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111 Cards in this Set
- Front
- Back
osteochondrosis: signalment
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dogs, pigs, horses, turkey, broilers, cattle
young animals, growing rapidly, M > F, esp. of large size |
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osteochondrosis: etiology
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hereditary factors
high plane of nutrition pushed for rapid growth trauma weight bearing Cu deficiency (horses) |
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osteochondrosis: pathogenesis
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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
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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) |
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main defect in osteochondrosis
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failure of endochondral ossification
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2 major types of dwarfs
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- non-pituitary dependent: disproportionate dwarfs
- pituitary dependent: proportionate dwarfs |
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main defect in non-pituitary dependent dwarfs
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failure of endochondral ossification
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chondrodysplasia (dwarfism) in cattle, dogs: main lesions
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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 |
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primary lesion in pituitary dependent dwarfs
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failure of adenohypophysis to develop --> panhypopituitarism --> secondary hypofunction of multiple endocrine organs
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osteopetrosis: major defect in mammals
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malfunctioning osteoclasts that fail to resorb bone (excess ENDOSTEAL bone)
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osteopetrosis: lesions
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excess mineralized bone & mineralized cartilage in bones --> solid but fragile bones that contain lacking medullary cavity
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osteopetrosis: prevalence & px
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rare
lethal |
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osteogenesis imperfecta: major defect
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defect in quantity &/or quality of type I collagen --> grossly normal but extremely fragile bones & hypermobility of joints
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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 |
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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 |
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angular limb deformities: pathogenesis
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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
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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 |
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calcitonin
a. secreted d/t: b. effects |
a. secreted d/t high calcium
b. effects: - inhibits osteoclasts - ↑ excretion of Ca & P by kidneys |
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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 |
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rickets: signalment
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young, growing animals
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rickets: etiology
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vitamin D deficiency: dietary, no sunlight, renal dz, etc.
OR phosphorous deficiency |
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rickets: main defect
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failure of endochondral ossification
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rickets: lesions
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- 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 |
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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 |
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fibrous osteodystrophy (FOD): pathogenesis
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increased PTH --> increased osteoclastic osteolysis --> extensive bone resorption & replacement w/ fibrous tissue & woven bone --> weak (but mineralized) bone
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FOD: etiology
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hyperparathyroidism
primary: parathyroid adenoma (rare) secondary: renal failure or nutritional imbalance |
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FOD secondary to renal failure: pathogenesis
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hypocalcemia, hyperphosphatemia d/t renal failure --> 2° hyperparathyroidism & ↑ in PTH secretion
uncommon to have clinical signs related to bone lesions |
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FOD secondary to nutritional imbalance: pathogenesis
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- low Ca diet
- high P diet (ex. bran “Big Head dz”, liver, nuts) |
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FOD: how to dx
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quantitate Ca/P in urine (fractional excretion study): esp. P; analyze feed (Ca:P ratio should be ~ 1:1)
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FOD: lesions
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- excessive fibrous tissue
- marked ↓ in bone density - bilateral swelling of maxillae &/or mandibles: “big head” |
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FOD: species affected
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-horses, pigs, goats: usually secondary nutritional
-dogs, cats: usually secondary renal -rare in cattle & sheep |
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osteoperosis: major defect
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↓ amt. of normally mineralized bone d/t ↓ bone production w/ normal or mildly ↑ resorption
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osteoperosis: etiology
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- 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 |
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osteoperosis: lesions
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- 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) |
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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 |
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vitamin A deficiency
a. pathogenesis b. prevalence |
a. failure of bone resorption along endosteal surface --> thick bones w/ ↓ central cavity
b. rare |
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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 |
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copper deficiency
a. pathogenesis b. prevalence |
a. abnormal collagen (Cu required for cross linkage) --> increased bone fragility
b. rare |
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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 |
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ddx for hyperostoses
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- vitamin A toxicity
- fluorine toxicity - HOD - HO - craniomandibular osteopathy - eosinophilic panosteitis - hepatozoonosis - Coccidiodes Immitis |
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canine hypertrophic osteodystrophy (HOD): signalment
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young, rapidly growing dogs (3-6 mos.), large breeds
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HOD: etiology
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probably infectious (bacterial, canine distemper)
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HOD: clinical signs
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intermittent fever, lameness, swollen metaphyses (esp. distal tibia, radius, ulna)
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HOD: lesions
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PNB
microfractures or osteomyelitis subadjacent to physis multiple bones involved |
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HOD: px
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good if dz is mild: ↓ plane of nutrition, cage rest --> lesions resolve (excess bone resorbed)
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hypertrophic osteopathy (HO): pathogenesis
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likely neurogenic or vascular
pulmonary or abdominal lesion (ore some other space occupying mass) stimulates production of periosteal new bone |
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HO: lesions
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markedly thickened distal limbs d/t excessive PNB formation along diaphysis & metaphyses
usually long bones (appendicular skeleton), not axial (vertebrae) |
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HO: px
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bone lesions resolve if mass removed
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craniomandibular osteopathy: signalment
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usually young dogs (~8 mo.), Westies, Scotties, Cairn Terriers, Labs, Dobermans
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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 |
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eosinophilic panosteitis: lesion
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increased ENDOSTEAL new bone --> ↑ radiodensity in DIAPHYSIS of long bones (usually forelimbs only)
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eosinophilic panosteitis: signalment
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usually young (6-18 mo.), large breed dogs, esp. GSD; M > F
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Hepatozoonosis
a. signalment b. lesion |
a. dogs in Texas (rare)
b. subperiosteal new bone along vertebral column & rarely along limbs |
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Coccidiodes immitis
a. signalment b. lesion |
a. dogs in southwest US
b. fungal osteomyelitis that produces excess PNB, often on vertebrae (lumbar most common) |
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top 2 causes of necrosis of bone
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1. infection
2. ischemia |
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What factors affect healing of necrotic bone?
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-volume of dead bone
-status of blood supply -presence of infection |
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Define sequestrum & involucrum
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sequestrum: necrotic pieces of bone isolated in middle of lesion
involucrum: surrounding granulation tissue & sclerotic bone |
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Legg-Perthes' dz: signalment
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small breed dogs 4-11 mos. of age; poodles, terriers, F > M
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Legg-Perthes' dz: pathogenesis
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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 |
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Legg-Perthes' dz: px
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removal of femoral head: good px
else, dog will develop DJD |
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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 |
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Examples of osteomyelitis caused by direct extension
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-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 |
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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 |
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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) |
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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) |
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osteosarcoma: signalment in dogs
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large breeds, males 2x more frequent than females, avg. age: 7.5 yrs
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osteosarcoma: most common sites in dogs
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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 |
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osteosarcoma: most common site in cats
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flat bones most common site (skull: #1 site)
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osteosarcoma: radiographic signs in dogs
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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 |
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osteosarcoma: radiographic signs in cats
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rads: lysis of metaphysis --> “moth eaten” appearance
NO PNB formation |
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osteosarcoma: px
a. cats b. dogs |
a. cats: good w/ amputation in appendicular OSA, poor in axial OSA
b. dogs: poor |
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osteosarcoma: keys for biopsy
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3 sites in metaphysis
choose lytic regions must enter medullary cavity |
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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 |
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fibrosarcoma: common sites in dogs
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periosteal surface of facial bones is most common site (nasal, oral fibrosarcomas are relatively common)
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mutilobular osteoma & chondroma
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head of dogs
locally aggressive may become malignant |
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multiple cartilaginous exostoses (osteochondromatosis)
a. prevalence b. signalment c. lesions |
a. rare
b. young animals c. multiple firm nodules near costochondral junctions & metaphyses |
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synovial sarcoma
a. prevalence b. site |
a. rare
b. in JOINT, yet may extend into bones on both sides of joint space |
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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 |
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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 |
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invertebral disc disease (IVDD): most common sites
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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 |
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IVDD: most common direction of disc protrusion
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dorsal most common b/c annulus is thinner dorsally
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possible sequelae to IVDD
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- 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 |
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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 |
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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) |
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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 |
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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 |
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degenerative joint dz (DJD): 2 types
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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 |
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DJD: gross lesions
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-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 |
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hip dysplasia: etiology
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-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 |
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hip dysplasia: lesions
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-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 |
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cervical vertebral stentoic myelopathy ("wobbler"): signalment
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horse: ataxia in young rapidly growing males (3x F)
- usually C3-C4 or C6-C7 dog: Great Danes, Dobermans, usually C6-C7 |
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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 |
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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 |
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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 |
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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 |
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hygroma
a. definition b. species affected |
a. enlarged bursa over carpi & tarsi
b. cows, goats, dogs |
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ddx for mineralization of muscle
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white muscle dz
exertional rhabdomyolysis vitamin D toxicity (d/t plants, rodenticides) |
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creatine kinase: kinetics
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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) |
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AST: kinetics
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increases more slowly than CPK and stays elevated longer (peak: 24-36 hrs post injury)
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ddx for red/brown urine
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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 |
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myoglobin: response to muscle injury
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released from dead/dying muscle
generally severe, acute injury (esp. in horses, wild animals) excreted in urine --> urine brown, plasma clear (cleared quickly) |
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myasthenia gravis: acquired
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Ab against Ach receptors in adult dogs
dysphagia, megaesophagus may be assoc. w/ thymoma |
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myasthenia gravis: congenital
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several breeds, incl. Jack Russell, Springer Spaniels, Smooth Fox Terriers
deficiency of Ach receptors: NOT immune mediated |
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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 |
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causes of bacterial myositis d/t direct extension
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-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 |
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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 |
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2 causes of muscle atrophy
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disuse: common
neurogenic: -roarers: horses (left recurrent laryngeal nerve injury) -radial n. injury |
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rhabdomyoma/rhabdomyosarcoma
a. classic location in dog b. other commonly affected locations |
a. laryngeal muscle
b. urinary bladder, cardiac muscle |
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leiomyoma
a. common locations b. lab finding |
a. GI, bladder, vagina
b. may have hypoglycemia |
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top ddx for discrete white mass in muscle
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LSA
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3 ddx for failure of endochondral ossification
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osteochondrosis
non-pituitary dwarfism rickets |