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FHB > Endocrinology 6- Calcium and Phosphate > Flashcards

Endocrinology 6- Calcium and Phosphate Flashcards

1
Q

Symptoms of hypocalceumia

A

muscle failure, tetany, convulsions, death

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2
Q

Symptoms of hypercalcemia

A

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

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3
Q

hyperphosphatemia and reason it often happens

A

usually result of severe crush injury, 10x more pi than Ca in soft tissue

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4
Q

What affects free calcium (ionized) in blood

A

changes in albumin and changes in pH

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5
Q

The 3 regulators of calcium, and which are the two main ones?

A

parathyroid hormone (PTH), vitamin D are the main two, calcitonin which is a thyroid hormone is potentially not important for humans

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6
Q

What cells in parathyroid gland synthesize PTH

A

chief cells

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7
Q

What kind of hormone is parathyroid hormone

A

peptide hormone

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8
Q

What is parathyroid hormone related peptide

A

You typically do not find in circulation but has paracrine effects in cells that make it - mimics action of PTH in bone and kidney if it gets into blood, but it usually isn’t a maor regulator of calcium because it isn’t in the blood. It can be made by tumors, however, and can lead to effect that seems like hyperparathyroidism. Sequences of PTH and PTHrP are very similar.

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9
Q

Both PTH and PTHrP bind to what receptor

A

PTH1

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10
Q

Does PTHrP bind to PTH2 receptor

A

Nno

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11
Q

Where is PTH1R

A

Osteoblasts, kidney, GPCR (Gs and Gq)

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12
Q

Net effects of PTH on bone and kidney

A

Increase plasma calcium, decrease plasma phosphate

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13
Q

Where is 99% of body calcium

A

bone

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14
Q

Osteoblasts

A

bone formation and mineralization, high expression of PTH recetpors, derived from mesenchymal stem cells

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15
Q

Osteoclasts

A

bone resorption, derived from hematopoietic stem cells, no PTH recetpors

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16
Q

Osteocytes

A

Make up bone matrix, terminally differentiated osteoblasts

17
Q

Is PTH’s affect on bone resorption direct or indirect

A

indirect

18
Q

How does PTH stimulate breakdown of bone?

A
  1. stimulates macrophate colony stimulating factor - stimulates hematopoietic stem cells to make more osteoclast precursors
  2. Stimulates RANK ligand - released from osteoblasts and important for maturation of osteoclasts
  3. Osteoblasts export calcium and phosphate into Extracellular space for bone mineralization
  4. RANK ligand binds to receptor, causes bone resorption.
19
Q

How can we protect bones from too much resorption

A

Osteoprotegrin is also released and binds up RANK ligand and prevents it from being stimulated, which prevents bones from being broken down. After menopause this protective effects no longer exists. Cortisol also inhibits osteoprotegrin which can lead tobones breaking down in stress

20
Q

How does PTH target kidney

A

Stimulates calcium channel insertion into apical membrane of distal tubule into kidney, leads to calcium reabsorption
* happens in TAL

Stimulates CYP1a - which encodes 1-a-hydroxylase which converts active form of Vitamin D

21
Q

What is the enzyme that converts vit D to be active

A

1-a hydroxylase

22
Q

How is PTH regulated

A

Regulated by calcium
Low calcium - lots of PTH released
High calcium - not a lot of PTH released

Sensing of calcium is done by chief cells in parathyroid gland

23
Q

What is the receptor on PTH chief cells, kidney tubules, and C cells that sense calcium

A

calcium sensing receptor (CaSR)

24
Q

What does vitamin D bind

A

Vitamin D receptor (nuclear receptor)

25
Q

how does vitamin D regulate PTH

A

inhibits PTS synthesis at promoter level, stimulates CaSR gene transcription (indirect regulation of PTH)

26
Q

What is the other name for vitamin D

A

cholecalciferol

27
Q

What does vitamin D require to be active

A

light

28
Q

hat organs does vitamin D target

A

intestines, kidneys, bone

29
Q

how does vitamin D affect bone

A

mobilize calcium from bone because osteoblasts and osteoclasts have vitamin D receptors - vitamin D stimulates osteoclast proliferation and differentation, and vitamin D increases plasma calcium which promotes bone minearlization

30
Q

How does vitamin D target intestine

A

increses transcellular Ca absorption in duodenum and stimulates Pi reabsorption from small intestine - opposite of PTH

31
Q

Osteoporosis

A

reduced bone density, trabecular bone and osteocytes are not going to be maintained properly so bone density goes down. There is a genetic component but something like menopause would also play a role (loss of osteoprotegrin), as well as glucocorticoids. Txt is estrogens, calcitonin, bisphosphates. If you hve vitamin D and bisphosphates you might get increased risk in fractures

32
Q

PTH overproduction

A

primary - tumors of parathyroid gland, leads to hypercalcemia and kidney stones. Can have a secondary problem due to chronic renal failure – kidney cannot respond to PTH, cannot have 1-a hydroxylase enzyme so no active vitamin D –> lose negative feedback signal, get excess PTh

33
Q

Hypoparathyroidism

A

Hypocalcemic tetany, facial muscles will twitch in response to tapping of facial nerve (sign of this tetany)

34
Q

Chvostek sign

A

twitching of facial muscles in response to tapping of facial nerve

35
Q

Rickets and osteomalacia

A

Vitamin D deficiency, bowing of long bones, decreased bone strength

36
Q

Pseudohypoparathyroidism

A

Congenital defect in G protein that associates with PTHR1, so hormones that also use this g protein but aren’t PTH will also be affected (ex. PTH, TSH, LH, and FSH)
Clinical signs are low calcium, high phosphate, elevated PTH, and short stature

37
Q

Calcitonin

A

Inhibits calciumr resorption from bone? Maybe but physiological importance is unclear, because if taking thyroid glands out but parathyroids remain, the nrmal physiological range of calcium is unaltered. With very high C cell from tumors, which would produce a lot of calcitonin, calcium levels are also not affected

38
Q

how is calcitonin used therapeutically

A

to inhibit osteoclast resoprtion and slow burn turnover as a treatment for paget disease - however the rapid downregulation of calcitonin causes the antiosteoclastic ctions of calcitonin to diminish in a few hours, so this is not a very effective txt

FHB (54 decks)

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