Path- Bones and Joints 2

untimely's version from 2015-05-05 18:00

metabolic bone diseases

Question Answer
Deficiency of mineralized bone can relate to what 4 conditions?osteoporosis, rickets, osteomalacia, and fibrous osteodystrophy
Osteoporosis is bone ___ atrophy
osteoporosis is characterized by...a decrease in bone mass (osteopenia), enlargement of bone spaces, and increased fragility of affected bones (the remaining bone is normally mineralized)
what is the GENERAL etiology/pathogenesis of osteoporosis?imbalance between bone formation and resorption in favor of resorption
why is there reduced production of bone in osteoporosis?failure of normal osteoblastic activity, combined with increased removal of previously formed bone, the INC REMOVAL is due to excess stimulation of osteoclasts by excess parathyroid hormone production (1°or 2° hyperparathyroidism)
4 etiological causes (specific) of osteoporosis?(1) Ca++ deficiency (2) malnutrition (3) disuse (4) toxicity
explain pathogenesis of Ca++ defeciency in osteoporosishypocalcemia --> increased output of PTH -->increased bone resorption
explain pathogenesis of starvation and malnutrition in osteoporosisreduced bone formation due to deficiencies of protein and mineral, as well as malabsorption of nutrients
explain pathogenesis of physical inactivity (disuse osteoporosis)increased bone resorption and decreased bone formation mediated through changes in piezoelectrical activity and stretch receptors
what are the three toxicities which can cause osteoporosis? (explain how they cause the prob)(1) vitamin A tox (dec osteoblastic activity--> dec bone formation) (2) adriamycin/doxorubicin tox (chemo drug-- dec osteoblastic activity) (3) Fluoride tox (leads to abnormal osteocytes)
postmenopausal osteoporosis in women causes what two things?(1) vertebral deformity or collapse (2) pathologic fractures of the femoral neck
how does administration of glucocorticoids and osteoporosis relate? (etiology)administration of glucocorticoids decreases rate at which bone is formed as well as the amount produced, AND it interferes with differentiation to osteoblasts
4 reasons senility leads to osteoporosisdec activity, dec sex steroid hormones, dec formation of vitamin D metabolites, dec responsiveness to vitamin D metabolites
what are the lesions of CORTICAL bone in osteoporosis?reduced in thickness and increased in porosity (lack of normal density)
what are the lesions of TRABECULAR bone in osteoporosis?thinner with perforations, and loss of trabeculae lost due to imbalance between formation and resorption
what are the lesions of the medullary cavity in osteoporosis?enlarged due to endosteal resorption and removal of metaphyseal cancellous bone
what are sequale to osteoporosis?fractures
Rickets is a disease of ____ boneimmature
ricks it charaterized by a failure of ____, because it's a disease of _mineralization_, disease of bone and cartilage undergoing endochondral ossification
does rickets affect cartilage?YES
what are the etiological causes of rickets? (2, which is the main one)(1) hypovitaminosis D <--main cause (2) could also be a deficiency of calcium and phosphorus (dietary, malabsorption, renal dz)
rickets--> basic function of vit d?maintenance of serum levels of calcium required for mineralization
explain the pathogenesis of rickets due to deficiency of vitamin Ddec absorption, transport, and deposition of calcium and phosphorus--> Ca++ deficiency--> failure of mineralization + 2º fibrous osteodystrophy
the basic lesions of rickets are where?epiphyseal cartilage and bone
what's “rachitic rosary” and what's it assocaited with?RICKETS problem, enlarged costochondral junctions
explain how rickets affects the epiphyseal cartilagefailure of mineralization! chondrocytes in the growth plates fail to degenerate > retention of cartilage matrix. capillaries from the metaphysis are unable to penetrate the cartilage---> growth plates: thickened and irregular
explain how rickets affects the bonesexcessive production of osteoid (matrix) which fails to mineralise--> resistant to normal remodelling via osteoclasts. SOFT AND DEFORMED
which metabolic bone dz is YOUNG animals, which is OLDER?young= rickets, old=osteomalacia
overall summary: lesions of ricketsfailure of endochondral ossification, thickened physes, flared metaphyses due to excess unmineralized osteoid, wide seams of osteoid on bone-forming surfaces, hypocalcemia --> 2°fibrous osteodystrophy, bones: soft, deformed, fracture easily
Osteomalacia (softening of bones)--> happens at what age? characterized by failure of ___ with subsequent..disease only of bone in adults after endochondral bone growth has ceased. _mineralization_, bone deformities and fractures
osteomalacia causes an accumulation of excess___unmineralized osteoid
3 main etiological causes of Osteomalacia? (which is most common)(1) deficiency of vitamin D or phosphorus (most commonly) (2) chronic renal disease (3) chronic fluorosis
pathogenesis of hypovitaminosis D in osteomalaciadec absorption, dec transport, and dec deposition of Ca and P
explain the pathogenesis of how hypophosphatemia can cause osteomalacialack of P stimulates renal production of calcitriol (active D3), which increases intestinal absorption of phosphorus by a PTH-independent mechanism and provokes osteoclastic resorption of bone. both bone resorption and hypophosphatemia tend to increase plasma ionized Ca2+ thus, suppressingPTH release and decreasingrenal excretion of phosphorus
how does chronic renal disease lead to osteomalacia?decreased renal mass or phosphate retention causes altered vit D metabolism, leading to dec decreased synthesis of 1,25 (OH)2D3 (calcitriol), causing diminished intestinal absorption of calcium, decreased calcemic response of the skeleton to PTH, impaired suppression of PTH secretion for any increase in serum calcium level, and altered collagen synthesis
osteomalacia--> chronic renal dz leads to osteomalacia andsecondary hyperparathyroidism
what is the pathogenesis of chronic fluorosis causing osteomalacia?fluoride ions replace hydroxyl radicals in the apatite crystal resulting in abnormal osteoid. Bone is then defective and irregularly mineralized
what are lesions of osteomalacia like?similar to rickets except that physeal cartilage and associated lesions are not present in the adult skeleton! you will see wide seams of unmineralized osteoid, marrow cavity enlarged with extension into epiphysis, cortex is thin, spongy, and soft, there is bone pain, fractures, and kyphosis, scoliosis, or both
what is Fibrous osteodystrophy? what are some akas?widespread increased osteoclastic resorption of bone and replacement by fibrous tissue. AKA: osteitis fibrosa cystica, von Recklinghausen‟s disease, “bighead”, Simian bone disease, osteogenesis imperfecta, “bran disease”, renal rickets, “rubber jaw”
4 etiological causes of fibrous osteodystrophy?(1) deficiency of Ca and vitamin D (2) high dietary Ca:P ratio (3) severe renal disease (4) ingestion of high oxalate plants (bind Ca)
what problem can eating high oxalate plants cause?Fibrous osteodystrophy (bc binds up all the Ca so PTH spikes)
Fibrous osteodystrophy--> why does high P cause problems which lead to bone resorption?it dec intestinal absorption of Ca
Fibrous osteodystrophy--> examples of low-calcium-high-phosphorus dietsall-meat dietsfed to dogs and cats, unsupplemented cereal grain rations fed to swine, horses on high-grain/poor quality roughageor all-bran diets
lesions of fibrous osteodystrophyweakening of bones --> lameness, pathologic fractures, collapse of articular surfaces of bones, deformities (of ribs, vertebrae, etc.)
Renal osteodystrophy is basically bccant excrete P, P too high, and cant make calcatriol. leads to inc resorption of bone, dec calcitriol, and imparied mineralization
three types of hyperparathyroidism that lead to fibrous osteodystrophy(1) primary (tumors) (2) secondary (nutritional/renal) (3) Paraneoplastic
osteomalacia vs fibrous osteodystrophy?in osteomalacia, the osteoid is being laid down but for some reason it can't be mineralized, so the osteoclasts can't remodel cartilage so it's just all soft. In fibrous osteodystrophy, the osteoclasts are remodeling too much and taking away mineralized bone

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