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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
signs and symptoms of hypercalcemia
-stones (kidney stones) -groans ( PUD, pancreatitis, GI symptoms) -bones (high bone turnover, pain, arthralgia) -psychiatric overtones (fatigue, weakness, depressions)
26
osteitis fibrosa cystica
severe, generalized osteoclast activation, fibrous marrow replacement
27
histology of hyperparathyroidism
osteitis fibrosa cystica: - subperiosteal bone resorption -brown tumor/ cystic bone lesions
28
secondary hyperparathyroidism
- 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
29
lab findings for secondary hyperparathyroidism
low or normal calcium increased PTH (hyperphosphatemia) increased ALK phos
30
high turnover bone rate reflected by
elevated alk phos, creates pronounced bone symptoms
31
renal osteodystrophy
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
32
most common cause of secondary hyperparathyroidism
renal osteodystrophy
33
dysregulated calcification of rapidly turning over cancellous bone
osteosclerosis (rugger jersey spine)
34
soft tissue calcification
CaPo4 products become very elevated and precipitate in soft tissues
35
hemodialysis utilizes _____ which is deposited at bone mineralization sites
aluminum
36
aluminum impairs ___ and ____ function, preventing proper bone mineralization
osteoblast and osteoclast
37
Tx for renal osteodystrophy
-phosphate binding agents - aluminum chelators -vit d replacement
38
low serum Ca/ elevated PO4
hypoparathyroidism
39
defective mineralization of otherwise normal osteoid
osteomalacia/rickets
40
Ca level in osteomalacia
low
41
hyperparathyroidism - brown tumor pathology
42
etiology of secondary hyperparathyroidism
chronic renal disease, vit D definiciency, corticosteroids
43
causes of Vit D definiciency
malabsorption, malnutrition, renal failure, lack of sun exposure
44
clinical presentation of RICKETS
- diffuse bone pain - limp - growth impairment - deformities (varus leg) rachitic rosary
45
rachitic rosary
46
osteomalacia
for adults - bone pain, local tenderness, pathologic fractures
47
looser zones
pseudofractures in osteomalacic bone (stress fracture that gets repaired improprly with an osteomalacic bone)
48
intrinsic bone disease
primary pathology is wihtin the skeletal system
49
ex of intrinsic bone disease
- osteoporosis - osteogenesis imperfecta (formation - osteopetrosis (resorption) - paget disease (remodelling)
50
intrinsic bone disease does not present with
serum calcium abnormalities
51
normal mineralization and decreased bone quantity
osteoporosis
52
peak bone mass achieved at ages
16-25
53
faster decline of bone mass seen in
women especially post menopause
54
higher peak bone mass means ____ osteoporosis risk
decreased
55
normal bone and osteoporotic bone
56
types of primary osteoporosis
- type 1 = post menopausal - type 2 = age related
57
presentation of post menopausal osteoporosis
- distal radius fractures - vertebral factures (wedging of vertebrae) - high turnover - more trabecular resorption than cortical
58
age related osteoporosis presentation
- proximal femur fractures - vertebral fractures - low turnover - uncoupling of osteoblasts from osteoclasts - travecular = cortical involvement
59
secondary osteoporosis causes
- hyperthyroidism - steroid induced - prolonged inactivity - parathyroid disease, hypogonadism, HIV, multiple myeloma, leukemia
60
disorder of bone formation
osteogenesis imperfecta
61
type ___ collagen defect leads to bone weakness and multiple fractures in bone formation
1
62
associated findings of osteogenesis imperfecta
blue sclera, hearing loss, tooth abnormalities
63
type 1 osteogenesis imperfecta inheritance
autodomal dominant
64
disorder of bone resorption
osteopetrosis (osteoclast failure)
65
failure of ruffled border to form or carbonic anhydrase deficiency preventing acidification of howships lacunae
osteopetrosis
66
osteopetrosis can lead to ____ from obliteration of marrow spaces
anemia - if marrow is suppressed, could be immunocompromised
67
"erlenmeyer flask" characteristic of osteopetrosis
68
disoder of bone remodeling
Paget disease
69
paget disease
high bone turnover (elevated alk phos) due to increased osteoclast function
70
pagetoid bone
71
clinical presentations of pagets disease
- majority asymptomatic - bone pain - secondary arthritis - deformity - pathologic fracture - high output heart failure
72
Pagets disease - high OC activity replaced with woven bone of weaker mechanical properties
73
Paget disease malignant transformation into
sarcoma
74
- low Ca - low PO4 - low PTH
not a thing! low PTH and low Ca we'd have elevated serum PO4
75
- Low Ca - Low PO4 - high PTH
secondary hyperparathyroid
76
- Low Ca - High PO4 - high PTH
renal osteodystrophy
77
- high Ca - low PO4 - high PTH
primary hyperparathyroid
78
- noraml Ca, - normal PO4, - normal PTH
osteoporosis
79
bone involvement in age related osteoporosis
cortical = trabecular
80
post menopausal osteoporosis bone involvement
trabecular \> cortical involvement
81
bowing of long bones in legs characteristic of
rickets

MSK final (11 decks)

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