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Endo/Repro > Regulation of Calcium and Phosphate Metabolism > Flashcards

Regulation of Calcium and Phosphate Metabolism Flashcards

1
Q

What is the Chvostek sign?

what is it indicative of?

Trousseau sign? sign of?

A
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2
Q

Symptoms of Hypercalcemia?

A

decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethary, coma

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3
Q

Distribution of calcium in the body

  • what is the active form?
  • what can cross the membranes?
A

free ionized is active, ultrafilterable is able to cross membranes

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4
Q

Hypocalcemia does what to membrane excitability?

plasma calcium=?

what is hypocalcemic tetany?

-symptoms?

high plasma calcium does what to membranes, CNS?

A
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5
Q

What can change calcium concentration?

A

Changes in plasma protein concentration–> increase in plasma protein concentration produces increase in total calcium concentration that is protein bound, not the ionized calcium

changes in anion concentration–> change the fraction of calcium +2 complexed with anions (increased phosphate concentration decreases ionized Ca+2 concentration)

Acid base abnormalities

-change in binding sites available in albumin

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6
Q

how do acid base abnormalities alter ionized calcium concentrations?

A

in acidemia there is more hydrogen fighting for binding sites to albumin, opposite in alkalemia

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7
Q

What organ systems regulate homeostasis of calcium?

what three hormones?

A

bone, kidney, intestine

pth, calcitonin, vitamin D

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8
Q
A

stimulate bone resorption, leading to the release of calcium into the plasma

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9
Q

how are Extracellular concentrations of Pi related to Ca+2?

A
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10
Q

What cells secrete PTH?

A

secreted by chief cells in the parathyroid glands

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11
Q

What part of PTH does most of the biological activity?

A

1-34 aa

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12
Q

what is main stimulus of secretion of PTH?

A

low plasma Ca+2

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13
Q

Regulation of PTH gene expression and secretion:

  • feedback mechanism
  • how does chief cell sense levels of calcium?
  • what does vitamin D do?
A

The mechanism of PTH secretion is explained as follows: The parathyroid cell membrane contains Ca 2+ sensing receptors that are linked, via a G protein (G q), to phospholipase C. When the extracellular Ca 2+ concentration is increased, Ca 2+ binds to the receptor and activates phospholipase C. Activation of phospholipase C leads to increased levels of IP 3 /Ca 2+ , which inhibitsPTH secretion. When extracellular Ca 2+ is decreased, there is decreased Ca 2+ binding to the receptor, whichstimulates PTH secretion.

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14
Q

Chronic hypercalcemia leads to?

-affect on synthesis/storage of PTH, breakdown of PTH/ release

Chronic hypocalcemia leads to?

-synthesis/storage affects, PTH glands?

What role does magnesium have?

-alcoholism?

A
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15
Q

How does PTH act?

  • via what type of protein receptor?
  • affect on bone?
  • affect on Kidney?
  • affect on intestine?

Overall goal?

A
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16
Q

How does Vitamin D promote mineralization of new bone?

  • What does it do?
  • What must happen for it to be activated?
A

Coordinated actions in the regulation of both Ca+2 and Pi plasma concentrations

Increases plasma Ca+2, Pi plasma concentrations

Must be hydroxylated to an active metabolite

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17
Q

what is the mechanism of vitamin D synthesis?

  • what is converted in the skin and what does it require?
  • Where can you also get this product?
  • what process and where produces the main circulating form of vitamin D?
  • what happens in the kidney?
  • what is the important enzyme in the kidney?

(what stimulates this enzyme)

A
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18
Q

what happens to cholecalciferol in the liver and what does it require?

A

As noted, cholecalciferol itself is physiologically inactive. It is hydroxylated in the liver to form 25-hydroxycholecalciferol, which also is inactive. This hydroxylation step occurs in the endoplasmic reticulum and requires NADPH, O 2 , and Mg 2+ , but not cytochrome P-450. 25-Hydroxycholecalciferol is bound to an α-globulin in plasma and is the principal circulating form of vitamin D.

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19
Q

what happens in the kidney to 25-OH-cholecalciferol

A

In the kidney, 25-hydroxycholecalciferol undergoes one of two routes of hydroxylation: It can be hydroxylated at the C1 position to produce 1,25-dihydroxycholecalciferol, which is the physiologically active form, or it can be hydroxylated at C24 to produce 24,25-dihydroxycholecalciferol, which is inactive. C1 hydroxylation is catalyzed by the enzyme 1α-hydroxylase, which is regulated by several factors including the plasma Ca 2+concentration and PTH. C1 hydroxylation occurs in the renal mitochondria and requires NADPH, O 2 , Mg 2+ , and cytochrome P-450.

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20
Q

Regulation of 1a-hydroxylase

  • Basolateral side pathways of Ca+2 levels and PTH
  • high levels of PTH promote transcription of what gene and what does it do?
  • negative feedback mechanism onto 1a-hydroxylase, what does it repress and what does it favor?
A

high levels of PTH stimulate CYP1a gene to transcribe 1a-hydroxylase

high levels of Vitamin D repress 1a-hydroxylase facors the transcription of CYP24 gene, the enzyme that promotes formation of inactive for 24,25-hydroxylase.

21
Q

Short term action of PTH on bones?

Long term action of PTH on bones?

how does Vitamin D work with PTH?

A
22
Q

Synergistic actions of PTH and vitamin D on bone formation and resorption

-pth binding to osteoblasts promotes what?

(why is this important)

-preosteoclasts have a receptor for what ligand?

binding of this ligand leads to what?

A

binding of PTH promotes M-CSF, important because it helps stem cells differentiate into preosteoclasts

-preosteoclasts (mononuclear osteoclasts) have receptors for RANK ligand, binding of ligand leads to multi-nucleated osteoclast

23
Q

What is OPG (osteoprotegerin)?

relationship of RANK ligand and OPG

A
24
Q

what does PTH do to RANKL and OPG?

what does Vitamin D do to RANKL

A
  • PTH: increases RANKL, decreases OPG
  • Vitamin D increases RANKL
25
Q

Mechanism of action of PTH on kidney

A

The action of PTH on the renal proximal tubule begins at the basolateral membrane, where the hormone binds to its receptor. The receptor is coupled, via a G s protein, to adenylyl cyclase (Step 1). When activated, adenylyl cyclase catalyzes the conversion of ATP to cAMP (Step 2), which activates a series of protein kinases (Step 3). Activated protein kinases phosphorylate intracellular proteins (Step 4), leading to the final physiologic action at the luminal membrane, inhibition of Na + -phosphate cotransport (Step 5). Inhibition of Na + -phosphate cotransport results in decreased phosphate reabsorption and phosphaturia (increased phosphate excretion).

26
Q

Actions of vitamin D on kidney?

(stimulates what two things to be reabsorbed)

-PTH promotes…

A

pth promotes calcium absorption and phosphate secretion but vitamin D stimulates reabsorption of both

27
Q

What is the mechanism of action of Vitamin d on the intestine?

A
  • vitamin d is involved in the generation of calbindin, which is a shuttle protein that takes calcium intracellularly
  • vitamin D binds to the receptors, dimerizes with retinoid receptor, binds to response elements in particular genes. can either lead to synthesis of calbindin, or promote the synthesis of the sodium phosphate transport, which leads to taking phosphate from the luminal side into the basolateral side.
  • another product of gene transcription activation by vitamin D is the generation of the sodium calcium transporter. also the generate of calcium atpase on basolateral side.
  • promote the absorption of calcium from lumen into the basolateral side.
28
Q

Summary of PTH actions on Ca+2 and Pi homeostasis in:

Small intestine

Bone

Kidney

Parathyroid gland

A
29
Q

Summary of Vitamin D actions on Ca2+ and Pi homeostasis in:

Small intestine

Bone

Kidney

Parathyroid gland

A
30
Q

Calcitonin actions:

  • Primary acts on what?
  • affect on blood Ca+2 and Pi and how?
  • role in chronic regulation of plasma calcium?

thyroidectomy does what to calcitonin?

Thyroid tumors generally do what?

A
31
Q
A
32
Q

Regulation of calcium and phosphate metabnolism by gonadal and adrenal steroid hormones

  • Estradiol-17B does what to Calcium and where
  • Estradiol-17B is potent regulator of what?
  • Adrenal glucocorticoids have what affect on bone, kidney, and intestinal calcium?
A
33
Q

Primary hyperparathyroidism

  • patients excrete lots of what?
  • classic signs
  • treatment?
  • Effects on PTH, Ca2+, Pi, Vitamin D?
A

PTH increased, Calcium increased, Phosphate decreased, Vitamin D increased.

34
Q

Secondary Hyperparathyroidism:

increase in what secondary to what decrease in blood?

causes for low blood calcium?

A
35
Q

Secondary hyperparathyroidism:

Renal failure effect on PTH, Ca, Pi, Vitamin D

Vitamin D deficiency effect on PTH, Ca, Pi, Vitamin D

A
36
Q

Hypoparathyroidism:

  • causes?
  • what are most symptoms associated with?
  • Treatment?
  • effect on PTH, Ca, Pi, Vitamin D
A

decreases PTH, Ca, increases Pi, decreases Vitamin D

37
Q

Albright hereditary osteodystrophy (pseudohypoparathyroidism type 1a)

  • genetic inheritance and what is defective?
  • what happens to calcium and phosphate?
  • what happens to PTH
A
38
Q

Pseudohypoparathyroidism type 1a effect on:

PTH, Ca, Pi, Vitamin D

phenotype

A
39
Q

Humoral hypercalcemia of malignancy:

  • PTHrP and its pathophysiology
  • where does pTHrp come from?
  • what receptor does it activate?
  • produces similar affects to what disease?

how is it different from this disease?

-what is the treatment?

A
40
Q

Effects of humoral hypercalcemia of malignancy on PTH, Ca, Pi, Vitamin D

A
41
Q

Familial hypocalciuric hypercalcemia (FHH)

  • mutations that inactivate what?
  • result of those mutations?

FHH effect on PTH, serum Ca, Urine Ca, Pi, Vitamin D

A

FHH has either No effect on PTH or an increase

it increases serum Ca but decreases Urine Ca

no effect on Pi and Vitamin D

42
Q
A

D. reduced renal activity of 1a-hydroxylase activity

43
Q
A

D. Muscle spasms and tetany

44
Q

Pathophysiology of Vitamin D: rickets osteomalacia:

-what is impaired? (reasons)

Rickets in children vs rickets in adults?

A
45
Q

Rickets:

Congenital disorders:

-Pseudovitamind D-deficient rickets or vitamin D-dependent rickets type I vs type II

A
46
Q

Vitamin D deficiency:

effect on PTH, Ca, pi, urine pi/camp, vitamin D, bone

A
47
Q

Treatment for Rickets-Osteomalacia

A

Vitamin D2 (ergocalciferol) or D3 (cholecalciferol)

Ca+2

sunlight

1,25-(OH)2-D3 (calcitriol)

48
Q

Treatment of osteoporosis:

anabolic therapy, antiresorptive therapy

A

Endo/Repro (10 decks)

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