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126 Cards in this Set
- Front
- Back
Contents of haversian canals
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Arterioles, Venules, Capillaries, Nerves, Lymphatics
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Contents of canals/canaliculi
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Osteocyte cell processes
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Cement lines
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Define border of osteon
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Characteristics of cortical bone
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Slow turnover, high Young modulus, higher resistance to torsion and bending
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Characteristics of cancellous bone
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Less dense, more remodeling according to Wolff's law, higher turnover, smaller Young modulus, more elastic
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Characteristics of woven bone
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Random organization (not oriented according to stress), increased turnover, weak, flexible. Can be immature or pathologic
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Osteoblasts
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Form bone by generating organic, non-mineralized matrix. Mesenchymal origin. More active cells line bone, less active trapped in resting regions- maintain ionic mileiu of bone.
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Growth factor effects on osteoblasts
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Differentiation increased by PDGF/ IDGF
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PTH effects on osteoblasts
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Secondary messenger-->activates adenyl cyclase-->Produce ALK Phos, type I collagen, osteocalcin, bone sialoprotein
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Osteoblast receptors
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1. PTH 2. 1,25- dihydroxyvitamin D 3. glucocorticoids 4. prostagalndins 5. estrogen
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Osteocytes
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Maintain bone. Most common cell in mature bone. Made from osteoblasts. Important for control of calcium/phosphorous balance. Stimulated by calcitonin/ inhibited by PTH
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Osteoclasts
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Resorb bone. Multinucleated giant cells. Monocyte origin. Ruffled brush border used for bone resorption. Osteoclast formation inhibited by IL-10
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RANKL
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On surface of osteoblasts and tumor cells. Stimulate RANK on osteoclasts--> differentiation into mature osteoclasts/ increases bone resorption. Inhibited by osteoprotegrin
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Osteoclast bone resorption
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Occurs in Howship's lacunae. Carbonic anhydrase creates H+ ions--> lower pH-->increases solubility of hydroxyapatite. Organic matrix removed via proteolytic digestion. Stimuated by IL-1.
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Bisphosphonate effects
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Inhibit osteoclast resorption. Prevents formation of ruffled border.
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Osteoprogenitor differentiation in different environments
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low strain/ high O2--> osteoblasts. Intermediate strain/low O2--> cartilage. High strain--> fibrous tissue
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Calcitonin
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From parafollicular cells of thyroid. Stimulated by high Ca+. Inhibits osteoclastic bone resorption-> transient decreased Ca+. Analgesic properties in pathologic fractures
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Vitamin D3 effects on osteoblasts
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stimulates matrix and ALK Phos synthesis/ bone protein synthesis
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Glucocorticoid effects on bone
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inhibits synthesis of DNA/ collagen production/protein synthesis by osteoblast. Cancellous affected more than cancellous.
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Prostaglandin effects on osteoblasts
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activates adenylyl cyclase--> stimulates resorption of bone
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Estrogen effects on bone
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Anabolic/ anticatabolic. Increases mRNA levels for ALK Phos and inhibits adenyly cyclase activation. Side effect: inc risk of heart disease/ breast CA
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Collagen structure
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Triple helix of one alpha 2/ 2 alpha 1 chains. Hole zone: within fibril between ends of molecules. Pores between sides of parallel molecules
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Collagen cross-linking
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decreases solubility/ increases strength
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Most abundant non-collageneous protein in bone
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Osteocalcin. Note: VERY popular question on OITE
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Osteocalcin
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Most abundant protein in bone (except collagen). Attracts osteoclasts, regulates bone density. Marker of bone turnover. Inhibited by PTH/ stimulated by vit D
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Proteoglycans in bone
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Compressive strength. Composed of GAG complexes. Inhibit mineralization
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Osteonectin
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Secreted by platelets and osteoblasts. Role in regulating calcium/ matrix
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Osteopontin
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Cell-binding protein similar to an integrin
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Ca hydroxyapatite
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Compressive strength. Most of inorganic matrix.
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Location of mineralization of bone
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Primary mineralizatin occurs in collagen gaps. Secondary at periphery
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Osteocalcium phosphate
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Remainder of inorganic matrix of bone
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Wolff's Law
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Bone remodels in response to mechanical stress. Increased stress--> increased bone density. Immobilization--> loss of bone mass
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Ionic properties of bone
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Compression side: electronegative--> stimulates osteoblasts. Tension side: electropositive--> stimulates osteoclasts
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Hueter-Volkman law
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remodeling occurs in basic multicellular units (BMU's) modulated by hormones/ cytokines. Compression inhibits growth/ tension facilitates growth
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Cortical bone remodeling
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Osteoclastic tunneling (cutting cones)--> layering of osteoblasts and deposition of laemllae. Head of cutting cone made of osteoclasts followed by capillaries/osteoblasts
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Cancellous bone remodeling
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Osteoclastic resorption--> osteoblastic formation
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Blood flow to bone
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5-10% of cardiac output
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Nutrient artery
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branch from major arteries--> diaphyseal cortex through nutrient foramen--> medullary canal-->arterioles in endosteal cortex. Suplly inner 2/3 of diaphyseal cortex. High pressure
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Periosteal blood supply
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Primarily capillaries--> outer 1/3 diaphyseal cortex. Low pressure
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Direction of blood flow in bone
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Normal bone: centifugal (in to out). Displaced fracture: centripetal (in to out)- disrupt high flow endosteal supply and flow reverses. Immature bone: centripetal (highly vascularized periosteum). Venous flow: centripetal
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Physiologic states that increase blood flow to bone
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hypoxia, hypercapnia, sympathectomy (SCI)
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Effect of fracture on blood flow to bone
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immediate: decreased. Hours-days: increases. 2wks: peak blood flow. 3-5 months: normal
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Effect of reaming on endosteal blood supply
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devascularizes inner 50-80%
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Periosteum
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Inner layer: cambium- loose/vascular/contains cells capable of becoming osteoblasts. Responsible for increaseing diameter o f bone/ forming callus. Outer layer: fibrous/less cellular/contiguous with joint capsules
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Bone marrow
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Red: Hematopoietic (40% H20/40%fat/20% protein). Changes to yellow marrow. Yellow marrow: inactive: 80% fat
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Enchondral ossification
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Replaces cartilage model. Locations: embryonic long bones. Physis. Callus. Disrupted in achondroplasia
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Intramembranous ossification
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Aggregates of undifferentiated mesenchymal cells become osteoblasts--> bone. Locations: embryonic flat bones. Distraction osteogenesis. Blastema bone. Disrupted in cledicranial dysostosis
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Appositional ossification
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Osteoblasts lay new bone on old bone. Locations: periosteal bone enlargement. Bone remodeling.
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Physeal nutrition
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primarily from perichondrial artery
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Physis physiology: reserve zone
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cells store material. Low O2 tension. Effected by lysosomal storage diseases
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Physis physiology: proliferative zone
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longitudinal growth. Increased O2 tension. Inc PG--> inhibits calcification. Effected by achondroplasia
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Physis physiology: hypertrophic zone
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Three zones. Maturation/degeneration/provisional calcification. Matrix mineralization occurs. Low O2 tension. Low PG. Widened in rickets
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Indian hedgehog
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produced by physeal chondrocytes. Regulates expression of PTHrP
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Physeal layer affected by SCFE
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Hypertrophic zone- idiopathic. Metaphyseal spongiosa- renal failure
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Groove of Ranvier
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supplies chondrocytes to periphery of growth plate--> increased width
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Perichondrial ring of LaCroix
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Dense fibrous tissue. Anchors and supports physeal periphery. Affected in Salter Harris VI injuries
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Stages of fracture repair
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Inflammation, repair, remodeling
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Inflammatory phase of fracture healing
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Hematoma--> cells release growth factors--> attract cells-->granulation tissue at fracture ends-->osteoblasts/fibroblasts proliferate
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Repair phase of fracture healing
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primary callus within 2wks. Soft callus replaced by hard callus by enchondral ossification. Cellular differentation depends on local strain and O2 tension.
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Effects of ultrasound on fracture healing
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Low intensity/ pulsed- accelerates healing and improves callus strength.
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Electrical stimulation effects on bone
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DC: stimulates inflammatory like response. AC: affects cAMP/colalgen synthesis/calcification during repair stage. Pulsed electromagnetic fields: initiate calcification of fibrocartilage
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Location with highest risk of pathologic fracture
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Subtrochanteric femur
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Osteoconductive
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scaffold for bone formation
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Osteoinductive
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Growth factures- stimulate bone formation
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Osteogenic
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Cells that make bones
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Bone graft antigenicity
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mediated by cell surface glycoproteins. Method of rejection: cellular
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Cortical bone graft
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Slower incorporation through remodeling of haversian systems. Resorption occurs first--> weakens graft.
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Cancellous bone grafts
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Revascularize and incorporate quickly. Osteoblasts lay down new boneon old trabeculae (creeping substitution)
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Silicate grafts
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bioactive glasses
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Ca-phosphate based grafts
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capable of osseoconduction/ osseointegration. Biodegrade at very slow rate. Ceramics
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BMP effects on bone
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Osteoinductive. Induces metaplasia of mesenchymal cells into osteoblasts. Target cesll: undifferentiated perivascular mesenchymal cells. Signal via serine/threonine kinase
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TGF-beta effects on bone
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induces production of type II collagen/ PG. Induces osteoblasts to synthesize collagen. Regulates cartilage/bone formation in fracture callus. Serine/threonine kinase signalling
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IGF-II effects on bone
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Stimulates type I collagen/ cellular proliferation/cartilage matrix and bone formation. Tyrosine kinase signalling
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PDGF effects on bone
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Chemotactic for inflammatory cells to fracture site. Released by platelets. Tyrosine kinase signalling
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Distraction osteogenesis phaes
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Latency: 5-7 days. Distraction: 1mm/day. Consolidation: 2x duration of distraction phase
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Most osteoconduction bone graft
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cancellous autograft
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Most osteogenic bone graft
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cancellous autograft
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Best structuaral bone graft
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cortical autograft
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Effects of bisphosphonates on HO
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inhibits mineralization but does not prevent osteoid matrix. Will mineralize when medication stopped
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Calcium metabolism
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Absorbed in duodenum (active transport-regulated by vit D3) and passive diffusion in jejunum. Kidney resorbs most Ca @ proximal tubules.
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Calcium intake needs
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600mg/day- kids. 1300 mg/day- adolescents. 750mg/day- adults. 1500mg/day-pregnant. 2000mg/day- lactating. 1500mg/day- healing fracture
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PTH
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Secreted by chief cells in parathyroid glands. Stimulated by low Ca conc. Inhibited by high Ca/ high 1,25(OH)2 vit D. Directly activates osteoblasts/modulates renal phosphate filtration. Stimulates 1,25(OH)2 vit D production in kidney, increaes renal Ca resorption, increases excretion of Phos. Net: inc Ca/dec Phos
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1,25(OH)2 vit D
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Secreted by proximal tubule of kidney. Stimulated by PTH. Inhibited by low PTH/high Ca/high phos. Stimulates intestinal absorption of Ca/phos. Stimulates osteoclastic resorption of bone.
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Phenytoin effects on bone
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impairs vitamin D metabolizms
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Effects of menopause on calcium
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decreased intestinal absorption/ increased urinary excretion
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Markers of bone resorption.
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Urinary hydroxyproline, pyridinoline cross-links.
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Markers of bone formation
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Serum alk phos.
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Hypercalcemia symptoms
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polyuria/polydipsia/nephrolithiasis/osteotis fibrosa cystica/confusion/constipation/anorexia/nausea
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Primary hyperparathyroidism
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Usually due to parathyroid adenoma. Result: inc Ca/dec phos. Increased bone resorption/ poor mineralization. Labs: high ca/PTH/urinary phos. Bony changes: osteopenia/fibrous replacement of marrow/brown tumors- destructive metaphyseal lesiosn.
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Pseudohypoparathyroidism
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PTH receptor abnormality. Decreased levels of active form of vitamin D. Normal serum Ca
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hypoparathyroidism
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low ca/ high phos. Low 1,25(OH)2 vit D. Usually iatrogenic
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Renal osteodystrophy- high turnover
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Decreased renal phos excretion-->hyperphosphatemia--> low Ca/ high PTH--> secondary hyperparathyroidism. Osteitis fibrosa cystica/amyloidosis. Tx: treat renal dz, restrict dietary phos, phosphate biding antacids, 1,25(OH)2 vit D supplementation
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Renal osteodystrophy- low turnover
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secondary to aluminum toxicity. No hyperparathyroidism
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Hypophosphatemic rickets
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Most common type. Inborn error in phosphate transport--> renal phosphate loss. Ca nml/PTH nml/vit D nml. Classic triad: hypophosphatemia/lower limb deformities/ stunted growth
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Hypophosphatasia
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Inborn error in alkaline phosphatase. High Ca/phos. Low serum alk phos. Osteomalacia. Early loss of teeth. Dx: elevated urinary phosphoethanolamine. Tx: none available
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Nutritional rickets
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low or nml ca/high phos. Hihg alk phos/PTH. Sx: Osteomalacia/hypotonia/weakness/tetany. Bowing of long bones. Tx: vitamin D/Ca/Phos supplementation depending on etiology
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Vitamin D dependent rickets- type I
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Pseudo vitamin D deficiency. Defect in renal 25-(OH) vatimin D 1alpha hydroxylase-->inhibits activation of vitamin D. More severe than vit D deficiency rickets
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Vitamin D dependent rickets- type II
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intracellular receptor deficit for 1,25 (OH)2. Very very high levels of vitamin D diagnostic
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treatment of hypercalcemia
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1. Saline hydration 2. loop diuretics 3. dialysis-severe
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Hypocalcemia sx
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increased neuromuscular irritability (tetany/seizures/Chvostek's sign). Cataracts. Onychomycosis. Prolonged QT.
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pseudo-pseudohypoparathyroidism
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looks like pseudoparathyroidism except Ca normal and normal response to PTH
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Amyloidosis
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Accumulation of beta-2-microglobulin. Assocaited with carpal tunnel syndrome, arthropathy, pathologic fractures.
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Definition of osteoporosis/osteopenia
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WHO: L2-L4 density at least 2.5 SD below peak bone mass of 25yo. Osteopenia- 1.0-2.5 SD
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Risk factors osteoporosis
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sedentary thin caucasian female age smokers heavy drinkers northern european h/o breast feeding poor diet phenytoin use
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Strongets predictor of future vertebral fracture
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2+ prior vertebral fractures
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Type I osteoporosis
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Postmenopausal. Primarily affects trabecular bone. Vertebral/distal radius fractures
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Type II osteoporosis
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Age related. >75yo. Affects trabecular and cortical bone. Related to poor calcium absorption. Hip/pelvic fractures.
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Degree of osteoporosis necessary to be visible on XR
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>30%
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Idiopathic transient osteoporosis of hip
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third trimester of pregnancy. Presents with groin pain/ dec ROM/ localized osteopenia. Tx: PWB. Resolves after 6-8mo.
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Osteomalacia
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Defect in mineralization. Qualitative deficit. Associated with Vit d deficiency/ GI disorders/ phenytoin/alcoholism. RA: Looser's zones, biconcave vertebral bodies, trefoil pelvis. Bx: widened osteoid seams. Tx: high dose vitamin D theraphy
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Scurvy
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Vitamin C deficiency-->dec chondroitin sulfate synthesis--> defective collagen growth/impaired hydroxylation of collagen. Sx: gum bleeding/ecchymosis/joint effusion/iron deficiency. RAD: thin cortices. Histo: widened zone of provisional calcification. Metaphyseal bone affected first
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Osteopetrosis
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Decreased osteoclast/chondroclast function-->failure in bone resorption. Histo: osteoclasts lack ruffled border/clear zone. Marrow filled with necrotic calcified cartilage.
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Infantile AR form of osteopetrosis
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Most severe form. Bone within bone appearance. Hepatosplenomegoly. Aplastic anemia. Fatal during infancy. Tx: BMT. High dose calcitriol +/- steroids
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AD form of osteopetrosis
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Albers-Schonberg disease. Generalized osteosclerosis. Rugger jersey spine. Pathologic fractures
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Osteopoikolosis
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Spotted bone disease. Islands of deep cortical bone within medullary cavity and cancellous bone. Asymptomatic. No malignant degeneration
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Paget's disease
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Dx: Elevated alk phos/urinary hydroxyproline/ virus-like inclusion bodies in osteoclasts. Active phase: intense resorption. Mixed phase. Sclerotic phase: osteoblastic formation. Inactive phase.
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Caisson's disease
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osteonecrosis secondary to dysbarism (SCUBA)
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Osteonecrosis
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Bony necrosis due to loss of blood supply. Hip commonly affected. Associated with steroid use/alcoholism/blood dyscrasias/radiation. Path: grossly necrotic bone. Bilateral in hip in 50% (80% if associated with steroids). MRI best study- most sens/spec and positive earliest. Pressure measurements: >30mmHg abnormal
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Legg-Calve-Perthe's disease
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osteonecrosis of femoral head
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Osgood-Schlatter disease
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Osteochondrosis of tibial tuberosity
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Sinding-Larsen-Johannson disease
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Osteochondrosis of inferior pole of patella
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Blount disease
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Osteochondrosis of proximal tibial epiphysis
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Sever's disease
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Osteochondrosis of calcaneus
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Kohler's disease
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Osteochondrosis of tarsal navicular
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Freiberg's infarction
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Osteochondrosis of metatarsal head
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Kienbock's disease
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osteochondrosis of lunate
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