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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
26
27
What is the clinical use of teriparatide? Side effects?
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
What is the mechanism of calcitonin?
acts through GPCR on osteoclasts to inhibit bone resorption
29
What is the mechanism of FGF-23?
inhibits calcitriol production in the kidney and inhibits phosphate resorption
30
What is the effect of estrogen on bone?
it inhibits bone resorption via decreased production of resorptive cytokines (IL-6, RANKL) increases bone formation by decreasing sclerostin
31
What are SERMS? What are their clinical uses?
selective estrogen receptor modulators that antagonize estrogen effects on the preast and have estrogenic agonist action on the bone
32
What is the mechanism of bisphosphonates?
they accumulate at the site of active resorption and inhibit activity of osteoclasts
33
What are the clinical uses of bisphosphonates?
osteoporosis, Paget's disease, breast and prostate tumor metastases, multiple myeloma, hypercalcemia
34
What are the adverse effects of bisphosphonates?
heartburn, esophageal irritation, esophagitis
35
What is the mechanism of denosumab?
monoclonal antibody against RANKL ## Footnote *leads to suppresion of resorption and increased bone mineral density*
36
What is the effect of glucocorticoids on bone?
interferes with intestinal calcium absorption, increases renal calcium excretion, stimulation of PTH secretion, decreased estrogen and testosterone, inhibition of osteoblasts
37
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) stimulate the anabolic activities of the osteoblast
38
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
c) antagonizes RANKL
39
The net effect of PTH action is to _________ serum calcium and _________ serum phosphorous.
The net effect of PTH action is to **increase** serum calcium and **decrease** serum phosphorous.
40
What 3 factors regulate PTH production?
1) serum calcium concentration (negative feedback) 2) serum 1,25 OH2 Vitamin D levels (inhibitory) 3) serum phosphorous concentration (stimulatory)
41
What is the mechanism of familial hypocalciuric hypercalcemia?
inactivating mutation of the calcium sensing receptor gene, leading to mildly elevated calcium and PTH levels with low urine calcium
42
Where is vitamin D converted to the active form? What enzyme converts it?
in the kidney by 1-alpha hydroxylase
43
Primary hyperparathyroidism leads to _________ calcium, __________ phosphorous, and _________ PTH levels.
Primary hyperparathyroidism leads to **high** calcium, **low** phosphorous, and **high** PTH levels.
44
What is the mechanism of primary hyperparathyroidism?
hyperplasia and adenoma formation of parathyroid glands often associated with MEN I and IIa syndromes
45
What are the clinical manifestations of primary hyperparathyroidism?
hypercalcemia symptoms fibrosa cystica skeletal condition, brown tumors of long bones, increased urinary calcium (nephrolithiasis)
46
What is the most common cause of hypercalcemia in hospitalized patients?
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
What is "false hypocalcemia"?
a lab result suggesting hypocalcemia when calcium levels are actually normal that is an artifact of decreased serum albumin
48
What are the symptoms of hypocalcemia?
neuromuscular irritability leading to paresthesias ## Footnote *includes chvostek's sign, Trousseau's sign, laryngospasm, seizures, and tetany*
49
What are the causes of hypoparathyroidism? What serum levels are associated with it?
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
What are the causes of non-hypoparathyroid hypocalcemia?
severe magnosemia (decreases PTH production and increased PTH resistance) acute pancreatitis hyperphosphatemia vitamin D deficiency
51
How does renal failure lead to hypocalcemia?
it leads to increased serum p hosphorous levels and decreased vitamin D production --\> leads to secondary hyperparathyroidism and subsequent hypocalcemia
52
What is pseudohypoparathyroidism?
a disease represented by tissue unersponsiveness to PTH due to inappropriate PTH/PTHrP signaling
53
How does phosphorous affect PTH levels?
low phosphorous triggers 1-alpha-hydroxylase production, which increases absorption of Ca and phosphorus and decreases PTH values
54
What is the role of FGF-23 in phosphorous regulation?
excess FGF-23 leads to hypophosphatemia (renal phosphate wasting)
55
What is the mechanism of osteomalacia?
defective bone mineralization due to vitamin D deficiency (or less frequently due to deficiency in calcium or phosphorous) ## Footnote *diagnosed with a serum D 25 OH level*
56
What is the mechanism of osteoporosis?
low bone mass, micro-architectural deterioration of bone ## Footnote *commonly due to peri/post-menopause or old age*
57
What are anti-resorptive agents to treat osteoporosis?
estrogen, bisphosphonates, raloxifene, calcitonin, denosumab
58
What are anabolic agents to treat osteoporosis?
teriparatide, abaloparatide, romosozumab
59
What is the mechanism of Paget's disease?
hyperdynamic bone remodeling leading to bony overgrowth
60
b) osteomalacia secondary to vitamin D deficiency ## Footnote * 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
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
c) obtain a 24 hour urine calcium ## Footnote *could check for familial hypocalciuric hypercalcemia*
62
a) familial hypocalciuric hypercalcemia b) primary hyperparathyroidism c) perimenopause d) vitamin D deficiency e) malignancy
b) primary hyperparathyroidism ## Footnote *serum calcium is high with an inappropriately normal PTH level*

ENDO (19 decks)

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