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Clinical Biochemistry > Lab Investigation of Disorders of Calcium & Phosphate Metabolism > Flashcards

Lab Investigation of Disorders of Calcium & Phosphate Metabolism Flashcards

1
Q

Where is calcium and phosphate obtained from?

A

Calcium and phosphate are obtained through diet and absorbed in the gut

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2
Q

What substances are required for ca and Phosphate absorption in the gut?

A

Requires calcitriol (Vit. D)

Vitamin D requires PTH and activation occurs in kidneys

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3
Q

How does PTH effect Ca and phosphate metabolism?

A

PTH promotes Ca absorption and Phosphate excretion

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4
Q

What is FGF-23?

A

Hormone released from osteocytes involved in phosphate regulation

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5
Q

How does FGF-23 effect phosphate metabolism?

A

Promotes phosphate excretion through kidneys via -ve feedback
Also has a negative effect on Vit. D conversion

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6
Q

What is the most common cause of osteomalacia?

A

Vitamin D deficiency

Usually due to combination of low dietary intake and lack of exposure to sunlight

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7
Q

Which members of the population are most at risk of Vit. D?

A

Elderly at risk, especially if in nursing home and not taking supplements

Breast-fed babies kept out of sunlight

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8
Q

What is vitamin D?

A

Calcitriol really a steroid hormone, not a vitamin!

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9
Q

Where is vitamin d synthesised?

A

Synthesised in skin in response to exposure to UV (‘sunshine vitamin’)

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10
Q

Outline the steps of vitamin D synthesis

A

Activated by 2 metabolic steps

25 hydroxylation in liver to form 25OH D3, major circulating metabolite

1α hydroxylation of 25 OH D3 in kidney produces 1,25(OH)2 D3, or calcitriol, the active hormone

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11
Q

Outline the serum mineral levels in Vit. D deficiency

A 
Ca - low
Pi - Low
25OHD - low
1,25(OH)2D - normal 
PTH - high
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12
Q

Why are there normal 1,25(OH)2D levels in vit. D deficiency?

A

Low 25OH D3 = less conversion to active form (calcitriol)

Low calcitriol = less absorption of Ca and P from gut ⇒ increased PTH secretion (due to low Ca)

PTH secretion also increases activation of Vit. D

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13
Q

Outline the expected serum minerla levels in 1OH mutation patients

A 
Ca - low
Pi - low
25OHD - normal
1,25OHD - V. low
PTH - high
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14
Q

In Vit.D receptor mutations, what are the serum endocrine molecule levels?

A 
Ca - low
Pi - low
25OHD - normal
1,25OHD - v.high 
PTH - high
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15
Q

What is hypophosphataemia?

A

mineral deficiency of phosphate

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16
Q

What are Hypophosphatemic rickets?

A

rare phosphate-wasting conditions leading to bone mineralization defects (osteomalacia)

17
Q

What is the role of FGF-23?

A

FGF-23 promotes phosphate excretion

18
Q

What are the causes of phosphate wasting rickets?

A
  1. Mutation leading to excess FGF-23 activity

2. Ectopic FGF secretion (benign tumour)

19
Q

Outline the serum levels in hypophophataemic rickets

A 
Ca - low/normal
Pi - low
25OHD - normal 
1,25OHD - low / normal 
PTH - high / normal 
FGF-23 - high
20
Q

What is FGF-23?

A

a hormone secreted by osteocytes; discovered in 2000

21
Q

How is FGF-23 activity mediated?

A

FGF-23 regulated by its short half life due to enzymatic cleavage

22
Q

Outline the normal regulation of FGF-23

A

Active peptide with a cleavage recognition sequence that is identified by an enzyme and cleaved to produce 2 inactive fragments

23
Q

How does FGF-23 mutations lead to hypophosphataemic rickets?

A

Mutation in cleavage recognition sequence causes site not to be recognised - active peptide remains in circulation ⇒ phosphate wasting

24
Q

How does serum phosphate levels interact with FGF-23?

A

Inc. serum phosphate = increased FGF-23 secretion from osteocytes

FGF-23 causes phosphate excretion via -ve feedback

25
Q

What are the effects of FGF-23 on vit d?

A

FGF-23 has an inhibitory effect on the conversion of precursor to calcitriol 1,25(0H)2D

26
Q

Outline the relationship between PTH and calcitriol

A

PTH activates calcitriol; calcitriol self regulates via -ve feedback to inhibit PTH release
-ve feedback between PTH and FGF-23

27
Q

How does renal disease effect calcium metabolism?

A

Renal disease can also lead to hypocalcemia

As renal failure progresses to severe stages it may lead to renal osteodystrophy

28
Q

What is the endocrine function of kidneys?

A

Endocrine renal function to activate Vit.D

29
Q

How does renal failure lead to renal osteodystrophy?

A

As renal failure occurs, all renal functions are affected

Less absorption/filtration etc. ⇒ low Ca and low P excretion ⇒ increases PTH which will try to increase calcitriol but is limited due to renal failure

30
Q

How does renal failure cause bone lesions?

A

Secondary HPT, high PTH, prolonged leads to bone reabsorption. In addition, impaired acid excretion, acidosis exacerbating mineral loss from bone = bone lesions

Clinical Biochemistry (7 decks)

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