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Calcium homeostasis Flashcards

1
Q

5 processes involving calcium?

A
  • Bone mineral formation as hydroxyapatite – 1kg calcium as Ca10(PO4)6(OH)2
  • blood clotting
  • Muscle contraction activation
  • inhibition of enzymes
  • excitability at neuromuscular junction
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2
Q

What are the reference nutrient intake of calcium?

A

Men - 11-18 1 g/day

Women - 11-18 0.8 g/day

Women - 19+ 0.7 g/day

Lactating women - 1.25 g/day

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3
Q

How are relative calcium absorption values in childhood?

A

High

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4
Q

How are relative calcium absorption values in pregnancy?

A

High

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5
Q

How are relative calcium absorption values in lactation?

A

High

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6
Q

How are relative calcium absorption values in calcium high intake?

A

Low

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7
Q

How are relative calcium absorption values in ageing?

A

Low

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8
Q

How does lactose affect calcium absorption?

A

Increases absorption?

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9
Q

How do basic amino acids affect calcium absorption?

A

Increase absorption

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10
Q

How does vitamin D affect calcium absorption?

A

Increases absorption

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11
Q

How does phytic acid (inositol hexaphosphate) affect calcium absorption?

A

Decreases absorption

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12
Q

See notes for diagram of daily calcium balance

A

-

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13
Q

What is the normal plasma concentration of calcium?
What is the plasma concentration of calcium that is in the free ionic form (biologically active)?
What is the concentration that is bound to plasma proteins?
What is the concentration in complexes?

A
  • plasma Ca 2.5 mM (2.2-2.6 mM)
  • 1.2 mM free ionic form (biologically active)
  • 1mM bound to plasma proteins
  • 0.3 mM in complexes e.g. with citrate
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14
Q

Hypocalcaemia?

A

– Hyperexcitable nervous system
– tetany
– <1.5 mM lethal

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15
Q

Hypercalcaemia?

A

– sluggish nervous responses
– ectopic calcification e.g. kidneys, synovial fluid etc
– >3.75 mM lethal

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16
Q

What is the effect of parathyroid hormone on blood calcium and phosphate levels?

A

↑blood Ca2+

↓ blood Pi

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17
Q

What is the effect of Cholecalciferol (vitamin D) on blood calcium and phosphate levels?

A

↑ blood Ca2+

↑ blood Pi

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18
Q

What is the effect of calcitonin on blood calcium and phosphate levels

A

↓ blood Ca2+

↓ blood Pi

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19
Q

What is the molecular mass of parathyroid hormone and how is it released and in response to what?

A
  • MM 9500
  • packaged in vesicles in the parathyroid glands
  • released in response to low blood Ca2+
  • increase cAMP - PTH secretion
  • increased PLC (+IP3) - inhibition of secretion
20
Q

See diagrams in notes for details of mechanism of PTH hormone release modulation

21
Q

What are the effects of PTH on bone?

A
  • PTH receptors on osteoblasts only
  • PTH binds and activates AC which produces c AMP
  • osteoblast collagen synthesis inhibited
  • osteoblasts release cytokines which affect osteoclast activity
  • Osteoclasts release their calcium and phosphate content and release H+ and collagenase in lacuna
  • bone mineral is resorbed
  • blood calcium and phosphate are increased
22
Q

Given that PTH causes the release of Ca and Pi into the bloodstream - why does PTH overall cause a decrease in plasma Pi?

A

• decreases Pi reabsorption in the kidneys, thereby increasing Pi excretion

23
Q

What are the actions of PTH on the kidney?

A
  • increases calcium reabsorption in the distal tubule
  • decreases Pi reabsorption thereby increasing Pi excretion
  • activates 1α hydroxylase which is needed to activate vitamin D (which increase gut absorption of calcium)
24
Q

What is hyperparathyroidism and what does it lead to?

A

Gland hyperfunction or hyperplasia
leads to :
• hypercalcaemia through excessive bone resorption
• ectopic calcification (heart, pancreas, kidney, uterus, synovial membranes

25
What is hypoparathyroidism and what does it lead to?
* usually due to surgical removal of parathyroid glands during thyroidectomy * leads to hypocalcaemia
26
Where is calcitonin made and when is it release to do what action?
* formed in the C or parafollicular cells of the thyroid. * secreted when blood calcium is high * acts on osteoclasts via cAMP and suppresses their activity
27
What do you know about rickets (in terms of history and geography of it etc.?
* Rickets described by Whistler and Gibson in 1650 in the UK * affected children • in temperate climates • not in the tropics, not in Scandinavia * common in the UK in 19th C esp. in urban slums • protruding forehead • pigeon chest • kyphosis • bending of long bones particularly weight bearing • ‘rickety rosary'
28
What are the signs of rickets?
* protruding forehead * pigeon chest * kyphosis * bending of long bones particularly weight bearing * ‘rickety rosary'
29
How could rickets be treated?
* consumption of fish oils | * exposure to the sun
30
Do plants contain vitamin D?
* vitamin D is not present in plants | * vegan diets contain no vitamin D
31
What is vitamin D3?
* cholecalciferol | * naturally occurring
32
What is vitamin D2?
* ergocalciferol | * commercial production from ergosterol
33
How does the body handle exogenous vitamin D?
* exogenous vit D absorbed * circulates in chylomicrons * delivered to the liver as chylomicron remnants
34
Upon what does the dietary requirement of vitamin D depend?
* Dietary requirement of vitamin D depends on exposure to sunlight, (synthesised in skin as inactive form) * NB no radiation 290-310 nm in UK October-March (in UK)
35
What groups are at risk of vitamin D deficiency?
* Infants and children in north England & Scotland (especially those born in winter and breast fed) * Asian children and women (especially on vegetarian diets and depending on exposure to sunlight) * All elderly and housebound people
36
What is the recommended supplementation for groups at risk of vitamin deficiency?
• recommendation: supplement 10µg /day
37
How is vitamin D metabolism activated?
Activated by 2 hydroxylations in liver and kidney
38
Mechanism of vitamin D action in the intestine?
``` • Genomic: – acts as a steroid hormone – binds to intracellular receptor, – transported to DNA – promotes synthesis of proteins (calbindins) ``` • Non genomic: – direct effect on cell membranes to increase calcium absorption
39
• vitamin D action on bone?
* receptors only in osteoblasts * on calcium free diet, bone resorption is net effect by osteoclasts activated by cytokines produced by osteoblasts * production of calcium binding proteins may relate to mineralisation of bone * differentiation of precursors into osteoblasts and differentiation of precursors into osteoblasts and osteoclasts
40
• vitamin D action on kidney
• increases reabsorption of calcium and phosphate ions
41
What are the causes of vitamin D deficiency (rickets/osteomalacia)?
rickets/osteomalacia - primary: • dietary deficiency • low synthesis in the skin ``` - secondary (vitamin D resistant): • bile duct obstruction • coeliac disease • liver disease • renal disease ```
42
vitamin D intoxication?
* 25OH CC conc high, 1,25 diOH CC conc low. * 25OH CC at high conc has enough activity to have toxic effects • nausea, vomiting, hypercalcaemia, ectopic calcification * infants most at risk * can be lethal
43
How do oestrogen, testosterone, glucocorticoids and thyroid hormones affects calcium homeostasis?
* oestrogen deficiency (menopause) leads to osteoporosis * testosterone deficiency * glucocorticoids (decrease calcium glucocorticoids (decrease calcium absorption and increase excretion) * thyroid hormones (increase bone resorption) * DO NOT CONFUSE OSTEOMALACIA WITH OSTEOPOROSIS
44
What differs between osteomalacia and osteoporosis?
Osteomalacia: - amount of bone - normal - Mineral/matrix ratio - reduced Osteoporosis: - amount of bone - reduced - Mineral/matrix ratio - normal
45
What are the risk factors for osteoporosis?
* menopausal status (oestrogen deficiency) * race: – bone density black>white>Asian * family history * physical activity * nutrition – (calcium, sodium, protein, caffeine) * corticosteroids – (inhibit osteoblasts)
46
What are the treatments for osteporosis?
* Calcium? – intake should be 1200mg/d * oestrogen replacement therapy * oestrogen receptor modulators * Strontium * Bisphosphonates (inhibit osteoclast activity) new ones to be taken every few weeks orally or by injection * Synthetic PTH preparations (low doses) * Clinical trials on monoclonal Ab that bind cytokines released by osteoblasts and do not allow them to activate osteoclasts

Endocrinolgy (8 decks)

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