Path 2 - Bone - Review

sihirlifil's version from 2017-05-02 02:42

Quick & Dirty

Question Answer
Osteopetrosis: aka? inherited in? what's going on?Marble bone disease, METAPHYSEAL dysplasia
Inherited in angus cattle (also seen in dogs, pigs, sheep, horses, catle, avian, mice, human)
Failure of osteoclasts to resorb primary spongiosa
Osteopetrosis: what does it look like?Bony spicules with central cores of calcified cartilage fill the medullary cavity
Osteopetrosis: what often happens as a result?Increased bone density, aplastic anemia
Osteopetrosis: lesionsDense bones, no medullary cavity, susceptible to fracture
Congenital cortical hyperostosis: aka? inherited in? what's going on?DIAPHYSEAL dysplasia
Newborn pigs (autosomal recessive)
New periosteal bone formation on long bones, EDEMA from lymph blocakge
Congenital cortical hyperostosis: lesionsThick, swollen, hard, rigid bones; stillbirth/early neonatal death (starvation, cardiac insufficiency)
Chondrodystrophy: what is it? what's going on?Inherited/idiopathic
Primary lesion in growth cartilage: physis, articular epiphyseal complex, epiphyseal cartilage
Chondrodystrophy: what does it look like? types?Disproportionate dwarfism (short legs, normal heads)
Deter (bulldog calves), Telemark (brachygnathia, cleft palate, protruding tongue, short neck), short-headed
Osteochondrosis: what is it? what's going on?Focal or multifocal failure / delay of endochondral ossification involving metaphyseal growth plate & AE complex --> cartilage retention
Osteochondrosis: etiologyInterference w/ vascular flow to cartilage; bred to achieve max body weight at young age; Cu deficiency + Zn excess; high-Ca diets (Greater incidence)
Osteochondrosis: LesionsDysplasia (wedge of hyaline cartilage at AE complex or physis), stages of resolution or 2ry necrosis, hemorrhage & mineralized debris in adjacent bone
Osteochondrosis: sequelaeProgression; resolution (endochondral ossification); necrosis & cystic cavitation)
Osteochondritis dissecans (OCD): what is it? what's going on?Dysplasia at AE COMPLEX --> fracture of articular cartilage --> flap (JOINT MOUSE)
Osteochondritis dissecans (OCD): what is a joint mouse?Fracture of cartilaginous or osteochondral flap, free in joint space
Interferes with mechanical movement of the joint
Osteochondritis dissecans (OCD): sequelaeDJD; ulceration & exposure of subchondral bone; lameness
Hypertrophic osteodystrophy (HOD): what is it? who gets it?METAPHYSEAL osteopathy
Young, growing, large & giant breed dogs
Hypertrophic osteodystrophy (HOD): what causes it?Increased Ca, Vit D; Decreased Vit C--> Bilaterally symettrical physitis (inflammation of growth plates of long bones)
Hypertrophic osteodystrophy (HOD): what's usually the result?Spontaneous recovery
Hypertrophic osteopathy (HOP): aka? most common in? what is it?Hypertrophic pulmonary osteopathy (HPO), dogs
Progressive, bilateral, periosteal new bone formation in DIAPHYSEAL regions of distal limbs
Hypertrophic osteopathy (HOP): what other lesions are commonly seen?Intrathoracic (neoplasms, pneumonia, endocarditis, heartworms, spirocercosis)
Hypertrophic osteopathy (HOP): pathogenesisIncreased blood flow to extremities increases arterial pressure in the periosteum (thickens by fibrosis, exostosis)
Hypertrophic osteopathy (HOP): associated with?Rhabdomyosarcoma of urinary bladder (young giant breed dogs)
Ovarian neoplasms (horses)
Hypovitaminosis A: in who? what happens?Calves and pigs fed unsupplemented grain/old hay
Abnormal intramembranous ossification (skull, ribs etc) with defective remodelling and reduces resorption of endosteal bone (bone produced at sites where resorption should be occurring)
Hypovitaminosis A: lesionsSmall brain case
Pressure on CNS
Increased ICP
Blindness (stenosis of optic canal)
Hypervitaminosis A: aka? common in? what happens?Vit A toxicity; seen in cats fed mainly bovine livers
Injury to growth cartilage, osteoporosis, development of exostoses
Hypervitaminosis A: normal fxn? what changes?Vit A usually affects both osteoblasts AND clasts- lesions depend on which affected
Reduced chondrocyte proliferation (destruction of growth plates, long bones decrease in length), decreased number of osteoclasts (osteoperosis/penia), stimulation of peripheral osteoblasts
Exostoses/osteophytes --> ankylosis/spondylosis
Dental disease (alveolar bone changes, prolif gingivitis, cutaneous hyperesthesia)
Hypervitaminosis D: which action does Vit D usually favor?Stimulation of osteoclasts, favors, bone resorption (also stimulates osteoblasts --> osteogenesis)
Hypervitaminosis D: what happens with acute massive exposure?Excessive intestinal absorption --> hypercalcemia --> widespread mineralization (pericardium, heart, b.v., intestines)
Hypervitaminosis D: what happens with longterm exposure?Persistent hypercalcemia --> decrease PHT, increase calcitonin --> osteosclerosis
Direct stimulation of osteoblasts = exostosis
Osteofluorosis: what is it? whats going on?Fluoride poisoning
F- chelates Ca2+ --> hypocalcemia --> ricket-like lesions
Osteofluorosis: how does it happen?Ingestion of bedrock/pasture, forage contam w/ industrial waste high in F- (--> abnormal osteoid), which accumulates in periosteum (thickened periosteum)
Osteofluorosis: acute vs chronicAcute: CNS & GI
Chronic: Dental (young), Osteodystrophy (mature cattle & sheep)
Osteoporosis: characterized by? etiology?Decrease in bone mass, enlargement of bone spaces, increased fragility (remaining bone has NORMAL mineralization)
Favors resorption (imbalance w/ formation)
Osteoporosis: caused by?Calcium deficiency (decr PTH)
Starvation, malnutrition (not enough protein, mineral/malabsorption)
Inactivity (disuse)
Toxicity (Vit A, Doxorubicin, Fl-)
Glucocorticoids (interfere with osteocyte differentiation)
Senitily (decreased activity, sex steroids, vit D metabolites, responsiveness to D metab)
Osteoporosis: lesionsCortical & trabecular bone reduced thickness
Trabecular bone loses trabeculae (thin, perforated)
Medullary cavity enlarged (endosteal resorption)
Fibrous osteodystrophy: what happens? etiology?Increased osteoclastic resorption of bone, replacement by fibrous tissue
Ca/Vit D deficiency, low Ca:P, severe renal dz, high oxalate plants (bind Ca2+)
Fibrous osteodystrophy: primary vs secondary hyperPTH?Primary: PTH adenoma, carcinoma or hyperplasia
Secondary: Nutritional (low Ca/VitD, high P), renal
Fibrous osteodystrophy: lesions?Osteoclastic bone resorption, replacement by fibrous CT, failure of osteoid to mineralize
Weakness, lameness, pathologic fractures, deformities, collapse of articular surfaces
Renal: also teeth loss, maxilla/mandible deformities
Rickets: happens in who? what's going on?YOUNG animals
Failure of mineralization of bone, cartilage undergoing endochondral ossification
Rickets: caused by?Hypovitaminosis D (mainly) (also Ca, P)
Rickets: what does it look like?Retained cartilage matrix, excessive osteoid production, capillaries from metaphysis unable to penetrate cartilage, thick & irregular growth plates, rachitic rosary
Soft, deformed bones, resistant to remodeling by osteoclasts
Rickets: can lead to?Hypocalcemia --> secondary fibrous osteodystrophy
Osteomalacia: happens in who? what's going on?MATURE animals after endochondral bone growth has ceased
Failure of mineralization (same as rickets) --> excess unmineralized osteoid
Osteomalacia: caused by?VIt D or P deficiency, CRD, chronic fluoridosis
Osteomalacia: looks like?(Rickets EXCEPT:) Physeal cartilage and associated lesions are NOT present in adult skeleton (growth plates are closed)
Wide seams of unmin. osteoid, enlarged marrow cavity, thin spongy cortex, bone pain, pathologic fractures, kyphosis, scoliosis
Osteomyelitis: what happens?Localized inflammation where capillaries make sharp bend (metaphysis)
Accumulations and spread of purulent exudate in medullary cavity; thrombosis and infarction of fat, BM, bone; osteoclastic bone resorption
Osteomyelitis: sequelaeExudation, irregular new bone formation
Extension to adj bone
Hematogenous spread
Pathologic fractures
Fistulae draining to exterior
Sequestrum formation
Vertebral osteomyelitis (necrosis, cavitation)
Lysis of articular cartilage
Osteosarcoma: common in who? sites?Mature dogs (large, giant breeds) = 80% of all primary bone tumors
Metaphyses of distal radius/tibia, proximal humerus
Osteosarcoma: typesSimple (bone formed in collagenous matrix)
Compound (bone and cartilage present)
Pleomorphic (anaplastic)
Osteosarcoma: classified based onCell type & activity (osteoblastic, chondroblastic, fibroblastic)
Radiographic appearance (lytic, sclerotic, mixed)
Origin (central, juxtacortical, periosteal)
Osteosarcoma: behavior? lesions?Rapid growth, painful, aggressive with early pulmonary metastasis
Gray-white gritty masses w/ hemorrhage, cystic degeneration, necrosis
Reactive bone formation
Cytological pleomorphism (Cells must be evaluated to determine malignancy)

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