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ENDO > 189-190 PTH/Ca/PO4 > Flashcards

189-190 PTH/Ca/PO4 Flashcards

1
Q

What are the three forms of serum calcium?

A

ionized (50%), protein-bound - mostly to albumin (40%), polyvalent anion with phosphate and citrate (10%)

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2
Q

What are the symptoms of hypercalcemia?

A

dehydration, renal stones, pain, weakness, confusion, arrhythmias

bones, groans, stones, psychiatric overtones

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3
Q

What is the active form of vitamin D?

A

1,25-(OH)2D

also called calcitriol

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4
Q

How is calcium absorbed in the GI tract?

A

facilitated diffusion throughout the small intestine

Vitamin D dependent absorption in the proximal duodenum

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5
Q

How does parathyroid hormone impact calcium absorption?

A

it increases calcium absorption in the distal nephron

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6
Q

Calcium excretion is directly related to __________ excretion.

A

Calcium excretion is directly related to sodium excretion.

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7
Q

Which diuretics increase calcium excretion? Which decrease it?

A

increase: loop diuretics
decrease: thiazides

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8
Q

Which signals increase phosphate excretion?

A

PTH, FGF-23

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9
Q

What is the function of osteoclasts?

A

breakdown of the collagenous bone matrix

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10
Q

What signal leads to osteoclast differentiation and activity?

A

RANK-L interaction with RANK on osteoclast precursor cells

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11
Q

What is the function of osteoblasts?

A

synthesize collagen and non-collagenous proteins to rebuild bone

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12
Q

What osteoblast products are used as markers of bone formation?

A

alkaline phosphatase, osteocalcin

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13
Q

What type of signaling plays a role in osteoblast differentiation?

A

Wnt signaling, IGF-1

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14
Q

What is the relationship between osteoblasts and osteoclast formation?

A

osteoblasts can produce RANKL to activate osteoclasts and can also produce osteoprotegerin which blocks RANK and inhibits bone resorption

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15
Q

What are osteocytes? What do they produce?

A

cells native to bone after it is built

produces sclerostin, which inhibits wnt signaling and subsequently bone formation

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16
Q

What is the difference between osteoporosis and Paget’s disease in terms of osteoclast/osteoblast balance?

A

osteoporosis = osteoblast activity cannot keep up with osteoclast activity

Paget’s disease of bone = a local increase in osteoclast activity is followed by an increase in osteoblast activity

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17
Q

What is the storage form of vitamin D?

A

25-OH vitamin D3

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18
Q

What receptors do calcitriol bind to?

A

nuclear receptors

leads to upregulation of genes involved in calcium/phosphate absorption and bone formation

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19
Q

Inadequate vitamin D can lead to _______ (in kids) or ________ (in adults). Too much can lead to ________.

A

Inadequate vitamin D can lead to rickets (in kids) or osteomalacia (in adults). Too much can lead to hypercalcemia.

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20
Q

What is the treatment for excess vitamin D?

A

stop the vitamin, low calcium diet, glucocorticoids, fluid

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21
Q

How does calcium affect PTH secretion?

A

calcium provides negative feedback by stimulating a G-protein coupled Ca receptor (CaSR), which decreases PTH secretion from parathyroid glands

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22
Q

What are calcimimetics like cinacalcet used to treat?

A

used to suppress excess PTH in patients with hyperparathyroidism and in parathyroid carcinoma

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23
Q
A
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24
Q

What is the mechanism of PTH?

A

acts on GPCRs in bone and kidney to activate cAMP and PKC

in bone: stimulates resorption by increasing osteoblast production of RANKL (continuous in response to PTH) OR stimulates bone formation (pulsatile, intermittent exposure to PTH)

kidney: promotes calcium reabsorption, inhibits phosphate absorption, increases activation of vitamin D

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25
Q
A
26
Q
A
27
Q

What is the clinical use of teriparatide? Side effects?

A

clinical use: increases bone mineral density and reduces fracture risk in women with osteoporosis (PTH-like)

side effects: osteosarcomas in rats, but unlikely to in people

28
Q

What is the mechanism of calcitonin?

A

acts through GPCR on osteoclasts to inhibit bone resorption

29
Q

What is the mechanism of FGF-23?

A

inhibits calcitriol production in the kidney and inhibits phosphate resorption

30
Q

What is the effect of estrogen on bone?

A

it inhibits bone resorption via decreased production of resorptive cytokines (IL-6, RANKL)

increases bone formation by decreasing sclerostin

31
Q

What are SERMS? What are their clinical uses?

A

selective estrogen receptor modulators that antagonize estrogen effects on the preast and have estrogenic agonist action on the bone

32
Q

What is the mechanism of bisphosphonates?

A

they accumulate at the site of active resorption and inhibit activity of osteoclasts

33
Q

What are the clinical uses of bisphosphonates?

A

osteoporosis, Paget’s disease, breast and prostate tumor metastases, multiple myeloma, hypercalcemia

34
Q

What are the adverse effects of bisphosphonates?

A

heartburn, esophageal irritation, esophagitis

35
Q

What is the mechanism of denosumab?

A

monoclonal antibody against RANKL

leads to suppresion of resorption and increased bone mineral density

36
Q

What is the effect of glucocorticoids on bone?

A

interferes with intestinal calcium absorption, increases renal calcium excretion, stimulation of PTH secretion, decreased estrogen and testosterone, inhibition of osteoblasts

37
Q

The therapeutic effectiveness of PTH (teriparatide) for the treatment of osteoporosis derives its action to:

a) stimulate the anabolic activities of the osteoblast
b) increase calcium reabsorption at the distal convoluted tubule
c) increase RANKL expression
d) stimulate the renal 25-hydroxyvitamin D3 1-alpha-hydroxylase
e) act on intestinal G protein linked membrane receptors to increase calcium absorption

A

a) stimulate the anabolic activities of the osteoblast

38
Q

Denosumab is a human monoclonal antibody that:

a) is directed against the T-cell CD3 component
b) prevents the formation of isoprenyl groups
c) antagonizes RANKL
d) blocks calcitonin receptors on osteoclasts
e) decreases interleukin-6 in osteoblasts

A

c) antagonizes RANKL

39
Q

The net effect of PTH action is to _________ serum calcium and _________ serum phosphorous.

A

The net effect of PTH action is to increase serum calcium and decrease serum phosphorous.

40
Q

What 3 factors regulate PTH production?

A

1) serum calcium concentration (negative feedback)
2) serum 1,25 OH2 Vitamin D levels (inhibitory)
3) serum phosphorous concentration (stimulatory)

41
Q

What is the mechanism of familial hypocalciuric hypercalcemia?

A

inactivating mutation of the calcium sensing receptor gene, leading to mildly elevated calcium and PTH levels with low urine calcium

42
Q

Where is vitamin D converted to the active form? What enzyme converts it?

A

in the kidney by 1-alpha hydroxylase

43
Q

Primary hyperparathyroidism leads to _________ calcium, __________ phosphorous, and _________ PTH levels.

A

Primary hyperparathyroidism leads to high calcium, low phosphorous, and high PTH levels.

44
Q

What is the mechanism of primary hyperparathyroidism?

A

hyperplasia and adenoma formation of parathyroid glands

often associated with MEN I and IIa syndromes

45
Q

What are the clinical manifestations of primary hyperparathyroidism?

A

hypercalcemia symptoms

fibrosa cystica skeletal condition, brown tumors of long bones, increased urinary calcium (nephrolithiasis)

46
Q

What is the most common cause of hypercalcemia in hospitalized patients?

A

humoral hypercalcemia of malignancy

3 mechanisms: ectopic production of PTH by malignant cells, bone resorption associated with malignancy, ectopic production of 1-alpha hydroxylase

47
Q

What is “false hypocalcemia”?

A

a lab result suggesting hypocalcemia when calcium levels are actually normal that is an artifact of decreased serum albumin

48
Q

What are the symptoms of hypocalcemia?

A

neuromuscular irritability leading to paresthesias

includes chvostek’s sign, Trousseau’s sign, laryngospasm, seizures, and tetany

49
Q

What are the causes of hypoparathyroidism? What serum levels are associated with it?

A

causes: iatrogenic destruction of a parathyroid gland by surgery, radiation, or autoimmune destruction

low serum calcium, inappropriately low serum PTH, low vitamin D, high phosphorous

50
Q

What are the causes of non-hypoparathyroid hypocalcemia?

A

severe magnosemia (decreases PTH production and increased PTH resistance)

acute pancreatitis

hyperphosphatemia

vitamin D deficiency

51
Q

How does renal failure lead to hypocalcemia?

A

it leads to increased serum p hosphorous levels and decreased vitamin D production –> leads to secondary hyperparathyroidism and subsequent hypocalcemia

52
Q

What is pseudohypoparathyroidism?

A

a disease represented by tissue unersponsiveness to PTH due to inappropriate PTH/PTHrP signaling

53
Q

How does phosphorous affect PTH levels?

A

low phosphorous triggers 1-alpha-hydroxylase production, which increases absorption of Ca and phosphorus and decreases PTH values

54
Q

What is the role of FGF-23 in phosphorous regulation?

A

excess FGF-23 leads to hypophosphatemia (renal phosphate wasting)

55
Q

What is the mechanism of osteomalacia?

A

defective bone mineralization due to vitamin D deficiency (or less frequently due to deficiency in calcium or phosphorous)

diagnosed with a serum D 25 OH level

56
Q

What is the mechanism of osteoporosis?

A

low bone mass, micro-architectural deterioration of bone

commonly due to peri/post-menopause or old age

57
Q

What are anti-resorptive agents to treat osteoporosis?

A

estrogen, bisphosphonates, raloxifene, calcitonin, denosumab

58
Q

What are anabolic agents to treat osteoporosis?

A

teriparatide, abaloparatide, romosozumab

59
Q

What is the mechanism of Paget’s disease?

A

hyperdynamic bone remodeling leading to bony overgrowth

60
Q
A

b) osteomalacia secondary to vitamin D deficiency

  • his serum calcium corrects to a level that is not hypocalcemia (8.9), but PTH is high indicating hyperparathyroidism (secondary cause)*
  • vitamin D is probably low overall if you measure the 25 OH form*
61
Q

A 29 yo female presents to you in clinic with fatigue and pain in her shins. She is found to have a calcium of 10.7, phosphorous 2.8 and PTH 99 (elevated). Vitamin D 25-hydroxy is 38 ng/ml (normal). She thinks her grandfather had hypercalcemia but is unsure about her parents. The next best step is:

a) give her vitamin D supplementation
b) obtain a CBC with differential
c) obtain a 24 hour urine calcium
d) obtain a parathyroid scan (sestamibi)
e) obtain a neck ultrasound

A

c) obtain a 24 hour urine calcium

could check for familial hypocalciuric hypercalcemia

62
Q

a) familial hypocalciuric hypercalcemia
b) primary hyperparathyroidism
c) perimenopause
d) vitamin D deficiency
e) malignancy

A

b) primary hyperparathyroidism

serum calcium is high with an inappropriately normal PTH level

ENDO (19 decks)

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