Regulation of Calcium and Phosphate Metabolism Flashcards

1
Q

As you age, what happens to the amount of calcium absorbed and the amount of calcium consumed?

A

Decreases

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2
Q

What happens to bone cells as you age?

A

Existing bone cells are absorbed by the body faster than new bone is made

Aging also contributes to osteopenia and osteoporosis

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3
Q

What is hypocalcemia? What are the symptoms and indicators?

A

Decreased plasma Ca2+ concentration; symptoms include hyperreflexia, spontaneous twitching, muscle cramp, tingling, numbness; indicators are Chvostek sign or Trousseau sign

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4
Q

What is a Chvostek sign?

A

Twitching of the facial muscles elicited by tapping on the facial nerve

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5
Q

What is a Trousseau sign?

A

Carpopedal spasm upon inflation of a blood pressure cuff

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6
Q

What is hypercalcemia? What are the symptoms?

A

Increased plasma Ca2+ concentration; symptoms are decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy, coma

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7
Q

What do changes in plasma protein concentrations do to calcium?

A

Alters total calcium concentration in the same direction (both either increase or decrease); no change in Ca2+ ionized

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8
Q

What do changes in anion concentrations do to calcium?

A

Change the fraction of Ca2+ complexed with anions (if phosphate concentration increases, ionized Ca2+ concentration decreases

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9
Q

What do acid-base abnormalities do to calcium?

A

Alter the ionized Ca2+ concentration by changing the fraction of Ca2+ bound to albumin

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10
Q

What is acidemia?

A

Free ionized Ca2+ concentration increases because less Ca2+ is bound to albumin

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11
Q

What is alkalemia?

A

Free ionized Ca2+ concentration decreases, often accompanied by hypocalcemia

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12
Q

What is the relationship between Ca2+ and phosphate?

A

Extracellular concentration of Pi is inversely related to that of Ca2+; extracellular concentration of Pi is regulated by the same hormones that regulates Ca2+ concentration

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13
Q

What is the normal range of extracellular Pi concentration?

A

2.5-4.5 mg/dL

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14
Q

Where is most of the Pi found in the body?

A

Bone (85%)

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15
Q

What does chronic hypercalcemia cause?

A

Causes decreased synthesis and storage of PTH, increased breakdown of stored PTH and release of inactive PTH fragment into the circulation

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16
Q

What does chronic hypocalcemia cause?

A

Causes increased synthesis and storage of PTH and hyperplasia of parathyroid glands (secondary hyperparathyroidism)

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17
Q

What effect does magnesium have on PTH secretion?

A

Parallel but less significant effects on PTH secretion; however, with severe hypomagnesemia (as in alcoholism), causes inhibition of PTH synthesis, storage, and secretion

18
Q

What is the function of vitamin D?

A

Promotes mineralization of new bone through its coordinated actions in the regulation of both Ca2+ and Pi plasma concentrations; acts synergistically with PTH to stimulate osteoclast activity and bone resorption

19
Q

What are the short-term actions of PTH?

A

Bone formation (via direct action on osteoblast); basis for the use of intermittent synthetic PTH administration in osteoporosis treatment

20
Q

What role does M-CSF (macrophage colony stimulating factor) have in bone formation and resorption?

A

Induce stem cells to differentiate into osteoclast precursors, mononuclear osteoclasts, and finally mature, multinucleated osteoclasts

21
Q

What role does RANKL have in bone formation and resorption?

A

Cell surface protein produced by osteoblasts, bone lining cells, and apoptotic osteocytes; primary mediator of osteoclast formation

22
Q

What role does RANK have in bone formation and resoprtion?

A

Cell surface protein receptor on osteoclasts and osteoclast precursors

23
Q

What role does OPG (osteoprotegerin) have in bone formation and resorption?

A

Soluble protein produced by osteoblasts; decoy receptor for RANKL; inhibits RANKL/RANK interaction

24
Q

What does PTH cause in terms of bone formation and resportion?

A

Increased RANKL and decreased OPG

25
Q

What does vitamin D cause in terms of bone formation and resorption?

A

Increased RANKL

26
Q

What action does PTH have in the bone on Ca2+ and Pi?

A

Promotes osteoblastic growth and survival; regulates M-CSF, RANKL, and OPG production by osteoblast; sustained elevated levels of PTH shift the balance to a relative increase in osteoclast activity, thereby increasing bone turnover and reducing bone density

27
Q

What action does PTH have in the kidney on Ca2+ and Pi?

A

Stimulates 1-alpha-hydroxylase activity; stimulates Ca2+ reabsorption by the thick ascendinglimb of Henle’s loop and the distal tubule; inhibits Pi reabsorption by proximal nephrons

28
Q

What action does PTH have in the small intestine and parathyroid gland on Ca2+ and Pi?

A

No direct actions

29
Q

What action does vitamin D have in the small intestine on Ca2+ and Pi?

A

Increases Ca2+ and Pi absorption

30
Q

What action does vitamin D have in bone on Ca2+ and Pi?

A

Sensitizes osteoblasts to PTH; regulates osteoid production and calcification

31
Q

What action does vitamin D have in the kidneys on Ca2+ and Pi?

A

Promotes Pi reabsorption by proximal nephrons; minimal actions on Ca2+

32
Q

What action does vitamin D have in the parathyroid glands on Ca2+ and Pi?

A

Directly inhibits PTH gene expression; directly stimulates CaSR gene expression

33
Q

What are the actions of calcitonin on Ca2+ and Pi?

A

Decreased blood Ca2+ and Pi concentrations by inhibiting bone resorption (only at high circulating levels of hormone); decreased activity and number of osteoclasts; major stimulus is increased plasma Ca2+ concentration

34
Q

What does a thyroidectomy cause?

A

Decreased calcitonin but no effect in Ca2+ metabolism

35
Q

What does a thyroid tumor cause?

A

Increased calcitonin but no effect in Ca2+ metabolism

36
Q

What is vitamin D dependent rickets type 1?

A

Decreased 1-alpha-hydroxylase

37
Q

What is vitamin D dependent rickets type 2?

A

Decreased vitamin D receptor

38
Q

What is osteomalacia?

A

Nutritional osteomalacia that could originate from either a GI disorder or suboptimal nutrition and inadequate sun exposure; could be suspected in cases of bone pain associated with malabsorption

39
Q

What are some clinical manifestations of osteomalacia?

A

Bone pain, muscle weakness, bone tenderness, fracture, muscle spasms, cramps, positive Chvostek’s sign, tingling/numbness

40
Q

How can you treat osteoporosis?

A

Anabolic therapy (PTH) or antiresorptive therapy with bisphosphonates, estrogen, selective estrogen receptor modulators, calcitonin, RANKL inhibitors