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164 Cards in this Set
- Front
- Back
Bone is what type of tissue? |
Connective tissue
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Main inorganic component of bone
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calcium hydroxyapatite
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2 functions of calcium hydroxyapatite in bone
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gives bone strength and hardness
stores: - calcium - phosphorus - sodium - magnesium |
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What proportion of the following minerals in a healthy human are found in the bone?
Calcium: Phosphorus: Sodium: Magnesium: |
Calcium: 95%
Phosphorus: 85% Sodium: 65% Magnesium 65% |
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Osteoid
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unmineralized bone
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Organic components of bone
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cells
matrix proteins |
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3 types of bone-forming cells
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osteoprogenitor cells
osteoblasts osteocytes |
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Osteoprogenitor cells
what: where: why: |
Osteoprogenitor cells:
what: pluripotent mesenchymal stem cells where: vicinity of all bony surfaces why: produce osteoblast cell lineage |
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2 factors important in the differentiation of osteoblasts
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BMPs - stimulate osteoprogenitor cells to produce offspring
TF core binding factor a1 - osteoblastic differentiation |
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Where are osteoblasts located?
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surface of bone
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3 functions of osteoblasts
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- synthesize, transport, arrange matrix proteins
- initiate mineralization - express hormone binding cell-surface receptors (CSRs) |
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What binds hormone binding CSRs on osteoblasts?
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PTH
vit. D estrogen cytokines growth factor ECM proteins |
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2 molecules involved in lipid metabolism recently found to influence osteoblast activity
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leptin
LDL receptor-related protein 5 |
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life span of metabolically active osteoblasts
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3 months
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3 fates of osteoblasts
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apoptosis
quiescent, flattened, bone surface lining cells osteocytes surrounded by matrix |
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How do osteocytes communicate?
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cell processes traverse caniculi
contacts along gap junctions allow travel of surface membrane potentials and substrates |
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Osteocytes are important in the homeostatic control of what?
Mechanism? |
Osteocytes help control serum levels of calcium and phosphorus
by altering their concentrations in the local ECM compartment |
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Osteocytes can do what with the mechanical forces they detect?
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translate mechanical forces into biological activity
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Which bone-forming cell is the most numerous?
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osteocytes
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Function of osteoclasts
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bone resorption
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Osteoclasts are derived from which cell lineage
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hematopoietic progenitor cells that give rise to monocytes & macrophages
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Member of TNF superfamily involved in osteoclast function
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RANK
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Where is RANKL expressed?
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membrane of osteoclasts
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What does RANK-RANKL binding signal?
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Onset of osteoclastogenesis
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Function of osteoprotegrin (OPG)
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competitively inhibits RANK-RANKL binding
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mature multinucleated osteoclasts
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fusion of circulating mononuclear precursors
limited life span - 2 weeks |
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Howship lacunae
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scalloped resorption pits produced by mature osteoclasts
ruffled border – part of osteoclast mb w/ many villi overlying pit mb bordering this region forms seal w/ underlying bone |
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What occurs within Howship lacunae?
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osteoclast acidifies bone w/ H+ pump system
digestive enzymes, eg: collagenase, disassemble matrix prtns elemental units recycled for bone renewal |
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2 types of bone proteins
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Collagen type I
noncollagenous proteins derived from osteoblasts |
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Backbone of bone matrix
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type I collagen
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collagen deposited by osteoblasts in what 2 patterns?
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woven bone (random weave)
lamellar bone (orderly, layered pattern) |
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where is woven bone found?
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in fetal skeleton
at growth plates in pathological lesions of adults (e.g.: fx sites) |
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4 types of lamellar bone
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3 in cortex:
- circumferential - concentric - interstitial trabecular lamellae (parallel to long axis) |
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noncollagenous proteins of bone are bound to _____
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matrix
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4 functional groups of noncollagenous proteins in bone
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adhesion
Ca2+ binding mineralization enzymes, hormones, growth factors |
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only noncollagenous protein unique to bone
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osteocalcin
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Osteocalcin is a specific and sensitive marker of ____?
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osteoblastic activity
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BMU
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basic multicellular unit
functional unit of bone osteoblasts & osteoclasts coordinating |
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how much of skeleton is replaced annually?
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10%
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5 bone growth factors
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bone morphogenic proteins (BMPs)
fibroblast growth factor (FGF) platelet-derived growth factor (PDGF) insulin-like growth factor transforming growth factor-β (TGF-β) |
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skeletal morphology encoded by what type of gene?
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Homeobox
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In what week of gestation does enchondral ossification begin?
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8th week
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physis
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aka: growth plate
plate of cartilage model trapped btw expanding centers of ossification |
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appositional growth
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deposition of new bone on preexisting surface
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2 regulators of bone growth, especially at physis
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Indian hedgehog gene
PTH-related protein (PTHRP) |
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Dysostoses
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developmental anomalies from local problems in migration of mesenchymal cells
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Dysplasias
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mutations in regulators of skeletal organogenesis affect cartilage & bone globally
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most common disease of physis
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achondroplasia
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Achondroplasia
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most common cause of nonlethal dwarfism
caused by defect in paracrine cell signaling --> reduced chondrocyte prolifereation |
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Genetics of achondroplasia
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point mutation (Arg for Gly375) in FGF receptor 3 gene
-- on chromosome 4p -- FGFR3 inhibits cartilage proliferation -- causes FGFR3 to be constantly activated, suppressing growth -- AD transmission -- 80% cases spontaneous mutation |
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Achondroplasia: clinical picture
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- shortened proximal extremities
- trunk relatively normal length - enlarged head w/ bulging forehead & depression of root of nose - not assoc. w/ Δ longevity, intelligence, reproductive status |
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most common type of lethal dwarfism
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Thanatophoric dwarfism
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Thanatophoric dwarfism
etiology fatality |
mutation of FGFR3 --> much more severe phenotype
death by resp. insufficiency 2° underdeveloped thoracic cavity |
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Osteogenesis imperfecta
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group of type I collagen disorders
aka: brittle bone disease |
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structures affected in osteogenesis imperfecta
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significant skeletal involvement
also: joints, eyes, ears, skin, teeth |
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Osteogenesis imperfecta
pattern of inheritance genes affected |
AD inheritance
genes coding for a1 & a2 chains of collagen polypeptide |
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2 types of mutations leading to osteogenesis imperfecta
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mutations yielding qualitatively normal collagen (but less of it) give rise to mild to moderate phenotypes
mutations yielding abnormal collagen give rise to severe and lethal phenotypes |
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morphological definition of all types Osteogenesis imperfecta
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too little collagen:
- extreme skeletal fragility - type of osteoporosis - marked cortical thinning - attenuation of trabeculae |
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Type I Osteogenesis Imperfecta
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- normal life span
- increased number fractures in childhood (decr. post puberty) - usu. acquired, not inherited - blue sclerae, allow part visualization underlying choroid - hearing loss --- sesnroineural deficit --- abnormal mechanical condxn - dental imperfections --- small, misshapen, blue-yellow teeth --- 2° decreased dentin |
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Type II Osteogenesis Imperfecta
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- uniformly fatal in utero or perinatally
- extraordinary bone fragility w/ multiple fractures in utero |
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Mucopolysaccharidoses
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group of lysosomal storage diseases
- caused by deficiencies in enzymes that degrade dermatan, herpan & keratan sulfates - implicated enzymes mainly acid hydrolases - mesenchymal cells, esp. chondrocytes, particularly affected - abnormalities in hyaline cartilage --> --- short stature --- chest wall abnormalities --- malformed bones |
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Osteopetrosis
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group of rare, genetic disorders
decreased osteoclast bone resorption diffuse, symmetrical skeletal sclerosis |
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Osteoporosis
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increased bone porosity from reduced bone mass
- changes predispose bone to fx - may be localized to certain bone or region, e.g.: disuse osteoporosis of a limb - may involve entire skeleton – metabolic bone ds |
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4 factors of aging that contribute to senile osteoporosis
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- decreased replicative actiivty of osteoprogenitor cells
- decreased synthetic activity of osteoblasts - decreased biological actiivty of matrix-bound growth factors - reduced physical acitivty |
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4 factors that contribute to post-menopausal osteoporosis
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- decreased serum estrogen
- increased IL-1, IL-6, TNF levels - increased expression of RANK, RANKL - increased osteoclast activity |
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3 overall factors contributing to senile and post-menopausal osteoporosis
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genetic factors
physical activity nutrition |
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Paget's disease, aka:
|
osteitis deformans
|
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3 stages of Paget's disease
net effect: |
(1) initial osteolytic stage
(2) mixed osteolytic-osteoblastic stage, ending with osteoblastic predominance (3) burnt-out quiescent osteosclerotic stage net effect: gain of bone mass |
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Epidemiology of Paget's disease
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usually occurs in mid-adulthood
relatively common in Whites from W. Europe |
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Clinical features of Paget's disease
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most affected individuals are asymptomatic
clinical course extremely variable - axial skeleton or proximal femur involved in up to 80% cases - enlarged calvarium - involvement of ribs, fibula, small bones of hands/feet unusual - pain most common prob - 2° comb. μfx & bone overgrowth compressing nn roots - variety of tumor & tumor-like conditions develop in pagetic bone |
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radiographic characteristics of Paget's disease
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radiography frequently diagnostic
Pagetic bone typically enlarged w/ thick, coarsened cortices & cancellous bone |
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biochemical abnormalities associated with Paget's disease
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increased serum level of alkaline phosphatase
increased urinary excretion of hydroxyproline |
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Hyperparathyroidism
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increased serum PTH causes hyperstimulation of osteoclast activity
unabated osteoclast bone resorption w/ entire skeleton affected |
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Primary hyperparathyroidism
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autonomous hyperplasia or a tumor,
usu. adenoma, of parathyroid gland |
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Secondary hyperparathyroidism
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prolonged states of hypercalcemia cause compensatory hypersecretion of PTH
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osteitis fibrosa cystica
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anatomic changes of severe, late-stage hyperparathyroidism
rarely seen in industrialized countries |
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Which form of hyperparathyroidism is usually more severe and prolonged?
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primary
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Classifications of fractures
closed - compound - communited - displaced - |
complete vs. incomplete
closed (simple) – overlying tissue intact compound – fx site communicates with the skin surfact communited – bone is spintered displaced – ends of bone at fx site not aligned |
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Pathologic fracture
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occurs at a site already altered by disease process
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Stress fracture
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slowly developing fracture following a period of increased activity with new, repetitive loads on the bone
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Process of fracture repair
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fracture --> ruptured vessels --> hematoma
clotted blood --> fibrin mesh --> enclosed inflammatory site PDGF, TGF-b, FBF activate osteoprogenitors, BMU end week 1: procallus - fusiform, soft tissue, anchors fractured ends osteoprogenitors deposit subperiosteal trabeculae of woven bone end week 2/3 - repair tissue at maximum girth last step: endochondral ossification of new cartilage |
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Complications of fracture repair
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- deformities from displaced and -comminuted fx, esp. w/ inadequate immobilization
- infection in comminuted and open fx - derailed bone repair 2° inadequate Ca2+, P, vit D; DM; sys. infxn; vasc. insufficieny |
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All forms of osteonecrosis result from what process?
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ischemia
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6 mechanisms producing ischemia in bone
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- mechanical vascular interruption (fx)
- corticosteroids - thrombosis & embolism (N bubbles in dysbarism) - vessel injury 2° vasculitis, radiation therapy - increased intraossesous pressure w/ vascular compression - venous HTN |
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Clinical course following subchondral infarcts in bone
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- chronic pain initially assoc. only w/ physical activity (then constant)
- subchondral infarcts often collapse - may predispose to severe, 2° OA |
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Clinical course following medullary infarcts in bone
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- clinically silent, exc. large ones (Gaucher ds, dysbarism, Hgbopathies)
- usu. remain stable over time - rarely site of malignant transformation |
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Degenerative joint disease, aka:
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osteoarthritis
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Osteoarthritis
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progressive degredation of articular cartilage
intrinsic disease involving mechanical and biochemical factors |
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Risk of OA increases with increased _____
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bone density
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morphological characteristics of early OA
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degenerating cartilage contains
- increased water - decreased proteoglycans weakening of collagen network - degradation of preexisting collagen |
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chronic osteoarthritic cartilage has increased levels of what molecules?
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IL-1, TNF, NO (--> PCD)
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symptoms characteristic of OA
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- deep, achy pain, worse w/ use
- morning stiffness - crepitus - limited ROM |
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joints characteristically involved in OA
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hips, knees, lumbar & cervical vertebrae
PIP, DIP, 1st CMC, 1st TMT joints |
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Heberden nodes
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in fingers
characteristic in women, not men prominent osteophytes in DIPs |
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Rheumatoid arthritis
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- chronic, systemic inflammatory disorder
- principally attacks joints --> nonsuppurative, proliferative, inflammatory synovitis - progresses to destruction of articular cartilage & ankylosis of the joints - also affects skin, blood vessels, heart, lungs, muscles - autoimmunity heavily involved |
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morphology of RA joints
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Synovium
- edematous - thickened - hyperplastic - bulbous fronds - Inflammatory cells - densely perivascular -. B cells, TH cells, Mφ Increased vascularity Hemosiderin deposits Fibrin aggregation PMNs in synovial fluid Ostoclastic activity allows synovium to penetrate bone --> juxta-articular erosisons, subchondral cysts, osteoporosis pannus formation |
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pannus
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mass of synovium & synovial stroma
consists of inflamm cells, granulation tissue, fibroblasts grows over articular cartilage, causing its erosion then bridges apposing bones --> fibrous ankylosis --> bony ankylosis |
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skin involvement in RA
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rheumatoid nodules
- most common cutanous lesions in RA - firm, nontender, round to oval - arise in s.c. tissue - central zone fibrinoid necrosis w/ prom. rim epithlioid histiocytes & many lymphocytes |
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common vascular complications of RA
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vasculititides
obstruction of vasa nervorum obstruction of digital arteries |
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clinical course of RA
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- initial malaise, fatigue, generalized musculoskeletal pain
- followed by clear joint involvement ~10% pts have acute onset w/ polyarticular involvement developing rapidly - usu. small joints affected first: MCP, DIP, PIP, MTP, IP - then wrists, ankles, elbows, knees - lumbosacral region usu. spared - involved joints swollen, warm, painful, particularly stiff on rising or s/p inactivity - large synovial cysts, e.g.Baker’s, may dev 2° ↑intra-articular P causing outpouchings synovium |
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diagnostic criteria for RA
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- morning stiffness
- arthritis in 3 or more joints - arthritis of typical hand joints - symmetric arthritis - rheumatoid nodules - serum RF - typical radiographic changes |
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5 ways JA differs from RA
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- oligoarthritis more common
- systemic onset more frequent - large joints affected more often than small joints - rheumatoid nodules & RF usu. absent - ANA seropositivity common |
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commonly targeted joints in JA
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knees, wrists, elbows, ankles
warm, swollen, typical symmetric involvement |
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describe systemic onset of JA
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may beg abruptly with...
- high spiking fever - migratory & transient rash - HSM - serositis |
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Seronegative spondyloarthritis
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immune-mediated, possibly by T cell response to unknown Ags
produce inflammatory peripheral or axial arthritis & inflammation of tendinous attachment types: ankylosing spondylitis, reactive arthritis, psoriatic arthritis, arthritis assoc w/ IBD |
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Ankylosing spondyloarthritism, aka:
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rheumatoid spondylitis, Marie-Strümpell disease
|
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end disease process of ankylosing spondyloarthritis in the spine
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- inflammation of tendinoligamentous insertion sites
- followed by ossification - ossification forms osteophytes - osteophytes create severe spinal immobility |
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Joint involvement in ankylosing spondyloarthritis
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axial joints, especially sacroiliac joints
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when does ankylosing spondyloarthritis usually become symptomatic?
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teens to 20s
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is there an association between spondyloarthritis and HLA-B27?
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Yes - 90% pts are HLA-B27 positive, although some subtypes not associated with disease
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characterize ankylosing spondyloarthritis
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chronic synovitis with destruction of articular cartilage & bony ankylosis, esp SI & apophyseal joints
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Reactive arthritis
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an episode of noninfectious arthritis of the appendicular skeleton
occuring within one month of infection localized elsewhere |
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Infections most commonly associated with reactive arthritis
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most infections are GUIs: Chlamydia
other common infections are GI: Shigella, Salmonella, Yersinia, Campylobacter |
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Reiter's syndrome triad:
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arthritis
nongonococcal urethritis or cervicitis conjunctivitis |
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arthritic symptoms associated with reactive arthritis
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- joint pain & low back pain common early symptoms
- ankles, knees, feet affected most often - usu. in asymmetric pattern - sausage finger (synovitis of digital tendon sheath) - calcaneal spurs & osteophytes --- from ossification of tendoligamentous insertion sites |
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Epidemiology of reactive arthritis
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Most patients in 20s, 30s
80% are positive for HLA-B27 |
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4 types of infectious arthritis
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Viral arthritis
Lyme arthritis Tuberculous arthritis Suppurative arthritis |
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Suppurative arthritis
etiology - presentation - systemic effects - |
bacteria seed joint during episode bacteremia
most common bacteria: - Staph, Strept, H. influenzae & G(-) bacilli classic presentation: sudden development of acutely painful, hot, swollen joint with restricted ROM systemic findings of fever, ↑WBCs, ↑ESR |
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endogenous crystals that cause pathology
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monosoidum urate,
calcium pyrophaophate dihydrate, calcium phosphate |
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exogenous crystals that cause pathology
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corticosteroid esters
talcum polyethylene mehtyl methacrylate |
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what do pathogenic crystals do?
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trigger cascade that leads to cytokine-mediated cartilage destruction
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Gout
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transient attacks of acute arthritis initiated by crystalization of urates in/around joints
leads eventually to chronic gouty arthritis tophi |
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tophi
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deposition of urate masses in joints form large aggregates with surrounding inflammatory reaction
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most common visceral complication of chronic gout
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urate nephropathy
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uric acid is the end product of what metabolic pathway?
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purine metabolism
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key enzyme deficiency in gout
|
HGPRT - involved in purine salvage pathway
deficiency causes - decrease in salvage pathway - increase in de novo pathway - increased production uric acid |
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Lesch-Nyhan Syndrome
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- rare, X-linked condition with complete absence of HGPRT
- only in males - hyperuricemia, severe neruological deficits with mental retardation & self-mutilation |
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factors contributing to conversion of asymptomatic hyperuricemia to primary gout
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- age
- genetic predisposition - heavy alcohol consumption predisposes to gout attack - obesity - certain drugs, e.g.: thiazides - lead toxicity predisposes to saturnine gout |
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plasma level of uric acid considered elevated
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plasma level > 7 mg/dL
b/c saturates plasma at normal core body temperature and blood pH |
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Why do urate crystals form in joints but not in blood vessels?
|
synovial fluid is a poorer solvent for uric acid than is plasma
temperature at the small, distal joints can be as low as 20*C |
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pathogenesis of gout attacks following urate crystal formation
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- some event (eg: trauma) initiates release of crystals into synovial fluid
- released crystals are chemotactic to WBCs & activate complement (yielding C3a, C5a) - phagocytsosis of crystals causes release toxic ROS & LTB4 - activated PMNs & Mφ produce inflammatory cytokines - acute arthritis eventually remits (days to weeks) even if untreated |
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four stages of gout
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(1) asymptomatic hyperuricemia
(2) acute gouty arthritis (3) intercritical gout (4) chronic tophaceous gout |
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length of time between first gout attack and development of chronic tophaceous gout
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average 12 years
|
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Pseudogout, aka:
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calcium pyrophosphate crystal deposition disease (CPPD)
or chondrocalcinosis |
|
epidemiology of pseudogout
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usually occurs in pts > 50 y/o
sexes & races equally affected |
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3 types of pseudogout
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sporadic (idiopathic)
hereditary secondary |
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hereditary pseudogout
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crystals dev relatively early in life - associated with severe OA
AD form related to ANKH gene mutation ANKH: transmembrane inorganic pyrophosphate transport channel |
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secondary pseudogout
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associated with various disorders:
- previous joint damage - hyperparathyroidism - hemochromatosis - hypomagnesemia - hypothyroidism - ochronosis - DM |
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pathogenesis of pseudogout
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crystals develop in articular matrix, menisci, intervertebral discs
may rupture & seed joint upon enlargement upon release into joint, elicit IL-8 production inflammatory infiltrate rich in PMNs |
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morphology of pseudogout crystals
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- chalky white friable deposits
- oval, blue-purple aggregates - individual xstals 0.5 to 5μm - geometrically shaped |
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Osteochondroma
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benign, cartilage capped outgrowth attached to skeleton by bony stalk
inactivation both copies of EXT gene in physis chondrocytes (sporadic & hereditary) occur in bones of endochondral origin arise in metaphysis near physis of long tubular bones, esp. near knee |
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Epidemiology of osteochondroma
|
solitary osteochondromas – late adolescence/early adulthood
multiples – usu. hereditary (AD) - childhood men > women |
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Chondroma
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benign tumors of hyaline cartilage
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endochondromas
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chondromas originating in medullary cavity
|
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subperiosteal chondromas
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chondromas originating on surface of bone
|
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Ollier disease
|
multiple endochondromas
|
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Maffucci syndrome
|
multiple endochondromas associated w/ soft tissue hemangiomas
|
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characteristic radiographic features of chondromas
|
unmineralized nodules of cartilage
O ring sign: well-circumsribed oval lucencies surrounded by thin rim radiodense bone |
|
Chondroblastoma
|
rare benign tumor
usually near knee, epiphyses/apophyses usu. painful rad: well-defined geographic lucency w/ spotty calcifications |
|
chondrosarcomas - common feature
|
production of neoplastic cartilage
|
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Characteristics of chondrosarcomas
|
usu. 40 y/o+
usu. in central portions of skeleton: pelvis, shoulder, ribs painful, progressively enlarging masses rad: prominent endosteal scalloping |
|
Fibrous cortical defect & nonossifying fibroma
|
Fibrous cortical defect & nonossifying fibroma
- very common: 30-50% kids > 2 y/o - DEVELOPMENTAL DEFECTS, not neoplasms - arise eccentrically in metaphysis of distal femur & proximal tibia - large defects yield nonossifying fibromas - radiography: elongated, sharply demarcated radiolucencies surry by thin zone of sclerosis - asymptomatic: limited growth φ & spontaneously resolve w/ replacement by normal bone |
|
Fibrous dysplasias (general)
|
benign tumor ~ localized developmental arrest
all components normal bone present, but do not differentiate into mature structures |
|
monostotic firbrous dysplasia
|
70% all cases, usu. in early teens & stops growing at time of physis closure
ribs, femur, tibia, jawbones, calvaria, humerus asymptomatic can cause marked enlargement & distortion of bone |
|
polyostotic fibrous dysplasia without endocrine dysfunction
|
- 27% all cases, manifests earlier than monostotic & con’t causing probs into adulthd
- femur, calvaria, tibia, humerus, ribs, fibula, radius, ulna, mandible, vertebrae - craniofacial involvment in 50% pts - propensity shoulder & pelvic girdle involvement severe, crippling deformities - spontaneous, often recurrent, fx |
|
McCune-Albright Syndrome
|
polyostotic fibrous dysplasia w/ café au lait skin pigmentation & endocrinopathies
sexual precocity, hyperthyroid, pit. adenomas secrete GH, 1° adrenal hyperplasia radiographic: ground-glass appearance & well-defined margins |
|
Fibrosarcoma & Malignant fibrous histiocytoma
|
- fibroblastic collagen-producing sarcomas of bone
- usu affect middle-aged to elderly - usu arise de novo - large, hemorrhagic, tan-white masses - destroy underlying bone & freq. ext. into soft tissues - enlarging, painful masses arising in metaphyses of long bones & pelvic flat bones - propensity to pathologic fx |
|
Ewing & PNET
|
- malignant small round cell tumors of bone & soft tissue
Ewing – youngest age presentation of all bone sarcomas - diaphyses of long tubular bones, esp. femur & flat bones of pelvis painful, enlarging masses affected site tender, warm, swollen xrays: destructive lytic tumor w/ permeative margins & ext. into soft tissues characteristic periosteal reactions --> layers reactive bone in onionskin pattern |
|
Giant Cell Tumor
|
profusion of multinucleated osteoclast-type giant cells (aka: osteoclastoma)
in adults: epiphyses & metaphyses in teens: confined by physis & limited to metaphysis arise around knee – often causes arthritic symptoms rad: large, purely lytic, eccentric, erode into subchondral bone plate |
|
most common form of skeletal malignancy
|
metastatic bone tumors
|
|
modes of spread to bone metastases
|
direct extension
lymphatic or hematogenous dissemination intraspinal seeding (Batson plexus of veins) |
|
most metastatic bone tumors involve which bones?
|
most involve axial skeleton, prox. femur, humerus
(rich capillary network, slow blood flow, nutrient environment) |
|
mode by which bone metastases cause bone resorption
|
metastatic cells produce PGs, IL, PTHRP
-- signal osteoclastic bone resorption -- tumor cells themselves do not resorb bone most elicit mixed lytic & blastic reaction |
|
What does increased urinary excretion of hydroxyproline indicate?
|
increased collagen breakdown
|