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Endocrinology - Chapters > Chap.73 Bone&Min A&P > Flashcards

Chap.73 Bone&Min A&P Flashcards

0
Q

Serum calcium concentrations regulate the degree of membrane excitability in muscle and nervous tissue.

  1. _____ in serum calcium lead to refractoriness to stimulation of neurons and muscle cells, which translates clinically into ______ and _____.
  2. _____ in serum calcium lead to increases in neuromuscular excitability that translate clinically into _____ and ____ and ____.
A
  1. increases ; coma and muscular weakness

2. reductions ; convulsions and spontaneous muscle cramps and contractions referred to as *carpopedal spasm or *tetany

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1
Q

Calcium is the major structural component in the _____

A

skeleton

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2
Q

Specifically, the mineral phase of the skeleton is composed of a calcium salt called _____, and reductions in bone mineral content lead to spontaneous ____.

A

hydroxyapatite

fractures

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3
Q

______ has a major intracellular signaling role, and control of this is essential to the survival of all cells.

A

intracellular calcium

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4
Q

THe serum total calcium concentration is normally _____. Of this about _____ is bound to serum proteins, albumin mostly, and about 0.5 mg/dL circulates as insoluble complexes such as calcium sulfate, phosphate, and citrate. THe remaining about ____ circulates as free or unbound or ionized calcium.

A
  1. 5 mg/dL
  2. 5 mg/dL bound to albumin
  3. 5 mg/dL free
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5
Q

The free, ionized calcium,1) is available to be filtered at the _____, 2) to interact with cell membranes to regulate ______, 3) to enter and exit the _____.

A
  1. glomerulus
  2. electrical potential or excitability
  3. skeletal hydroxyapatite crystal lattice
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6
Q

From a clinical standpoint, it is important to know that total serum calcium can change without a change in the ionized calcium. For example, if a decline in serum albumin occurs as a result of ______ or the _____, a corresponding decline in the total serum calcium will ensue, but the ionized serum calcium will remain normal. Thus, at times, measuring the ionized serum calcium directly is important.

A

hepatic cirrhosis or the nephrotic syndrome

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7
Q

The three critical regulatory fluxes that maintain normal serum calcium concentration are with the ___, ____, and ____.

A

intestine, kidney, and the skeleton

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8
Q

What is the normal dietary intake for an adult human?

A

1000 mg per day

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9
Q

About 300 mg of the 1000 mg of normal diatary calcium is absorbed in the ____ and _____

A

duodenum and proximal jejunum

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10
Q

T/F About 150 mg per day of calcium is secreted by the liver (in bile), the pancreas (in pancreatic secretions), and the intestinal glands such that net absorption (called fractional absorption) of calcium is about 15% of intake.

A

true

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11
Q

The efficacy of calcium absorption is regulated at the level of the small intestinal epithelial cell (enterocyte) by the active form _______, 1,25-dihydroxyvitamin D ( 1,25[OH]2D, also called calcitriol).

A

Vitamin D
*dietary calcium absorption can be increased, at least over short term, by increasing calcium intake, by increasing plasma 1,25 (OH)2D concetrations, or by both measures.

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12
Q

______ in serum calcium can be caused by increases in circulating 1,25 (OH)2D , as in sarcoidosis.

A

increase

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13
Q

_____ in serum calcium can be caused by excessive calcium intake , as in milk-alkali syndrome

A

increase

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14
Q

______ can occur as a result of a decline in 1,25[OH]2D , as in chronic renal failure and hypoparathyroidism.

A

hypocalcemia

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15
Q

If an individual consumes 1000 mg of calcium per day, and if net _______ is 150 mg per day, then he or she will ____ 850 mg of calcium in feces per day.

A

net absorption = 150 mg per day

net excretion = 850 mg per day

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16
Q

the normal ionized serum calcium concentration is about 4.5 mg/dL. The normal glomerular filtration rate is 120 mL per minute. Multiplying these two numbers produces the ______.

A

filtered load of calcium

*which proves to be about 10,000 mg per day

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17
Q

The ____ is the most important moment to moment regulator of the serum calcium concentration.

A

kidney

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18
Q

Disorders of renal calcium handling (e.g. _____) can be expected to lead to significant abnormalities in ______ homeostasis.

A

e.g. thiazide diuretics, hypoparathyroidism

serum calcium homeostasis

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19
Q

9000 mg of the 10,000 mg filtered at the glomerulus each day is absorbed proximally. The remaining 10% that arrives at the distal tubule on a daily basis is subject to regulation, with ______.

A

PTH

PTH stimulates renal calcium reabsorption

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20
Q

PTH is vital in conditions of calcium deprivation (vitamin D deficiency). Why?

A

It acts at the distal tubule and stimulates renal calcium reabsorption

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21
Q

T/F PTH is anticalciuric.

A

true

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22
Q

About 150 mg of calcium is excreted by the kidney in the final ___ daily basis in a healthy individual. If the kidney filters 10,000 mg of calcium each day, and if 150 mg is excreted, 9850 mg is reabsorbed at _______.

A

urine excretion = 150 mg per day
9850 reabsorbed at proximal and distal sites each day

***98.5% of filtered calcium is reabsorbed by the nephron. Conversely, the normal *fractional excretion of calcium is about 1.5%

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23
Q

The skeletal compartment contains about 1.2 kg of calcium in a ______ and 1.0 kg in a _____.
male vs female

A

male =1.2

female = 1.0

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24
Q

what are the two types of bone

A
  1. cortical (lamellar)

2. trabecular (cancellous)

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25
Q

Which type of bone predominates in the skull and the shafts of long bones?

A

cortical (lamellar)

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26
Q

Which type of bone predominates at other sites, such as the distal radius, vertebral bodies, and the trochanters of the hip?

A

trabecular

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27
Q

The adult skeleton is completely remodeled every ____ years.

A

3 - 10 years
**this is perhaps best appreciated by recalling that orthopedic surgeons routinely and intentionally set fractures imperfectly, knowing that the normal processes of bone remodeling will lead to restoration of the original shape of a given bone with the passage of time.

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28
Q

_____ cells that remove old bone

A

osteoclasts

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29
Q

Osteoclasts deposit themselves on the surface of bone and form a *sealing zone over the bone surface into which they secrete what?

A
  1. protons (acid)
  2. proteases (collagenase)
  3. proteoglycan-digesting enzymes (hyaluronidase)
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30
Q
  1. What does the acid released by osteoclasts solubulize? What does this release?
  2. What does the enzyme released by osteoclasts digest? What component of the bone does this constitute?
A
  1. acid solubilizes *hydroxyapatite crystals releasing *calcium
  2. enzyme digests *proteins and proteoglycans (collagen, osteocalcin, osteopontin), which constitute the non-mineral or *OSTEOID component of bone
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31
Q

Osteoclasts literally move along the surface of trabecular bone plates and drill tunnels in cortical bone, periodically releasing the digested contents within their sealed zones into the bone marrow space and thereby creating resorption lacunae, called ______, on the trabecular bone surface.

A

Howship lacunae

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32
Q

Osteoclasts:
The released calcium contributes to the ECF calcium pool, and the released proteolytic products, such as _________ , can be used clinically as indices of bone resorption.

A

deoxypyridinoline cross-links (collagen fragments and hydroxyproline)

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33
Q

_____ = new bone formation

A

osteoblasts

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34
Q

Osteoblasts synthesize and secrete components of the nonmineral phase of the bone, called ______.

A

osteoid

35
Q

_____ = serve a critical role in sensing biomechanical strain within bone, and through their cellular extensions to the cell surface, also communicate signals that attract, activate, or repress osteoclasts and osteoblasts. That is, they determine which area of the skeleton require new bone formation and which need to be targets of osteoclastic bone remodeling.

A

osteocyte

36
Q
  1. _____ = derived from the fusion of macrophages
  2. _____ = derived from marrow stromal cells or bone surface lining cells
  3. _____ = descendants of osteoblasts
A
  1. osteoclasts
  2. osteoblasts
  3. osteocyte
37
Q

the principal therapy for ______ is with so called antiresorptives such as estrogens, estrogen like drugs, and bisphosphonates, which dramatically reduce bone turnover and yet appear to improve not only bone mass but bone mechanical properties.

A

osteoporosis

38
Q

Which type of cell can be used to access calcium from the skeleton in times of need to maintain a normal serum calcium concentration?

A

osteoclasts

39
Q

Which type of cell can be used to access calcium at appropriate times as a sink into which excess serum calcium can be deposited?

A

osteoblasts

40
Q

What are the two key metabolic regulatory hormones that coordinate the osteoclast, osteoblast, and osteocytes of the bone?

A

PTH and the active form of Vitamin D 1,25[OH]2D

41
Q

______ = peptide hormone produced by the four parathyroid glands.

A

PTH

42
Q

Through the _______ - a G protein coupled receptor for calcium that is located on the surface of the parathyroid cell - the serum ionized calcium concentration is continuously monitored.

A

calcium sensor

43
Q

A minor _______ in serum ionized calcium leads to PTH secretion.

A

decrease

44
Q

A minor _____ in serum calcium lead to suppression of PTH secretion.

A

increase in normal serum calcium

45
Q

What is the half life of PTH?

A

3 to 5 minutes

46
Q

PTH is secreted as an 84 amino acid peptide hormone that is rapidly cleaved by the _____ in the _____ into what?

A

Kupffer cells in the liver into amino-terminal and carboxy-terminal species

47
Q

T/F 84-amino acid peptide and carboxy-terminal are biologically active.

A

FALSE!!!
active = 84-amino acid peptide & amino-terminal
*caboxy-terminal IS NOT active

48
Q

What is the function of PTH in the kidney?

A
  1. inhibition of renal calcium excretion
  2. inhibits phosphate & bicarbonate reabsorption; which produce phosphaturia and hypophophatemia, as well as a proximal renal tubular acidosis
  3. stimulates the production of the active form of vitamin D, 1,25(OH)2D, at the PROXIMAL TUBULE
49
Q

What is the function of PTH on the skeleton?

A
  1. PTH has the ability to mobilize calcium immediately from the skeleton through activation of osteoclastic bone resorption.
  2. Over the longer term (days to weeks), PTH also stimulates the activity of steoblasts to produce new bone and thereby removes calcium from the circulation.
    * **the ability to stimulate osteoclasts acutely without activating bone formation is important for the rapid delivery of calcium to the ECF.
50
Q

How does PTH have the indirect effect of increasing intestinal calcium absorption?

A

by increasing renal synthesis of 1,25[OH]2D

51
Q

REVIEW SLIDE :)
PTH is secreted in response to hypocalcemia, and the actions of PTH combine to restore a low serum calcium to normal by
1. preventing renal calcium loss
2. by adding calcium to the ECF from the skeleton
3. by stimulating, indirectly through 1,25[OH]2D,increases in intestinal absorption

A

YAY!!! :)

52
Q

Vitamin D is really two different compounds. What are they?

A
  1. ergocalciferol (vitamin D2)

2. cholecalciferol (vitamin D3)

53
Q
  1. ______ = derived principally from skin exposed to sunlight
  2. ______ = derived from plant sterols
A
  1. cholecalciferol (V3)

2. ergocalciferol (V2)

54
Q

Both V2&V3 precursors are converted passively by the enzyme vitamin D-25 hydroxylase in the ____ to the respective 25-hydroxyvitamin D (25-OH D).

A

liver

55
Q

The conversion to make 25-OH- D is prevented in cirrhosis, and leads to _____

A

vitamin D deficient syndrome, collectively called hepatic osteodystrophy

56
Q

What is the standard clinical laboratory measure of the vitamin D status (repletion versus deficiency) in a patient with hypocalcemia, osteomalacia or rickets, osteoporosis or intestinal malabsorption, and other similar conditions?

A

25-OH D

57
Q

where is 25-OH D converted, or activated by the 25-hydroxyvitamin D 1 alpha hydroxylase?
what is it converted to?

A

renal proximal tubule

vitamin 1,25(OH)2D , called calcitriol**

58
Q

25-OH D is also called ____

A

calcidiol

59
Q

Because 1,25(OH)2D is the active form of vitamin D, its production is necessarily regulated, and this is accomplished primarily by _____ , with ____ increase stimulating 1,25(OH)2D production and the decrease of ____ diminishing synthesis.

A

PTH

60
Q

what is the primary action of active Vitamin D?

A

regulate intestinal calcium absorption

***Thus, PTH, through 1,25[OH]2D, indirectly regulates calcium absorption from the diet by the intestine.

61
Q

T/F Hypocalcemia of Hypoparathyroidism is a result of inadequate intestinal calcium resorption. Conversely, hyperparathyroidism is associated with hypercalcemia and nephrolithiasis both of which are direct results of increases in circulating 1,25[OH]2D.

A

true

62
Q

T/F Measurement of activated Vitamin D can be used as an index of both parathyroid function and intestinal calcium absorption.

A

true

63
Q

_____ = produced by the parafollicular or C cells of the thyroid gland in response to hypercalcemia.

A

Calcitonin

64
Q

Does calcitonin have homeostatic relevance?

A

NO
*clearly, pharmacologic doses of calcitonin may reduce the serum calcium, and although everyone agrees that it is secreted in response to hypercalcemia, little evidence exists that calcitonin has homeostatic relevance in humans.

65
Q

T/F Malignant tumors of the parafollicular cell (medullary carcinomas of the thyroid) routinely overproduce calcitonin and lead to enormous long term (years or decades) elevations in circulating calcitonin concentrations. This has no effect on serum calcium or any apparent skeletal effect.

A

true

66
Q

Stephanie just ate cheese, milk, ice cream, and yogart. This leads to a mild rise in serum calcium followed by what?

  • PTH?
  • Osteoblasts, Osteoblasts, Osteocytes?
A
  • Immediate suppression of the PTH, this action leads to immediate OPENING of the renal distal tubular calcium flood gates.
  • immediate reduction of osteoclastic activity, prevents continued bone resorption, but also allows continuation of calcium entry from ECF to an unmineralized osteoid sink.
67
Q

If stephanie continues to eat like this for months what will happen?
-the long term effects?

A

If the high calcium diet is maintained over the long term, the immediate adaptations are insufficient; therefore continued renal calcium wasting would lead to

  • hypercalciuria (nephrolithiasis and nephrocalcinosis)
  • excessive skeletal mineralization (osteopetrosis)
68
Q

What are the two additional responses that are required to prevent these potential long term adverse effects of a high calcium diet?

A
  1. subacute or chronic suppression of PTH results in a reduction in circulating 1,25[OH]2D. THis action in turn leads to a reduction in the efficiency of calcium absorption from the intestine and a reduction of calcium entry into the ECF and hence a reduction of urinary calcium excretion.
  2. A chronic decrement in PTH leads to a chronic decline in osteoblastic activity such that no osteoid is formed, and the ability to deposit calcium into the skeletal sink is lost.
69
Q

Between meals, you have brief periods of dietary calcium deficiency, what happens to PTH? Osteoclasts, Osteoblasts, Osteocytes?

A
  • serum calcium declines, PTH rises
  • the increase in PTH immediately prevents renal calcium losses from continuing.
  • acute activation of osteoclasts occurs, and this action delivers calcium into the ECF
  • ***Thus, the acute response to low calcium entry intake is the appropriate elimination of renal calcium losses and the development of a new source of calcium entry into the ECF.
  • **Over long term, this response doesnt work, so SKELETAL DEMINERALIZATION occurs.
70
Q

For a chronic low calcium intake, what adaptations must take place, for example in a person with lactose intolerance?

A
  1. chronic elevation of PTH, and this, over a matter of days to weeks, leads to an increase in 1,25[OH]2D. This increase in turn, leads to an increase in the efficiency of calcium absorption from the intestine (an increase in the fractional absorption of calcium) to compensate for the reduction in dietary intake.
  2. Second, a chronic elevation in PTH will lead to an increase in osteoblast activity and osteoid synthesis, with resultant increase in skeletal calcium deposition.
    * **In this new steady state adaptation to low calcium diet, PTH will be elevated, and coupled increases in both osteoclastic and osteoblastic activities will take place (an increase in bone turnover), but net skeletal calcium loss will be negligible or normal.
71
Q

______ is the more clinically relevant form that most laboratories measure rather than the more biologically active phosphate ion.

A

Phosphorus

72
Q

Is phosphorus primarily an intracellular or extracellular ion?

A

intracellular

73
Q

T/F The phosphate ions pairs with calcium in the hydroxyapatite crystal lattice that provides structural integrity to the skeleton.

A

true

74
Q

Does chronic alcoholism cause dietary phosphorus deficiency?

A

yes, because most alcoholic beverages do not contain phosphorus

75
Q

Skeletal destruction in multiple myeloma or severe immobilizaiton syndromes leads not one to hypercalcemia, but also ______.
Osteoblastic metastases in prostate cancer and breast cancer and the hungry bone syndrome following parathyroidectomy all lead to clinically significant ________.

A
  1. hyperphosphatemia, which, with the concomitant hypercalcemia, leads to nephrocalcinosis and renal failure
  2. hypophosphatemia
76
Q

What happens to phosphorus in acidic environements? Alkalosis?

A

acidic - phosphate leaves the intracellular compartment and may lead to hyperphosphatemia
alkalosis -serum phosphate concentrations decline, and hypophosphatemia develops as phosphate enters the intracellular compartment

77
Q

Crush injury (rhabomyolysis) and the tumor lysis syndrome, in both of which large intracellular loads of phosphate are delivered into the ECF and result in _____, _______ , _______, and _____.

A

hypocalcemia, seizures, nephrocalcinosis, and renal failure

78
Q

Glucose shifts phosphate ____ the cells as glucose 6-phosphate and overzealous intravenous or oral caloric restitution in the undernourished patient can result in severe hypophosphatemia and sudden death.

A

into the cell

79
Q
  1. Hypophosphatemia is associated with _________parathyroidism.
  2. Hyperphosphatemia is assocaited with ________parathyroidism.
A
  1. Hyperparathyroidism w/ hypophophatemia

2. Hypoparathyroidism w/ hyperphophatemia

80
Q
  1. ___ PTH lowers the TmP

2. ____ PTH raises the TmP

A
  1. excessive PTH lowers the TMP

2. low PTH values allow the TMP to rise to supranormal levels

81
Q

How does PTH effect phosphate?

A

PTH has been appreciated to be phosphaturic, that is , to LOWER the TmP or, more accurately, to INHIBIT PROXIMAL RENAL TUBULAR PHOSPHATE REABSORPTION.

82
Q

Does magnesium homeostasis have a closer parallel with calcium or phosphorus?

A

even tho calcium and magnesium are both DIVALENT cations; magnesium homeostasis has closer parallels with PHOSPHORUS HOMEOSTASIS

83
Q

Magnesium is primarily intracellular. What is magnesium involved in?

A

DNA replication and transcription, translation of RNA, the use of ATP, regulates peptide hormone secretion

84
Q

T/F Magnesium deficiency, like phosphate, is frustrating to recognize because the symptoms are so nonspecific: weakness, respirator dependence, diffuse neurologic syndromes including seizures, and cardiovascular collapse.

A

true

85
Q

In what situations do you see magnesium deficiency?

A
  • alcoholism (a pure alcohol diet contains no magnesium)
  • intensive care unit settings in which adequate nutrition is often not provided
  • intestinal malabsorption
86
Q

Many instances of Magnesium deficiency are caused by excessive renal losses. Examples include ______.

A
  • magnesuria that accompanies saline infusions
  • diuretic use
  • alcohol use
  • secondary hyperaldosteronism states such as CIRRHOSIS & ASCITES

Endocrinology - Chapters (20 decks)

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