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NE Exam 3 > 13 - Calcium-Phosphate Homeostasis > Flashcards

13 - Calcium-Phosphate Homeostasis Flashcards

1
Q

What is the distribution of calcium in the body?

A

ECF - 0.1 percent
Plasma - < 0.5 percent
ICF - 1 percent
Bones and teeth - 99 percent

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2
Q

Free, ionized Calcium (Ca2+) is the biologically (ACTIVE/INACTIVE) form.

A

Active

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3
Q

During aging, there are decreases in the amount of calcium absorbed from dietary intake, and in dietary intake of calcium. Existing bone cells are reabsorbed by the body faster than new bone is made, resulting in ________ or _______.

A

Osteopenia

Osteoporosis

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4
Q

This is decreased plasma calcium concentration. Symptoms include hyperreflexia, spontaneous twitching, muscle cramps, and tingling and numbness.

A

Hypocalcemia

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5
Q

What are some indicators for Hypocalcemia?

A

Chvostek sign – twitching of facial muscles elicited by tapping facial nerve

Trousseau sign – carpopedal spasm upon inflation of a blood pressure cuff

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6
Q

This is increased plasma calcium concentration. Symptoms include decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy, and coma.

A

Hypercalcemia

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7
Q

Plasma calcium concentration influences membrane excitability. Plasma calcium is the same as _________ calcium.

A

Extracellular

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8
Q

(HIGH/LOW) extracellular Calcium will reduce the activation threshold for Na+ channels, making it easier to evoke AP. This results in an increase in membrane excitability (spontaneous APs).

A

Low (hypocalcemia)

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9
Q

In hypocalcemia, generation of spontaneous AP is the physical basis for hypocalcemic ________ (spontaneous muscle contractions due to low extracellular Calcium). Produces tingling and numbness (on sensory neurons).

A

Tetany

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10
Q

High extracellular Calcium (hypercalcemia) acts the exact opposite of hypocalcemia. It will (INCREASE/DECREASE) the membrane excitability. The nervous system becomes depressed and reflex responses are slowed.

A

Decrease

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11
Q

What are the ways to alter the forms of Calcium in plasma?

A

Change in plasma protein concentration
Change in anion concentration
Acid-Base abnormalities

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12
Q

T/F. If there is a change in plasma protein concentration, it will alter the total Calcium concentration in the same direction (i.e., increase in protein then increase in total Calcium). There is NO change in ionized Calcium.

A

True

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13
Q

If there is changes in anion concentration, it will change the fraction of Calcium complexed with anions (remember that of total Calcium, 60 percent is ultra filterable, and of this 60 then 10 percent is complexed to anions and 50 percent is ionized calcium). So, if there is an increased anion concentration, then that will (INCREASE/DECRASE) the ionized Calcium concentration.

A

Decrease

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14
Q

For Acid-Base abnormalities, it alters the ionized Calcium concentration by changing the fraction of Calcium bound to ________.

A

Albumin

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15
Q

In ________ there is an increased concentration of free ionized Calcium because less is bound to Albumin.

A

Acidemia

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16
Q

In ________ there is a decreased concentration of free ionized Calcium because more is bound to Albumin. Often accompanied by Hypocalcemia.

A

Alkalemia

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17
Q

To maintain Calcium balance, the ________ must excrete the same amount of Calcium that is absorbed by the GI tract.

A

Kidneys

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18
Q

What activates and inhibits bone resorption?

A

Activate – PTH and Vitamin D

Inhibit – Calcitonin

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19
Q

What promotes calcium absorption by the intestines?

A

Vitamin D

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20
Q

The extracellular concentration of ________ is inversely related to that of Calcium. It is regulated by the same hormones that regulate Calcium concentration.

A

Phosphate (Pi)

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21
Q

What is the body distribution of Phosphate?

A

Bone – 85 percent
Plasma – < 1 percent (of this, most is ionized)
ICF – 15 percent

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22
Q

The _______ cells of the Parathyroid glands synthesize and secrete ________.

A

Chief

PTH

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23
Q

This regulates the concentration of Calcium and Phosphate in plasma.

A

PTH

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24
Q

Briefly explain the synthesis of PTH.

A

Synthesized on ribosome as preproPTH –

Cleaved to proPTH –

Transported to Golgi and cleaved to PTH –

Packaged in secretory granules

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25
Q

When is PTH secreted?

A

If there is decreased plasma Calcium.

***Remember, if there is increased plasma Calcium then Calcitonin is stimulated.

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26
Q

Chronic __________ causes decreased synthesis and storage of PTH, increased breakdown of stored PTH and release of inactive PTH fragment into the circulation.

A

Hypercalcemia

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27
Q

Chronic __________ causes increased synthesis and storage of PTH, and hyperplasia of parathyroid glands (secondary hyperparathyroidism).

A

Hypocalcemia

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28
Q

This has parallel effects of Calcium on PTH, just less significant.

A

Magnesium

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29
Q

Severe ____________ is a result of chronic Magnesium depletion (as in Alcoholism) and results in inhibition of PTH synthesis, storage, and secretion!

A

Hypomagnesemia

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30
Q

PTH acts via what type of receptor?

A

GPCR

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31
Q

What will increased PTH secretion cause the bone, kidney, and intestine to do?

A

Bone – increased bone resorption

Kidney – decreased Phosphate reabsorption, increased calcium reabsorption, increased urinary cAMP

Intestine – increased calcium absorption (indirect via Vitamin D)

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32
Q

This promotes mineralization of new bone through its coordinated actions in the regulation of both Calcium and Phosphate plasma concentrations.

A

Vitamin D

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33
Q

Vitamin D will increase both ________ and ________ plasma concentrations, and the increased products of these will promote mineralization of new bone. Like PTH, Vitamin D also has actions in intestine, kidney, and bone.

A

Calcium

Phosphate

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34
Q

Vitamin D (cholecalciferol) is a prohormone and is physiologically inactive as is. It must be successfully _______ to an active metabolite. Regulated by negative feedback mechanisms.

A

Hydroxylated

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35
Q

Decreased Calcium, increased PTH, and decreased Phosphate will induce the kidney to form the active from of ________ in the proximal tubule.

A

Vitamin D

36
Q

This enzyme is what converts Vitamin D to its active form in the proximal tubule (from 25-OH-cholecalciferol).

A

1a-hydroxylase

***This enzyme tightly regulated at transcription level

37
Q

______ receptors are located on Osteoblasts, not Osteoclasts. Its short-term action is bone formation via direct action on the Osteoblasts.

A

PTH

***This is basis for synthetic PTH treatment in Osteoporosis treatment!

38
Q

PTH long-term actions on bone is increased bone resorption by indirectly eating on Osteoclasts mediated by ________ released from Osteoblasts.

A

Cytokines

39
Q

This acts synergistically with PTH to stimulate Osteoclast activity and bone resorption.

A

Vitamin D

40
Q

Osteoblasts will stimulate this to induce stem cells to differentiate into Osteoclast precursors, mononuclear Osteoclasts, and finally, mature into multinucleated Osteoclasts.

A

M-CSF (Macrophage Colony-Stimulating Factor)

41
Q

This is a cell surface protein produced by Osteoblasts, bone lining cells, and apoptotic Osteocytes. It is the primary mediator of Osteoclast formation.

A

RANKL

42
Q

This is a cell surface protein receptor on Osteoclasts and Osteoclast precursors.

A

RANK

43
Q

This is a soluble protein produced by Osteoblasts that acts as a decoy receptor for RANKL. It inhibits the interaction of RANK and RANKL.

A

OPG (Osteoprotegerin)

44
Q

This cytokine is also released from Osteoblasts.

A

IL-6 (binds to IL-6R on Osteoclast precursors)

45
Q

PTH will (INCREASE/DECREASE) RANKL and (INCREASE/DECREASE) OPG. Vitamin D will (INCREASE/DECREASE) RANKL also.

A

Increase
Decrease
Increase

46
Q

In the kidney, the inhibition of _______ _______ transport by PTH causes _________ (increased excretion of Phosphate in urine).

A

Sodium
Phosphate
Phosphaturia

47
Q

The cAMP generated in the cells of the proximal tubule is excreted in urine, called _______ _______.

A

Urinary cAMP

48
Q

The second renal action of PTH is on the distal convoluted tubule and complements the increase in plasma _________ that resulted from the combination of resorption and phosphaturia.

A

Calcium

49
Q

PTH actions on Calcium and Phosphate homeostasis in bone are the following —

– Promotes ________ growth and survival.

– Regulates ______, ______, and ______ production by Osteoblast

– Sustained elevated levels of PTH shift the balance to a relative increase in ________ activity, thereby increasing bone turnover and reducing bone density.

A 
Osteoblast
M-CSF
RANKL
OPG
Osteoclast
50
Q

PTH actions on Calcium and Phosphate homeostasis in the kidney are the following —

– Stimulates _________ activity

– Stimulates _________ reabsorption by the thick ascending limb of Henle’s loop and the distal tubule

– Inhibits _________ reabsorption by proximal nephrons (represses NPT2a expression)

A

1a-hydroxylase
Calcium
Phosphate

51
Q

What does PTH action on Calcium and Phosphate homeostasis have no direct effect on?

A

Small intestine

Parathyroid gland

52
Q

What does Vitamin D action on Calcium and Phosphate homeostasis in the small intestine cause?

A

Increased calcium and phosphate absorption

53
Q

What does Vitamin D action on Calcium and Phosphate homeostasis in bone cause?

A

Sensitizes osteoblasts to PTH

Regulates osteoid production and calcification

54
Q

What does Vitamin D action on Calcium and Phosphate homeostasis in the kidney cause?

A

Promotes phosphate reabsorption by proximal nephrons (stimulates NPT2a expression)

Minimal actions on Calcium

55
Q

What does Vitamin D action on Calcium and Phosphate homeostasis in the parathyroid gland cause?

A

Directly inhibits PTH gene expression

Directly stimulates CaSR gene expression

56
Q

This acts primarily on bone and kidney by decreasing blood calcium and phosphate concentrations by inhibiting bone resorption (effects occur only at high circulating levels of the hormone).

A

Calcitonin

57
Q

Calcitonin receptors are located on _________, which when bound will decrease the activity and decrease numbers of ________.

A

Osteoclasts

Osteoclasts

58
Q

What is the major stimulus for Calcitonin production?

A

Increased plasma Calcium

59
Q

Calcitonin has no role in chronic (minute-to-minute) regulation of plasma Calcium. A _________ will result in decreased Calcitonin but no effect in Calcium metabolism. A _______ _______ will result in increased Calcitonin but no effect in Calcium metabolism.

A

Thyroidectomy

Thyroid tumor

60
Q

_________ is a gonadal hormone that stimulates intestinal Calcium absorption and renal tubular Calcium reabsorption. It is one of the most potent regulators of Osteoblast and Osteoclast function. _________ promotes survival of Osteoblasts and apoptosis of Osteoclasts, favoring bone formation over resorption.

A

Estradiol-17B

Estrogen

61
Q

Adrenal _________ (i.e., Cortisol) promote bone resorption and renal Calcium wasting, and inhibit intestinal absorption. Patients treated with high levels of this can develop __________-induced Osteoporosis.

A

Glucocorticoid

Glucocorticoid

62
Q

This occurs when patients excrete excessive amounts of Phosphate, Calcium, and cAMP. It often results in Calcium-Oxalate stones (kidney stones) from hypercalciuria. There is increased bone resorption and constipation (due to increased calcium absorption from intestines). Treatment usually requires a parathyroidectomy.

A

Primary hyperparathyroidism

  • **Remember “Stones, Bones, and Groans”
  • **Primary problems are caused by the gland itself, so there is parathyroid adenoma!
63
Q

What type of hyperparathyroidism results in hypercalcemia and hypophosphatemia?

A

Primary hyperparathyroidism

***The kidney will reabsorb Calcium while it excretes Phosphate, has inverse relationship!

64
Q

Describe levels in PTH, Calcium, Phosphate, and Vitamin D in Primary Hyperparathyroidism.

A

PTH – increased
Calcium – increased
Phosphate – decreased
Vitamin D – increased

65
Q

In this type of hyperparathyroidism, the increase in PTH levels is secondary to low Calcium in the blood. Causes for the low Calcium in the blood is due to renal failure or Vitamin D deficiency.

A

Secondary hyperparathyroidism

66
Q

Chronic kidney disease (renal failure) causes increased ________ and decreased _________, which leads to decreased Calcium. This signals PTH to increase and secrete.

A

Phosphate
Vitamin D

***Secondary hyperparathyroidism

67
Q

Describe levels in PTH, Calcium, Phosphate, and Vitamin D in Secondary Hyperparathyroidism.

A

Renal Failure –

    • PTH increased
    • Calcium decreased
    • Phosphate increased
    • Vitamin D decreased

Vitamin D deficiency –

    • PTH increased
    • Calcium decreased
    • Phosphate decreased
    • Vitamin D decreased

***In renal failure, there is low Vitamin D because the kidney can’t activate it. PTH also normally inhibits the reabsorption of Phosphate by the kidney, and when they’re failing they already can’t remove the excess Phosphate in the body.

***In Vitamin D deficiency, the increased PTH is doing its job of decreasing the Phosphate. Vitamin D levels are low due to diet, aging, etc. (common in elderly)

68
Q

This can be caused by thyroid or parathyroid surgery, or autoimmune or congenital (less common). Most symptoms are associated with decreased Calcium levels, like muscle spasms or cramping, numbness, tingling, or burning, especially around the mouth and fingers. Seizures and in kids there is poor teeth development and mental deficiency.

A

Hypoparathyroidism

69
Q

What is the treatment for Hypoparathyroidism?

A

Oral Calcium supplement

Active form of Vitamin D

70
Q

This presents as hypocalcemia and hyperphosphatemia.

A

Hypoparathyroidism

***Kidney will reabsorb more Phosphate and less Calcium, has inverse relationship!

71
Q

Describe levels of PTH, Calcium, Phosphate, and Vitamin D in Hypoparathyroidism.

A

PTH – decreased
Calcium – decreased
Phosphate – increased
Vitamin D – decreased

72
Q

This is an inherited autosomal dominant disorder where the Gs for PTH in bone and kidney is defective. Hypocalcemia and hyperphosphatemia develop. PTH levels are increased, but their receptor is defective (Gs). Phenotype presents as short stature, short neck, obesity, subcutaneous calcification, and shortened metatarsals and metacarpals.

A

Albright hereditary osteodystrophy (Pseudohypoparathyroidism type 1a)

73
Q

Describe levels of PTH, Calcium, Phosphate, and Vitamin D in Pseudohypoparathyroidism.

A

PTH – increased
Calcium – decreased
Phosphate – increased
Vitamin D – decreased

74
Q

This is a hypercalcemic syndrome associated with malignancy.

A

Humoral hypercalcemia of malignancy

75
Q

This is a peptide produced by tumors with close homology in the N-terminal to PTH (product of gene duplication of PTH). This peptide binds and activates the same receptor as PTH (type 1 PTH receptor).

A

PTH-related peptide (PTHrP)

76
Q

This produces a similar profile to Primary Hyperparathyroidism. It has hypercalcemia and hypophosphatemia. The only thing different is that it has decreased levels of PTH.

A

Humoral hypercalcemia of malignancy

77
Q

Describe levels of PTH, Calcium, Phosphate, and Vitamin D in Humoral hypercalcemia of malignancy.

A

PTH – decreased
Calcium – increased
Phosphate – decreased
Vitamin D – decreased

78
Q

This is an autosomal dominant disorder that is caused by mutations that inactivate CaSR in parathyroid glands and parallel Calcium receptors in the ascending limb of the kidney. This results in decreased urinary Calcium excreting (hypocalciuria) and increased serum Calcium (hypercalcemia).

A

Familial hypocalciuric hypercalcemia (FHH)

79
Q

Describe levels of PTH, Calcium, Phosphate, and Vitamin D in Familial hypocalciuric hypercalcemia (FHH).

A 
PTH -- normal or increased
Serum Calcium -- increased
Urine Calcium -- decreased
Phosphate -- normal 
Vitamin D -- normal
80
Q

This is the impaired metabolism of Vitamin D. GI disorders, chronic renal failure, and Phosphate depletion can lead to pathophysiological changes in Vitamin D metabolism.

A

Rickets (children)

Osteomalacia (adults)

81
Q

What are examples of impairment in Vitamin D metabolism?

A

Dietary deficiency of Vitamin D

Deficit in synthesis of active Vitamin D (i.e., absence of 1a-hydroxylase)

Vitamin D resistance (mutations affecting Vitamin D receptor)

82
Q

In this type of Vitamin D problem, there is insufficient amounts of Calcium and Phosphate available to mineralize growing bone. Characterized by growth failure and skeletal deformities.

A

Rickets (children)

83
Q

In this type of Vitamin D problem, new bones fail to mineralize. Characterized by bending and softening of weight-bearing bones.

A

Osteomalacia (adults)

84
Q

This type of rickets is due to decreased 1a-hydroxylase. Can’t produce active form of Vitamin D.

A

Vitamin D-dependent rickets type I

Pseudovitamin D-deficient rickets

85
Q

This type of rickets is due to decreased Vitamin D receptors.

A

Vitamin D-dependent rickets type II

Pseudovitamin D-deficient rickets

86
Q

Nutritional _________ could originate from either a GI disorder or suboptimal nutrition and inadequate sun exposure (vitamin D deficiency). Could be suspected in cases of bone pain associated with malabsorption (i.e., gastric bypass surgery). Presents as bone pain and muscle weakness, bone tenderness, fracture, muscle spasms and cramps.

A

Osteomalacia

87
Q

Increased _______ occurs secondary to Vitamin D deficiency.

A

PTH

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