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Endo/Repro Midterm > Regulation Of Calcium And Phosphate Metabolism > Flashcards

Regulation Of Calcium And Phosphate Metabolism Flashcards

1
Q

How is Ca compartmentalized?

A

ECF: 0.1%
Plasma: 0.5%
ICF: 1%
Bones and teeth: 99%

Ca exists in ionized form, bound to plasma proteins or in nonionized form

Protein-bound: 40%
Ultrafilterable: 60% -> complexed non-ionized form 10%, ionized 50%

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2
Q

Describe how total and ionized Ca is altered in the plasma?

A

Total Ca is altered by changing the plasma protein concentration to alter the total Ca concentration in the same direction as protein conc

Ionized Ca is altered by changing the fraction of Ca complexed with anions:

Increasing plasma Pi, increases the fraction of complexed Ca and decreases ionized Ca

Albumin binds Ca and H; in academia (high H+) albumin binds more H+, increasing ionized Ca
In alkalemia (low H+) albumin binds more Ca, decreasing ionized Ca)
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3
Q

How do Ca levels influence membrane excitability?

What regulates this?

A

Hypocalcemia: increases neuromuscular excitability -> hypocalcemic tetany/spasticity (lowers RMP, so easier to reach threshold)

Hypercalcemia: depresses neuromuscular excitability (raises RMP, so harder to reach threshold)
PTH, calcitonin, calcitriol

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4
Q

What diseases are associated with elevated Ca?

Low Ca?

A

Primary hyperparathyroidism, malignancy

Hypoparathyroidism, renal disease, vitamin D deficiency

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5
Q

Ca homeostasis is tightly regulated and involves the actions of what organs?

What hormones?

A

Bone, kidney, intestines

PTH, calcitriol, calcitonin

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6
Q

Where is phosphate stored?

How is it stored in serum?

A

85% bone
14% cells
< 1% serum -> 84% ionized, 10% protein-bound, 6% complexed to cations

Extracellular concentration of Pi is inversely correlated to that of Ca. Extracellular concentration of Pi is regulated by same hormones that regulate Ca concentration

(High Pi, low Ca and vice versa)

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7
Q

Fine-tuning circulating Pi is under the control of ____.

A

Renal excretion

Na/Pi cotransporters in the apical membrane

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8
Q

Four regulators of phosphate metabolism

A

Dietary: Pi intake and absorption

Calcitriol: increase phosphorus resorption from bone and absorption from intestine; increases Pi reabsorption in kidneys

PTH: Pi resorption directly from bone; indirectly activates intestinal absorption through stimulation of calcitriol production

Renal tubular: reabsorption of Pi, stimulated by tubular filtered load of Pi and inhibited by PTH

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9
Q

What are fibroblast growth factors?

A

Promote to growth of fibroblasts

Role in growth, development, cell survival, endocrine signaling

Bind to FGF-receptors (FGFRs)

Mutation in FGFR3 causes achondroplasia

FGF-23 is an endocrine growth factor and uses Klotho as a cofactors

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10
Q

What is FGF-23 and where is it from?

What regulates it?

What are its three renal effects?

A

Derived from bone

Phosphate and vitamin D levels regulate expression of FGF-23 and therefore regulate phosphate homeostasis

  1. Directly downregulates NaPi transporters in the kidney
  2. Stimulates PTH to downregulates NaPi transporters in the kidney
  3. Decreases calcitriol production in the kidney

Used in hyperphosphetemia because it decreases Pi

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11
Q

What does PTH do?

What secretes it?

A

Regulator of Pi and Ca homeostasis

Synthesized and secreted from chief cells of parathyroid gland

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12
Q

Cleavage of PTH

A

Chief cells store PTH in vesicles

Can regulate Ca levels minute by minute

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13
Q

How does low plasma Ca simulate PTH secretion?

Mutation in CaSR causes what?

A

Though Ca-sensing receptor (CaSR): uses G protein to activate PTH genes

Increased ECF Ca inhibits PTH secretion

Low Ca will stimulate PTH secretion

Hypocalciuric hypercalcemia (FHH)

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14
Q

Chronic hypercalcemia

Chronic hypocalcemia

A

Decreases synthesis/storage of PTH and breaks down any stored PTH

Increases synthesis/storage of PTH resulting in hyperplasia of parathyroid glands

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15
Q

Magnesium effects on PTH

A

Similar to Ca

Severe hypomagnesemia inhibits PTH synthesis, storage, and secretion

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16
Q

PTH signals through a ____.

A

GPCR

17
Q

Actions of PTH on bone, kidney, and intestine

A

Low Ca -> increase PTH ->

Bone: increase bone resorption; increase Ca and Pi in blood

Kidney: decrease Pi reabsorption; increase Ca absorption; increase urinary cAMP (biomarker of PTH secretion)

Intestine: increase Ca absorption

18
Q

Actions of vitamin D

A

Promotes mineralization of new bone through Ca/Pi

Opposing effects on Pi levels

Increase Ca/Pi products to promote mineralization of new bone

19
Q

Names for biologically active forms of vitamin D

A

1,25-dihydroxycholecalciferol

1,25 hydroxy vitamin D

1,25(OH)2D3

Calcitriol

20
Q

Synthesis of vitamin D

A

?????

1alpha-hydroxyase

21
Q

Regulation of 1alpha-hydroxylase is tightly regulated

A

Feedback loop dihyroxyvitamin D inhibits 1alpha-hydroxylase

High Ca inhibits the enzyme

22
Q

Trrty

A

Utyu

23
Q

PTH receptors are located on ___.

Short-term actions?
Long-term actions?

What acts synergistically with PTH to simulate osteoclast activity?

A

Osteoblasts

Direct effect on osteoblasts bone formation

Indirect effect on osteoclast bone resorption

Vitamin D

24
Q

Agents involved in bone formation and resorption

A

M-CSF: simulates stem cells to become osteoclast precursors

RANKL: cell surface protein produced by osteoblasts; primary mediator of osteoclast formation

RANK: cell surface protein on osteoclasts and osteoblasts precursors

OPG: soluble protein produced by osteoblasts; decoy receptor for RANKL; inhibits RANKL/RANK interaction

25
Q

PTH inhibits ____ on the apical membrane of the kidney.

What does this cause?

PTH also stimulates reabsorption of ____ in the distal tubule.

PTH stimulates what enzyme to make vitamin D?

A

Na/Pi absorption (NPT)

Phosphaturia

Ca

1alpha-hydroxylase

26
Q

Action of vitamin D on the intestines

A

Kolkka

27
Q

Function of calcitonin

A

Released from thyroid gland

Lowers Ca and Pi levels by inhibits bone resorption

Parafollicular C cells of the thyroid express CaSR -> senses elevated extracellular Ca -> synthesis and secretion of calcitonin

Decreases activity of osteoclasts

Promotes renal excretion of Ca/Pi

28
Q

Primary hyperparathyroidism

A

Hypersecretion of PTH

Results in hypercalcemia and hypophosphatemia due to bone demineralization, increased GI and renal Ca reabsorption

Stones

29
Q

Secondary hyperparathyroidism

What can cause low blood Ca?

A

Increased PTH secondary to low blood Ca

Renal failure, vitamins D deficiency

30
Q

Hypoparathyroidism

Symptoms?

A

Caused by thyroid/ parathyroid surgery

From low Ca: muscle cramps, increased neuromuscular excitability

31
Q

Pseudohypothyroidism type I (Albright hereditary osteodystrophy, AHO)

Phenotype

A

Tissues are PTH resistant because problem with PTH receptor

Defective cAMP signal transduction

Increases PTH secretion, low Ca levels

Short neck

32
Q

Humoral hypercalcemia of malignancy

Treatment?

A

High PTH-related peptide which is produced by tumors

Decrease bone formation, PTH, vitamin D

Furosemide

33
Q

Problems due to vitamin D

Treatment?

A

Impaired vitamin D metabolism: vitamin D resistant

Rickets: low Ca/Pi, growth failure

Osteomalacia: new bone fails to mineralize

Vitamin D

34
Q

Peudovitamin D deficiency

A

Rickets

35
Q

Osteoporosis

A

Depends on age, sex

Decrease bone mass

36
Q

What directly or indirectly controls Pi activities?

What increases renal Pi reabsorption?

What decreases renal Pi reabsorption?

A

PTH, vitamin D, FGF-23
PTH reduces Na/Pi activity leading to Na excretion

Insulin, GH, TH

Calcitonin, glucocorticoids, ANP

Endo/Repro Midterm (11 decks)

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