close proximity to a joint in dogs
-frequently met to regional ln’s & occasionally to lungs & other visceral organs
multiple myeloma

a. lesions
b. lab findings
a. mutiple lytic lesions in BM of multiple bones, esp. ribs & vertebrae

b. hypercalcemia in ~10% of dogs, monoclonal spike on electrophoresis
invertebral disc disease (IVDD): most common sites
lumbar (75% b'twn T-12 & L-2) & cervical vertebrae (15%)

rare in thoracic vertebrae d/t intercapital ligaments connecting heads of ribs across top of annulus fibrosus
IVDD: most common direction of disc protrusion
dorsal most common b/c annulus is thinner dorsally
possible sequelae to IVDD
- if mild, pain, or if severe, paraplegia w/ hemorrhage & necrosis of spinal cord

-fibrocartilaginous embolism: emboli of nucleus pulposus enters vascular spaces --> acute necrosis of spinal cord (ischemic myelopathy); primarily in giant breeds of dogs

-ankylosing spondylosis: ventral herniation, usually not a problem
IVDD: chondrodystrophic breeds

a. age of onset
b. pathogenesis
a. degeneration starts by 1 year of age, see problems b’twn ages 1-3

b. nucleus pulposus loses fluid & pliability  becomes mineralized, “cheesy” --> crumbles --> annulus fibrosus starts progressive degeneration
IVDD: non-chondrodystrophic breeds

a. age of onset
b. pathogenesis
a. degeneration starts during middle age (~5 yrs)

b. degeneration starts in annulus fibrosus --> nucleus pulposus gradually becomes dried out, but never mineralizes (fibrotic)
ankylosis spondylosis

a. species
b. pathogenesis
a. cats: vit A toxicity (very rare), bulls, dogs (incidental finding)

b. tearing of annulus from ventral margin of vertebral body --> osteophyte formation on ventral & lateral margins of vertebrae, may bridge IV disc & fuse
discospondylitis

a. pathogenesis
b. dogs: common organisms, site
c. dogs: signalment
a. IV disc infection & inflammation that extends into adjacent vertebra --> osteomyelitis
b. Staph auerus, Brucella; lumbosacral vertebrae
c. large breed dogs, M > F
degenerative joint dz (DJD): 2 types
primary: aging changes in cartilage + wt. bearing --> lesions is large joints

secondary:
- developmental: d/t OCD, hip dysplasia, conformational defects, etc. (common)
- acquired: d/t trauma, fx, infections, metabolic bone dz, necrosis of bone, idiopathic
DJD: gross lesions
-larger wt. bearing joints usually most severely affected
-soft, yellow cartilage
-fibrillation: fraying of cartilage
-exposure of subchondral bone
-eburnation: sclerosis of exposed subchondral bone
-joint mice
-proliferating synovial tissue
-ankylosis
-excess joint fluid of poor quality
-osteophytes
-pannus formation: extension of granulation tissue of articular cartilage from synovial membrane
hip dysplasia: etiology
-hereditary/development disorder
-ratio of muscle mass: pelvic size is a predicting index
-OC predisposes or is manifested as hip dysplasia in coxofemoral joint
-overnutrition, rapid growth may contribute
hip dysplasia: lesions
-shallow acetabulum
-flattened femoral head
-femoral neck lacks definition: filled w/ new bone
-osteophytes usually on bones adj. to joints
-degenerative changes on articular cartilage of femoral head
cervical vertebral stentoic myelopathy ("wobbler"): signalment
horse: ataxia in young rapidly growing males (3x F)
- usually C3-C4 or C6-C7

dog: Great Danes, Dobermans, usually C6-C7
cervical vertebral stentoic myelopathy ("wobbler"):

a. etiology
b. pathogenesis
c. px
a. mutifactorial (genetic, overnutrition, etc.)

b. variety of cervical vertebral malformations --> compression & injury of spinal cord & stenosis of vertebral canal

c. poor
arthritis/synovitis: direct extension

a. number of joints involved
b. causes
a. usually one 1 joint involved
b. puncture wound, extension from localized soft tissue lesion
arthritis/synovitis: hematogenous

a. source
b. why this is most common route (3 reasons)
c. number of joints involved
a. source in young animals: septicemia (often umbilicus (failure of passive transfer) or surgical procedure)
-if old, often d/t endocarditis

b.
-synovial membrane has tiny vessels to trap emboli
-synovial fluid is a good nutrient
-difficult for host defense mechanisms to enter joint

c. usually a polyarthritis
non-infectious arthritis

a. species usually affected
b. joint fluid
c. number of joints affected
d. pathogenesis
a. dogs, cats
b. fluid contains mostly neutrophils even though etiology in non-infectious
c. polyarthritis
d. inflammation 2º to persistence of antigenic material in synovium
hygroma

a. definition
b. species affected
a. enlarged bursa over carpi & tarsi

b. cows, goats, dogs
ddx for mineralization of muscle
white muscle dz
exertional rhabdomyolysis
vitamin D toxicity (d/t plants, rodenticides)
creatine kinase: kinetics
increases rapidly after muscle injury & returns to normal very quickly (peak 6-12 hrs, back to normal w/in 24-48 hrs)

magnitude of increase matters (will increase w/ slight muscle injury)
AST: kinetics
increases more slowly than CPK and stays elevated longer (peak: 24-36 hrs post injury)
ddx for red/brown urine
horse: think myoglobin 1st, dog: think Hb 1st

hematuria: hemorrhage

hemoglobinuria: hemolysis (ex. Red Maple)
-PCV: N to ↓, pink to icteric plasma, precipitate on ammonium sulfate test

myoglobinuria: exertion rhabdomyolsis
-PCV N to ↑, clear to icteric plasma, no precipitate on ammonium sulfate test
myoglobin: response to muscle injury
released from dead/dying muscle

generally severe, acute injury (esp. in horses, wild animals)

excreted in urine --> urine brown, plasma clear (cleared quickly)
myasthenia gravis: acquired
Ab against Ach receptors in adult dogs

dysphagia, megaesophagus

may be assoc. w/ thymoma
myasthenia gravis: congenital
several breeds, incl. Jack Russell, Springer Spaniels, Smooth Fox Terriers

deficiency of Ach receptors: NOT immune mediated
examples of ischemia in muscle

a. cat
b. horse
c. cow
a. cardiomyopathy --> saddle thrombi --> ischemic muscle necrosis in pelvic limbs (↑↑ CPK)

b. usually associated w/ prolonged anesthetic procedures

c. assoc. w/ obturator n. paralysis post-calving w/ dystocia
causes of bacterial myositis d/t direct extension
-IM injections: discolored muscle, muscle necrosis (ex. Banamine in neck of horses)
-cat bite: Pateurella
-wooden tongue: Actinobacillus lignieresii
-gas gangrene (Clostridium): spores introduced from soil via penetrating foreign body
-lumpy jaw: Actinomyces
-black leg: Clostridium chauvoei

myositis d/t septicemia is rare
masticatory muscle myositis

a. acute lesions
b. chronic lesions
c. etiology
d. species
a. eosinophilic, swollen, edematous, hard, painful

b. atrophic myositis

c. Ab to particular fiber type in masticatory muscle

d. dog
2 causes of muscle atrophy
disuse: common
neurogenic:
-roarers: horses (left recurrent laryngeal nerve injury)
-radial n. injury
rhabdomyoma/rhabdomyosarcoma

a. classic location in dog
b. other commonly affected locations
a. laryngeal muscle

b. urinary bladder, cardiac muscle
leiomyoma

a. common locations
b. lab finding
a. GI, bladder, vagina

b. may have hypoglycemia
top ddx for discrete white mass in muscle
LSA
3 ddx for failure of endochondral ossification
osteochondrosis
non-pituitary dwarfism
rickets