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61 Cards in this Set

  • Front
  • Back
Inorganic elements in bone (2)
Ca, PO4
Organic elements of bone
Type I collagen
pluripotent stem cells, turn into osteoblasts
osteoprogenitor cells
synthesize proteins, initiate mineralization of bone
osteoblasts
cells within bone, communicate through canaliculi
osteocytes
resorb bone
osteoclasts
*unmineralized bone
osteoid
bone seen in fetal skeleton and at growth plates
woven bone
bone that replaces woven bone and is stronger. Bone is in orderly layers
lamellar bone
when does skeletal mass begin to decline?
after 4th decade - amt of bone formed is less than amt of bone resorbed
central part of bone
diaphysis
3 characteristics of diaphysis
1. central part of bone
2. from primary ossification center
3. metaphysis is end of diaphysis
end of diaphysis before epiphysis is called
metaphysis
epiphysis (2)
1. end of long bones
2. from secondary ossification center
physis (2)
1. between diaphysis and epiphysis
2. responsible for growth until fusion
4 major parts of a long bone
diaphysis, metaphysis, epiphysis, physis
4 types of fractures
closed - overlying tissue intact
compound - communicates with the skin
comminuted - bone is splintered
pathologic - fracture in already diseased bone
5 steps in fracture healing
1. hematoma formation
2. procallus formation
3. soft callus
4. hard callus
5. remodeling
procallus
inflammation with granulation tissue, collagen forms between fractured ends
soft callus
osteoprogenitors deposit woven bone, may deposit cartilage.
Not weight bearing!
hard callus
mineralization through enchondral ossification
false joint due to untreated fracture
pseudoarthrosis
2 causes of osteomyelitis
1. hematogenous spread (MC. Long bones & vertibrae)
2. Direct spread or innoculation (surgery, open fracture)
osteomyelitis in a neonate is usually found in the...
metaphysis and/or epiphysis
osteomyelitis in a child is usually found in the...
metaphysis
osteomyelitis in an adult is usually found in the...
epiphysis & subchondral regions
MC organism in osteomyelitis
S aureus
osteomyelitis due to EtOH or IV drug use
Group G strep
osteomyelitis in neonate (causative organisms) (2)
Hib, Group B strep
osteomyelitis due to heroin use
p. aeruginosa
osteomyelitis in sickle cell patient
salmonella
osteomyelitis in an immunocompromised patient
All others + mycobacterium & fungal species
osteomyelitis due to GU infection
E. Coli,
Pseudomonas,
Klebsiella
*necrotic piece of bone from ischemic injury
sequestrum
*reactive or woven bone around sequestrum
involucrum
soft tissue abscess from periosteum rupture
draining sinus
small abscess surrounded by reactive bone
brodie abscess
Radiology:
bone destruction surrounded by zone of sclerosis
Dx: osteomyelitis
5 factors in primary osteoporosis
1. Vitamin D receptor polymorphisms—hereditary
2. Physical activity
3. Muscle strength
4. Diet
5. Hormonal state—loss of estrogen is bad
primary vs secondary osteoporosis?
Primary=loss of bone mass during agine
secondary=loss of bone mass due to something else (malabsorption, multiple myeloma, etc)
4 possible causes of seconday osteoporosis
1. Endocrine (hyperparathyroidism)
2. Multiple myeloma
3. Malabsorption
4. Corticosteroids
what is the rule of 2's?
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
how Dx osteoporosis? (3)
values outside of rule of 2's
DEXA scan
CT: lumbar spine
Rickets vs Osteomalacia?
(who gets? what causes?)
Rickets - children
osteomalacia - adults

due to lack of vitD or problem in metabolism
deranged bone growth & skeletal deformity in child
rickets
adult with undermineralized bone & predesposed to fractures
osteomalacia
mosaic pattern of lamellar bone what resembles jigsaw puzzle produced by prominent cement lines
paget's disease
increased abnormal bone mass
paget's disease
paramyxovirus infection with IL-6 induction --> ???
paget's disease
bone has many resporption pits. osteoclasts are larger than normal & have >10-12 nuclei
Lytic phase of paget's disease
osteoclasts persist with prominent osteoblasts lining the bone surfaces. marrow is replaced by loose connective tissue
mixed phase of paget's disease
bone becomes its own caricature but is larger than normal and hase hoarsely thickened trabeculae
osteosclerotic stage of paget's disease
paget's disease usually effects what bones
long bones of axial skeleton. especially femur
pagets disease in bones other than pelvus, skull
monostotic
pagets disease in pelvis, skull
polyostotic
increased alkaline phosphatase and urinary hydroxyproline
pagets disease!!!!
*3 major complications of paget's disease
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**
cause of primary hyperparathyroidism?
hyperplasia or tumor of parathyroid
*cause of secondary hyperparathyroidism?
prolonged hypocalcemia with increased PTH secretion
anatomic changes of skeleton due to hyperparathyroidism
osteitis fibrosa cystica (aka: von Recklinghausen disease of bone)
*morphology of osteitis fibrosis cystica (due to hyperparathyroidism)
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**)