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Clinical biochemistry > Calcium and phosphate metabolism > Flashcards

Calcium and phosphate metabolism Flashcards

1
Q

What does bone turnover serve and in conjunction with what?

A 
• Bone turnover serves homeostasis of serum calcium and phosphate, in conjunction with:
	○ Parathyroid hormone (PTH)
	○ Vitamin D (1,25-dihydroxy D3)
	○ Calcitonin
        ○ FGF-23
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2
Q

What does FGF-23 lower?

A

Lowers serum phosphate levels

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3
Q

What does bone remodelling release in the short term?

A

In the short term, bone remodelling releases minerals, notably calcium, into the circulation

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4
Q

What percentage of body calcium is in bone?

A

• 99% of body calcium is in bone

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5
Q

Where is 1% of calcium mainly found?

A

Mainly found intracellularly

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6
Q

What is normal plasma Ca levels?

A

plasma Ca 2.2-2.6 mmol L-1

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7
Q

How is extracellular calcium found?

A

• About half of extracellular is free [Ca2+] (physiologically active), half protein bound (mainly albumin)

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8
Q

What does PTH increase?

A

Increases bone remodelling

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9
Q

How is PTH at low doses?

A

○ At low doses, PTH is anabolic: promotes formation of new bone

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10
Q

What happens when there is prolonged higher levels of PTH and what does this result in?

A

Prolonged higher level = excess of resorption over formation
Results in rise in extracellular calcium

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11
Q

What does a persistent raised level of PTH result in and why?

A

§ Persistent raise

Results in hypercalcaemia because it promotes/increases resorption of Ca from kidney tubule

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12
Q

What does PTH lower?

A

Lowers phosphate

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13
Q

What does PTH increase expression of what is it responsible for?

A

○ Increases expression α hydroxylase enzyme that is responsible for converting precursor of vitamin D to 1,25 dihydroxy D3

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14
Q

What percentage of body phosphorous is found in the bone and in what form?

A

• 85% of body phosphorus is in bone

-Mainly in the form of hydroxyapatite

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15
Q

What is normal levels of phosphate extracellularly?

A

2.5-4.5 mg dL-1

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16
Q

Why do phosphate levels fluctuate more than calcium levels?

A

Less tightly controlled

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17
Q

What are clinical features of hypercalcaemia?

A

• May be asymptomatic for a while
• Depression, fatigue, anorexia, nausea, vomiting,
• Abdominal pain, constipation
• Renal calcification (kidney stones)
• Bone pain
○ “painful bones, renal stones, abdominal groans, and psychic moans”
• Severe: cardiac arrhythmias, cardiac arrest

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18
Q

What is the most common cause of hypercalcaemia in ambulatory patients?

A

primary hyperparathyroidism
§ Involves benign tumour of one or more of the parathyroid glands
§ parathyroid tumour = excess PTH = excess resorption = high calcium

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19
Q

What is the cause of hypercalcaemia in hospitalised patients?

A

Malignancy

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20
Q

What are the less common causes of hypercalcaemia?

A

○ Hyperthyroidism

○ Excessive intake of vitamin D

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21
Q

Serum biochemistry in hypercalcaemia

A
  • Serum calcium - modest to marked increase
  • Serum phosphate - low or low normal
  • Serum alkaline phosphatase raised in ~ 20% of cases
  • Serum creatinine may be elevated in longstanding disease (kidney damage)
  • Serum PTH concentration should be interpreted in relation to calcium
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22
Q

What is the most common cause of hypercalcaemia in hospitalised patients?

A

• Most common cause of hypercalcaemia in hospitalized patients
○ Humoral, e.g., lung carcinoma secreting PTHrP
○ Metastatic
○ Haematological
§ Myeloma

23
Q

What is the most common cause of hypocalcemia?

A
  • Vitamin D deficiency

- Renal failure

24
Q

What are the less common causes of hypocalcemia?

A

Hypoparathyroidism

25
Q

What does vitamin D promote and what does a lack of it cause?

A

Promotes calcium uptake so lack of it causes hypocalcemia

26
Q

What are rickets in children?

A

Failure of bone mineralisation and disordered cartilage formation

27
Q

What is osteomalacia in adults?

A

Impaired bone mineralisation

28
Q

What are the features of osteomalacia?

A
  • Diffuse bone pain
  • Waddling gait, muscle weakness
  • On X-ray, stress fractures
29
Q

What is the serum biochemistry of osteomalacia?

A

○ Low/normal calcium
○ Hypophosphataemia
○ Raised alkaline phosphatase
○ Secondary hyperparathyroidism

30
Q

What is osteoporosis?

A
  • loss of bone mass/density

- Increase in bone resorption over formation

31
Q

What are the causes of osteoporosis?

A 
○ Endocrine
○ Malignancy
○ Drug-induced
○ Renal disease
○ Nutritional
○ Age-related
32
Q

What is there an increased risk of in osteoporosis?

A

Increased fracture risk

33
Q

What is osteomalacia?

A

loss of bone mineralization

34
Q

What do we measure for the diagnosis of osteoporosis?

A

Measurement of bone mineral density (BMD)

35
Q

What scan do we use in the diagnosis of osteoporosis?

A

• Dual-energy X-ray absorptiometry (DEXA or DXA scan)

36
Q

What is the T score?

A

Number of SDs below average for young adult at peak bone density

37
Q

What is the Z score?

A

A Z-score compares your bone density to the average values for a person of your same age and gender.

38
Q

What are the endocrine causes of osteoporosis?

A

• Hypogonadism – notably any cause of oestrogen deficiency
○ Oestrogen is essential for bone health
○ Needed in males as well
○ inactivation of aromatase enzyme in men leads to failure of oestrogen production = osteoporosis
• Excess glucocorticoids – endogenous or exogenous
• Hyperparathyroidism
• Hyperthyroidism

39
Q

What are the different treatments for osteoporosis?

A
  • HRT
  • Bisphosphonates
  • PTH analogues
  • Denosumab
40
Q

What do bisphosphonates do?

A

inhibit function of osteoclasts leading to inhibition of bone resorption

41
Q

What is Denosumab?

A

An antibody against RANK ligand

42
Q

What is RANK and what does it stimulate?

A

○ Surface receptor on pre-osteoclasts

○ Stimulates osteoclast differentiation

43
Q

What are RANK ligands produced by?

A

○ Produced by pre-osteoblasts, osteoblasts and osteocytes

44
Q

What do RANK ligands do?

A

○ Bind to RANK and stimulates osteoclast differentiation

45
Q

What is OPG and what is it produced by?

A

○ Decoy receptor produced by osteocytes

46
Q

How do OPG works?

A

Binds to RANK-L, preventing activation of RANK

47
Q

What determines osteoclast differentiation rate?

A

Ratio of RANK-L to OPG is what determines osteoclast differentiation rate

48
Q

What is wnt signalling pathway required for?

A

• Required for osteoblast differentiation

49
Q

What is the wnt signalling pathway negatively regulated by and how?

A

Negatively regulated by DKK (dickkopf) and sclerostin (SOST)

-Interact with LRP5 receptor preventing interaction

50
Q

Steps involved in WNT signalling pathway

A
  1. WNT has GPCR
    ○ Frizzled
    ○ Requires co-receptor – LRP5/6
    ○ Both of these interact to activate WNT signaling
  2. Effector: beta-catenin
    ○ Locked in a network of interacting proteins until WNT binds
  3. Binding causes complex set of events freeing β-catenin
    4.Beta-catenin accumulates in cytoplasm and translocates to nucleus where it initiates transcription
51
Q

What is sclerostin highly expressed in?

A

Sclerostin (SOST) is highly expressed in osteocytes

52
Q

How does sclerostin work?

A

○ Secreted, makes its way to surface

○ Prevents osteoblast differentiation

53
Q

What must be downregulated for bone formation?

A

○ Must downregulate RANK-l secretion and SOST to allow osteoblast differentiation

54
Q

What must be upregulated to resorb bone?

A

○ Upregulate RANK-l and SOST to prevent osteoblast differentiation

Clinical biochemistry (6 decks)

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