AP: Metabolic Bone Disease Flashcards Preview

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Flashcards in AP: Metabolic Bone Disease Deck (30)
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1
Q

Causes of hypercalcemia.

A
  • Primary hyperparathyroidism.
  • Malignancy.
  • Sarcoidosis.
  • Vit D intoxication.
  • Milk alkali syndrome.
  • Familial conditions.
  • Drugs.
  • Other endocrine disorders.
  • Immobilisation.
  • Renal disease.
2
Q

Describe osteoporosis

A

completely normal bone in terms of structure and cellularity, just less of it.

3
Q

What are the normal constituents of bones?

A
  • Cells: osteocytes, -blasts, -clasts
  • Mineral: calcium hydroxyapatite crystals
  • Organic matrix: collagen (type1), glycosaminoglycans
4
Q

What is osteoid?

A

The non-mineralised matrix synthesised by osteoblasts

5
Q

What does mineralisation require?

A
  • Adequate calcium, phosphate

- Normal cellular function

6
Q

What are the primary regulators of calcium and phosphate?

A
  • Parathyroid hormone

- Vitamin D

7
Q

What are the two principal functions of bone remodelling?

A
  1. Allows repair of microscopic areas of damage within bone to maintain skeletal strength
  2. Allows release of calcium to maintain serum calcium levels
8
Q

Where does trabecular bone loss tend to occur?

A

Women: spine, distal radius, hips

Men: spine and hips

9
Q

What factors influence osteoporosis development?

A
  • Peak bone mass
  • Rate of bone loss
  • Imbalance resorption and formation
  • Calcium metabolism
  • Hormonal status
10
Q

What are the 3 different types of osteoporosis?

A

Type 1 - post menopausal (trabecular, forearm, spinal fractures)

Type 2 - age related (cortical and trabecular, hip fracture)

Secondary - caused by some other endocrine disease (e.g. Cushing’s, hyperparathyroidism), drugs, malabsorption and rheumatological diseases

11
Q

How does osteoporosis present clinically?

A

Typically asymptomatic: presents with complications:

  • pain
  • microfractures
  • deformity
  • fractures
12
Q

How do you diagnose osteoporosis?

A

Densitometry: bone mineral density by dual x-ray absorptiometry (DEXA)

** X-ray can see fractures, cortical thinning, & reduced density but has low sensitivity.

13
Q

How are DEXA scans scored, and what are the WHO classifications?

Where are the scans taken?

A

T-score = number of standard deviations above/below the density of a young person (peak bone mass) of the same race as the patient.

Normal = T score > -1
Osteopenia = T score -1 to -2.5
Osteoporosis = T score < -2.5
Severe osteoporosis = T score

14
Q

What is osteomalacia?

A

Defective mineralisation of organic matrix; relative excess of osteoid.

Deficiency of both quality & quantity of bone. Loss of stiffness of bone and increased susceptibility to compressive forces.

15
Q

What is osteomalacia in children?

A

Rickett’s

16
Q

What are some causes of osteomalacia/ricketts?

A
  • Dietary deficiencies (Vit D, Ca, P)
  • Lack Vit D (no sun exposure, malabsorption, chronic renal or hepatic disease)
  • Vit D resistance (phosphate wasting)
  • Hypophosphatemia (renal tubular disorders, antacids)
  • Drugs (heavy metals)
  • Neoplasia (oncogenic osteomalacia)
17
Q

What are clinical presentations of osteomalacia?

A

May be asymptomatic: soft (deforms), fragile bone (fractures), bone pain, proximal muscle weakness (hypocalcemia)

Generalised osteopenia (reduced skeletal mass)

18
Q

What is a hallmark of Ricketts?

A

Abnormal, thickened epiphyses: often terrible deformities
If untreated causes reduced long bone growth
Patients show weakness & hypotonia

19
Q

Are we likely to see lots of Osteomalacia in Australia?

A

Tends to occur more in impoverished countries, mores in low SES contexts.

Most of developed world has adequate sunlight and/or fortified foods

20
Q

What is hyperparathyroidism and what are its consequences?

A

Excess of parathyroid hormone secrete by parathyroid

Excess activation of osteoclasts - chomp bone up

21
Q

What are the causes of primary hyperparathyroidism?

A
Parathyroid adenoma (80%)
Parathyroid hyperplasia (15-20%). Mostly sporadic, genetic conditions = small proportion of these. 

In both cases, pump out parathyroid hormone for no reason (autonomously)

22
Q

What are the causes of secondary hyperparathyroidism?

A
  • Chronic hypocalcaemia (perpetually low Calcium levels e.g. in chronic renal failure)
  • lack of negative feedback
    » Hypersecretion of PTH

Bone effects usually less severe than primary

23
Q

What are clinical manifestation of hyperparathyroidism?

A
  • Dissecting/tunnelling bone resorption
  • Diffuse osteopenia

Tunneling resorption: fibrosis and osteoclastic activity from the inside of the trabeculae
Dissecting resorption: Haversian systems expanded w irregular scalloping of walls

24
Q

What is Paget’s disease of bone?

A

Poorly understood idiopathic disorder where bone decides to remodel itself for some reason

25
Q

What are the 3 stages of Paget’s?

A

1) osteolytic
2) mixed (lytic and blastic)
3) osteoblastic/sclerotic phases

Results in thick, soft, porous bone, prone to compression and deformity

26
Q

What are the common sites and symptoms of Paget’s?

A
  • Skull: enlargement, cranial nerve compression
  • Thoraco-lumbar spine: pain, neurological, cord compression
  • Pelvis sacrum: pain, arthritis
  • Femur, tibia: pain, deformity, path fracture
27
Q

What is renal osteodystrophy?

A

Range of bone abnormalities seen in chronic renal disease and haemodialysis (basically combo of everything else in lecture)

28
Q

Explain the pathophysiology of renal osteodystrophy

A

renal failure = hypocalcaemia

Low serum calcium —> hyperparathyroidism = osteoclastic activity = Reduced skeletal mass

Renal failure —> vitamin D problem

29
Q

What are 3 types of localised osteoporosis?

A

Not caused by systemic metabolism issues like general osteoporosis, localised to area of neuro/vascular/mechanical issue.

  1. disuse, immobilised (ie plaster cast)
  2. vasomotor injury (complex regional pain syndrome = loss of density in one limb/area)
  3. Transient regional (similar to disuse but not immobilised)
30
Q

Laboratory & microscopic signs of osteomalacia

A

Vary according to the underlying cause of the disease process

  • low to normal serum calcium
  • low phosphate
  • high alkaline phosphatase

Microscopic = increased osteoid (unmineralised matrix) on surfaces of bone trabeculae.