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Biochem final > bone SG (schricker) > Flashcards

bone SG (schricker) Flashcards

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
Q

lays down collagen and a variety of different proteins to build bone

A

osteoblast upon activation by RANKL surface binding

26
Q

how do osteoblasts regulate osteoclasts?

A

since RANK L is expressed on the surface of osteoblasts, it can in turn activate and bind to RANK receptor on osteoclast

27
Q
  • primary regulator of calcium levels

- 84 aa protein synthesized by the PH gland

A

parathyroid hormone

28
Q

major consequences of increased PTH?

A
  • increase in serum calcium
  • mobilizes calcium
  • decreases excretion
  • stimulates osteoclast
29
Q

PTH production stimulated by:

A

low plasma calcium

30
Q

-increases serum calcium, gut adsorption of calcium, and bone adsorption

A

increased vitamin D levels

31
Q
  • precursurs are synthesized in the skin
  • stored in the liver
  • converted to active form I the kidney
A

vitamin D

32
Q

point of regulation for vitamin D production:

A

1-alpha-hydroxylase

33
Q
  • PTH
  • low calcium
  • low vitamin D
  • calcitonin
A

1-alpha-hydroxylase stimulation

34
Q
  • low PTH
  • high serum calcium
  • high vitamin D
  • 24 hydroxylase
A

1-alpha-hydroxylase inhibition

35
Q

can inactivate liver precursor to vitamin D; 25- hydroxycholecalciferol

A

24 hydroxylase

36
Q
  • increase in production of PTH

- diagnosed by bone, stones, and abdominal groans

A

Hyperparathyroidism (HPT)

37
Q

intact PTH indicator of:

A

hyperparathyroidism (HPT)

38
Q
  • increases bone remodeling
  • results in osteopenia
  • 6 mo after surgery most but not all bone density back to normal
A

Hyperparathyroidism (HPT) effect on bone

39
Q
  • 3rd leading cause of hpercalcemia

- normally obvious cause

A

vitamin D

40
Q
  • primary hyperparathryoidism
  • malignant disease
  • iatrogenic vitamin D
A

common causes of hypercalcemia

41
Q

symptoms of hypercalcemia

A

dehydration, vomiting, reduced renal perfusion

42
Q

treatment of hypercalcemia via inhibition of osteoclast activity (remodeling)

A

bisphosphates

43
Q
  • slow fracture healing
  • brittle bones
  • osteonecrosis in mandible
  • typified by oral lesions
  • long half times in bone
A

result of bisphosphates

44
Q

produced by tumors (common: breast, lung, kidney)

A

parathyroid hormone-related protein (PTHrP)

45
Q

primary cause of hypercalcemia

A

parathyroid hormone-related protein (PTHrP)

46
Q

Hypophosophatemia, phosphateuria, increased renal calcium resorption, osteoclast activation

A

sequence homology between PTH and PTHrP

47
Q
  • locally active
  • alters RANK/OPG balance
  • produces cytokines and growth factors
A

HCM (hypercalcemia) from bone tumor or metastases

48
Q

drop in serum albumin (adjusted calcium levels), changes in ionized calcium from pH change

A

hypocalcemia

49
Q

neuromuscular irritability , numbness, tingling, cramps, tetany, seizures

A

symptoms of hypocalcemia

50
Q

usually a result of damaged parathyroid gland (surgery, tumor, PT disease)

A

hypoparathryoidism

51
Q

needed for PTH to bind to secretory granules

A

magnesium

52
Q

usually a genetic defect due to G protein

A

PTH resistance

53
Q

causes increase in PTH, end organ resistance to PTH, hyopmagnesmia

A

PTH resistance

54
Q

observed with vitamin D deficiency, tissue resistance, or various clinical conditions (liver disease, renal failure)

A

abnormal metabolism of vitamin D

55
Q
  • defects in HA formation, due to vitamin D deficiency

- associated with rickets

A

osteomalacia

56
Q
  • inhibited vitamin D metabolism
  • bone and muscle weakness
  • skeletal deformity
  • cod liver oil
A

rickets

57
Q

hypothesized to cause gaps in dentin

A

rickets

58
Q
  • loss of mineral density with age
  • increased risk of fracture
  • relative rates of bone synthesis and resorption
A

osteoporosis

59
Q
  • estrogen
  • bisphosphonates
  • calcitonin
  • PTH
A

treatments of osteoporosis

60
Q
  • cause is unknown
  • most common in Europe, Australia, new zealand
  • some are asymptomatic
A

pagets disease

61
Q

bisphosphonates and calcitonin

A

treatments of pagets disease

Biochem final (3 decks)

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