Calcium and Bone physiology Flashcards

1
Q

What are the forms and abundance of Calcium?

A

Free ionized: 50%
Protein Bound 40%
Calcium bound to small difusible anion: 10%

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2
Q

What effect does pH have on calcium?

A

Calcium bound to protein
Akaline = More calcium bound to protein
Acidic = Less calcium bound to protein.

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3
Q

What effect does calcium have on nervous excitability?

A

Less calcium causes excitability easier

More calcium makes it harder to excite neurons.

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4
Q

Phosphate causes the release of PTH, what does PTH do to phosphate?

A

PTH causes the body to get rid of Phosphate.

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5
Q

What does FGF23 do?

A

Fibroblast gorwth factor 23 causes phosphate to be excreted and increased by calcitriol (Vitamin D)

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6
Q

What causes FGF23 release?

A

Calcitriol (Vitamin D)

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7
Q

What does Calcitriol/Vitamin D do?

A

Causes increase uptake of calcium in the small intestine, passive paracelular transport.

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8
Q

What does PTH do in the kidneys?

A

Causes phosphate excretion in the thick ascending limband calcium absorbtion via the proximal tubule and thick ascending loop/ DCT.

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9
Q

How does PTH act on vitamin D?

A

In the proximal tubules it converts 25-hydroxycholecalciferol into 1,25 hihydroxxycholecalciferol (most active form)

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10
Q

How does PTH act on the bones?

A

Upregulates osteoclasts to have bone resorption releasing calcium to plasma.

Helps mature preosteoclasts causing release of RANKL and macrophage colony stimulating factor.

Inhibits collagen synthesis by osteoblasts.

Active form of vitamin D further increases PTH bone resorption.

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11
Q

What does the PTH related peptide do? (PTHrP)

A

Can bind to PTH receptors in the bone and kidney and raise plasma Ca2+ levels even higher.

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12
Q

What are symptoms of hypocalcemia?

A

Easily excitable nerves

Tetany, latent tetanny, tresseaus sign, chvostek sign, numbness tingling, syncope, heart failure.

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13
Q

What are symptoms of hypercalcemia?

A

Fatigue, muscle weakness, constipation, polyuria, kidney stones, coma, cardiac arrest.

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14
Q

What does RANKL do?

A

Promoted by PTH binding osteblasts

Activates RANK receptors of preosteoclast cells.

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15
Q

What dos M-CSF do?

A

Released by osteoblasts and binds to preosteoclasts helping to mature them.

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16
Q

What does OPG do?

A

Osteoprotegrin is also release by osteoblasts and acts as a Decoy receptor for RANKL inhibiting bone resorption.

Estrogen also stimulates OPG.

17
Q

What receptor acts as a decoy for RANKL?

A

OPG = Osteoprotegrin

Released by osteoblasts and estrogen induced limits bone resorption.

18
Q

How does PTH effect OPG?

A

PTH inhibits the release of OPG Increasing bone resorption.

19
Q

what effect does Vitamin D have on bone resorption?

A

Promotes action of PTH on osteoblasts causing the maturation of osteoclasts.

PTH cannot directly interact with osteoclasts

20
Q

Can PTH act directly on osteoclasts?

A

No it must interact with Osteoblasts to interact with the osteoclasts through RANKL which then activates RANK on osteoclasts.

21
Q

where is Vitamin D precursors transformed into vitamin D3?

A

Occurs in the skin it then travels to the liver where it is transformed into 25-hydroxycholecerifol by 25-hydroxylase

22
Q

Where does Vitamin D3 become converted into its most active form?

A

Occurs in the proximal tubule again with PTH.

23
Q

What are the signs and symptoms of hyperparathyroidism?

A

Hypercalcemia and hypophosphatemia.

Symptoms would be calcium kindey stones, weak bones, hypercalcemia can lead to constipation.

24
Q

What are the symptoms of secondary hyperparathyroidsm?

A

Diseases that cuase low plasma calcium such as chronic renal disease and rickets.

25
Q

What are the signs and symptoms of hypoparathyroidism?

A

Due to parathyroidectormy (Too low PTH)

Causes steady decrease in calcium levels showing hyperexcitability leading to tetany.

26
Q

What is pseudohypoparathyroidism?

A

Pt has normal PTH levels but showing signs of hypoparathyroidism.

Likely due to receptor issues.

27
Q

How can renal disease cause osteomalacia (bone softening)

A

Caused by renal rickets due to failure of damaged kidney to produce active form of vitamin D.

28
Q

What cells make FGF23?

A

Osteoblasts and osteocytes

29
Q

What components cause calcitriol (vitamin D) to rise?

To lower?

A

FGF23 causes calcitriol to decrease

PTH causes calcitriol to increase.

30
Q

What two factors increase phosphate excretion?

What factor induces phosphate reabsorbtion?

A

PTH and FGF23 increase phosphate excretion

Calcitriol increases phosphate reabsorbtion.

31
Q

What factor is responsible for hypercalcemia of malignancy?

A

PTH-related peptide (PTHrP)

is not under normal endocrine control and is released by many tissues.