Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2: Musculoskeletal > Metabolic bone disease: Biochemistry > Flashcards

Metabolic bone disease: Biochemistry Flashcards

1
Q

symptoms of MBD

A

Metabolic

  • Hypocalacaemia
  • Hypercalcaemia
  • Hypo/Hyper phosphataemia

Specific to bone
- Bone pain –> deformity and fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the biochemical investigations in bone disease? What are the biochemical changes in bone disease?

A

See slides 16 and 17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Bone calcium

A

Is in the form of hydroxyapatite

Cancellous bone is metabolically active:

  • 5% is remodelling at anytime total
  • the whole skeleton is remodelled over 7 years
  • Continuous exchange of ECF with bone fluid reserve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Calcium balance

A

See endocrinology

Bone acts as the compensatory mechanism when everything goes wrong in the calcium homeostasis.
Post menopausal women are less efficient at getting Ca because lack of oestrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the serum levels of calcium and how are they corrected?

A

46% protein bound (to albumin)
47% Free ionized
7% complexed (to P and citrate)

So the corrected calcium a lab gives you compensates for the protein level; if protein levels are HIGH they compensate down; o.o2 for each g/l of albumin

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

Alkalosis changes ionized to protein bound –> more Ca binds to protein so free levels of Ca2+ drop = tingling sensation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the role of PTH?

A

Acts on 2 systems

  1. Bone acute release of available calcium; not in hydroxyapatite crystals
    more chronically INCREASED osteoclast activity to reabsorb bone
  2. Kidney increased Ca reabsorption in the distal conv tubule. Also activates renal 1-alpha hydroxylase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the clinically relevant points about PTH?

A

See slides

1 - 84 amino acid peptide but N1-34 active

  1. Mg dependent
  2. plsma half life 1/2 8 mins
  3. PTH1 receptor is actvated by…
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the clinically relevant points about PTH?

A
  1. 84 amino acid peptide
    but N1-34 active
  2. Mg dependent
  3. T 1/2 8 min
  4. PTH receptor is activated
    also by PTHrP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does PTH drive in terms of the kidney?

A

It drives active calcium absorption in the distal tubule of the kidney.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does PTH affect bone reabsopriton?

A

Causes bone reaborption through the RANK ligand system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the causes of HPT?

A
  • Parathyroid adenoma
  • Parathyroid hyperplasia
  • Parathryoid cancer
  • Familial syndrome (under age 40 –> higher chance of familial syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do you diagnose primary HPT?

A

Primary hyperthryoidism is diaignosed by:

An elevated total/ionised calcium with PTH levels fankly elevated or in the upper half of the normal range.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the clinical features of hyperthyroidism?

A

These features are mainly due to the high calcium - hypercalcaemia

Thirst, polyuria, tiredness, fatigue, muscle weakness.

Stones, adbominal moans and psychic groans.

1) Renal colic, nephrocalcinosis, CRF
2) Dyspepsia, pancreatitis, constipation, nausea, anorexia
3) Depression , impaired concentration, drowsy and coma

Patients may also supper fractures secondary to bone resorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why does hypercalcaemia cause diuresis?

A

Na/Cl/K co transporter transports these ions into cells of the ascending loop. K+ is then recycled out.

High levels of Ca2+ –> shuts down the counter current system. The K+ transport stops moving K+ out of the cell which means the co transporter can not bring ions in. Water moves out by osmosis. Viscous cycle

The diuresis results in hypercalciuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does chronic elevated PTH cause?

A

Causes increased cortical bone resorption
Increased bone turnover
The cortical bone > cancellous

Increases fracture risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the biochemical findings in primary HPT?

A

1) Increased serum calcium
2) Decreased serum phosphate
3) PTH in the upper half
4) Creatinine may be elevated

17
Q

Describe the metabolism of the vitamin D

A

See slides and endocrinology

18
Q

How do you define vitamin D deficiency?

A

You define it as the level where PTH starts to rise

See slides

19
Q

Define rickets?

A

Inadequate vitamin D activity leads to defective mineralisation of the cartilagenous growth plate (before a low calcium)

Severe rickets may have hypocalcaemia (this is serious because hypocalcaemia has many neuromuscular problems) chovestek sign + Trousseaus’s sign

See slides for symptoms and signs

20
Q

Causes of rickets/osteomalacia?

A

Vitamin D related

1) Dietary
2) GI - small bowel malabsorption/bypass, pancreatic insufficiency, liver/biliary disturbance, drugs
3) Renal - Chronic renal failure
4) Rare hereditary - Vitamin D dependent rickets
Type I = Deficiency of 1 alpha hydroxylase
Type II = Defective vitamin D receptor for calcitriol

21
Q

Describe the biochemistry of rickets?

A

Serum:

  • calcium = N/low
  • Phosphate = N/low
  • 25(OH) Vita D = low
  • PTH = high
  • Alk phos = high

Urine:
- phosphate = high

22
Q

Bone and phosphate?

A

see slide

If phosphate levels are low and they have rickets there are probably problems with the kidney

The PCT is where phosphate resorption occurs with Na+PO4^3- cotransporter. Damage to the PCT results in phosphaturia and stops the 1 alpha hydroxylation of vitamin D.

Fanconi syndrome = see slides

23
Q

What is FGF-23

A

See endocrinology - from osteocytes

  • Inhibits calcitriol = less phosphate resorption in the gut
  • Inhibits Na+/PO4^3- co-transporter = more phosphate excretion like PTH
24
Q

What can FGF-23 cause?

A

Excess can cause rickets/osteomalacia as normal phosphate levels are required for bone and cartilage mineralisation.

Kidneys are forced to lose phosphate. Isolated hypophophataemia: X linked mutations in PHEX = high levels of FGF-23. Autosomal dominant: Mutation of FGF-23 cleavage site = high FGF-2

Oncogenic osteomalacia - mesenchymal tumours produce FGF-23

25
Q

Describe the effect of the menopause on bone?

A

Menopause results in an estrogen deficiency which:

Increases the number of remodelling units

  • Causes remodelling imbalance with increased bone resorption (90%) compared to bone formation (45%) Enhanced osteoclast survival and activity
  • Remodelling errors. Deeper and more resorption pits lead to
    1) Trabecular perforation
    2) Cortical excess excavation
  • Decreased osteocyte sensing

Year 2: Musculoskeletal (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions