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LCRS Musculoskeletal > Clinical and biochemical features of metabolic bone disease > Flashcards

Clinical and biochemical features of metabolic bone disease Flashcards

1
Q

What serum investigations would you carry out for metabolic bone disease?

A

Calcium, corrected calcium, albumin, phosphate, PTH, 25-hydroxy vitamin D

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2
Q

What urine investigations would you carry out for metabolic bone disease?

A

NTX (n-terminal telopeptide; indicator of bone turnover rate) and calcium phosphate

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3
Q

What biochemical changes are there in osteoporosis?

A

Increased or normal bone formation and increased bone resorption
Calcium, phosphate and ALP are all normal

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4
Q

What biochemical changes are there in osteomalacia?

A

Calcium is decreased or normal
Phosphate is decreased
Alk P is increased

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5
Q

What biochemical changes are there in Pagets?

A

Ca and P are normal
ALP is greatly increased
Bone formation increases

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6
Q

What biochemical changes are there in primary hyperparathyroidism?

A

Increased calcium
Decreased phosphate
Normal or increased ALP
Increased bone resorption

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7
Q

What biochemical changes are there in renal osteodystrophy?

A

Decreased or normal calcium
Increased P
Increased ALP

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8
Q

What biochemical changes are there in metastases?

A

Increased Ca, P and ALP

Increased bone resorption

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9
Q

What happens to calcium as we age?

A

We have less in our diet

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10
Q

Where is calcium mainly absorbed and how?

A

Mainly in jejunum and ileum
It is either:
Passive (inefficient and not controlled)
Active (Vit D controlled)

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11
Q

What is the calcium that we measure in serum?

A

Total calcium

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12
Q

What percentage of calcium is free ionised?

A

47%

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13
Q

What percentage of calcium is bound to albumin?

A

46%

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14
Q

How does the remaining 7% of circulating calcium exist?

A

Complexed to phosphate and citrate

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15
Q

What does the state of calcium in the blood lead to?

A

Calcium levels are corrected in the blood to compensate for changes in protein levels; if the protein levels are high, they compensate down

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16
Q

When does the amount of protein-bound calcium increase?

A

During alkalosis

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17
Q

What does PTH have the predominant role in?

A

Minute by minute regulation of plasma calcium levels- if plasma Ca drops, within seconds there is secretion of PTH from pre-formed stores

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18
Q

What are the two systems that PTH acts on?

A

Bone- Acute release of available calcium; not in hydroxyapatite crystals- also increased osteoclast activity to reabsorb bone
Kidney- increased calcium re-absorption in the distal convoluted tubule; the only site where ca reabsorption is under active hormonal control. Stimulation of enzyme activity so increasing activated vit D production which leads to increased gut reabsorption of calcium; decreases enzyme activity and increases phosphorous excretion by inhibiting the NAP co-transporter in the proximal tubule

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19
Q

What is PTH as a molecule?

A

84 amino acid peptide hormone

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20
Q

What is the active form of PTH that is used to build bone?

A

N1-34

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21
Q

What is PTH dependent on?

A

Magnesium- low magnesium leads to low PTH and hypocalcaemia

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22
Q

What patients is the PTH dependence on magnesium important to remember in?

A

Alcoholics

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23
Q

What is the half life of PTH like?

A

Short of about 8 minutes which allows intraoperative sampling

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24
Q

What can also activate PTH receptors?

A

PTHrP which is produced by some tumours

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25
Q

What does PTHrP binding to PTH mean?

A

Hypercalcaemia may be a first presenting feature for example in small cell carcinoma of the lung

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26
Q

What does the calcium sensing receptor do?

A

Links serum calcium to PTH gland

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27
Q

What is the graph of the relation between PTH levels and Ca2+ in vivo like?

A

Steep inverse sigmoidal

28
Q

What is the set point of the graph between PTH and Ca2+?

A

Point of half of the maximal suppression of PTH; it is the steep part of the slope. A small perturbation causes a large change in PTH

29
Q

How does PTH release calcium from the bone?

A

Activating the RANK system

30
Q

Where is the RANK ligand found?

A

On osteoblast membrane

31
Q

What does vit D do in the intestine?

A

Activates Ca and P absorption in the duodenum (TRPV6, calbindin)

32
Q

What does Vit D do in bone?

A

Synergises with PTH acting on osteoblasts to increase formation of osteoclasts through RANKL

33
Q

What does Vit D do in the kidneys?

A

Facilitates PTH action to increase Ca reabsorption in the distal tubule

34
Q

What is Vit D’s effect on the parathyroid glands?

A

Negative feedback- reduces PTH secretion

35
Q

What is primary hyperparathyroidism?

A

Common disorder in which there is increase in serum calcium by absorption from the bone, gut and kidneys

36
Q

What are the causes of primary hyperparathyroidism?

A

Parathyroid adenoma is responsible for 80% of cases

Parathyroid hyperplasia is responsible for 20%

37
Q

What are the clinical features of primary hyperparathyroidism mainly due to?

A

High calcium

38
Q

What are the key clinical features of primary hyperparathyroidism?

A

Stones- renal colic
Bones
Abdominal groans- constipation
Psychic moans

39
Q

What is osteomalacia?

A

Inadequate vit D activity leads to defective mineralisation of the cartilaginous growth plate

40
Q

What are the signs and symptoms of osteomalacia?

A 
Bone pain
Tenderness
Muscle weakness
Age dependent deformity
Myopathy
Hypotonia
Short stature
Tenderness on percussion
41
Q

What is the difference between healthy bones and aged bones in terms of trabecular meshwork?

A

Healthy bones show thick plates within trabecular meshwork but ageing leads to loss of connections between the trabecular network- plate thins and continuity breaks

42
Q

As women age, which bones does fracture rate greatly increase for?

A

Vertebrae, hip and colles

43
Q

What happens due to menopausal bone changes?

A

Increase in the number of remodelling units and causes remodelling imbalance with increased bone resorption (90%) compared to bone formation (45%) due to enhanced osteoclast survival and activity

44
Q

What do the remodelling errors lead to?

A

Deeper and more resorption pits which leads to trabecular perforation and cortical excess excavation and decreased osteocyte sensing

45
Q

What effect does oestrogen have on bone?

A

Oestrogen increases the action of OPG therefore causing inhibition of the RANK pathway (which usually activates osteoclasts)

46
Q

How do menopausal changes lead to osteoporosis?

A

Menopausal changes include a decrease in oestrogen leading to reduced inhibition of the RANK pathway which leads to increased osteoclast action

47
Q

What causes high turnover of bone (bone resorption>formation)?

A 
Oestrogen deficiency
Hyperparathyroidism
Hyperthyroidism
Hypogonadism
Heparin
48
Q

What causes low turnover of bone (decreased bone formation)?

A

Liver disease
Heparin
Age

49
Q

What causes increased bone resorption and decreased formation?

A

Glucocorticoids

50
Q

What does high PTH and high free thyroxine indicate?

A

Primary hyperparathyroidism

51
Q

What is the best predictor of fracture risk?

A

Bone density

52
Q

What is the gold standard test for BMD?

A

DXA (Duel energy Xray absorptiometry)

53
Q

Why is DXA the gold standard?

A

It has good precision, short scan times and stable calibration in clinical use

54
Q

How does DXA work?

A

It measures transmission through the body of X-rays of two different photon energies. This enables densities of two different tissues to be inferred

55
Q

What do the WHO use to define osteoporosis?

A

T score- Measured BMD minus young adult mean BMD divided by the young adult mean BMD
Score less than -2.5 is indicative of osteoporosis
-1 - -2.5 is indicative of osteopenia
Score of over -1 is normal

56
Q

What site is commonly used to measure BMD?

A

Vertebrae because they’re a common place for fractures

57
Q

Whose BMD should be measured?

A 
People with risk factors:
Oestrogen deficiency
Corticoid steroid treatment
Maternal history of hip fracture
Low BMI
Other endocrine diseases
Malabsorption
Radiographic evidence of osteopenia and vertebral deformity
58
Q

What is disrupted in most bone diseases?

A

The bone cycle

59
Q

What gives us an insight into bone activity?

A

Bone markers

60
Q

What types of collagen are produced by osteoblasts?

A

Alpha 1 and 2 chains of type 1 collagen with proline and lysine residues being hydroxylated to form tropocollagen. 3 hydroxylysine molecules on adjacent tropocollagen fibrils condense to form a pyridinium ring linkage.

61
Q

What are good markers of bone resorption?

A

Collagen breakdown products as they’re directly linked

Serum CTX, NTX and tartrate resistant acid phosphatase can also be used

62
Q

How can osteoclast activity be measured?

A

Measuring urine hydroxyproline or urine collagen cross links

63
Q

What are bone markers used for?

A

Diagnosis of osteoporosis
Prediction of fracture risk
Monitoring of treatment

64
Q

What is tertiary hyperparathyroidism due to?

A

Chronic renal impairment

65
Q

What is the mechanism of tertiary hyperparathyroidism?

A

Nephron loss > Reduced production of active calcitriol > Reduced Vit D levels > Osteomalacia and hypocalcaemia>secondary PTH increase > increased bone resorption
There is also phosphate retention so hyperphosphataemia>combines with calcium to form metastatic calcifications around tissues and all vessels>atherosclerosis and further drop in Ca levels

LCRS Musculoskeletal (7 decks)

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