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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
Q

low turnover osteoporosis

A
  • age related changes

- due to accumulation of bone loss with each turn over

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26
Q

clinical course of osteoporosis

A
  • depends on bones involved
  • vertebral fx common
  • complications of fx of femoral neck, pelvis or spine -> PE or pneumonia
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27
Q

endocrine disorders associated with secondary osteoporosis

A
  • diabetes
  • hyperparathyroidism
  • hyper/hypothyroidism
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28
Q

pagets disease

A
  • aka osteitis deformans
  • increased but disordered and structurally unsound bone mass
  • usually begins in late adulthood
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29
Q

phases of paget disease

A
  • initial osteolytic stage
  • mixed osteoclastic- osteoblastic stage
  • osteosclerotic stage (silent)
30
Q

pathogenesis of paget disease

A
  • genetic and enviornmental factors
  • mutations in SQSTM1 gene - increased NK-kB
  • RNA virus infections -> modifies vit D sensitivity and IL-6 secretion
31
Q

clinical course of paget disease

A
  • 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
Q

leontiasis ossea

A
  • lion face

- associated with paget disease

33
Q

platybasia

A
  • invagination of skull base

- associated with paget disease

34
Q

chalk stick type fx

A
  • occurs in long bones of lower limb in pts with paget disease
35
Q

renal osteodystrophy

A
  • skeletal changes that occur in chronic renal disease
  • osteopenia/porosis
  • osteomalacia
  • secondary hyperparathryoidism
  • growth retardation
36
Q

impact of tubular dysfunction on bones

A
  • renal tubular acidosis -> decreased pH
  • dissolves the hydroxyappatite
  • results in osteomalacia
37
Q

impact of renal failure on bones

A
  • decreased phosphate excretion
  • causes chronic hyperphsphatemia hypocalcemia
  • causes secondary hyperparahtyroidism
38
Q

BMP-7 and Klotho

A
  • normally secreted by kidneys

- play role in osteoblast activity and Ca homeostasis

39
Q

pathologic fx

A
  • involving bone weakened by a underlying disease process like a tumor
40
Q

steps of healing fractures

A
  • 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
Q

osteomyelitis

A
  • inflammation of bone secondary to infection

- most common causes= pyogenic (s. aureus) bacteria and mycobacteria

42
Q

how can organisms reach bone and cause infection

A
  • hematogenous spread
  • extension from contiguous site
  • direct implantation
43
Q

sequestrum

A
  • dead bone in osteomyelitis
44
Q

involucrum

A
  • newly depositied bone

- forms shell of living tissue around segment of infected bone during osteomyelitis

45
Q

clinical course of osteomyelitis

A
  • malaise, fever, chills
  • leukocytosis
  • pain over affected region
  • destruction of discs and vertebrae -> scoliosis or kyphosis and neurological deficits
46
Q

complications of osteomyelitis

A
  • chronic osteomyelitis
  • pathologic fx
  • secondary amyloidosis
  • endocarditis
  • sepsis
  • carcinoma
47
Q

osteoid osteoma

A
  • benign bone producing tumor
  • < 2cm in diameter
  • common in teens and 20s
  • occurs in appendicular skeleton
  • malignant transformation rare
48
Q

osteoblastoma

A
  • benign bone producing tumor
  • > 2cm
  • involves posterior spine most frequently
  • malignant transformation rare
49
Q

osteosarcoma

A
  • 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
Q

predisposing conditions for osteosarcoma

A
  • paget disease
  • bone infarcts
  • prior radiation
51
Q

pathogenesis of osteosarcoma

A
  • mutation in RB
  • TP53 mutations
  • inactivated INK4a- encodes two tumor suppressors p16 and p14
  • MDM2 and CDK4- cell cycle regulators
52
Q

non-synovial joints

A
  • solid
  • provide structural integrity
  • allow minimal movement
  • lack joint space
  • i.e. cranial sutures
53
Q

synovial joints

A
  • have joint space

- allow for wide ROM

54
Q

osteoarthritis

A
  • 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
Q

what is the most common site for OA in women

A
  • knees

- hands

56
Q

what is the most common site of OA in men

A

hips

57
Q

clinical features of OA

A
  • 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
Q

pathogenesis of OA

A
  • 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
Q

most common sites for OA overall

A
  • hips
  • knees
  • lower lumbar and cervical vertebrae
  • proximal and distal IP joints of fingers
  • first CMC joints
  • first TMT joints
60
Q

rheumatoid arthritis

A
  • chronic inflammatory disorder
  • autoimmune
  • non-suppurative, proliferative, and inflammatory synovitis
  • can involve other parts of body
61
Q

extra-articular involvement in RA

A
  • skin (nodules)
  • heart (MI)
  • blood vessels (atherogenesis)
  • lungs
62
Q

clinical features of RA

A
  • inflammation
  • articular cartilage destruction
  • bone erosion
  • angiogenesis
  • ankylosis and joint enlargement
  • symmetrical joint involvment
  • swollen, warm, painful joints
  • morning stiffness lasts longer
63
Q

swan neck deformity

A
  • in RA
  • flexion at distal IP joint
  • extension and proximal IP joint
64
Q

boutonniere deformity

A
  • in RA
  • extension at distal IP joint
  • flexion at proximal IP joint
65
Q

diagnosis of RA

A
  • radiographic findings
  • turbid synovial fluid with decreased viscosity, poor mucin clot formation, and inclusion bearing neutrophils
  • RA factor and anti-CCP antibody
66
Q

pathogenesis of RA

A
  • 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
Q

RA factor

A
  • most pts have serum IgM or IgA antibodies that bind to Tc portion of own IgG
68
Q

gout

A

transient attacks of acute arthritis

  • initiated by crystallization of monosodium urate within and around joints
  • due to hyperuricemia
69
Q

hyperuricemia

A

plasma urate > 6.8 mg/dL

70
Q

risk factors for gout

A
  • age
  • genetics
  • heavy alcohol consumption
  • obesity
  • drugs- thiazides
  • lead toxicity
71
Q

morphologic changes with gout

A
  • acute arthritis
  • chronic tophaceous arthritis
  • tophi in various sites
  • gouty nephropathy

Patho 2 (15 decks)

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