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Endo Final > Parathyroid Gland- Regulation of Ca and PO4 Metabolism > Flashcards

Parathyroid Gland- Regulation of Ca and PO4 Metabolism Flashcards

1
Q

Where are most of the body’s calcium found in?

A

Bones and teeth.

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2
Q

Positive Chvasotek sign, and Trouseau sign, hyperreflexia, spontaneous twitching, muscle cramps and tingling and numbness are also associated with _

A

Hypocalcemia.

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3
Q

Decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muslce weakness, hyporeflexia, lethargy, and coma are all assoicated with _

A

hypercalcemia

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4
Q

What is the mechanism by which hypocalcemia causes tetany?

A

hypocalcemia reduces the activation threshold for Na channels and thus is easier to evoke AP and generation of spontaneous AP is the physical basis for hypocalcemic tetany (spontanous muscle contraciton due to low exracellular Ca)

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5
Q

Which of the following will increase plasma Ca concentration.

a. increase plasma protein concentration
b. increase phosphate concentration
c. Alkalemia
d. decrease H concentration

A

A.

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6
Q

In acidemia, ionized Ca concentration in the blood decrease or increases?

A

Increase. Decreases in alkalemia.

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7
Q

What three organs, and what three hormones are needed to regulate Ca.

A

Organs: bone, kidney, intestine
Hormones: PTH, Calcitonin, Vit D.

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8
Q

True or False: When excess Ca from diet that is not used by cells, is stored in bones.

A

False. Kidneys excrete out the same amount of Ca that is absorbed by the Gi tract.

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9
Q

Most of the inorganic phosphate is in what form in our body: ionized, protein bound, or complex?

A

Ionized as phaphate (PO4-) = 84%

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10
Q

If extracellular Ca levels was to increase, how would Pi concentration change?

A

Pi levels would decrease. Extracellular concentration of Pi is inversely related to that of Ca.

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11
Q

what cells produce PTH?

A

chief cells of they parathyroid gland

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12
Q

What is the stimuli for PTH secretion?

A

decreased Ca.

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13
Q

What sends the signal to parathyroid gland to make PTH?

A

1,25 vit D.

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14
Q

Explain the pathway of how PTH is released and inhibited.

A

1,25 Vit D enters parathyroid cell nucleus and causes transcription of PTH mRNA. PTH is released. Vit D also stimulates the synthesis of CaSR which after production goes to cell surface and will sense any Ca++. If they sense Ca++ then it will feedback inhibit PTH.

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15
Q

In chronic hypercalcemia, what happens to PTH levels?

A

decreased synthesis and storage of PTH and increased breakdown of stored PTH and release of inactive PTH fragment into the circulation.

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16
Q

What causes secondary hyperparathyroidism?

A

Chronic hypocalcemia leading to increased synthesis and storage of PTH leading to hyperplasia of the parathyroid glands.

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17
Q

What happens to PTH levels, and CaSR receptor during hypermagnesemia?

A

PTH inhibited. CaSR senses Mg++ and feedsback to inhibit PTH.

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18
Q

A patient comes in severe dehydration and faints unconscious. You notice that his blood alcohol levels is severely elevated. What happens to patient’s PTH levels?

A

PTH synthesis storage and secretion is inhibited.

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19
Q

VIa what G protein does PTH receptor work and what is the second messenger?

A

Gs –> cAMP

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20
Q

During hypocalcemia, how does the kidney function to bring Ca levels back up?

A

It increases Ca reabsorption and Pi secretion. As a resut urinary cAMP is also elevated.

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21
Q

What factors stimulates 1a-hydroxylase?

A
  1. Decreased Ca
  2. Increased PTH
  3. decreased Phosphate
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22
Q

What is the main form of vitamin D that is found in circulation?

A

25-OH-cholecalciferol

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23
Q

What effect would 1,25 Vit D have on CYP1a-gene, on CYP25 gene?

A

inhibitory on CYP1a gene and stimulatory on CYP24 gene.

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24
Q

What is the short term action of PTH on bone?

A

Bone formation via direct action.

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25
Q

What is the long term action of PTH on bone?

A

increased bone resorption indirectly by actions of osteoclasts activity mediated by cytokines released from osteoblasts.

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26
Q

Does vitamin D work with, or against PTH?

A

Vit D and PTH work synergistically to stimulate osteoclast activity and bone resorption.

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27
Q

On what cell is RANKL located on and it is RANKL?

A

It is a receptor activator for NF-kB ligand that is a cell surface protein produced by osteoblasts, bone lining cells, and apoptotic osteocytes.

28
Q

On what cells are RANK located?

A

osteoclasts and osteoclast precursor

29
Q

How is RANKL/RANK interaction inhibited in a normal bases when bone resorption is not needed?

A

OPG (osteoprotegerin) which is a decoy receptor that binds to RANKL thus blocking the RANKL/RANK interaction

30
Q

what stimulates RANKL activity but decreases OPG

A

PTH

31
Q

PTH acts directly to increase which RANKL or RANK?

A

RANKL

32
Q

Explain the mechanism of action of PTH on kidney

A

in proximal tubule, PTH binds to Gs receptor and via AC converting ATP to cAMP. cAMP can’t act on Na/Phosphate transporter cuz PTH blocks it by repressing NPT2a expression and so cAMP is excreted in urinary (urinary cAMP). The second action of PTH is on the distal convoluted tubule where it increases Ca reabsorption.

33
Q

Unlike PTH in the kidney, Vitmin D stimulates Ca and Pi _ (reabsorption or secretion)

A

Stimulates reabsorption of both. PTH stimulates Ca reabsortpion but Pi secretion

34
Q

What function does Vitamin D have on Ca and Pi homeostatin in the small intestine?

A

Increase Ca and Pi absorption by increasing calbindin expression

35
Q

Calcitonin inhibits bone resorption by _

A

decreasing activity and the number of osteoclasts

36
Q

In thyroid tumors, calcitonin levels are increased. How does this effect Ca metabolism?

A

No effect

37
Q

What effect does estradiol 17b have on intestinal Ca absorption and renal tubular Ca reabsorption?

A

Stimulates in both

38
Q

What effect does estradiol 17b have on osteoblast and osteoclast activity?

A

Increases osteoblast activity and inhibits osteoclast activity. overall promotes bone formation vs over resorption

39
Q

What effects do adrenal glucocorticoids have on bone resorption, renal Ca, and intestinal Ca?

A

Increases bone resorption, inhibit renal ca and intestinal ca reabsorption.

40
Q

Patients treated with high level os glucocorticoids can develop what bone disease?

A

osteoporosis

41
Q

Patients with primary hyperparathyroidsim will excrete excessive levels of _, _, and _.

A

Pi, cAMP, and Ca++

42
Q

What are some clinical symptoms of Primary hyperparathyroidism?

A

Stones, Bones, and groans. Hypercalciuria - stones; increased bone resorption - bones; and consitpation - groans.

43
Q

What would be the levels of the following in primary parathyroidism: ;PTH, Ca, Pi, and Vit D

A

PTH = increased
Ca = increased
Pi = decreased
Vit D = increased

44
Q

What is secondary hyperparathyroidism?

A

increased in PTH levels secondary to low Ca.

45
Q

What would be the levels of the following in secondary parathyroidism due to renal failure: PTH, Ca, Pi, and Vit D

A

PTH = increased
Ca = decreased
Pi = increased
Vit D = decreased

46
Q

What would be the levels of the following in secondary parathyroidism due to vit deficiency: PTH, Ca, Pi, and Vit D

A

PTH = increased
Ca = decreased
Pi = decreased
Vit D = decreased

47
Q

Hypoparathyroidism symptoms are mostly associated with _

A

symptoms of Decreased Ca, such as muscle spasm or cramping, numbness, tingling, or burning, seizures, poor teeth develoment, and mental deficiency.

48
Q

Hypoparathyroidism can be treated by:

A

oral Ca supplement and active form of vitamin D

49
Q

During hypoparathyroidism, what would be levels of the following: PTH, Ca, Pi, and Vitamin D

A

PTH = decreased
Ca = decreased
Pi = increased
vitamin D = decreased

50
Q

What is albright hereditary osteodystrophy?

A

It is a psudoehypoparathyroidism type 1a which is a inherited autosomal dominant disorder, Gs, for PTH in bone and kidney is defective.

51
Q

How can you diagnose someone with pseudohypoparathyroidism typa 1a?

A

Increased PTH levels. and if you give them exogensous PTH, will not produce phosphaturic respone and no urinary cAMP.

52
Q

In albright hereditary osteodystrophy, what would you expect the levels of the following to be: PTH, Ca, Pi, vit D

A

PTH = increased
Ca = decreased
Pi = increased
vita D = decreased

53
Q

what are phenotypes associated with Albright hereditary osteodystrophy?

A

Short stature, short neck, obesity, subcutenous calcification, shortentend metarsal and metacarpals.

54
Q

General symptoms of hyperparathyroidism?

A
  • kidney stones
  • osteoporosis
  • GI disturbances, peptic ulcers, nausea, constipation
  • muslce weakness, decreased muscle tone
  • depression, letharyg, fatigue, mental confusion
  • polyuria,
  • low serum phosphate concentration; high serum calcium concentration
55
Q

In general symptoms of hypoparathyroidism are:

A

-tetany, convulsions, paresthesias, muscle craps, deceased myocardial contractility, 1st degree heart block, CNS problems, including irritability and psychosis, intestinal maabsorption, low serum calcium concentraiton; high serum phosphate concentration

56
Q

What is humoral hypercalcemia of malignancy?

A

It is a hypercalcemia syndrome associated with malignancy where PTH-related peptide (PTHrP) is produced by tumors with close homology in the N-terminal to PTH –> dene duplication of PTH which binds and activaates the same receptors as PTH.

57
Q

In Humoral hypercalcemia of malignancy, with PTHrP levels increased, the signs are mostly similar to primary hyperprathyroidism, but differ in what ways?

A

Similar in that Urinary Ca, Urinary Pi, and cAMP, Blood Ca are all increased; blood pi is decreased. Differ in that bone formation, PTH levels and Vit D levels are all decreased

58
Q

In humoral hypercalcemia of maignancey, what would the levels of the following: PTH, Ca, Pi, and Vit D

A

PTH = decreased
Ca = Increased
Pi = decreased
Vit D = decreased

59
Q

What is familial hypocalciuric hypercalcemia (FHH)

A

An autosomal dominant disorder where there is a mutation in CaSr in the parathyroid gland and parallel Ca receptors in the ascending limb of the kidney, leading to decreased Ca excretion and increased serum Ca.

60
Q

In familial hypocalciuric hypercalcemia (FHH) what would be the levels of the following: PTH, Serum Ca, Urine Ca, Pi, Vitamine D

A 
PTH = N / increased
serum Ca = increased
Urine Ca = decreased
Pi = N
Vit D = N
61
Q

What are some causes that can lead to Vit D deficiency as seen in Rickets-Osteomalacia

A
  1. Dietary deficiency of Vit D
  2. Vitamin D resistance - deficit synthesis of active vitamin D (absence of 1a-hydroxylase)
  3. Mutation affecting vitamin D receptor
62
Q

What is the difference between Rickets and Osteomalacia besides age differences.

A

Rickets (in children) is due to insufficiency amount of Pi and Ca for mineralization of growing bone. In osteomalacia it is the failure to mineralize new bone.

63
Q

Rickets Type I is due to

A

decreased 1a-hydroxylase

64
Q

Rickets Type II is due to

A

decreased vitamin D receptors

65
Q

With Vitamin D deficiency what would be the expected levels of PTH, Ca, Pi, Urine Pi and cAMP, Vit D, Bone resorption

A 
PTH = increase (2ndary)
Ca = N or decreased
Pi = decreased
Urine Pi = increased
Urine cAMP = increased
Vitamin D = decreased
Bone resorption = increased in osteomalacia
66
Q

What are some treatments for Rickets - Osteomalacia

A
  • ergocalciferol
  • cholecalciferol
  • Ca
  • sunlight
  • Calcitriol
67
Q

What are some treatment options for Osteoporosis?

A

Antiresorptive therapy like bisphosphonates, estrogen, selective estrogen receptor modulators (SERMs) like raloxifene, tamoxifen), calcitonin, RANKL inhibitor (denosumab)

Anabolic therapy - PTH

Endo Final (14 decks)

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