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Endocrinology and Reproduction > Regulation of Calcium and Phosphate Homeostasis II > Flashcards

Regulation of Calcium and Phosphate Homeostasis II Flashcards

1
Q

E2 and the anabolic androgens (testosterone and dihydrotestosterone) stimulate bone growth and increase and/or maintain

A

Bone density

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2
Q

Exerts a number of effects that collectively affect Ca2+ and PO4 homeostasis to maintain bone density

A

Estrogen

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3
Q

Stimulates the expression of VDR in the duodenum and may also directly increase Ca2+ absorption

A

E2

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4
Q

What is the predominant ER receptor in humans?

A

ER-alpha

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5
Q

Estrogen receptors are expressed by

A

Growth plate chondrocytes

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6
Q

Acts in a biphasic manner to first stimulate longitudinal bone growth, but then over time induces epiphyseal closure, thus terminating longitudinal growth

A

ER

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7
Q

In osteocytes, E2 blocks apoptosis and stimulates the secretion of

A

TGFB

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8
Q

Blocks osteoclast differentiation

A

TGFB

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9
Q

Impairs osteoclast differentiation and RANKL synthesis

A

Estrogen

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10
Q

Which three things does estrogen promote in bones?

A
  1. ) Osteoclast apoptosis
  2. ) Osteoblast proliferation
  3. ) Osteoprotegerin production
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11
Q

Collectively, these actions support the maintenance of bone density by thwarting

A

Osteoclast-mediated reabsorption

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12
Q

Is by and large sequestered to the epiphyseal chondrocytes, growth plate cartilage, osteocytes, and osteoblasts

A

Androgen Receptor (AR) expression

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13
Q

Men with total E2 deficiency due to mutations in either ERa or CYP19 exhibit severe

-Despite normal testosterone levels

A

Osteopenia

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14
Q

Thus, we may not receive a direct effect on bone growth from

A

AR expression

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15
Q

Aromatase, i.e. the enzyme which aromatizes testosterone into E2

A

CYP19

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16
Q

We can treat these men with osteopenia in order to induce epiphyseal closure and longitudinal bone growth by giving them

A

Exogenous Estrogen

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17
Q

Since the predominant circulating anabolic androgen, testosterone, can be aromatized into E2 by a variety of tissues, the anabolic effects of androgens in bone are possibly due to

A

E2

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18
Q

The best indicator of fracture risk in aging men

A

E2

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19
Q

21-carbon steroids produced by the adrenal cortex

-produced in zona fasciculata and zona reticularis

A

Glucocorticoids

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20
Q

In the context of bone, function to enhance reabsorption

A

Glucocorticoids

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21
Q

Thus, prolonged glucocorticoid excess can result in

A

Glucocorticoid-induced osteoporosis

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22
Q

Glucocorticoid-induced osteoporosis can lead to the development of

A

Osteonecrosis

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23
Q

The rapid focal deterioration of bone, often occuring within the femoral head

A

Osteonecrosis

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24
Q

Has complex effects in bone, involving both direct (via effects within osteoblasts, osteoclasts, and osteocytes), as well as indirect mechanisms within the kidneys and the small intestine where Ca2+ reabsorption and absorption, respectively, are impaired

A

Glucocorticoids

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25
Q

Impede skeletal muscle function by increasing catabolism

A

Glucocorticoids

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26
Q

Muscle wasting and the deleterious effects within bone can be exacerbated by the inhibitory effect of glucocorticoids on

A

Gonadal estrogen and androgen production

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27
Q

Osteoblasts, osteoclasts, and osteocytes all express

A

Glucocorticoid receptors

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28
Q

Within osteoblasts and osteocytes, glucocorticoids upregulate

A

Apoptosis

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29
Q

Actually extend the life of osteoclasts

A

Glucocorticoids

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30
Q

The production of RANKL is promoted by

A

Glucocorticoids

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31
Q

The production of RANKL is promoted by glucocorticoids, thereby increasing the ratio of
RANKL:osteoprotegerin; a mechanism that promotes

A

Osteoclast-mediated bone reabsorption

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32
Q

Predominantly synthesized by the liver in response to GH

A

IGF-I

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33
Q

However, it has been shown that IGF-I is also synthesized in

A

Osteocytes and chondrocytes

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34
Q

Postnatally and through adolescence, GH and IGF-1 together stimulate

A

Longitudinal bone growth

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35
Q

In long bones, exerts mitogenic effects in chondrocytes within the epiphyseal cartilages (epiphyseal lengthening) concomitant with stimulating local IGF-1 expression

A

GH

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36
Q

Due to their anabolic effects, GH and IGF-I can also regulate modeling and remodeling of

A

Trabecular and cortical bone

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37
Q

Note that the anabolic effects of GH depend on

A

IGF-I

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38
Q

Osteoblast activity is upregulated by

A

GH

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39
Q

GH promotes osteoblasts to express

A

IGF-I

40
Q

The expression of IGF-I in osteoblasts is also stimulated by

A

PTH and E2

41
Q

IGF-I expression is reduced by

A

Glucocorticoids

42
Q

In children, hypothyroidism is associated with

A

Blunted growth

43
Q

Has been shown to increase the activity of both osteoblasts and osteoclasts

A

Thyroid Hormone

44
Q

In adult hyperthyroidism, an upregulation in bone mineralization is in fact linked with increased

A

Reabsorption

45
Q

A wasting of the bone matrix that is associated with the age dependent drop in E2, and perhaps androgen, production that occurs in older men and women

A

Osteoporosis

46
Q

In women, the loss of ovarian function that defines menopause results in a profound decline in bioavailable

A

E2

47
Q

The hallmark sign of osteoporosis is the demineralization of bone leading to decreased bone density in the

A

Spine, hip, pelvis, and/or wrist

48
Q

Serum Ca2+, PO4, and PTH generally remain normal in

A

Osteoporosis

49
Q

Increases bone mineral density and thus exerts anti-osteoporotic effects in properly nourished post menopausal women

A

Estrogen Replacement Therapy (ERT)

50
Q

Commonly prescribed for osteoporosis

A

Bisphosphonates

51
Q

Act to prevent bone absorption by impairing osteoclast activity and accelerating osteoclast apoptosis

A

Bisphosphonates

52
Q

Another treatment treatment for osteoporosis is

A

Selective Estrogen Receptor Modulators (SERM)

53
Q

A SERM which functions as an E2 agonist in bone, while antagonizing E2 in breast and uterine tissue

A

Raloxiphene

54
Q

A human monoclonal antibody against RANKL that is used to treat osteoporosis

A

Denosumab

55
Q

The third most common endocrine disorder

A

Primary hyperparathyroidism

56
Q

Approximately 75-80% of the time, results from a single parathyroid adenoma causing hypersecretion of PTH from parathyroid glands

A

Primary hyperparathyroidism

57
Q

Elevated PTH results in

A

Hypercalcemia

58
Q

In severe cases of hyperparathyroidism, we see loss of cortical bone and deposition of

A

Trabecular bone

59
Q

The chief complaint in symptomatic hyperparathyroid patients is usually bone pain and

A

Arthralgias

60
Q

More frequent in those over 50 years of age and is 3x more common in women

A

Hyperparathyroidism

61
Q

If present, symptoms from pathologic hypercalcemia only appear at serum levels greater than

A

12 mg/dL

62
Q

In an electrocardiogram, hypercalcemia will show as a

A

Shortened QT

63
Q

During phase 2 depolarization (i.e. the plateau phase; of the cardiac myocyte action potential, calcium slowly enters the cell. The duration of phase 2 is directly correlated with the duration of the

A

ST segment

64
Q

When the extracellular Ca2+ levels are elevated, the Type L channels become

-activate and inactivate more frequently

A

Irritated

65
Q

Although rare with hypercalcemia, disruption of cardiac electrical activity can lead to serious

A

Arrythmias

66
Q

With regard to skeletal muscle, experimental evidence has shown that excess extracellular Ca2+ raises the membrane potential necessary to open the motor neuron voltage-gated Na+ channels, thus inducing

A

Hypoexciteability

67
Q

Patients with hypercalcemia due to primary hyperparathyroidism have increased renal excretion of

A

Ca2+ and PO4

68
Q

The hypercalciuria predisposes the formation of

A

Kidney stones

69
Q

Also, the abnormal increase in Ca2+ concentration within the forming urine can induce aberrant CaSR activity which can lead to a form of

A

Ca2+ Dependent nephrogenic diabetes insipidus

70
Q

The most common cause of true hypocalcemia is the loss of calcitriol synthesis that results from the advanced stages of

A

Chronic kidney disease

71
Q

Signs and symptoms of this condition are associated with the increase in nerve and muscle excitability that accompanies

A

Hypocalcemia

72
Q

It appears that extracellular Ca2+ aids in somehow stabilizing membrane Na+ channels within

A

Skeletal muscle and neurons

73
Q

With low extracellular Ca2+, membrane permeability to Na+ is increased and the result is

A

Hyperexciteability

74
Q

If severe enough, hypocalcemia can impair ventricular conductivity and ventricular myocyte contractility and is shown on an ECG as

A

Prolonged QT interval

75
Q

Skeletal muscle cramping and/or tetany, and perioral and distal extremity paresthesias can occur with

A

Hypocalcemia

76
Q

There are two signs that can be used in the diagnosis of hypocalcemia. The first is

A

Trousseau’s sign

77
Q

Shows as a carpal spasm due to the loss in brachial artery circulation that occurs upon inflation of a BP cuff above systolic BP

A

Trousseau’s sign

78
Q

Approximately what percent of patients with hypocalcemia will show Trousseau’s sign?

A

94%

79
Q

The second test for hypocalcemia is known as

A

Chvostek’s sign

80
Q

This is observed as ipsilateral facial muscle contraction when the facial nerve is tapped anterior to the ear

A

Chvostek’s sign

81
Q

Which test has a higher specificity, Trousseau’s or Chvostek’s?

A

Trousseau’s

82
Q

Hyperphosphatemia is indicated by serum PO4 above

A

5mg/dL

83
Q

Most often due to acute and chronic renal failure, when GFR falls under 30 mL/min

A

Hyperphosphatemia

84
Q

Abnormally elevated PO4 tends to precipitate

A

Ca2+

85
Q

Tends to precipitate Ca2+, impairs calcitriol synthesis, and impedes PTH mediated bone resorption

A

Abnormally elevated PO4

86
Q

Thus, the signs and symptoms of hyperphosphatemia are actually attributed to the ensuing

A

Hypocalcemia

87
Q

If prolonged, hyperphosphatemia and the associated Ca2+ imbalances can progress to the formation of metastatic calcifications which tend to develop within the vascular walls, ventricular myocardium, as well as

A

Atrial and mitral valves

88
Q

The most common etiology of hypophosphatemia is due to an increase in PO4 excretion that accompanies

A

Hyperparathyroidism

89
Q

During severe hypophosphatemia (≤1 mg/dl), the affinity of hemoglobin for O2 is increased due to a decrease in

A

2,3 DPG

90
Q

Since O2 cannot be effectively offloaded to tissues,

skeletal muscle cell weakness and sometimes skeletal muscle necrosis can occur. This necrosis is also known as

A

Rhabdomyolysis

91
Q

A condition of childhood calcitriol deficiency or resistance prior to epiphyseal plate closure

A

Rickets

92
Q

The adult form of Rickets is called

A

Osteomalacia

93
Q

The calcitriol deficiency induces increased PTH-dependent elimination of PO4 in the urine, and the inability to absorb

A

Dietary Ca2+

94
Q

SIgns and symptoms of Rickets/osteomalacia would then include bone pain and tenderness, diminished bone density/mineralization, as well as

A

Hypophosphatemia, hypocalcemia, and hypocalciuria

95
Q

If this condition is not corrected, we can see severe bone weakening and

A

Tetanic respiratory failure

Endocrinology and Reproduction (15 decks)

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