metabolic bone disease Flashcards

1
Q

two main physiological functions of bone

A

-structural -endocrine

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2
Q

structural functions of bone

A

-scaffold for the body -remodels in response to stress

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3
Q

endocrine functions of bone

A
  • main storage site for calcium - perturbations in serum Ca or or calcium regulatory hormones lead to bone
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4
Q

bone turnover releases

A

calcium

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5
Q

mild decreases in serum calcium

A

increase bone resorption activity at the lining cell/osteocyte complexes (LCOCs)

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6
Q

lining cell/osteocyte couples LCOCs

A

compensate for small fluctuations in serum Ca

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7
Q

when the ability to compensate for low Ca is overcome, _____ acts to increase the number of active BMUs

A

PTH

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8
Q

BMU

A

bone multicellular units

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9
Q

PTH is released from ___ cells within the PT gland in response to _____ in serum Ca

A

-chief cells - decreases

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10
Q

Vitamin D and its affect on PTH

A

inhibits

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11
Q

what does PTH bind to?

A

PTH receptors on osteoblasts, then the osteoblasts secrete something in return

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12
Q

osteoblasts secrete

A

osteoclast activating factor OAF which includes RANK

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13
Q

RANK binds to

A

RANK receptor is on osteoclasts (which activates bone resorption)

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14
Q

do osteoclasts have PTH receptors?

A

no! only osteoblasts

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15
Q

steroid hormone synthesized in inactive form in the skin

A

cholecalciferol (vitamin D3)

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16
Q

Vit D3/cholecalciferol is converted to its active form by

A

hydroxylation in the liver and proximal renal tubule

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17
Q

function of cholecalciferol/vit D3

A

-increases available Ca2+/PO4 3- for mineralization -also enhances monocyte innate immune response

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18
Q

Vitamin D3 becomes ____ after hydroxylation in the liver

A

25 VitD3

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19
Q

UVB light is required to synthesize the inactive form of this

A

vit D3

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20
Q

bone disease primary pathway external to the skeletal system

A

extrinsic bone disease

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21
Q

serum calcium levels are often ____ in extrinsic bone disease

A

affected

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22
Q

etiology of primary hyperparathyroidism

A

adenoma (85%)

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23
Q

lab findings of primary hyperparathyroidism

A

increased Ca increased PTH increased normal alk phos

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24
Q

in both primary and secondary hyperparathyroidism, ____ become hormonally activated

A

osteoclasts

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25
Q

signs and symptoms of hypercalcemia

A

-stones (kidney stones) -groans ( PUD, pancreatitis, GI symptoms) -bones (high bone turnover, pain, arthralgia) -psychiatric overtones (fatigue, weakness, depressions)

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26
Q

osteitis fibrosa cystica

A

severe, generalized osteoclast activation, fibrous marrow replacement

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27
Q

histology of hyperparathyroidism

A

osteitis fibrosa cystica: - subperiosteal bone resorption -brown tumor/ cystic bone lesions

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28
Q

secondary hyperparathyroidism

A
  • parathyroid hyperplasia in response to chronic increase in phosphate and/or decreased calcium
  • (no bones,groans,tones, rhyme) -chronic renal disease, vit D deficiency, corticosteroids
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29
Q

lab findings for secondary hyperparathyroidism

A

low or normal calcium increased PTH (hyperphosphatemia) increased ALK phos

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30
Q

high turnover bone rate reflected by

A

elevated alk phos, creates pronounced bone symptoms

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31
Q

renal osteodystrophy

A

spectrum of bone pathology seen with CKD -decreased renal phosphate excretion, so increase it in serum, binds with serum ca and depletes serum ca, which ultimately inhibits renal hydroxylation of vitd3 and decreases Ca absorption, further decreasing serum Ca

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32
Q

most common cause of secondary hyperparathyroidism

A

renal osteodystrophy

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33
Q

dysregulated calcification of rapidly turning over cancellous bone

A

osteosclerosis (rugger jersey spine)

34
Q

soft tissue calcification

A

CaPo4 products become very elevated and precipitate in soft tissues

35
Q

hemodialysis utilizes _____ which is deposited at bone mineralization sites

A

aluminum

36
Q

aluminum impairs ___ and ____ function, preventing proper bone mineralization

A

osteoblast and osteoclast

37
Q

Tx for renal osteodystrophy

A

-phosphate binding agents - aluminum chelators -vit d replacement

38
Q

low serum Ca/ elevated PO4

A

hypoparathyroidism

39
Q

defective mineralization of otherwise normal osteoid

A

osteomalacia/rickets

40
Q

Ca level in osteomalacia

A

low

41
Q
A

hyperparathyroidism

  • brown tumor pathology
42
Q

etiology of secondary hyperparathyroidism

A

chronic renal disease, vit D definiciency, corticosteroids

43
Q

causes of Vit D definiciency

A

malabsorption, malnutrition, renal failure, lack of sun exposure

44
Q

clinical presentation of RICKETS

A
  • diffuse bone pain
  • limp
  • growth impairment
  • deformities

(varus leg) rachitic rosary

45
Q
A

rachitic rosary

46
Q

osteomalacia

A

for adults

  • bone pain, local tenderness, pathologic fractures
47
Q

looser zones

A

pseudofractures in osteomalacic bone

(stress fracture that gets repaired improprly with an osteomalacic bone)

48
Q

intrinsic bone disease

A

primary pathology is wihtin the skeletal system

49
Q

ex of intrinsic bone disease

A
  • osteoporosis
  • osteogenesis imperfecta (formation
  • osteopetrosis (resorption)
  • paget disease (remodelling)
50
Q

intrinsic bone disease does not present with

A

serum calcium abnormalities

51
Q

normal mineralization and decreased bone quantity

A

osteoporosis

52
Q

peak bone mass achieved at ages

A

16-25

53
Q

faster decline of bone mass seen in

A

women especially post menopause

54
Q

higher peak bone mass means ____ osteoporosis risk

A

decreased

55
Q
A

normal bone and osteoporotic bone

56
Q

types of primary osteoporosis

A
  • type 1 = post menopausal
  • type 2 = age related
57
Q

presentation of post menopausal osteoporosis

A
  • distal radius fractures
  • vertebral factures (wedging of vertebrae)
  • high turnover
  • more trabecular resorption than cortical
58
Q

age related osteoporosis presentation

A
  • proximal femur fractures
  • vertebral fractures
  • low turnover
  • uncoupling of osteoblasts from osteoclasts
  • travecular = cortical involvement
59
Q

secondary osteoporosis causes

A
  • hyperthyroidism
  • steroid induced
  • prolonged inactivity
  • parathyroid disease, hypogonadism, HIV, multiple myeloma, leukemia
60
Q

disorder of bone formation

A

osteogenesis imperfecta

61
Q

type ___ collagen defect leads to bone weakness and multiple fractures in bone formation

A

1

62
Q

associated findings of osteogenesis imperfecta

A

blue sclera, hearing loss, tooth abnormalities

63
Q

type 1 osteogenesis imperfecta inheritance

A

autodomal dominant

64
Q

disorder of bone resorption

A

osteopetrosis

(osteoclast failure)

65
Q

failure of ruffled border to form or carbonic anhydrase deficiency preventing acidification of howships lacunae

A

osteopetrosis

66
Q

osteopetrosis can lead to ____ from obliteration of marrow spaces

A

anemia

  • if marrow is suppressed, could be immunocompromised
67
Q
A

“erlenmeyer flask” characteristic of osteopetrosis

68
Q

disoder of bone remodeling

A

Paget disease

69
Q

paget disease

A

high bone turnover (elevated alk phos) due to increased osteoclast function

70
Q
A

pagetoid bone

71
Q

clinical presentations of pagets disease

A
  • majority asymptomatic
  • bone pain
  • secondary arthritis
  • deformity
  • pathologic fracture
  • high output heart failure
72
Q
A

Pagets disease

  • high OC activity replaced with woven bone of weaker mechanical properties
73
Q

Paget disease malignant transformation into

A

sarcoma

74
Q
  • low Ca
  • low PO4
  • low PTH
A

not a thing!

low PTH and low Ca we’d have elevated serum PO4

75
Q
  • Low Ca
  • Low PO4
  • high PTH
A

secondary hyperparathyroid

76
Q
  • Low Ca
  • High PO4
  • high PTH
A

renal osteodystrophy

77
Q
  • high Ca
  • low PO4
  • high PTH
A

primary hyperparathyroid

78
Q
  • noraml Ca,
  • normal PO4,
  • normal PTH
A

osteoporosis

79
Q

bone involvement in age related osteoporosis

A

cortical = trabecular

80
Q

post menopausal osteoporosis bone involvement

A

trabecular > cortical involvement

81
Q

bowing of long bones in legs characteristic of

A

rickets