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Musculoskeletal > Metabolic bone disease: Biochemistry > Flashcards

Metabolic bone disease: Biochemistry Flashcards

1
Q

What are biochemical investigations used in bone disease?

A

Bone profile: calcium, albumin, phosphate, alkaline phosphate

Renal function: PTH, 25-OH vitD

Urine: Calcium, phosphate, NTX

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2
Q

What 3 systems control calcium?

A

Kidney
GI tract
Bones

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3
Q

How do we correct serum calcium calculations?

A

[calcium] + 0.02(45-[albumin])

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4
Q

How does PTH control calcium?

A

Low plasma Ca -> Release of PTH
PTH increases bone resorption
Acts on the kidney to increase calcium absorption/reabsorption and increase calcitriol formation, while increasing phosphate excretion in the urine

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5
Q

How does parathyroid gland monitor serum Ca?

A

Via calcium-sensing receptor

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6
Q

Diagnosis of Primary hyperthyroidism?

A

Hypercalcaemia with PTH in the upper half of the normal range

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7
Q

Chronically elevated PTH causes?

A

Gall stones
Increased cortical bone resorption
Increased fracture risk

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8
Q

Biochemical findings in Primary HPT?

A
  1. Increased serum calcium (by absorption from bone/gut)
  2. Decreased serum phosphate (renal excretion in proximal tubule)
  3. PTH in the upper half of the normal range or elevated
  4. Increased urine calcium excretion
  5. Cr may be elevated
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9
Q

What are the actions of vitamin D in the intestine, bone and kidney? What is its feedback mechanism?

A

Intestine: activates Ca/P absorption
Bone: Synergises with PTH - act on osteoblasts, increases formation of osteoclasts via RANKL. Also increases osteoblast differentiation/bone formation
Kidney: Facilitates PTH action to increase Ca reabsorption in DCT

Direct feedback on parathyroid to reduce PTH secretion
Feedback on bone to increase FGF-23 production

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10
Q

How is vit D deficiency defined?

A

Serum 25(OH)D = 21-29ng/ml

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11
Q

Define rickets

A

Vit D deficiency leading to defective mineralisation of growth plates (BEFORE hypocalcaemia)
Severe rickets may have hypocalcaemia

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12
Q

Biochemical findings in rickets/osteomalacia

A 
Serum:
Ca NORMAL (low in osteomalacia)
Phosphate NORMAL (low in osteomalacia)
Alk Phosphates HIGH
25(OH)D LOW
PTH high (secondary effect, to compensate)

Urine:
Phosphates HIGH

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13
Q

Where is FGF-23 produced and what does it do?

A

Produced by osteoblast lineage cells in long bones
Causes LOSS of phosphates in PCT -> phosphaturia (same as PTH)
Inhibits 1-alpha hydroxylase -> inhibits vit D activation (unlike PTH)

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14
Q

Name conditions which involve loss of phosphate leading to osteomalacia

A

X-linked hypophosphataemic Rickets
- High levels of FGF-23

Autosomal Dominant Hypophosphataemic Rickets
- High FGF-23

Oncogenic osteomalacia - mesenchymal tumours producing FGF-23 (phosphaturia + inhibit 1a-hydroxylase)

PCT damage -> phosphaturia and stops activation of vit D

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15
Q

What are the 4 Ms that make a bone strong?

A

Mass
Material properties
Microarchitecture
Macroarchitecture

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16
Q

Describe changes in bone mass with age in men and women

A

Women have lower bone mass in general
Both attain Peak bone mass at around 28-30yrs age
Followed by consolidation stage until early 40s (i.e. no change in BM)
Then age-related bone loss

Women have further decrease in bone mass (endocortical bone resorption) during menopause, meaning they could go below the fracture threshold at EARLIER age than men

17
Q

Significance of Peak Bone Mass? What factors affect it?

A

Important predictor of osteoporosis

Genetics, gender, nutrition (Ca), exercise levels, ethnic origin

18
Q

Lifespan of remodelling units, osteoclast, osteoblasts? How long does it take to replace whole skeleton?

A

remodelling units = 6-9 months
Osteoclast = 2 weeks
Osteoblast = 3 months
10 years

19
Q

What causes menopausal bone loss?

A

Estrogen deficiency
Increases number of remodelling units
Causes increased bone resorption (bone formation also increased but only half as much)
Causes remodelling errors - more/deeper remodelling pits
Decreased osteocyte sensing

20
Q

What is the likelihood of women having osteoporotic fracture?

A

HALF of women aged over 50

21
Q

Biochemical findings of osteoporosis

A 
Serum should all be NORMAL if primary osteoporosis
If secondary:
1. Check Vit D deficiency
2. Check secondary endocrine causes
3. Exclude multiple myeloma
4. May have high urine Ca

Diagnosis using bone density DEXA scan
T score less than -2.5 = Osteoporosis

22
Q

Which bone is measured for Fracture Risk Assessment Tool? (FRAX)

A

Hip bone

23
Q

Commonest fractures?

A
  1. Vertebral - measure of cancellous bone

2. Hip

24
Q

What are the bone formation/resorption markers?

A

Formation markers: P1NP - propeptide formed during collagen synthesis by osteoblasts

Resorption markers: Serum CTX, urine NTX
3-hydroxylysine condenses to form PYRIDINIUM linkage

25
Q

How do you monitor anti-resorptive drug treatment?

A

BMD change during 18 months
Bone resorption markers FALL in 4-6 weeks
Expect 50% drop of urine NTX by 3 months

26
Q

Problems with crosslink (resorption) markers

A

Increases with age

Fluctuates during day (peak 4-8am)

27
Q

Clinical use of bone markers?

A

Alkaline phosphatase
Used in diagnosis/monitoring of:
Paget’s, osteomalacia, boney metastases

P1NP being used for bone formation treatments
(e.g. PTH treatment - P1NP peaks at 3 months)

28
Q

What is BSAP?

A

Bone-specific Alkaline Phosphatase
Essential for mineralisation
Half-life 40hrs (so levels constant in individual)

29
Q

What conditions would you see an increase in BSAP?

A

Paget’s
Osteomalacia
Bone metastases

Possibly HPT and hyperthyroidism

30
Q

How do alkaline phosphatase levels change with age?

A

In both men and women: peaks mid-10s, stays consistently low for rest of life

31
Q

Biochemical findings of Renal osteodystrophy

A

Increased serum phosphate

Reduced calcitriol

32
Q

What are the consequences of renal osteodystrophy?

A

Secondary HPT develops to compensate but FAILS
Hypocalcaemia develops
Long-term: Parathyroids become autonomous (TERTIARY HPT) causing HYPERCALCAEMIA

Musculoskeletal (11 decks)

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