Osteomalacia and rickets

Question 1

Definition

Answer 1

condition where the bones become soft and weak. Meaning they can bend and break more easily.

There is normal quantity of bone tissue but reduced quantity of mineral content = excess of uncalcified osteoid and cartilage.

after fusion of epiphyses- osteomalacia
In younger children during phase of growth- rickets

Question 2

Aetiology

Answer 2

Problems with metabolism of vitamin D (liver/kidney disease)

Deficiency of vitamin D-
– poor intake
– poor absorption
– lack of sunlight

Drug induced disease (E.g: anticonvulsants leading to break down of 25-hydroxycholecalciferol from enzyme induction)

Resistance to vitamin D metabolism (e.g: hypophosataemic)

Question 3

Osteomalacia clinical features

Answer 3

Bone pain

Deformity of bone (curved long bones)

proximal myopathy (symmetrical weakness of proximal upper and/or lower limbs)

waddling gait

easy fracturing

pelvic flattening

Question 4

Rickets clinical features

Answer 4

Poor general health

Retarded skeletal growth, long bones curved, enlarged epiphyses, chest deformity with transverse sulcus

Reduced skeletal density

Curved bones

Epiphyseal cartilage:
– increased, ragged, cupped

Widened metaphysis

Question 5

Investigations

Answer 5

Radiographic features:
- plasma biochemistry-
– normal or low calcium, low phosphate with raised ALP

• urine stool may be taken
• bone biopsy
• technetium bone scan

Question 6

Treatment

Answer 6

Calcium/vitamin D tablets dependant upon the cause

Question 7

Pathophysiology

Answer 7

Vitamin D acts on the liver and kidney to eventually form 1,25 dihydroxycholecalciferol (calcitriol)

Calcitriol acts on the GIT to increase calcium into the blood, and because the bone is constantly being rebuilt and broken down, having less calcium available will mean the new bone that forms will be less mineralised