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PMCOL 200 Final > bone mineral homeostasis > Flashcards

bone mineral homeostasis Flashcards

1
Q

what are the control sites for plasma Calcium and PO4

A

gut, blood, bone. kidney

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2
Q

which bone cell is responsible for deposition of bone

A

osteoblasts

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3
Q

which bone cell is responsible for resorption of bone

A

osteoclasts

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4
Q

how are osteoclasts activated? draw a flowchart.

A

hormones activate osteoblasts
osteoblasts secrete RANK ligand
RANK ligand activates osteoclasts

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5
Q

Parathyroid hormone promotes or inhibits

______ bone resorption
_______ Ca absorption in the kidney
_______ PO4 excretion

A

promotes
promotes
promotes

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6
Q

What is the net affect of PTH on Calcium and PO4`

A

increase calcium

decrease (sort of) PO4

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7
Q

what is PTH 1-34

A

synthetic parathyroid hormone

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8
Q

what is teriperatide ?

what is it used for?

A

PTH 1-34, synthetic hormone

osteoperosis

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9
Q

how does PTH affect the kidney ASIDE from affecting the Ca and PO4 concentrations?

A

stimulation of vitamin D processing

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10
Q

T or F
PTH directly promotes bone resorption.
explain

A

FALSE
not directly, INDIRECTLY.
PTH –> osteoblast —–> RANKL ——> osteoctye ——> resorption

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11
Q

where is vitamin D metabolized

A

liver then kidney

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12
Q

what is vitamin D metabolized into? (2)

A

calcitriol (active form)

secalciferol

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13
Q

Vitamin D3: (fill in the blanks)

________ Ca excretion
_______ PO4 excretion
________ Ca concentration through bone resorption
_________ PO4 concentration through bone resorption

A

decrease
decrease
increase
increase

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14
Q

how does vitamin D affect Ca and PO4 in the gut?

A

promotes uptake

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15
Q

what are Ca levels sense by?

A

Ca receptors in the parathyroid

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16
Q

PTH exerts effects on PTH receptors in the _______ and _______

A

kidney and osteoblasts

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17
Q

PTH stimulation of vitamin D metabolism leads to vitamin D effects in _____, _____ and _____

A

gut, kidney and bone

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18
Q

what is the active form of Vitamin D

19
Q

what are the effects of FGF23?

A

inhibits phopshate uptake
inhibits D3 metabolism
inhibits PTH production

20
Q

what are the effects of calcitonin?

A

INHIBITS bone resoprtion

inhibits calcium and phosphate reabsorption in kidney

21
Q

where was calcitonin discovered, and by whom?

A

UBC, D.H Copp

22
Q

what effects do glucocorticoids have on bones? why?

A

osteoporosis

because it blocks calcium uptake in gut and promotes excretion in the kidney

23
Q

how do estrogens affect bones?

A

PREVENT bone loss in postmenopausal women

direct effects in bone, prevents PTH stimulated resorption

24
Q

what is hypocalcemia?

A

too little calcium

25
Q

how can hypocalcemia be treated?

A

calcium (oral, iv or im)

or an active vitamin D3 metabolite

26
Q

what are the negative effects of hypocalcemia?

A

hyperexcitability in cells

seizures, muscle tetany, spasms

27
Q

what is the long-term danger of hypocalcemia:?

what does it cause?

A

HYPERPARATHYROIDISM

weakening of bones

28
Q

what is the long term underlying defect causing hypocalcemia?

A

hypoparathyroidism

vitamin D deficiency

29
Q

how can hypoparathyroidism be treated?

A

vitamin D OR calcium supplements

30
Q

how can vitamin D deficiency be treated

A

ingestion of active vitamin D3 metabolites (like calcitrol)

sunshine

31
Q

how does hypercalcemia affect cellular excitability

A

loss of cellular excitability

32
Q

lethargy is caused by _____

hyper or hypocalcemia

A

hypercalcemia

33
Q

what is the long-term cause of hypercalcemia usually?

A

primary hyperparathyroidism

34
Q

what are calciimimetics? what do they treat?

A

synthetic calcium, mimic calcium affect on receptors to increase excitability
hypercalcemia

35
Q

name 3 modes of therapy for hypercalcemia?

A
  1. resection of PT gland
  2. protect the bone
  3. calcimimetics
36
Q

which demographic is most affected by osteoperosis?

A

aging females

37
Q

what is teriparatide?

what does it treat?

A

recombinant fully active PTH fragment

osteoporosis

38
Q

why is teriparatide strange?

how does it work despite this feature?

A

it is meant to fix osteoporosis, but it is a PTH fragment.

must be timed correctly to tip balance to osteoblast activity rather than RANKL activation of osteoclasts

39
Q

what are biphosphates used for clinically?
how do they work?
what is the side affect that they are speculated to have?

A

osteoporosis
inhibition of osteoclast resorption of bone
inhibit glucocorticoid effects

40
Q

what is alendronate?

A

biphosphate

41
Q

what structure do all biphosphates have?

A

2 phosphonate groups

42
Q

what is osteoprotegerin ? how does it work?

A

binds to RANKL to inhibit RANK

43
Q

PTH is a _____

peptide or steroid hormone

PMCOL 200 Final (11 decks)

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