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*Neuroendocrine Exam 3 > 15. Regulation of Calcium and Phosphate Metabolism > Flashcards

15. Regulation of Calcium and Phosphate Metabolism Flashcards

1
Q

Ca2+ distribution in the body

A

40% is bound to protein.

60% is “ultrafilterable”, with 10% being attached to anions and 50% being free Ca2+

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2
Q

Sx of hypocalcemia

A

Hyporeflexia, twithcing. tingling, numbness.
+ Chvostek sign (facial twitching via facial n.)
+ Trousseau sign (carpopedal spasm upon inflation of BP cuff).

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3
Q

Sx of hypercalcemia

A

Lowered QT int., constipation, decreased appetite, polyuria, weakness, hyporeflexia.

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4
Q

How does low Ca2+ lead to numbness, tingling and twitching?

A

Low Ca2+ lowers the threshold for Na+ channels making it easier to fire an AP –> increased excitability –> spontaneous APs –> tetany.

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5
Q

How does increased Ca2+ affect membrane excitability?

A

Increases threshold for Na+ channels –> decreased excitability.

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6
Q

What does acidemia mean for free Ca2+ levels?

A

More H+ is bound to albumin, so more Ca2+ is free.

Increases plasma [Ca2+].

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7
Q

What does alkalemia mean for free Ca2+ levels?

A

Less H+ is bound to albumin, so less Ca2+ is free.

Decreases plasma [Ca2+].

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8
Q

How does bone remodeling change Ca2+ levels?

A

It doesn’t.

Amt of Ca2+ resorbed = Amt of Ca+ deposited

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9
Q

What must occur at the kidneys and GI tract to maintain Ca2+ balance?

A

Kidneys must excrete the same amt of Ca2+ as is absorbed by the GI.

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10
Q

How are Ca2+ levels and PO4- levels related?

A

Inversely

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11
Q

What secretes and produces PTH?

A

Chief cells of the PTG.

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12
Q

How does PTH become secreted by the PTG?

A

PreproPTH (115 aa) –> proPTH (90 aa) –> PTH (84 aa) –> Golgi secretes PTH via granules.

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13
Q

What happens in chronic hypercalcemia?

What is another name for it?

A

A decrease in synthesis/storage of PTH.
Increased breakdown of stored PTH and it releases fragmented PTH into circulation.

Secondary hypoparathyroidism.

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14
Q

What happens in chronic hypocalcemia?

What is another name for it?

A

An increase in synthesis/storage of PTH.
Hyperplasia of the PTG.

Secondary hyperparathyroidism.

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15
Q

What is the “general” effect of Mg2+ on PTH secretion?

A

Usually follows PTH rules.

Low Mg2+ triggers an increase in PTH.

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16
Q

What is the exception of Mg2+ and PTH secretion?

A 
Severe hypomagnesemia (alcoholism).
Inhibits PTH synthesis/storage.
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17
Q

PTH effects on bone, kidneys, GI tract:

A

Bone: + bone resorption.
Kidneys: + Ca2+ reabsorption, - Pi reabsorption, increase urinary cAMP.
GI: indirectly + Ca2+ absorption by activating Vit D.

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18
Q

What is the goal of Vit D?

A

To increase Ca2+, Pi.

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19
Q

What kind of hormone is Vit D?

A

Steroid.

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20
Q

What is the main circulating form of Vit D, which is inactive?

A

25-OH-cholecalciferol

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21
Q

What is the Vit D we get from diet?

A

Cholecalciferol.

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22
Q

What enzyme activates Vit D?

A

1a-hydroxylase

AKA CYP1a

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23
Q

What is the stimuli for 1a-hydroxylase activity? (3)

A

Low Ca2+
Low Pi
High PTH

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24
Q

Where is 1a-hydroxylase regulated? What level is it regulated at?

A

Kidneys at the transcriptional level.

25
Q

Where is the PTR R located?

A

On osteoblasts.

26
Q

S-T actions of PTH on bone:

What can PTH be used as a therapy for, then?

A

Bone formation.

Osteoporosis.

27
Q

L-T actions of PTH on bone:

A

Increased bone resorption by indirect action on osteocytes by cytokines from osteoblasts.

28
Q

What is the function of M-CSF?

A

Activates stem cells to differentiate into osteoclasts.

29
Q

What is the function of RANKL and RANK?

A

Primary mediators of osteoclast formation.

RANKL is a protein produced by bone cells to + remodeling. RANK is the R on osteoclasts.

30
Q

What is the function of OPG?

What produces it?

A

To inhibit RANKL/RANK.

Produced by osteoblasts.

31
Q

Osteoclast formation can be approximated by:

A

RANKL/OPG

32
Q

What effects does PTH have on RANKL and OPG?

A

PTH: + M-CSF, increases RANKL, decreases OPG.

33
Q

How does PTH inhibit Pi reabsorption in the PT?

A

PTH binds and triggers GPCR. cAMP activates a protein kinase that inhibits the NPT2a channel (symport w/ Na+ and Pi) on the luminal membrane.

34
Q

How does PTH increase urinary cAMP?

A

cAMP in the PT is excreted in the urine –> increase urinary cAMP.

35
Q

Besides the PT, where else can PTH act along the nephron to increase Ca2+? Why?

A

DT/TAL to complement the increase in [Ca2+] from bone resorption and phosphaturia.

36
Q

What protein is upregulated in the GI by Vit D to increase Ca2+ and Pi absorption?

A

Calbindin

37
Q

How does Vit D stimulate Pi reabsorption in the kidneys? What kind of effect does it have on Ca2+ reabsorption?

A

+ NPT2a

MInimally affects Ca2+ in the kidney.

38
Q

How does Vit D affect the PTG?

A

+ CaSR expression, which increases Ca2+ secretion.

39
Q

Where does calcitonin act?

A

Bone and kidney.

40
Q

What is the goal of calcitonin and how does it do that?

A

To lower Ca2+ and Pi.

Inhibits bone resorption (binds its R on osteoclasts) and reabsorption at the kidney.

41
Q

What kind of role does calcitonin play in chronic regulation of plasma Ca2+?

A

It does NOT play a role.

42
Q

What happens to calcitonin levels post thyroidectomy?

A

Lowers calcitonin but does not change Ca2+ metabolism.

43
Q

What happens to calcitonin levels w/ a thyroid tumor?

A

Increases calcitonin but does not change Ca2+ metabolism.

44
Q

What is the effect of Estradiol-17B on Ca2+ regulation?

A

+ GI to absorb Ca2+ and kidneys to reabsorb.

Promotes survival of osteoblasts (favors bone formation > resorption).

45
Q

What is the effect of glucocorticoids (cortisol) on Ca2+ regulation?

A

Promotes bone resorption, + renal Ca2+ wasting, and inhibits Ca2+ absorption in the GI.
Pt can develop osteoporosis.

46
Q

What do patients excrete in high quantities with Primary HyperPTHism? (3)
What are symptoms?
What is the treatment?
What effect does it have on PTH, Ca2+, Pi and VitD levels?

A

Increased excretion of Pi, cAMP, Ca2+.
Ca2+ stones, constipation.
PT-ectomy.
+PTH, +Ca2+, -Pi, +VitD.

47
Q

What happens in Secondary HyperPTHism?

What are the causes? (2)

A

Increase in PTH is secondary to decrease [Ca2+].

Renal failure, Vit D deficiency.

48
Q

Effects on PTH, Ca2+, Pi, Vit D in a patient with:
RF
Vit D deficiency

A

RF: +PTH, -Ca2+, +Pi, -Vit D

Vit D deficiency: +PTH, -Ca2+, -Pi, -Vit D

49
Q

Causes of hypoPTHism:
Sx of hypoPTHism:
TTM of hypoPTHism:
HypoPThism effects on PTH, Ca2+, Pi, Vit D

A

Thyroid or Pt surgeries. Rarely autoimmune/genetic dz.
Same as those associated with low Ca2+.
TTM is oral Ca2+.
-PTH, -Ca2+, +Pi, -Vit D

50
Q

Albright hereditary osteodystrophy (AKA Pseudohypoparathyroidism type 1a) effects PTH levels how?
What do patients develop?

A

The Gs for PTH is ineffective in bone and kidneys.

Pts develop HYPOcalcemia and HYPERphosphaturia.

51
Q

How do patients develop hyperphosphaturia in Pseudohypoparathyroidsm?

A

PTH cannot activate the Gs to activate cAMP/AC to inhibit NPT2a, so the reabsorption of Pi is accelerated.

52
Q

What is the phenotype of a pt w/ Pseudohypoparathyroidism?

What is its effects on PTH, Ca2+, Pi, Vit D?

A

Short stature, obese, shortened hands/feet.

+ PTH, -Ca2+, +Pi, -Vit D

53
Q

What happens in Humoral Hypercalcemia of Malignancy physiologically?
What is its effect on PTH, Ca2+, Pi, Vit D?
What is the TTM?

A

PTHrP is produced by tumor cells and binds and activates PTH R.
Causes inhibition of PTH.-
-PTH, +Ca2+, -Pi, -Vit D
Lasix or Etidronate to inhibit Ca2+ absorption/reabsorption/resorption).

54
Q

What happens in Familial Hypocalciuric Hypercalcemia?

How does it effect serum and urinary Ca2+ levels?

A

Mutations arise that inhibit CaSR in the PTG.

There is an increase serum Ca2+ and a decrease in urinary Ca2+

55
Q

What are 2 causes of Rickets?

A

Dietary deficiency in Vit D.

Vit D resistance by inhibition of 1a-hydroxylase or mutations in the Vit D R.

56
Q

Main problem in Rickets:

Osteomalacia:

A

Rickets - not enough Ca2+ or Pi to mineralize bone.

Osteomalacia - new bone cannot mineralize.

57
Q

What causes Vit D-dependent Rickets type I?

What causes Vit D-dependent Rickets type II?

A

I: Low activity of 1a-hydroxylase.
II: Problems w/ Vit D R

58
Q

What happens to levels of PTH, Ca2+, urinary Pi, urinary cAMP and Vit D in a patient w/ Rickets?

A

+PTH (secondarily), -Ca2+, +urinary Pi, +urinary cAMP, -Vit D.

59
Q

TTM for Osteoporosis includes:
Anabolic therapy (1):
Anti resorptive therapy (5):

A

Anabolic therapy: PTH

Anti resorptive therapy: biophosphonates, estrogen, SERMs, calcitonin, RANKL inhibitors.

*Neuroendocrine Exam 3 (27 decks)

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