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Pharm > Lecture 30: Bone Minerals > Flashcards

Lecture 30: Bone Minerals Flashcards

1
Q

What is the principal reservoir for calcium and phosphate?

A

Bone

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2
Q

Why is regulation of Calcium and Phosphate important?

A
  • Health/strength of bones
  • Ca balance has effects on electrical excitability of cells
  • Ca is an essential intracellular signal
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3
Q

What are the major targets of Ca2+ and PO43- control?

A

The Gut, Kidney and Bone

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4
Q

What is resorption?

A

The breakdown of bone which allows calcium to go into the bloodstream

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5
Q

what do Osteoblasts cause?

A

Deposition of bone

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6
Q

What do osteoclasts cause?

A

Resorption of bone

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7
Q

What are the major regulators of bone remodelling?

A

Vitamin D metabolites and PTH

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8
Q

How can Osteoclasts be activated?

A

Osteoclasts must be activated by osteoblasts that release the Rank Ligand which binds to osteoclasts and binds to the Rank receptor on osteoclasts

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9
Q

What are Parathyroid Hormones effects on the bone?

A

It promotes bone resorption indirectly through RANKL so it increases Ca and PO4 levels

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10
Q

What are Parathyroid Hormones effects on the Kidney?

A

It promotes Ca absorption and promotes PO4 excretion

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11
Q

What is the net effect of Parathyroid hormone?

A

It increases calcium and PO4 in the blood

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12
Q

Where is parathyroid hormone released from?

A

The parathyroid gland

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13
Q

What is PTH made is response to?

A

Reduced levels of circulating calcium

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14
Q

Why does PTH promote phosphate excretion in the kidneys?

A

So it doesn’t form precipitates, crystals and stones

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15
Q

How does PTH affect vitamin D in the kidneys?

A

It promotes the processing of vitamin D to its active form

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16
Q

What causes PTH to be released?

A

Decreased levels of circulating calcium

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17
Q

How does the parathyroid gland sense the level of circulating calcium?

A

It has calcium-sensitive receptors

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18
Q

What kind of Hormone is Vitamin D?

A

A steroid hormone

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19
Q

What is vitamin D metabolized in the liver to form?

A
  • Calcitriol (1,25-hydroxy vitamin D3)

* Calciferol (24,25-hydroxy D3)

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20
Q

What is the active form of the Vitamin D metabolites?

A

Calcitriol (1,25-hydroxy vitamin D3)

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21
Q

How is vitamin D metabolized?

A

First the liver converts vitamin D3 to 25-OH-D3 and then the kidney converts this to Calcitriol and Secalciferol

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22
Q

What causes Secalciferol (24,25-hydroxy D3) to be produced?

A

High circulating levels of calcium or high levels of the calcitriol form

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23
Q

What does Vitamin D do?

A

Promotes the resorption of calcium to increase levels in the blood

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24
Q

What promotes the kidneys to produce Calcitriol (1,25-hydroxy vitamin D3)

A

High levels of PTH and low levels of circulating calcium

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25
Q

How does Vitamin D3 affect the kidney?

A

It increases calcium reabsorption from bones and promotes phosphate excretion

26
Q

How does vitamin D3 affect the bone?

A

It promotes bone resorption and increases calcium and phosphate levels in the blood

27
Q

How does vitamin D3 affect the gut?

A

It promotes the uptake of calcium and phosphate from the gut to increase circulating levels

28
Q

What is the net effect of the active form of vitamin D3?

A

It increases circulating calcium and phosphate

29
Q

Where does PTH exert it effects?

A

In kidneys and osteoblasts

30
Q

What does PTH stimulation of vitamin D do?

A

It leads to vitamin D effects in gut, kidney and bone

31
Q

What are the normal circulating levels of calcium?

A

2.2 mM total calcium, 1mM free caclcium

32
Q

How can hypocalcemia be resolved short term?

A

The patient can be given calcium or an active D3 metabolite that will increase blood calcium levels

33
Q

What can Hypocalcemia cause?

A

Hyperactivity of cells

34
Q

What is an early symptom of Hypocalcemia?

A

Trousseau’s sign

35
Q

what is a longer-term danger of Hypocalcemia?

A

Secondary hyperparathyroidism

36
Q

What is secondary hyperparathyroidism?

A

A hyperactive parathyroid due to low plasma calcium due to kidney failure that stops reabsorption of Ca2+. So the parathyroid wants to increase circulating hormone by releasing PTH but there is no calcium being absorbed so its consistently being released

37
Q

What does secondary hyperparathyroidism lead to?

A

The breakdown and weakening of bones

38
Q

What usually causes long term Hypocalcemia?

A
  • Hypoparathyroidism

* Vitamin D deficiency

39
Q

How does Hypoparathyroidism cause Hypocalcemia?

A

A defect in the parathyroid gland that doesn’t allow it to produce parathyroid hormone

40
Q

How is secondary hypoparathyroidism caused by hypocalcemia treated?

A

With vitamin D and calcium supplementation

41
Q

How can Vitamin D deficiency cause Hypocalcemia?

A

The inability to generate vitamin D metabolites

42
Q

How can hypocalcemia caused by vitamin D deficiency be resolved?

A

By dietary correction or ingestion of active Vit D3 metabolites (calcitriol), sunshine

43
Q

What is Hypercalcemia?

A

Too much circulating calcium

44
Q

What does acute hypercalcemia cause?

A

Loss of cellular excitability, lethargy, coma, pain in bones due to excessive PTH

45
Q

What causes Hypercalcemia long-term?

A

Primary hyperparathyroidism

46
Q

What can primary hyperparathyroidism be due to?

A

A tumor

47
Q

What is treatment form primary hyperparathyroidism?

A
  • Resection of the gland
  • Bisphosphonates, calcitonin, inhibitors of bone resorption
  • Calcimimetics
48
Q

What are Calcimimetics?

A

Drugs that mimic the effects of calcium on the calcium receptors causing negative feedback and decrease the amount of parathyroid hormone released

49
Q

What is Osteoporosis?

A

A loss in bone density

50
Q

Why is osteoporosis seen in post-menopausal women?

A

because estrogen promotes bone deposition

51
Q

What is one of the ways the osteoporosis can be treated and what are their downsides?

A

Hormone replacement - but they have serious adverse effects like cancers

52
Q

What are other common causes of osteoporosis aside from hormones?

A
  • Glucocorticoid administration

* Hyperparathyroidism

53
Q

What is Teripide used to treat?

A

Osteoporosis

54
Q

How does Teriparatide work?

A

It acts on osteoblasts to activate them but because it doesn’t give enough for them to activate osteoclasts causing deposition

55
Q

What are Bisphosphonates used to treat?

A

Osteoporosis

56
Q

How do Bisphosphonates work?

A

They inhibit osteoclast resorption of bone through inhibiting glucocorticoids. They also have a toxic effect on osteoclasts

57
Q

How do glucocorticoids affect the deposition of bone?

A

They tend to promote the activity of osteoclasts which cause resorption of bones and suppress the activity of osteoblasts

58
Q

Why do bisphosphonates have a toxic effect on osteoclasts?

A

The phosphonate groups of the bisphosphonates have a high affinity for Ca2+ so they accumulate in bone allowing osteoclasts to target them

59
Q

What is Osteoprotegerin used to treat?

A

Osteoporosis

60
Q

How does Osteoprotegerin work?

A

It competes with RANK by binding to RANKL and inhibiting activation which inhibits bone resorption by osteoclasts

61
Q

What is Denosumab used to treat?

A

Osteoporosis

62
Q

How does Denosumab work?

A

It is an antibody against RANKL, and mimics osteoprotegerin

Pharm (31 decks)

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