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Sophie - Applied Physiology & Pharmacology Year 2 > 51.3 Regulation of Extracellular Calcium > Flashcards

51.3 Regulation of Extracellular Calcium Flashcards

1
Q

How much calcium is in the body?

A

1kg: teeth/ CT/ bones (99% Ca3(PO4)2)

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2
Q

What is the intake of Ca2+?

A

diet (daily 200 -1500 mg). Western - dairy/ flour (Ca salts added)

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3
Q

What are the three main primary sources of calcium?

A

Diet
Bone
Kidney

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4
Q

How is Ca2+ absorbed?

A

Gastrointestinal absorption
*Transcellular in duodenum + upper jejunum. Calcitriol ↑.
*Paracellular across entire length of intestines.
- Calcitriol ↑ (FGF-23 potent antagonist)
*↑ Ca2+ demands promote (e.g. growth/ pregnancy/ lactation/ physical activity)
*Ageing ↓ Ca2+ transport.

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5
Q

How is Ca2+ excreted/ reabsorbed?

A

renal reabsorption/excretion
*~ 98% ultrafiltrate Ca2+ reabsorbed
- Paracellularly in PT + TAL of LoH (bulk)
- Transcellularly in DCT
*100–200 mg of Ca2+ excreted /day in urine

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6
Q

How much EC Ca2+ is there?

A

2.3-2.4 mmol l-1, 1.4 mmol l-1 free

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7
Q

How much IC Ca2+ is there?

A

1-2 mmol kg-1, 0.1μmol l-1 free

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8
Q

What are the IC functions of Ca2+?

A

*Exocytosis activation → stimulus-secretion coupling
*Muscle contraction → stimulus-contraction coupling
*AP propagation
*2nd messenger → enzyme regulation/ regulating cellular processes

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9
Q

What are the EC functions of Ca2+?

A

*Plasma membrane integrity + functioning → Ca2+ imp. Co-factor in proteins (e.g. adhesion molecules, clotting factors + secreted enzymes)
*Mineral phase of Skeleton → critical (also PO43-). Collagenous matrix + insoluble mineral phase = Tensile + compressive strength of bone. Protection/ ambulation.

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10
Q

What are the effects of hypercalcaemia? (rhyme)

A

Bones, stones, moans, groans

Bones = fractures
Stones = kidney stones
Moans = lower mood
Groans = abdominal discomfort

along with decreased excitability of nerves

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11
Q

What are the effects of hypocalcaemia? (mnemonic)

A

CATs go numb: Convulsions, Arrhythmias, Tetany, Numbness

  • Muscle hyperexcitability
  • Confusion
  • Arrhythmia
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12
Q

Why does hypocalcaemia cause muscle hyperexcitability?

A

There is less Ca2+ to block sodium channels –> lowered threshold for depolarisation

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13
Q

What is the difference between osteoporosis and osteomalacia?

A

Osteoporosis = decreased bone formation (less bone)
Osteomalacia = decreased calcification (bone softening)

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14
Q

What is the role of osteoblasts?

A

deposits new bony matrix

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15
Q

What are the functions of osteocytes?

A

secrete sclerostin which recruits osteoclasts.
Maintenance.

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16
Q

What is the function of osteoclasts?

A

resorbs bony matrix

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17
Q

How do osteoblasts activate osteoclasts?

A

By interaction of RANK-L on osteoblasts with RANK on osteoclasts

18
Q

Osteoblasts [increase/decrease] Ca2+ levels while osteoclasts [increase/decrease] Ca2+ levels

A

Osteoblasts decrease plasma Ca2+ levels while osteoclasts increase plasma Ca2+ levels

19
Q

Why are people at increased risk of osteoporosis as they age?

A
  • Decreased vit D - less Ca2+ absorbed
  • Women have less oestrogen which usually activates osteoblasts
20
Q

What is the action of calcitriol?

A

↑absorption of ingested Ca2+ when ↓ plasma Ca2+.

21
Q

How does calcitriol increase absorption?

A

Direct effect on intestinal mucosa.
Nuclear receptors → ↑ expression of Ca2+ channels + Na+/Ca2+X + Ca2+ATPase

22
Q

How does calcitriol stimulate calcification of the bone matrix?

A

Stimulates calcification of bone matrix (observed from Vit.D deficiency) → bone remodelling
*Indirectly: ↑ Ca2+ in plasma
*Directly: stimulating osteoclast + osteoblast activity

23
Q

What happens to calcitriol during pregnancy/ lactation/ ageing?

A

*Pregnancy → sig ↑ to ↑ maternal Ca2+ absorption so sufficient Ca2+ for foetal growth.
*Lactation → ↑ to help maintain Ca2+ homeostasis.
*Ageing → ↓ synthesis efficiency (↑ by ↓ sunlight exposure/ ↓ renal function)

24
Q

What is the action of PTH?

A

most broad activity: mobilises Ca2+ from bone + ↑ Ca2+ reabsorption in kidneys. ↑ when plasma Ca2+ ↓

25
Q

What are the anabolic effects of PTH, when do they happen?

A

Continuous basal secretion rate (5 min ½ life) → maintains bony skeleton
*Promotes osteoblastogenesis + osteoblast survival + ↑ calcification of bone matrix

26
Q

What are the catabolic effects of PTH?

A

Effect on bone: ↑PTH → biphasic action
*Initially - rapid Ca2+ loss from readily releasable Ca2+ pool on bone surface
*Long-term - resorption of stable bones by osteoclasts → + minerals to ECF

27
Q

What is the effect of PTH on the kidneys?

A

↑ Ca2+ + ↓ PO43- reabsorption
*Ca2+ → In Cortical ascending Thick LoH + DT
By stimulating Calcitriol synthesis
*↓ PO43- → ↑ ionised Ca2+/ ↓ [Ca3(PO4)2] - an insoluble salt.

28
Q

What happens to PTH in hypocalcaemia?

A

hypocalcemia → PTH biosynthesis + PT cell proliferation
*most potent PTH stimulator. ↑ Ca2+ inhibits PTH release.

29
Q

What happens to PTH during pregnancy?

A

↓ in 1st trimester (maintain ca2+ balance), ↑ throughout 2nd/ 3rd.

30
Q

What happens to PTH during lactation?

A

PTHrp produced by lactating breast. ↑ bone resorption to ensure adequate Ca2+/ PO43- in breast milk.

31
Q

What happens to PTH during development?

A

compensatory PTH ↑ drive Calcitriol production + enhance Ca2+absorption during ↑ demand.

32
Q

What happens to PTH during ageing?

A

PTH ↑ w/ age. (due to ↓ renal function/ ↓ Ca2+ absorption frequency/ ↓ calcitriol)

33
Q

What is the function of calcitonin?

A

↓ free plasma Ca2+

34
Q

What are the actions of calcitonin?

A

*Inhibits osteoclast activity → ↓ bone resorption, Ca/P not released into plasma
*↑ Ca2+ + PO43- excretion by kidneys. Also other ions such as K+, Mg2+ and Na+

35
Q

What happens to calcitonin in pregnancy?

A

↑ (protect skeleton against PTH-induced resorption?)

36
Q

What happens to calcitonin during lactation?

A

role in development of enteric neurons in breastfed infants?

37
Q

What happens to calcitonin in development?

A

↑ opposes PTH action to limit skeletal loss during ↑ Ca2+ demand

38
Q

What happens to calcitonin during ageing?

A

↓ (due to ↓ sunlight exposure etc)

39
Q

What is osteomalacia?

A

*caused by a Vitamin D deficiency –> X calcification of bone matrix + impaired bone remodelling → hypocalcaemia
*In adults
*↓ bone density, lots of non-mineralised osteoid. ↑ susceptibility to fracture, bone pain + proximal muscle weakness

40
Q

What is osteoporosis?

A

unbalanced resorption(↑) and deposition. Results in porous bones/ lost density/ deterioration of architecture. 3 types. (1/ 2) 10 and 20.
Type I primary osteoporosis → postmenopausal women due to ↓oestrogen. Sever long term effects as presents earlier

41
Q

What is a common side effect of corticosteroid therapy?

A

Osteoporosis

Sophie - Applied Physiology & Pharmacology Year 2 (32 decks)

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