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61 Cards in this Set
- Front
- Back
Inorganic elements in bone (2)
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Ca, PO4
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Organic elements of bone
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Type I collagen
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pluripotent stem cells, turn into osteoblasts
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osteoprogenitor cells
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synthesize proteins, initiate mineralization of bone
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osteoblasts
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cells within bone, communicate through canaliculi
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osteocytes
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resorb bone
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osteoclasts
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*unmineralized bone
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osteoid
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bone seen in fetal skeleton and at growth plates
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woven bone
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bone that replaces woven bone and is stronger. Bone is in orderly layers
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lamellar bone
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when does skeletal mass begin to decline?
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after 4th decade - amt of bone formed is less than amt of bone resorbed
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central part of bone
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diaphysis
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3 characteristics of diaphysis
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1. central part of bone
2. from primary ossification center 3. metaphysis is end of diaphysis |
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end of diaphysis before epiphysis is called
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metaphysis
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epiphysis (2)
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1. end of long bones
2. from secondary ossification center |
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physis (2)
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1. between diaphysis and epiphysis
2. responsible for growth until fusion |
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4 major parts of a long bone
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diaphysis, metaphysis, epiphysis, physis
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4 types of fractures
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closed - overlying tissue intact
compound - communicates with the skin comminuted - bone is splintered pathologic - fracture in already diseased bone |
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5 steps in fracture healing
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1. hematoma formation
2. procallus formation 3. soft callus 4. hard callus 5. remodeling |
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procallus
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inflammation with granulation tissue, collagen forms between fractured ends
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soft callus
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osteoprogenitors deposit woven bone, may deposit cartilage.
Not weight bearing! |
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hard callus
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mineralization through enchondral ossification
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false joint due to untreated fracture
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pseudoarthrosis
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2 causes of osteomyelitis
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1. hematogenous spread (MC. Long bones & vertibrae)
2. Direct spread or innoculation (surgery, open fracture) |
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osteomyelitis in a neonate is usually found in the...
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metaphysis and/or epiphysis
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osteomyelitis in a child is usually found in the...
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metaphysis
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osteomyelitis in an adult is usually found in the...
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epiphysis & subchondral regions
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MC organism in osteomyelitis
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S aureus
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osteomyelitis due to EtOH or IV drug use
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Group G strep
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osteomyelitis in neonate (causative organisms) (2)
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Hib, Group B strep
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osteomyelitis due to heroin use
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p. aeruginosa
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osteomyelitis in sickle cell patient
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salmonella
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osteomyelitis in an immunocompromised patient
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All others + mycobacterium & fungal species
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osteomyelitis due to GU infection
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E. Coli,
Pseudomonas, Klebsiella |
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*necrotic piece of bone from ischemic injury
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sequestrum
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*reactive or woven bone around sequestrum
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involucrum
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soft tissue abscess from periosteum rupture
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draining sinus
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small abscess surrounded by reactive bone
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brodie abscess
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Radiology:
bone destruction surrounded by zone of sclerosis |
Dx: osteomyelitis
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5 factors in primary osteoporosis
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1. Vitamin D receptor polymorphisms—hereditary
2. Physical activity 3. Muscle strength 4. Diet 5. Hormonal state—loss of estrogen is bad |
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primary vs secondary osteoporosis?
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Primary=loss of bone mass during agine
secondary=loss of bone mass due to something else (malabsorption, multiple myeloma, etc) |
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4 possible causes of seconday osteoporosis
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1. Endocrine (hyperparathyroidism)
2. Multiple myeloma 3. Malabsorption 4. Corticosteroids |
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what is the rule of 2's?
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the normal ranges of bone values all have "2" in them:
bone volume - >20% osteoid surface - ~20% osteoid vol - ~2% mean trabecular width = 200um osteoclasts - .2/mm2 bone calcification rate = 1/2 um/day mineralization lage time=20 days |
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how Dx osteoporosis? (3)
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values outside of rule of 2's
DEXA scan CT: lumbar spine |
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Rickets vs Osteomalacia?
(who gets? what causes?) |
Rickets - children
osteomalacia - adults due to lack of vitD or problem in metabolism |
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deranged bone growth & skeletal deformity in child
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rickets
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adult with undermineralized bone & predesposed to fractures
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osteomalacia
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mosaic pattern of lamellar bone what resembles jigsaw puzzle produced by prominent cement lines
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paget's disease
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increased abnormal bone mass
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paget's disease
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paramyxovirus infection with IL-6 induction --> ???
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paget's disease
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bone has many resporption pits. osteoclasts are larger than normal & have >10-12 nuclei
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Lytic phase of paget's disease
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osteoclasts persist with prominent osteoblasts lining the bone surfaces. marrow is replaced by loose connective tissue
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mixed phase of paget's disease
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bone becomes its own caricature but is larger than normal and hase hoarsely thickened trabeculae
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osteosclerotic stage of paget's disease
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paget's disease usually effects what bones
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long bones of axial skeleton. especially femur
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pagets disease in bones other than pelvus, skull
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monostotic
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pagets disease in pelvis, skull
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polyostotic
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increased alkaline phosphatase and urinary hydroxyproline
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pagets disease!!!!
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*3 major complications of paget's disease
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1. compression of cranial or spinal nerve roots (ex: hearing loss)
2. high output cardiac failure due to increased blood flow (bone acts like A-V shunt) 3. **malignancy - usually osteosarcoma** |
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cause of primary hyperparathyroidism?
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hyperplasia or tumor of parathyroid
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*cause of secondary hyperparathyroidism?
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prolonged hypocalcemia with increased PTH secretion
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anatomic changes of skeleton due to hyperparathyroidism
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osteitis fibrosa cystica (aka: von Recklinghausen disease of bone)
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*morphology of osteitis fibrosis cystica (due to hyperparathyroidism)
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1. Thinned cortices and loss of lamina dura around teeth
2. Cortical cutting cones—spearhead arrangement of osteoclasts 3. Railroad tracts (dissecting osteitis) in cancellous bone 4. Microfractures with hemorrhages are common 4a. Influx of macrophages with fibrosis (**brown tumor**) |