Metabolic Bone Disease Flashcards

1
Q

Osteoporosis

A

Clinical disease to reduce bone mass

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2
Q

Osteopenia

A

reduced bone mass without clinical disease

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3
Q

Causes of osteoporosis

A

humans–estrogen loss at menopause
animals–protein calorie malnutrition; low calcium with normal phosphorus diets (usually experiemental in mammals); localized due to disuse

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4
Q

Pathogenesis of osteoporosis–post menopausal

A

increased resorption due to loss of protective effect of estrogen; formation is normal or decreased

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5
Q

Ovariectomy and osteopenia

A

ovariectomy induces osteopenia mostly in animals with monthly estrous cycles–so does NOT affect ovariectomized dogs and cats

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6
Q

Pathogenesis protein calorie malnutrition

A

decreased formation due to overall anti-antibolic effects of malnutrition; normal resorption

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7
Q

Pathogenesis localized disuse

A

Increased resorption and decreased formation.

Osteocytes sense mechanical use and signal osteoblasts concerning what bone mass they think is appropriately needed

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8
Q

Structural Changes

A
  • *Less bone: thin, less connected and fewer trabeculae (in long appendicular bones of adults) –trabecular bone should span from epiphysis to metaphysis–increased porosity of cortices and thin cortices in advanced stages
  • *Increased microcracks
  • *pathologic fractures
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9
Q

Clinical Consequences of Osteoporosis/osteopenia

A
  • -Pathologic fractures=force to fracture was not as high as is necessary to fracture normal bone
  • -bone pain
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10
Q

What is Osteomalacia/Rickets

A

Failure of mineralization in adults=osteomalacia

Failure of mineralization of bone and growth plate in young=rickets

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11
Q

Causes of Osteomalacia/rickets

A

Vitamin D deficiency

phosphorus deficiency

xenobiotics that inhibit mineralization

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12
Q

Pathogenesis of osteomalacia/rickets

A

Inadequate calcium/ phosphorus product at the mineralization site

vitamin D metabolites needed at mineralization site or just for calcium absorption from intestine??

Inhibition of mineralization process by drugs

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13
Q

Structural changes with osteomalacia/rickets

A

accumulation of osteoid (young/adult)

retention of chondrocytes in the growth plate due to failure of mineralization

deformity due to bone softness

accumulation of microcracks secondary to reduced ability to remodel bone because unmineralized surfaces are resistant to osteoclasis

pathologic fracture

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14
Q

Retention of chondrocytes in growth plate (osteomalacia/rickets)

A

causing flaring of the metaphysis due to the thickened growth plate and failure of osteoclasts to taper the bone at the cut back zone OSTEOCLASTS CAN ONLY BIND TO AND RESORB MINERALIZED BONE MATRIX

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15
Q

Clinical consequences of osteomalacia/rickets

A

1) deformity
2) pathologic fracture
3) Bone Pain

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16
Q

Fibrous osteodystrophy (FOD)

A

response of bone pathologic levels of PTH

17
Q

Causes of FOD

A

PTH stimulates osteoclastic bone resorption and fivrous differentiation and hyperplasia of osteoprogenitor cells

18
Q

Stuctural changes with Fibrous osteodystrophy

A

1) less than normal bone mass
2) dimensions may be reduced due to bone resorption or increase. due to proliferation of fibrous/fibro-osseous tissue in the marrow spaces and periosteum by osteoprogenitor cells
3) bone may be pliable due to bone loss and replacement with fibrous tissue
4) pathologic fractures/deformity

19
Q

Clinical consequences of Fibrous osteodystrophy

A
  • -deformity
  • -pathologic fracture
  • -bone pain