Midterm - Lecture 9 Flashcards

1
Q

What grows at the physe?

A

long bone

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2
Q

How does long bone grow at the physe?

A
  • Cartilage cells undergo proliferation, hypertrophy, and programmed cell death causing provisional calcification of cartilage cells
  • Invasion of calcified cartilage by blood vessels is accompanied by movement of osteoblasts into area from meta physis
  • Resorption of calcified cartilage followed by laying down of bone matrix – calcified primary bone
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3
Q

What happens to bone growth with an animal that has rickets?

A

failure to mineralize growth plates of the bone

rubbery widened cartilage remains which makes bones bendable

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4
Q

What is the cause for rickets?

A

can be due to calcium deficiency but more commonly die to vitamin D or phosphate deficiency

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5
Q

What happens within the bone with an animal that has rickets?

A

the hypertrophic cartilage cells fail to undergo apoptisis eventually undergo necrotic death
zone of calcified cartilage fails to calcify

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6
Q

Why can piglets get rickets?

A

poor transfer of vitamin D across the placenta and there is little to no Vitamin D in milk

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7
Q

What happens within the bone with an animal that has osteomalacia?

A

during the reversal phase of bone remodeling the newly laid down matrix fails to mineralize

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8
Q

What are the phases of remodeling?

A

activation, resorption, and reversal

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9
Q

What occurs during the activation phase of remodeling?

A

osteoblasts retract from the surface of the area of bone to be remodeled, osteoclasts move toward the site of exposed bone

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10
Q

What occurs during the resorption phase of remodeling?

A
  • Osteoclasts develop a ruffled border and form a tight seal with the exposed bone
  • Secretion of acids and enzymes cause dissolution of the organic matrix freeing the minerals which enter extracellular fluid
  • Osteoclasts scoop out bone matrix and mineral to a depth of approximately 50 microns
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11
Q

What occurs during the reversal phase of remodeling?

A
  • Osteoclasts leave the area and become inactive
  • Osteoblasts from among the endosteal bone lining cells at the edge of the resorption site now enter the depths of the resorption cavity
  • Osteoblasts begin producing new bone matric to fill in the resorption cavity; Some become trapped within the matrix to give rise to new osteocytes
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12
Q

When does osteoporosis occur?

A

when the diet fails to supply calcium

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13
Q

How does osteoporosis affect bone remodeling?

A

the low supply of calcium causes a disconnect between the resorption phase

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14
Q

How does lactational osteoporosis affect bone remodeling?

A

the need for calcium to support lactation causes a disconnect between the resorptive and reversal phases of the remodeling process
the resorbed bone is not replaced

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15
Q

How does the body respond to nutritional secondary hyperparathyroidism?

A
  • Increases renal reabsorption of Ca; Only a limited amount of Ca can be recovered
  • Increases osteoclastic bone resorption; Resorption and bone formation uncoupled, eventually reduces bone calcium content
  • Increases production of vitamin D
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16
Q

What causes nutritional secondary hyperparathyroidism? (NSHP)

A
  • diet that is inadequate in calcium
  • diet that is low in vitamin D
  • diet that has excessive phosphrus
17
Q

Why can a diet with excessive phosphorus cause NSHP?

A

reduce solubility of Ca in gut decreasing availability for absorption

18
Q

What are the causes of osteodystrophy?

A

calcium deficiency accompanied by excessive phosphorus

19
Q

What are symptoms of osteodystrophy?

A

no calcification of the bone matrix occurs

renal failure

20
Q

What happens during renal failure in patients with osteodystrophy?

A
  • fail to make Vitamin D
  • leads to inability to absorb diet Ca and secondary hyperparathyroidism
  • failure to excrete phosphate