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Patho 2 > Ch 26- Bone and Joints > Flashcards

Ch 26- Bone and Joints Flashcards

1
Q

constituents of bone

A
  • ECM -> osteoid and mineral components

- Cells -> osteocytes, osteoblasts, osteoclasts

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2
Q

osteocytes

A
  • derived from osteoblasts
  • have projecting dendrites for cell to cell communication
  • perform mechanotransduction
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3
Q

osteoid ECM

A
  • made up of type 1 collagen and osteopontin

- osteopontin- Ca homeostasis and marker for osteoblast activity

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4
Q

hydroxyapatite

A
  • mineral component of ECM

- stores Ca and P

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5
Q

diaphysis

A
  • shaft of bone

- made of compact tissue that encloses medullary cavity

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6
Q

epiphysis

A
  • enlarged end of bone
  • made of spongy tissue and articulates with neighboring bones
  • covered with articular cartilage to reduce friction and absorb shock
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7
Q

metaphysis

A
  • between epiphysis and diaphysis
  • contains cartilage to enable bone to grow
  • disappears in adulthood
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8
Q

periosteum

A
  • dense layer of vascular CT enveloping bones

- not found on surfaces of joints

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9
Q

compact bone

A
  • aka cortical bone

- dense bone in which bony matrix is solidly filled with organic ground substances and inorganic salts

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10
Q

endosteum

A
  • covers insides of bones

- surrounds medullary cavity

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11
Q

medullary cavity

A
  • central cavity of bone shafts

- where red and/or yellow marrow is stored

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12
Q

how much of the skeleton is replaced annually

A
  • 10%

- regulated by cell-cell interactions and cytokines

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13
Q

osteoclast activation

A
  • primary pathway= NFkB
  • activated NFkB -> RANKL binding to RANK receptor
  • RANK receptor located on stromal cells and osteoblasts
  • also get MCSF release causing differentiation of osteoblasts to osteoclasts
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14
Q

osteoclast inactivation

A
  • maturation of osteoblasts to osteoclasts is stopped by producing osteoprotegrin
  • osteoproegrin is “decoy receptor” to prevent RANKL from binding to receptor
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15
Q

achondroplasia

A
  • most common cause of dwarfism
  • autosomal dominant
  • retarded cartilage growth
  • due to mutation if FGF3 causing excessive suppressed bone growth
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16
Q

clinical features of achrondroplasia

A
  • shortened proximal extremities
  • normal trunk length
  • enlarged head with bulging forehead
  • depression of bridge of nose
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17
Q

osteogenesis imperfecta

A
  • type 1 collagen disease
  • most common inherited disorder of CT
  • affects bones*, eyes, ears, skin, teeth
  • autosomal dominant
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18
Q

pathphysiology of osteogenesis imperfecta

A
  • collagen subunit assembly is disturbed- defective assembly of collagen peptides
  • results in too little bone and very fragile skeleton
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19
Q

types of osteogenesis imperfecta

A
  • type 1- normal life span but experiences childhood fx

- type 2- fatal in uteru

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20
Q

osteopenia

A
  • decreased bone mass
  • bone mass < 1 or 2.5 SD
  • normal bone mineral content
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21
Q

osteoporosis

A
  • severe osteopenia
  • bone mass < 2.5 SD
  • classified as either localized or generalized
  • normal bone mineral content
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22
Q

causes of primary generalized osteoporosis

A
  • idiopathic
  • post- menopausal*
  • senile*
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23
Q

causes of secondary osteoporosis

A
  • endocrine disorders
  • neoplasia
  • drugs- corticosteroids
  • manutrition and vit C or D def
  • immobilization
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24
Q

estrogen and osteoporosis

A
  • estrogen required for proper functioning of osteoblasts and clasts
  • decreased estrogen -> increased cytokine release
  • cytokines activate osteoclasts
  • called high turnover osteoporosis
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25
low turnover osteoporosis
- age related changes | - due to accumulation of bone loss with each turn over
26
clinical course of osteoporosis
- depends on bones involved - vertebral fx common - complications of fx of femoral neck, pelvis or spine -> PE or pneumonia
27
endocrine disorders associated with secondary osteoporosis
- diabetes - hyperparathyroidism - hyper/hypothyroidism
28
pagets disease
- aka osteitis deformans - increased but disordered and structurally unsound bone mass - usually begins in late adulthood
29
phases of paget disease
- initial osteolytic stage - mixed osteoclastic- osteoblastic stage - osteosclerotic stage (silent)
30
pathogenesis of paget disease
- genetic and enviornmental factors - mutations in SQSTM1 gene - increased NK-kB - RNA virus infections -> modifies vit D sensitivity and IL-6 secretion
31
clinical course of paget disease
- mostly asymptomatic - often involves axial skeleton and proximal femur - pain localized to affected bone - leontiasis ossea - platybasia - compression of posterior fossa of skull - anterior bowing of legs - chalk-stick fx - compression fx of vertebra -> kyposis - osteosarcoma and fibrosarcoma rare
32
leontiasis ossea
- lion face | - associated with paget disease
33
platybasia
- invagination of skull base | - associated with paget disease
34
chalk stick type fx
- occurs in long bones of lower limb in pts with paget disease
35
renal osteodystrophy
- skeletal changes that occur in chronic renal disease - osteopenia/porosis - osteomalacia - secondary hyperparathryoidism - growth retardation
36
impact of tubular dysfunction on bones
- renal tubular acidosis -> decreased pH - dissolves the hydroxyappatite - results in osteomalacia
37
impact of renal failure on bones
- decreased phosphate excretion - causes chronic hyperphsphatemia hypocalcemia - causes secondary hyperparahtyroidism
38
BMP-7 and Klotho
- normally secreted by kidneys | - play role in osteoblast activity and Ca homeostasis
39
pathologic fx
- involving bone weakened by a underlying disease process like a tumor
40
steps of healing fractures
- hematoma - necrosis of broken bone ends - fibroblasts invade clot - fibroblasts secrete collagen fibers which form callus - callus bridges broken bone ends over 2-6 weeks - osteoblasts invade callus and convert it to bone over 3-6 weeks
41
osteomyelitis
- inflammation of bone secondary to infection | - most common causes= pyogenic (s. aureus) bacteria and mycobacteria
42
how can organisms reach bone and cause infection
- hematogenous spread - extension from contiguous site - direct implantation
43
sequestrum
- dead bone in osteomyelitis
44
involucrum
- newly depositied bone | - forms shell of living tissue around segment of infected bone during osteomyelitis
45
clinical course of osteomyelitis
- malaise, fever, chills - leukocytosis - pain over affected region - destruction of discs and vertebrae -> scoliosis or kyphosis and neurological deficits
46
complications of osteomyelitis
- chronic osteomyelitis - pathologic fx - secondary amyloidosis - endocarditis - sepsis - carcinoma
47
osteoid osteoma
- benign bone producing tumor - < 2cm in diameter - common in teens and 20s - occurs in appendicular skeleton - malignant transformation rare
48
osteoblastoma
- benign bone producing tumor - > 2cm - involves posterior spine most frequently - malignant transformation rare
49
osteosarcoma
- most common primary bone tumor - produce osteoid matrix or mineralized bone - bimodal age distribution but most common in 20s-30s - painful, progressively enlarging mass - pathologic fxs
50
predisposing conditions for osteosarcoma
- paget disease - bone infarcts - prior radiation
51
pathogenesis of osteosarcoma
- mutation in RB - TP53 mutations - inactivated INK4a- encodes two tumor suppressors p16 and p14 - MDM2 and CDK4- cell cycle regulators
52
non-synovial joints
- solid - provide structural integrity - allow minimal movement - lack joint space - i.e. cranial sutures
53
synovial joints
- have joint space | - allow for wide ROM
54
osteoarthritis
- most common joint disease - degeneration of cartilage -> structural/ functional failure of joints - primary OA- aging - secondary OA- obesity or diabetes - joint deformity can occur but never fusion
55
what is the most common site for OA in women
- knees | - hands
56
what is the most common site of OA in men
hips
57
clinical features of OA
- asymptomatic until 50s - deep, achy pain that worsens with use - morning stiffness - crepitus - osteophyte formation - limited ROM - nerve root compression - radicular pain - muscle spasms or atrophy - neurologic deficits
58
pathogenesis of OA
- chondrocytes get activated d/t pressure or cartilage degen -> stimulate macrophages - macrophages release TNF alpha, IL6 and IL1 - accumulation of immune cells and more bone destruction
59
most common sites for OA overall
- hips - knees - lower lumbar and cervical vertebrae - proximal and distal IP joints of fingers - first CMC joints - first TMT joints
60
rheumatoid arthritis
- chronic inflammatory disorder - autoimmune - non-suppurative, proliferative, and inflammatory synovitis - can involve other parts of body
61
extra-articular involvement in RA
- skin (nodules) - heart (MI) - blood vessels (atherogenesis) - lungs
62
clinical features of RA
- inflammation - articular cartilage destruction - bone erosion - angiogenesis - ankylosis and joint enlargement - symmetrical joint involvment - swollen, warm, painful joints - morning stiffness lasts longer
63
swan neck deformity
- in RA - flexion at distal IP joint - extension and proximal IP joint
64
boutonniere deformity
- in RA - extension at distal IP joint - flexion at proximal IP joint
65
diagnosis of RA
- radiographic findings - turbid synovial fluid with decreased viscosity, poor mucin clot formation, and inclusion bearing neutrophils - RA factor and anti-CCP antibody
66
pathogenesis of RA
- CD4 cells initiate autoimmune response - T cells prod cytokines that stim other inflammatory cells - recruit and activate other immune cells -> cartilage damage - RANKL expressed on activated t cells stimulates bone resportion
67
RA factor
- most pts have serum IgM or IgA antibodies that bind to Tc portion of own IgG
68
gout
transient attacks of acute arthritis - initiated by crystallization of monosodium urate within and around joints - due to hyperuricemia
69
hyperuricemia
plasma urate > 6.8 mg/dL
70
risk factors for gout
- age - genetics - heavy alcohol consumption - obesity - drugs- thiazides - lead toxicity
71
morphologic changes with gout
- acute arthritis - chronic tophaceous arthritis - tophi in various sites - gouty nephropathy

Patho 2 (15 decks)

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