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NE Exam 3 > Ca Phosphate Homeostasis > Flashcards

Ca Phosphate Homeostasis Flashcards

1
Q

What is the distribution of Ca in the body?

A

99% of Ca is in the bones and teeth

The rest is in the ECF, ICF and plasma

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2
Q

What is the biologically active form of Ca?

A

Free ionized Ca

50% of the ultrafilterable total Ca in the body

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3
Q

What percentage of Ca is bound to protein?

A

40%

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4
Q

Extracellular Ca concentrations have a dramatic effect on what?

A

The excitability of cells (particularly nerve fibers)

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5
Q

Describe Ca homeostasis during the aging process

A

There are decreases in the amount of Ca absorbed from dietary intake and in dietary intake of Ca
Existing bone cells are reabsorbed by the body faster than new bone is made
Aging contributes to osteopenia or osteoporosis

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6
Q

What is Hypocalcemia and what are the sx?

A

Low plasma Ca concentration

Sx: hyperreflexia, spontaneous twitching, muscle cramp, tingling and numbness

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7
Q

What are the indicators of Hypocalcemia?

A

Chvostek sign and trousseau sign

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8
Q

What is the Chvostek sign?

A

Twitching of the facial muscles elicited by tapping on the facial nerve

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9
Q

What is the trousseau sign?

A

Carpopedal (muscle) spasm upon inflation of a BP cuff

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10
Q

What is hypercalcemia and what are the sx?

A

Elevates plasma Ca concentration
Sx: decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy and coma

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11
Q

How does Hypocalcemia effect membrane excitability of cells?

A

Reduces the activation threshold for Na channels -> easier to provoke AP
Results in increased membrane excitability (spontaneous APs)
Generation of spontaneous AP is the physical basis for hypocalcemic tetany (spontaneous muscle contractions due to low extracellular Ca)
Produces tingling and numbness (on sensory neurons) and spontaneous muscle twitches (on motorneurons and muscle)

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12
Q

How does hypercalcemia influence the membrane excitability of cells?

A

Opposite of hypocalcemia mechanism (decreased membrane excitability)
Nervous system becomes depressed and reflex responses are slowed

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13
Q

How can the forms of Ca in the plasma be altered?

A

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

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14
Q

How do changes in plasma protein concentrations alter the forms of Ca in the plasma?

A

Alter total Ca concentration in the same direction (e.g. increase plasma protein concentration, increase total Ca concentration)

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15
Q

How do changes in anion concentration alter the forms of Ca in the plasma?

A

Change in the fraction of Ca complexed with anions (eg. If phosphate concentrations increase, ionized Ca concentrations decrease)

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16
Q

How do acid-base abnormalities alter the forms of Ca in the plasma?

A

Alter the ionizes concentration by changing the fraction of Ca bound to albumin

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17
Q

What effects does acidemia have on Ca?

A

Free ionized Ca concentration increases because less Ca is bound to albumin

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18
Q

What effect does alkalemia have on Ca concentration?

A

Free ionized Ca concentration decreases and is often accompanied by hypocalcemia
(More bound to albumin)

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19
Q

In order to maintain ca balance the kidneys must excrete the same amount of Ca that is what?

A

Absorbed by the GI tract

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20
Q

What is the state of bone remodeling during Ca homeostasis?

A

No net gain or loss of Ca
New bone is formed (deposited)
Old bone is resorbed

21
Q

What level of Ca is maintained in the ECF?

22
Q

Ca homeostasis depends on the actions of which three organs?

A

Absorption and secretion in the intestines
Filtration and reabsorption in the kidneys
Bone deposition and resorption

23
Q

What is the relationship between Ca and phosphate?

A

Extracellular concentration of Pi is inversely related to that of Ca
Extracellular concentration of Pi is regulated by the same hormones that regulates Ca concentration
Normal range of extracellular Pi is 2.4-4.5

24
Q

What is the distribution of Pi in the body?

A

85% in bone, 15% in ICF and less than 1% in plasma (mostly ionized form)

25
What is the function of chief cells of the parathyroid gland?
Synthesize and secrete PTH
26
What is the function of PTH?
Regulate concentration of Ca and Pi in plasma
27
Describe the structure of PTH
PTH is a peptide hormone Single chain polypeptide with 84 aa (1-34 are the molecules biological activity) Synthesized on ribosomes as prepro-PTH then it is cleaved to form proPTH followed by transportation to Golgi and further cleavage into PTH which is then packaged in secretory granules
28
What stimulates the secretion of PTH from the parathyroid glands?
Decreased plasma Ca (below 10mg/dL)
29
Increased extracellular Ca concentration inhibits what process?
PTH synthesis and secretion
30
Describe the regulation of PTH gene expression and secretion
1. Ca binding to CaSR -> downstream signaling pathway via G proteins -> inhibit the PTH gene 2. 1,25 vitamin D enters nucleus and inhibits PTH gene and promotes CaSR gene
31
What effect does chronic hypercalcemia have on PTH?
Causes decreased synthesis and storage of PTH | Increases breakdown of stored PTH and release of inactive PTH fragment into the circulation
32
What effect does chronic hypocalcemia have on PTH?
Causes increased synthesis and storage of PTH and hyperplasia of parathyroid glands (2ndary hyperparathyroidism)
33
What are the actions of PTH on bone?
Increased bone resorption to increase plasma Ca
34
What are the actions of PTH on the kidneys?
Decreased Pi reabsorption Increased Ca reabsorption and urinary cAMP Done to increase Ca levels toward normal
35
What are the actions of PTH on the intestines?
Increased Ca absorption (indirect via vitamin D) to increase Ca levels
36
What are the actions of vitamin D?
Promotes mineralization of new bone through its coordinated actions in regulating both Ca and Pi concentrations Increases both Ca and Pi concentrations Increases Ca x Pi production to promote mineralization of bone Has actions in the intestine, kidney and bone
37
Describe the structure of vitamin D
Also known as cholecalciferol Is a prohormone Must be successively hydroxylated to an active metabolite Regulated by negative feedback mechanisms
38
Describe the signaling pathway of vitamin D
Vitamin D enters the cell nucleus and binds to a VDR VDR dimerizes with RXR and together with vitamin D bone to responses elements on DNA Lead to stimulation/suppression of gene transcription
39
What is the main circulating form of vitamin D?
25-OH-cholecalciferol | But has very low activity and is not the active form
40
Describe the synthesis of the active form of vitamin D
7-dehydrocholesterol —> via UV light becomes cholecalciferol (can also be obtained from diet) —> via liver 25 hydroxylase converts it to 25-OH-cholecalciferol —> gets converted to 1-alpha hydroxylase (CYP1a) into 1,25-OH(2)-cholecalciferol in the kidneys
41
What stimulates 1a hydroxylase in the renal proximal tubule?
Decreased Ca and phosphate | Increased PTH
42
How is kidney 1a-hydroxylase regulated at the transcriptional level?
1. Ca binding to CaSR which triggers a signaling pathway which inhibits the CYP1a gene 2. PTH which via a cAMP/PKA signaling pathway promotes the CYP1a gene 3. 25(OH) vitamin D which can form the active form of vitamin D which then inhibits the CYP1a gene and promotes the CYP24 gene to make 24 hydroxylase (makes inactive form in kidneys)
43
What are the short term actions of PTH on bone?
Bone formation via direct action on osteoblasts (contain PTH receptors) Basis for the use of intermittent synthetic PTH administration in osteoporosis treatment
44
What are the long term actions of PTH on bone?
Increase bone resorption (indirect action on osteoclasts mediated by cytokines like IL-6R released from osteoblasts)
45
What effect does vitamin D have on bone?
Acts synergistically with PTH to stimulate osteoclast activity and bone resorption
46
What is the role of macrophage colony stimulating factor (M-CSF) on bone formation/resorption?
Induces stem cells to differentiate into osteoclast precursors, mononuclear osteoclasts and finally mature multinucleated osteoclasts
47
What is the role of RANKL during bone formation and resorption?
Cell surface protein produced by osteoblasts, bone lining cells and apoptotic osteocytes Primary mediator of osteoclast formation Increased by PTH and vitamin D
48
What is the function of RANK during bone formation and resorption?
Cell surface protein receptor on osteoclast and osteoclast precursors
49
What is the role of osteoprotegerin (OPG) during bone formation and resorption?
Soluble protein produced by osteoblasts Decoy receptor for RANKL Inhibits RANK/RANKL interaction (preventing formation of osteoclasts) Decreased by PTH

NE Exam 3 (16 decks)

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