bone SG (schricker) Flashcards

(61 cards)

1
Q

chemical composition of bone?

A
  • collagen

- HA

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2
Q

a composite of HA and collagen, 50-60% of HA plates

A

bone

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3
Q

why is bone a composite of 2 materials?

A
  • collagen is tough but not strong

- HA strong but not tough

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4
Q

primary protein component of bone?

A

type 1 collagen

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5
Q

99% is contained in mineralized tissue, remaining 1% is circulated in bound or ionic form

A

calcium

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6
Q

bone is a:

A

calcium store

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7
Q

increase in bone mass leads too:

A

decrease in serum Ca2+, bone resorption

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8
Q

decrease in bone mass leads too:

A

increase in serum Ca2+, bone synthesis

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9
Q

non-diffusible, biologically inactive, not excreted

A

protein bound calcium (40%)

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10
Q

what percent of calcium is complexed with phosphate, bicarb, and citrate?

A

10%

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11
Q

percent of ionized calcium?

A

50%, biologically active

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12
Q

total serum calcium?

A

2.2-2.6 mmol/L (5 L of blood)

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13
Q
  • calcium
  • estrogens
  • calcitonin
  • tumor growth factor
  • I L 17
A

inhibit resorption (bone remodeling cycle)

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14
Q
  • parathyroid hormone
  • parathyroid hormone related protein
  • prostaglandin
  • IL 1, IL 6, TNF
  • prolactin
  • corticosteriods
  • vitamin D
A

promote resorption (bone remodeling cycle)

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15
Q
  • build bone via excreting matrix proteins
  • come from mesenchymal stem cells
  • will become osteocytes
A

osteoblasts

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16
Q
  • resorb bone

- from hematopoietic stem cell –> macrophage/monocyte

A

osteoclasts

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17
Q

from different lineages

A

osteoblasts and osteoclasts

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18
Q

when RANK L bound, osteoclast generates:

A

-lysosomal enzymes
-collagenases
-cathepsins
-acidic pH
(starting to degrade and resorb HA)

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19
Q

when RANK L binds to RANK receptor on osteoclast

A

osteoclast ACTIVATION to remodel bone

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20
Q

will result in bone thickening

A

lack of RANKL

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21
Q

precursor of OPG

A

estrogen

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22
Q

will block RANKL from binding to osteoclast, osteoclast INHIBITION

A

OPG

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23
Q

will result in osteoporosis

A

lack of OPG

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24
Q

RANKL binding to surface of osteoblast

A

ACTIVATION of osteoblast

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25
lays down collagen and a variety of different proteins to build bone
osteoblast upon activation by RANKL surface binding
26
how do osteoblasts regulate osteoclasts?
since RANK L is expressed on the surface of osteoblasts, it can in turn activate and bind to RANK receptor on osteoclast
27
- primary regulator of calcium levels | - 84 aa protein synthesized by the PH gland
parathyroid hormone
28
major consequences of increased PTH?
- increase in serum calcium - mobilizes calcium - decreases excretion - stimulates osteoclast
29
PTH production stimulated by:
low plasma calcium
30
-increases serum calcium, gut adsorption of calcium, and bone adsorption
increased vitamin D levels
31
- precursurs are synthesized in the skin - stored in the liver - converted to active form I the kidney
vitamin D
32
point of regulation for vitamin D production:
1-alpha-hydroxylase
33
- PTH - low calcium - low vitamin D - calcitonin
1-alpha-hydroxylase stimulation
34
- low PTH - high serum calcium - high vitamin D - 24 hydroxylase
1-alpha-hydroxylase inhibition
35
can inactivate liver precursor to vitamin D; 25- hydroxycholecalciferol
24 hydroxylase
36
- increase in production of PTH | - diagnosed by bone, stones, and abdominal groans
Hyperparathyroidism (HPT)
37
intact PTH indicator of:
hyperparathyroidism (HPT)
38
- increases bone remodeling - results in osteopenia - 6 mo after surgery most but not all bone density back to normal
Hyperparathyroidism (HPT) effect on bone
39
- 3rd leading cause of hpercalcemia | - normally obvious cause
vitamin D
40
- primary hyperparathryoidism - malignant disease - iatrogenic vitamin D
common causes of hypercalcemia
41
symptoms of hypercalcemia
dehydration, vomiting, reduced renal perfusion
42
treatment of hypercalcemia via inhibition of osteoclast activity (remodeling)
bisphosphates
43
- slow fracture healing - brittle bones - osteonecrosis in mandible - typified by oral lesions - long half times in bone
result of bisphosphates
44
produced by tumors (common: breast, lung, kidney)
parathyroid hormone-related protein (PTHrP)
45
primary cause of hypercalcemia
parathyroid hormone-related protein (PTHrP)
46
Hypophosophatemia, phosphateuria, increased renal calcium resorption, osteoclast activation
sequence homology between PTH and PTHrP
47
- locally active - alters RANK/OPG balance - produces cytokines and growth factors
HCM (hypercalcemia) from bone tumor or metastases
48
drop in serum albumin (adjusted calcium levels), changes in ionized calcium from pH change
hypocalcemia
49
neuromuscular irritability , numbness, tingling, cramps, tetany, seizures
symptoms of hypocalcemia
50
usually a result of damaged parathyroid gland (surgery, tumor, PT disease)
hypoparathryoidism
51
needed for PTH to bind to secretory granules
magnesium
52
usually a genetic defect due to G protein
PTH resistance
53
causes increase in PTH, end organ resistance to PTH, hyopmagnesmia
PTH resistance
54
observed with vitamin D deficiency, tissue resistance, or various clinical conditions (liver disease, renal failure)
abnormal metabolism of vitamin D
55
- defects in HA formation, due to vitamin D deficiency | - associated with rickets
osteomalacia
56
- inhibited vitamin D metabolism - bone and muscle weakness - skeletal deformity - cod liver oil
rickets
57
hypothesized to cause gaps in dentin
rickets
58
- loss of mineral density with age - increased risk of fracture - relative rates of bone synthesis and resorption
osteoporosis
59
- estrogen - bisphosphonates - calcitonin - PTH
treatments of osteoporosis
60
- cause is unknown - most common in Europe, Australia, new zealand - some are asymptomatic
pagets disease
61
bisphosphonates and calcitonin
treatments of pagets disease