By Thelma Robertson,2014-12-25 01:44
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     I. Diseases of Bone Framework

    Disease Etiology Clinical Features

    ; a group of diseases charac by a ? in bone ; Immobilization: confinement to bed > 6 months; OSTEOPOROSIS mass resulting in vulnerability to loss of 30% of initial bone. Lack of exercise leads fracture. Mostly a consequence of to ? in bone resorption and ? bone formation. aging, part. in post-menopausal ; Other: can occur in Cushings Syndrome, women. hypogonadism, hyperthyroid, hypopituitary, ; MORPH: Cortex; ? thickness pregnancy and lactation, malabsorption, Trabeculae of cancellous bone; ? in malnutrition, prolonged admin of heparin number and size. Bone mineralization is ; Clinical: bone pain, deformity, height loss, normal and osteoid seams are normal fractures of femoral neck and vertebrae width. Common in vertebrae, femoral ; Diagnosis: XRay with thin cortices. Osteopenia or neck, wrist. “little bone” seen in osteomalcia, OI, osteitis ; Aging: most imp. factor, esp > 40-50 fibrosa, renal osteodys, multiple myeloma. Serum when mass decreases at a faster rate Ca2+ and PO4- normal. and more pronounced in women. Cause ; Estrogen replacement, exercise, and Ca2+ help ? of ? mass and ? osteoclastic resorption risks. is unknown. Ca2+ absorption also ? with aging. ; ? Estrogenic activity post-menopause: ? loss of cortical bone in post-menopausal and post-oophorectomy. For men, androgen deficiency is imp.

    ; Vit. D deficiency or PO4- depletion in ; CLINICAL: pain, bone deform including rachitic RICKETS children. Can result from dietary rosary (swollen costochondral jxn of ribs), outward deprivation, fat malabsorption, curvature of sternum (pigeon chest), shortened and prolonged lack of sunlight, chronic renal deformed limbs with severe bowing of arms and failure. PO4- depletion can occur from legs, freq. fxs. Fanconi syndrome, heavy metal ; XRAY: thickened, irreg. and Lobulated epiphyseal poisoining, idiopathic PO4- leak. plate ; MORPH: defective mineralization of osteoid; wide osteoid seams and a decrease in calcified bone.

    ; Vit. D deficiency or PO4- depletion in ; CLINICAL: In dietary Vit D deficiency, serum levels OSTEOMALACIA adults. Can result from dietary of Ca2+ and PO3 are low due to diminished (Soft Bones) deprivation, fat malabsorption, absorption, esp. of Ca2+. Low Ca2+ stimulates prolonged lack of sunlight, chronic renal Parathyroid glands; Secondary HyperPTH failure. PO4- depletion can occur from ; XRAY: osteopenic patten with compression fxs, Fanconi syndrome, heavy metal decreased in bone thickness. poisoining, idiopathic PO4- leak. ; MORPH: defective mineralization of osteoid; wide osteoid seams and a decrease in calcified bone.

    ; “von Recklinghausen Disease” ; XRay shows “moth-eaten” in phalanges and OSTEITIS FIBROSA clavicles. ; ? parathyroid hormone; mobilizes Ca2+ CYSTICA ; Tumor like masses with giant cells, cysts, from bone; ? osteoclastic activity; (Hyperparathyroidism) subsequent fibrous replacement. hemorrhages, and fibrous tissue; Brown Tumors; reparative giant cell granulomas. ; ? resorption and fibrosis; formation of cysts and areas of hemorr.

    ; Changes include: osteitis fibrosa ; May be osteosclerosis if severe RENAL cystica, osteomalacia, osteoporosis OSTEODYSTROPHY

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    Disease Etiology Clinical Features

    ; disease of uncertain etiology assoc. with ; AGE: 40-60, most common in Caucasians PAGET DISEASE irreg. thickening and softening of ; MICRO: Osteolytic stage; resorption with (Osteitis Deformans) bones. increased osteoclasts Mixed Stage; new bone ; ETIOLOGY: paramyxovirus infection formation with abundant osteoblasts. Bone suggested, but not proven. Polyostotic haphazardly laid down mostly as woven bone, some 85% and monostotic 14% of cases converted to lamellar. Mosaic Pattern: minerlization lags and newly laid down bone well ; STAGES: 1) Initial Osteolytic: bone demarcated by osteoid seams or cement lines. resorption by osteoclasts 2) Mixed Marrow spaces filled with loose, vascular connective Osteolytic-osteoblastic: woven bone tissue Osteosclerotic Stage; predom. bone with mosaic pattern 3) Burnt-out, formation and osteosclerosis quiescent Osteosclerotic ; CLINICAL: Initially, bone pain, fxs, deformities. ; MACRO: most common in spine, pelvis, Deafness common when skull affected. Vertebral femur, skull, tibia, humerus. compression with height distortion. Coarsening of Spine ; thickening and softening of facial bones; leontiassi ossea (lion-like) Serum resulting in kyphosis, shortening of trunk ALP markedly ?. Can have high output cardiac and pressure on nerves in vertebral failure in polyostotic cases. Osteosarcoma may foramina. Skull ; prog. ? in size due to dev. in 1% thickening, the base may be involved with pressure in nerves. Femur ; ? ; XRAY: bone lysis and reformation thickness with coax vera and anterior bowing.

    ; benign replacement of bone by disorg ; Albright Syndrome: 5% most commonly in FIBROUS DYSPLASIA fibrous and osseus elements. Occurs in precocious puberty in females. Other endocrine children or adults and may be problems include acromegaly, Cushings Syndrome, monostotic. Polyostotic assocl with skin hyperthyroid. Skin Lesions: pigmented macules pigmentation and endocrine problems. (Café au lait spots) usually over buttocks, back, sacrum. ; Monostotic FD: most common (70%) and most common in prox femur, tibia, ; XRAY: lucent ground glass appearance with well-ribs, facial bones. Can lead to marginated borders and thin cortex pathologic fx. ; MICRO: benign fibroblastic tissue in a whorled ; Polyostotic FD: 25% usually in children pattern with haphazardly arranced trabeculae of with pthologic fxs, limb deformities, woven bone which lack osteblastic rimming and limb length discrepancies. Most common form configurations likened to Chinese charac. in females. RARELY, sarcomas may arise. ; Serum ALP elevated. Ca2+ and PO4- normal.

    ; non-neoplastic developmental lesion in ; MICRO: cellular fibroblastic tissue with scattered NONOSSIFYING children most commonly in femur, tibia, lipid-laden Macros and multinucleated giant cells. FIBROMA and fibula. Well-demarcated, ; CLINICAL: extremely common, usually asx and (Fibrous Cortical radiolucent defects of cortex with thin often disappears spontaneously within years. NO Defect) intact layer of subperiosteal cortical TX to sarcomas. bone.

    ; periosteal new bone formation, arthritis, ; New bone formation; distal ends of long bones, HYPERTROPHIC clubbing of digits usually in pts with metatarsals, metacarpals, and prox phalanges. OSTEOARTHROPATHY bronchial CA, pleural tumors, ; Arthritis; adjacent joints and is nonspecific with pulmonary METS, mediastinal Hodgkins, edematous thickening of synovium and mild Chronic Lung Infections, Chronic Liver lymphoplasmacytic infiltrate Dz. ; Clubbing; edematous fibrovascular overgrowth in ; Clubbing alone may occur secondary to tips of digits and appears dusky to cyanotic. same conditions but also with cyanotic ; Resection of underlying CA reverses changes. heart disease, infective endocarditis, UC, Crohns, CA of Eso and Colon.

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