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leiomyomaa. common locationsb. lab finding
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a. GI, bladder, vaginab. may have hypoglycemia
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vitamin D toxicitya. pathogenesisb. etiology
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a. excessive vitamin D effects GI, kidney --> hypercalcemia, hyperphosphatemia --> mineralization of soft tissue thru out bodyprogressive renal & cardiac mineralization --> death, often before bone lesions developb. plants (Solanum), rodenticides
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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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Define sequestrum & involucrum
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sequestrum: necrotic pieces of bone isolated in middle of lesioninvolucrum: surrounding granulation tissue & sclerotic bone
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synovial sarcomaa. prevalenceb. site
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a. rareb. in JOINT, yet may extend into bones on both sides of joint space
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2 causes of muscle atrophy
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disuse: commonneurogenic: -roarers: horses (left recurrent laryngeal nerve injury) -radial n. injury
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rickets: etiology
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vitamin D deficiency: dietary, no sunlight, renal dz, etc. ORphosphorous deficiency
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main defect in non-pituitary dependent dwarfs
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failure of endochondral ossification
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HO: px
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bone lesions resolve if mass removed
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osteochondrosis: signalment
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dogs, pigs, horses, turkey, broilers, cattleyoung animals, growing rapidly, M > F, esp. of large size
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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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main defect in osteochondrosis
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failure of endochondral ossification
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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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2 major types of dwarfs
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- non-pituitary dependent: disproportionate dwarfs- pituitary dependent: proportionate dwarfs
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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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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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osteosarcoma: pxa. catsb. dogs
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a. cats: good w/ amputation in appendicular OSA, poor in axial OSAb. dogs: poor
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masticatory muscle myositisa. acute lesionsb. chronic lesionsc. etiologyd. species
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a. eosinophilic, swollen, edematous, hard, painfulb. atrophic myositisc. Ab to particular fiber type in masticatory muscled. dog
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arthritis/synovitis: direct extensiona. number of joints involvedb. causes
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a. usually one 1 joint involvedb. puncture wound, extension from localized soft tissue lesion
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chondrosarcomaa. signalment in dogsb. common sites
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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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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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vitamin A deficiency a. pathogenesisb. prevalence
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a. failure of bone resorption along endosteal surface --> thick bones w/ ↓ central cavityb. rare
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lead toxicitya. pathogenesisb. lesions
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a. impaired osteoclastic & chondroclastic resorption --> persistence of mineralized cartilage in metaphysis b. lead line: double line in metaphysis; metaphyseal sclerosis
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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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HOD: clinical signs
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intermittent fever, lameness, swollen metaphyses (esp. distal tibia, radius, ulna)
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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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non-infectious arthritisa. species usually affectedb. joint fluidc. number of joints affectedd. pathogenesis
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a. dogs, catsb. fluid contains mostly neutrophils even though etiology in non-infectious c. polyarthritisd. inflammation 2º to persistence of antigenic material in synovium
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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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Coccidiodes immitisa. signalmentb. lesion
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a. dogs in southwest USb. fungal osteomyelitis that produces excess PNB, often on vertebrae (lumbar most common)
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top ddx for discrete white mass in muscle
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LSA
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FOD: etiology
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hyperparathyroidismprimary: parathyroid adenoma (rare)secondary: renal failure or nutritional imbalance
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3 ddx for failure of endochondral ossification
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osteochondrosisnon-pituitary dwarfismrickets
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FOD secondary to renal failure: pathogenesis
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hypocalcemia, hyperphosphatemia d/t renal failure --> 2° hyperparathyroidism & ↑ in PTH secretionuncommon to have clinical signs related to bone lesions
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osteomyelitis caused by hematogenous spreada. signalmentb. site of infection in bonec. causes
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a. young animalsb. usually lodges in metaphysis: (or epiphysis): caps patent at their endpoint in metaphyses --> bacteria exit soft tissue therec. compromised immune system ↑ likelihood of dz (ex. failure of passive transfer of colostrum), umbilicus, sx
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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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parathyroid hormone (PTH)a. secreted d/t:b. effects
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a. secreted d/t low calciumb. 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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ankylosis spondylosisa. speciesb. pathogenesis
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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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rhabdomyoma/rhabdomyosarcomaa. classic location in dogb. other commonly affected locations
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a. laryngeal muscleb. urinary bladder, cardiac muscle
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vitamin A toxicitya. lesionsb. etiologyc. prevalence
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a. exostoses: hip, stifle, shoulder, elbow, cervical vertebrae; fused cervical vertebraeb. primarily cats fed raw beef liver for several monthsc. rare
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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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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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osteogenesis imperfectaa. lesionsb. prevalencec. px
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a. blue sclera, fx bones, fx teeth, fx ribs in utero, translucent pink/gray teethb. rarec. terrible
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top 2 causes of necrosis of bone
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1. infection2. ischemia
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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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rickets: main defect
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failure of endochondral ossification
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IVDD: chondrodystrophic breedsa. age of onsetb. pathogenesis
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a. degeneration starts by 1 year of age, see problems b’twn ages 1-3b. nucleus pulposus loses fluid & pliability becomes mineralized, “cheesy” --> crumbles --> annulus fibrosus starts progressive degeneration
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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 chauvoeimyositis d/t septicemia is rare
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osteopetrosis: prevalence & px
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rarelethal
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HOD: lesions
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PNBmicrofractures or osteomyelitis subadjacent to physismultiple bones involved
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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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osteosarcoma: most common sites in dogs
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originates in medullary cavity of METAPHYSIS of long bonesmost common sites: proximal humerus, distal radius, distal femur, proximal tibiaif 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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mutilobular osteoma & chondroma
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head of dogslocally aggressivemay become malignant
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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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craniomandibular osteopathy: signalment
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usually young dogs (~8 mo.), Westies, Scotties, Cairn Terriers, Labs, Dobermans
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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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hypertrophic osteopathy (HO): pathogenesis
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likely neurogenic or vascularpulmonary 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 & metaphysesusually long bones (appendicular skeleton), not axial (vertebrae)
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IVDD: non-chondrodystrophic breedsa. age of onsetb. pathogenesis
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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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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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eosinophilic panosteitis: signalment
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usually young (6-18 mo.), large breed dogs, esp. GSD; M > F
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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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vitamin Da. secreted d/t:b. effects
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a. secreted d/t PTH, low phosphorousb. effects-increases serum Ca & P (esp. Ca) by increasing GI absorption of both-required for mineralization of bone
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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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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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Legg-Perthes' dz: signalment
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small breed dogs 4-11 mos. of age; poodles, terriers, F > M
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osteochondrosis: etiology
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hereditary factorshigh plane of nutritionpushed for rapid growthtraumaweight bearingCu deficiency (horses)
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osteosarcoma: radiographic signs in cats
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rads: lysis of metaphysis --> “moth eaten” appearanceNO PNB formation
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osteosarcoma: radiographic signs in dogs
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rads: lysis + sclerosiselevated 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 tissuepulmonary mets
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Hepatozoonosisa. signalmentb. lesion
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a. dogs in Texas (rare)b. subperiosteal new bone along vertebral column & rarely along limbs
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myasthenia gravis: congenital
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several breeds, incl. Jack Russell, Springer Spaniels, Smooth Fox Terriersdeficiency of Ach receptors: NOT immune mediated
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copper deficiencya. pathogenesisb. prevalence
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a. abnormal collagen (Cu required for cross linkage) --> increased bone fragilityb. rare
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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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arthritis/synovitis: hematogenousa. sourceb. why this is most common route (3 reasons)c. number of joints involved
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a. source in young animals: septicemia (often umbilicus (failure of passive transfer) or surgical procedure)-if old, often d/t endocarditisb.-synovial membrane has tiny vessels to trap emboli-synovial fluid is a good nutrient-difficult for host defense mechanisms to enter jointc. usually a polyarthritis
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cervical vertebral stentoic myelopathy ("wobbler"): a. etiologyb. pathogenesisc. px
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a. mutifactorial (genetic, overnutrition, etc.)b. variety of cervical vertebral malformations --> compression & injury of spinal cord & stenosis of vertebral canalc. poor
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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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histiocytic sarcoma1. prevalence2. px3. behavior
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1. relatively common in Rotties, Mastiffs, Retrievers2. poor3. 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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Legg-Perthes' dz: pathogenesis
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aseptic necrosis of femoral headblood 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 injurycontinued wt. bearing --> fragmentation or fx of necrotic bone --> deformed & malfunctioning femoral head
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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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ddx for mineralization of muscle
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white muscle dzexertional rhabdomyolysisvitamin D toxicity (d/t plants, rodenticides)
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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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multiple myelomaa. lesionsb. lab findings
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a. mutiple lytic lesions in BM of multiple bones, esp. ribs & vertebraeb. hypercalcemia in ~10% of dogs, monoclonal spike on electrophoresis
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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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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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rickets: signalment
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young, growing animals
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discospondylitisa. pathogenesisb. dogs: common organisms, sitec. dogs: signalment
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a. IV disc infection & inflammation that extends into adjacent vertebra --> osteomyelitisb. Staph auerus, Brucella; lumbosacral vertebraec. large breed dogs, M > F
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hygromaa. definitionb. species affected
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a. enlarged bursa over carpi & tarsi b. cows, goats, dogs
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osteomalaciaa. etiologyb. signalmentc. lesions
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a. impaired mineralization in osteoid (newly formed bone) d/t vitamin D or P deficiency b. adult animalsc. excess osteoid on bone spicules accumulates --> thick, weak, soft bone
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myoglobin: response to muscle injury
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released from dead/dying musclegenerally severe, acute injury (esp. in horses, wild animals)excreted in urine --> urine brown, plasma clear (cleared quickly)
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osteosarcoma: keys for biopsy
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3 sites in metaphysischoose lytic regionsmust enter medullary cavity
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malformation abnormalities: a. ameliab. syndactylyc. micromeliad. brachygnathia inferiore. polydactylyf. brachygnathia superiorg. adactyly
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a. absence of a limbb. fused digitsc. abnormally small limbd. undershot of jawe. extra digitsf. overshot of jawg. no digits
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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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myasthenia gravis: acquired
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Ab against Ach receptors in adult dogsdysphagia, megaesophagusmay be assoc. w/ thymoma
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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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2 routes of infectious osteomyelitisWhich is more common?How many bones involved in each?
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direct extension: 1 bonehematogenous: multiple bonesdirect extension more common
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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-C7dog: Great Danes, Dobermans, usually C6-C7
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most common sites of osteochondrosisa. dogb. pigc. horsed. poultry
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a. shoulderb. stifle, elbowc. stifle, shoulderd. tibia (tibial dyschondroplasia)
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Legg-Perthes' dz: px
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removal of femoral head: good pxelse, dog will develop DJD
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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 epiphysesossification centers don’t form in epiphyses --> epiphysis is a solid cap of cartilage
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non-infectous osteomyelitisa. causeb. sequelae
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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: most common site in cats
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flat bones most common site (skull: #1 site)
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craniomandibular osteopathya. etiologyb. lesionsc. pxd. ddx for lesion
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a. unknownb. excess PNB along mandibles, occ. occipital & temporal bonesc. good, lesions may regress by 11-15 mo.d. osteomyelitis, tooth abscess, trauma, CMO
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HOD: etiology
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probably infectious (bacterial, canine distemper)
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ddx for red/brown urine
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horse: think myoglobin 1st, dog: think Hb 1sthematuria: hemorrhagehemoglobinuria: hemolysis (ex. Red Maple) -PCV: N to ↓, pink to icteric plasma, precipitate on ammonium sulfate testmyoglobinuria: exertion rhabdomyolsis -PCV N to ↑, clear to icteric plasma, no precipitate on ammonium sulfate test
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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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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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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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multiple cartilaginous exostoses (osteochondromatosis)a. prevalenceb. signalmentc. lesions
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a. rareb. young animalsc. multiple firm nodules near costochondral junctions & metaphyses
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calcitonina. secreted d/t:b. effects
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a. secreted d/t high calciumb. effects:- inhibits osteoclasts- ↑ excretion of Ca & P by kidneys
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common etiologic agents for osteomyelitis caused by hematogenous spreada. foalsb. cattlec. dogsd. poultry
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a. E. coli, Strep, Salmonella, Klebsiellab. Actinomyces bovis (lumpy jaw)c. Coccididoes immitis, Hepatozoon canis, Brucellad. Staph aureus (green livers)
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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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examples of ischemia in musclea. catb. horsec. cow
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a. cardiomyopathy --> saddle thrombi --> ischemic muscle necrosis in pelvic limbs (↑↑ CPK)b. usually associated w/ prolonged anesthetic proceduresc. assoc. w/ obturator n. paralysis post-calving w/ dystocia
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