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Neuroendocrine Exam 3 > Calcium and Phosphate Homeostasis > Flashcards

Calcium and Phosphate Homeostasis Flashcards

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1
Q

what is the biologically active form of calcium?

A

free, ionized Ca2+

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2
Q

What effect does aging have on calcium levels?

A

during aging, there are decreases in the amount of calcium absorbed from dietary intake and in dietary intake of calcium

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3
Q

What effect does the decreased calcium absorption/intake levels have in association with aging?

A

aging contributes to osteopenia or osteoporosis

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4
Q

what are the symptoms of hypocalcemia?

A

hyperreflexia, spontaneous twitching, muscle cramp, tingling and numbness

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5
Q

what two signs are associated with hypocalcium?

A

Chvostek sign and trousseau

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6
Q

what are the symptoms of hypercalcemia?

A

constipation, lack of appetite, polyuria, muscle weakness, hyporeflexia, lethargy

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7
Q

what effect does a low extracellular Ca2+ level have on the action potential?

A

it reduces the activation threshold for Na+–> so its easier to evoke an AP

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8
Q

what effect does a high extracellular Ca2+ level have on the acton potential?

A

it raises the activation threshold–> decreased the membrane excitability–> harder to evoke an action potential

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9
Q

the forms of Ca2+ in the blood can be altered by what?

A

changes in plasma protein concentration, changes in anion concentration, acid-base abnormalities

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10
Q

what is the ionized Ca2+ concentration going to look like in an acidemia situation?

A

free ionized Ca2+ concentration increases (because less Ca2+ is bound to albumin

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11
Q

what is the ionized Ca2+ concentration going to look like in an alkalemia situation?

A

free ionized Ca2+ concentration decreases (because less Ca2+ is bound to albumin)

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12
Q

To maintain Ca2+, what must the kidneys do?

A

they must excrete the same amount of Ca2+ that is absorbed by the GI tract

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13
Q

Ca2+ homeostasis involves the coordinated interaction of three organ systems. What are they?

A

Bone, kidney, intestine

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14
Q

Ca2+ homeostasis involves the coordinated interaction of 3 hormones. What are they?

A

PTH, calcitonin, and vitamin D

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15
Q

How is extracellular phosphate (Pi) related to extracellular free ionized Ca2+?

A

they are inversely related

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16
Q

what is the role of the Parathyroid glands?

A

they secrete PTH

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17
Q

what specific cell type in the parathyroid gland secretes PTH?

A

chief cells

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18
Q

What type of hormone is PTH?

A

peptide hormone

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19
Q

what is the stimulus for secretion of PTH?

A

low plasma Ca2+ levels

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20
Q

What senses the amount of extracellular Ca2+ levels?

A

Calcium-sensing receptor (CaSR)

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21
Q

when is the CaSR activated?

A

whenever there are high levels of extracellular Ca2+

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22
Q

what happens when the CaSR is activated?

A

there is going to be a downstream signaling pathway that either shuts down the production of PTH or it can also inhibit the PTH gene

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23
Q

What effect does vitamin D have on PTH production?

A

the active form of vitamin D is going to exert a negative feedback mechanism on the regulation of PTH

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24
Q

Chronic hypercalcemia causes what to PTH?

A

causes decreased synthesis and storage of PTH and increased breakdown of stored PTH

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25
chronic hypocalcemia causes what to PTH?
causes increased synthesis and storage of PTH and hyperplasia of the parathyroid glands
26
what type of receptor is the PTH receptor?
it is a GPCR
27
what does recognition of PTH by the PTH GPCR lead to?
increased levels of cAMP through the activation of AC
28
where are PTH receptors mostly found?
in the bone and the kidney tubule
29
what is a byproduct of the activation of PTH?
cAMP
30
what is the significance of cAMP being a byproduct of activation of PTH?
you are going to see increased levels of cAMP in the urine, so therefore increased urine cAMP could indicate increased levels of PTH
31
what is the effect of PTH secretion on bone?
increased bone resorption
32
what is the effect of PTH secretion on the kidney?
decreased Pi reabsorption (phosphaturia), increased Ca2+ reabsorption, increased urinary cAMP
33
what is the effect of PTH secretion on the intestine?
increased Ca2+ absorption
34
What type of hormone is vitamin d?
steroid hormone
35
what is the stimulus for the production of the active form of vitamin D?
decreased levels of Ca2+, increased levels of PTH and decreased levels of Phosphate
36
what is the main circulating form of vitamin D?
25-OH-cholecalciferol but it is inactive
37
what converts 25-OH- cholecalciferol into its active form? and where does this occur?
CYP1 alpha (aka 1alpha-hydroxylase) and this occurs in the renal proximal tubule
38
how is kidney 1alpha-hydroxylase enxyme tightly regulated?
at the transcriptional level
39
where exactly on bones is the PTH receptor located?
on the osteoblasts
40
what are the short-term actions of PTH on bone?
bone formation (via direct action on osteoblast)
41
what are the long-term actions of PTH on bone?
increased bone resorption (due to indirect action on osteoclasts mediated cytokines released from osteoblasts)
42
What is M-CSF?
it induces stem cells to differentiate into osteoclast precursors
43
What is the primary mediator of osteoclast formation?
RANKL
44
Where is RANK found?
it is a cell surface protein receptor on osteoclasts and osteoclast precursors
45
What are the specific actions of PTH on bone formation and resorption?
increased RANKL and decreased OPG
46
what is OPG?
produced by osteoblasts- inhibits RANKL/RANK interaction
47
what are the specific actions of vitamin D on bone formation and resorption?
increased RANKL
48
how does PTH cause phosphaturia?
by inhibiting the Na+ Phosphate transporter
49
How does PTH stimulate the kidney?
it stimulates the 1alpha-hydroxylase activity
50
what is the effect of vitamin D on the intestines?
it is going to promote calcium absorption as well as Pi absorption
51
how does vitamin D promote calcium absorption in the intestines?
it promotes the protein synthesis of the TRPV6-Ca2+ channel
52
what is the stimulus for calcitonin release?
high levels of Ca2+ in plasma
53
where is calcitonin released from?
the parafollicular cell (c cells) in the thyroid gland
54
what are the effects of calcitonin on bone?
it inhibits bone resorption
55
where are calcitonin receptors found on bone?
osteoclasts
56
what is the main effect of calcitonin on bone?
it promotes bone formation
57
what would you expect the calcitonin levels to be after a thyroidectomy?
decreased, but no effect on Ca2+ levels
58
what would you expect the calcitonin levels to be with a thyroid tumor?
increased levels, but no effect on Ca2+ levels
59
what are the effects of Estradiol-17 B on the intestines and kidney?
it stimulates intestinal Ca2+ absorption and renal tubular Ca2+ reabsorption
60
what is the most potent regulator of osteoblast and osteoclast function?
estradiol-17B
61
what is the effect of estrogen on bone?
estrogen promotes the survival of osteoblasts and apoptosis of osteoclasts
62
what is the affect of the adrenal glucocorticoids (cortisol) on bone, kidney, and intestines?
they promote bone resorption, renal Ca2+ wasting, and inhibit intestinal Ca2+ absorption
63
patients treated with high levels of a glucocorticoid (aka a patient with addison disease) could develop what?
osteoporosis
64
what is primary hyperparathyroidism?
adenoma of the parathyroid gland- over secretion of PTH
65
what would expect to see with a patient with primary hyperparathyroidism?
stone, bones, and groans(constipation); hypercalciuria- leads to kidney stones; increased bone resorption
66
what levels would you expect to see with a patient with primary hyperparathyroidism?
increased PTH, increased Ca2+, decreased Pi, increased Vitamin D
67
what are some causes of low Ca2+ in the blood that could cause secondary hyperparathyroidism?
renal failure or vitamin d deficiency
68
what levels would you expect to see in a patient with renal failure?
increased PTH, decreased Ca2+, increased Pi, decreased vitamin D
69
what levels would you expect to see in a patient with vitamin d deficiency?
increased PTH, decreased Ca2+, decreased Pi, decreased vitamin D
70
what do the symptoms of hypoparathyroidism resemble?
hypocalcemia
71
What levels would you expect to see in a patient with hypoparathyroidism?
decreased PTH, decreased Ca2+, decreased vitamin D, increased Pi
72
what is the treatment of hypoparathyroidism?
oral Ca2+ supplement and active form of vitamin D
73
what is albright hereditary osteodystrophy?
an inherited autosomal dominant disorder where the Gs for the PTH receptor in the bones and kidneys is defective
74
what is the result of albright hereditary osteodystrophy?
hypocalcemia and hyperphosphatemia
75
what would you expect to the PTH levels to be in a patient with albright hereditary osteodystrophy?
high PTH levels (PTH resistance)
76
what would the treatment of albright hereditary osteodystrophy with PTH result in?
it would produce no response and no increase in urinary cAMP
77
what would you expect the levels to be in a patient with albright hereditary osteodystrophy (pseudohypoparathyroidism type 1a)
increased PTH levels, decreased Ca2+ levels, increased Pi levels, decreased vitamin D levels
78
what is the phenotype of pseduohypoparathyroidism?
short stature, short neck, obesity
79
some malignant tumors secrete what?
PTH-related peptide (PTH-rp)
80
what would you expect the levels of PTH and vitamin D to be in humoral hypercalcemia of malignancy?
low
81
what is familial hypocalciuric hypercalcemia (FHH)
a mutation that inactivates the CaSR in the parathyroid glands
82
what does familial hypocalciuric hypercalcemia
decrease in urinary Ca2+ excretion (hypocalciuria) and increased serum [Ca2+] levels
83
in children vitamin D deficiency causes what?
rickets
84
what is rickets?
there is an insufficient amount of Ca2+ and Pi available to mineralize growing bones
85
In adults vitamin D deficiency results in what?
osteomalacia
86
What is osteomalacia?
new bone fails to mineralize, resulting in bending and softening of the weight-bearing
87
what are two things you could use to treat osteoporosis?
estrogen and RANKL inhibitors (Denosumab)

Neuroendocrine Exam 3 (19 decks)

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