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FHB Hormone/Repro > 78 - Parathyroid and Ca2+ > Flashcards

78 - Parathyroid and Ca2+ Flashcards

1
Q

What % of the body’s Ca2+ is found in the bone?

A

99%

- Because of bone stores, it’s the most abundant cation in the body as well

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2
Q

What are the sx of hypocalcemia?

A

Muscle failure, tetany, convulsions, death

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3
Q

What are the sx of hypercalcemia?

A

Renal dysfunction, calcification of soft tissues, muscle weakness, coma

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4
Q

Hyperphosphatemia is rare. What’s the most common way people get it?

A

Severe tissue injury or “crush” injury

10x more Pi than Ca2+ in soft tissue

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5
Q

What is the ratio of ionized Ca2+ (free) to protein-bound Ca2+ in the serum?

A

50:45 (5% complexed)

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6
Q

What is the ratio of ionized Pi (free) to protein-bound Pi in the serum?

A

84:10 (6% complexed)

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7
Q

Because calcium is bound to it in blood, _______ is a good indicator of free Ca availability.

A

Albumin

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8
Q

What are the 2 primary mechs for Ca regulation in humans, and what is a 3rd that is probably not important?

A
  • Parathyroid hormone (PTH)
  • Vitamin D (skin, diet)
  • Calcitonin - potentially not important for humans
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9
Q

What produces calcitonin?

A

Thyroid (parafollicular cells)

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10
Q

What amount is the typical dietary intake of Ca?
What is the net uptake?
How much is excreted in urine?
How much is excreted in feces?

A

1000mg

  • 200mg
  • 200mg
  • 800mg
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11
Q

The kidney and bones change the levels of Ca2+ in the body’s __________________________.

A

Rapidly exchangeable pool

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12
Q

How many parathyroid glands are there, and where are they located?

A

4

- Located at posterior borders on lateral lobes of thyroid gland (usually embedded in capsule)

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13
Q

What are the parathyroid cells that synthesize PTH? (2 names)

A

Chief cells AKA Principle cells

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14
Q

Besides chief/principle cells, what other cells are found in the parathyroid gland? What are their function?

A

Oxyphil Cells: no known function, increase with age and chronic kidney disease

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15
Q

Recall: on the PTH preprohormone, what directs it to the ER?

A

Signal sequence/signal peptide

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16
Q

What part of the PTH preprohormone is biologically active?

A

N-terminal fragment 1-34: binds to PTH receptor

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17
Q

The PTH C-terminal fragment 35-84 has longer half-life than other fragments but is inactive. Therefore, what do we want to measure in the blood for best accuracy of current PTH levels?

A

The entire 1-84 fragment.

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18
Q

What is the 1/2-life of the 84AA PTH?

A

4 min

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19
Q

What is PTH-related peptide (PTHrP) and why is it important?

A
  • Mimics PTH in bone and kidney
  • produced by many tumors, resulting in hypercalcemia!

(normally, it’s very low conc and not a regulator of plasma Ca)

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20
Q

What are the names of the 2 PTH receptors?

Which is the primary receptor?

A
  • PTH R1 (primary)

- PTH R2

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21
Q

Where are PTH R1’s located?

A
  • Kidney

- Osteoblasts (not clasts!)

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22
Q

What is the 2nd msger pw of PTH R1 g-alpha-s?

What about G-alpha-q?

A

G-alpha-s: adenylyl cyclase/cAMP pathway

G-alpha-q: PLC/IP3/DAG

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23
Q

What hormones can bind PTH R1?

A

1-34, 1-84, and PTHrP

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24
Q

What binds PTH R2 and what’s its function?

A

1-34 only (unclear fcn)

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25
Q

What are the (2) net effects of PTH?

A

Increase plasma Ca2+, decrease plasma Pi

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26
Q

What do osteoblasts do?

What do osteoclasts do?

A
  • Bone formation and mineralization (Ca and Pi taken up)

- Bone reabsorption (Ca and Pi released into circulation)

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27
Q

What types of SC’s are osteoblasts derived from?

A

Mesenchymal stem cells

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28
Q

What types of SC’s are osteoclasts derived from?

A

Hematopoetic stem cells

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29
Q

Which express PTH R1 receptors: osteoclasts, osteoblasts, both or neither?

A

Just osteoblasts (osteoclasts is indirect thru the blasts)

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30
Q

What cell type makes up more of the bone matrix?

A

Osteocytes (terminally differentiated from osteoblasts)

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31
Q

What 2 important factors does PTH stimulate the production of? (just name, next questions focus on them)

A

M-CSF and RANK Ligand (RANK-L)

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32
Q

What does M-CSF stand for and what does it specifically do?

What stimulates its production?

A

M-CSF: macrophage colony stimulating factor (production stimulated by PTH)
- Stimulates differentiation of osteoclast precursors
(key concept: *PTH stimulate of osteoclasts is indirect!)

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33
Q

What does RANK ligand do?

A

(stimulated by PTH)

- Leads to maturation of osteoclasts and bone reabsorption

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34
Q

What does osteoprotegerin (OPG) do?

What is its net effect?

A

Antagonist of RANK-L, leading to less maturation of osteoclasts (therefore less Ca is reabsorbed from bone)

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35
Q

What 2 hormones affect OPG, and how do they affect it?

A
  • Estrogens stimulate OPG (v serum Ca)

- Cortisol inhibits OPG (^ serum Ca)

36
Q

In the kidney, what gene does PTH stimulate?

What protein does this gene encode?

A
  • CYP1alpha

- 1alpha-hydroxylase

37
Q

What is the function of 1alpha-hydroxylase?

A

Converts 25(OH) Vit D -> 1,25(OH)2 Vit D (active form)

38
Q

Besides stimulating CYP1alpha gene, what else does PTH do in the kidney?

A

Stimulates Ca reabsorption, reduces Pi reabsorption

39
Q

In what segments of the kidney does PTH act to increase Ca reabsorption and decrease Pi reabsorption?

A

PT, TAL, DT

40
Q

How do PTH act to increase Ca reabsorption in the DT, PT, and TAL?

A

Inserts Ca channel in apical membrane

41
Q

At blood [Ca] increases, how does blood [PTH] change?

A

Decreases

42
Q

What are the 2 mechanisms by which PTH is regulated?

A
  • Ca-sensing receptors (CaSR)

- Vit. D

43
Q

Where are CaSR’s located?

What do they bind?

A

Chief cells, kidney tubules, C cells

- Ca2+

44
Q

Once CaSR’s bind Ca, what 2 things do they do?

A

Inhibit PTH synthesis at promoter level and stimulate degradation of pre-existing PTH

45
Q

What types of receptors do vit D bind?

What is the name of the specific receptor?

A 
Nuclear receptors (they are fat soluble)
- VDR
46
Q

What are is the direct and indirect effect of Vit D binding a VDR?

A
  • Direct: inhibits PTH synthesis at promoter level

- Indirect: Stimulates CaSR gene TS

47
Q

What’s the general term for vitamin D and other natural structural analogs?
What term specifically refers to vitamin D3 (from animal tissues)?
What about from vegetable tissues?

A
  • Calciferol
  • Cholecalciferol
  • Ergocaliferol (Vitamin D2, not D3)
48
Q

What is the term for 25-hydroxy-vitamin D (25-D) = 25-hydroxy-cholecalciferol (immediate precursor)?

A

Calcidiol

49
Q

What is the term for 1,25-dihydroxy-vitamin D (1,25-D) = 1,25-dihydroxy-cholecalciferol?

A

Calcitriol

50
Q

Vit D3 is derived from:

A

Cholesterol

51
Q

What is the active form of vitamin D3?

A

1,25-dihydroxy-vitamin D or Calcitriol

52
Q

How is Vit D found in the blood?

A

Bound to vitamin D-binding protein

53
Q

What are the 2 ways we can obtain vit D?

A

From diet or from sunlight, requiring UV-B’s

54
Q

Where is Vit D from the skin sent to be converted to its active form precursor?
What enzyme is required?

A

Liver

- 25 Hydroxylase (makes 25-hydroxy Vit D3)

55
Q

Where is 25-hydroxy Vit D3 finally sent to be converted to its active form?
What enzyme is required?

A

Kidney

- 1alpha-hydroxylase

56
Q

If 25-hydroxy D3 isn’t converted to 1,25(OH) vit D3, what it is instead converted to in the “inactive default pw”?

A

24,25(OH)2-Vit D3

57
Q

W/r/t Ca and Pi levels, under what conditions would the inactive default pw be used?

A
  • Normocalcemia, hypercalcemia
  • Normophophatemia, hyperphosphatemia

(so w/hypocalcemia or hypophosphatemia, the active hormone is synthesized)

58
Q

What are some dz’s that vit D deficiency is linked to?

A
  • Multiple Sclerosis
  • Asthma
  • Cardiovascular disease
  • Type II Diabetes mellitus
  • Colorectal/breast cancer
59
Q

In terms of organs, what’s the difference b/w targets of PTH and the targets of Vit D?

A

They both target kidneys and bone, but vit D targets gut as well.

60
Q

What bone cells have VDRs?

A

Osteoblasts and osteoclasts (only osteoblasts have PTH R1s)

61
Q

What are the direct effects of Vit D in bone?

Indirect effects?

A
  • Direct: Mobilize Ca; osteoclast proliferation/differentiation
  • Indirect: increases plasma Ca which promotes bone mineralization

(*breaks down old bone at the expense of making new bone)

62
Q

What are the effects of vit D on the intestines?

A
  • Increases transcellular Ca absorption at duodenum

- Stimulates Pi reabsorption at small intestine (as opposed to PTH, which excretes Pi at kidneys)

63
Q

What channels are involved w/Ca xport on the luminal and basolateral sides of intestinal cells? (both are stimulated by vit D to mobilize Ca)
What does calcium bind to in cells?

A
  • Luminal: TRPV5/6
  • Basolateral: PMCA
  • Calbindin
64
Q

What 2 factors can feed back to negative inhibit PTH production? (slide 40, key slide)

A
  • Active form of Vit D3

- Increased blood Ca2+ (also inhibits CYP1alpha, gene that encodes for enzyme that makes active Vit D3)

65
Q

What is osteoporosis?

A

Reduced bone density, mainly trabecular bone

66
Q

Explain the main causes of osteoporosis.

A
  • Genetic, menopause (low estrogen which stimulates OPG), glucocorticoid therapy/chronic stress (high cortisol which inhibits OPG), low dietary Ca2+
67
Q

What are tx’s for osteoporosis?

A

Estrogens, calcitonin, biphosphonates (inhibit bone resorption), Vitamin D

68
Q

What is the difference b/w primary and secondary hyperparathyroidism?

A
  • Primary: hyperplasia, carcinoma of parathyroid gland

- Secondary: chronic renal failure (because vitamin D is activated by the kidney, so no negative feedback?)

69
Q

What are some sx of hyperparathyroidism?

A

Hypercalcemia, kidney stones

70
Q

How would PTH be affected w/reduced vit D?

A

Reduced Vitamin D leads to excess PTH synthesis (lack of negative feedback)

71
Q

What are the major signs/sx of hypoparathyroidism?

A

Hypocalcemic tetany

Chvostek sign

72
Q

What is Chvostek sign?

A

Twitching of facial muscles in response to tapping of facial nerve

73
Q

Vit D deficiency in children is called ___________, in adults it’s called ___________.
What are the major sx?

A
  • Rickets
  • Osteomalacia
  • “bowing” of long bones (children); decreased bone strength
74
Q

What is pseudohypoparathyroidism?

A

Congenital defect in G protein that associates with PTHR1 (hormone levels are nl)
- Generalized resistance to PTH, TSH, LH, and FSH

75
Q

What are the signs of pseudohypoparathyroidism?

A

Low Ca++, high phosphate, elevated PTH, short stature

76
Q

Low serum calcium and high serum phosphate are normalized by _________ infusion.

A

PTH

77
Q

As phosphate excretion increases, tubular reabsorption of phosphate (TRP) _________.

A

Falls

78
Q

What is elevated urinary hydroxyproline a marker of?

A

Enhanced bone resorption

79
Q

Serum [Ca+2] normal range:

A

2.2-2.6 mM or 8.8-10.3 mg/100mL (mg/dL)

80
Q

Serum [phosphate] normal range:

A

0.8-1.45 mM or 2.4-4.1 mg/100mL (mg/dL)

81
Q

How would a C cell tumor (calcitonin) affect Ca2+ levels?

A

Doesn’t effect them

82
Q

What is the therapeutic use of calcitonin?

What disease is it used to treat?

A

Inhibits osteoclasts, therefore decreases reabsorption of and slows bone turnover (net effect = hypocalcemic action)
- Paget disease

83
Q

What is Paget disease?

A
  • Excessive localized regions of bone resorption and reactive sclerosis.
  • Very high bone turnover
  • Cause is unknown.
84
Q

What is calcitonin a less effective tx option that we want?

A

“Escape” phenomenon – rapid downregulation of calcitonin receptors cause the antiosteoclastic actions of calcitonin to diminish within a few hours (so it’s typically given locally)

85
Q

Positive Chvostek sign could indicate what disease?

A

Hypoparathyroidism

FHB Hormone/Repro (16 decks)

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