Hypophosphataemic rickets and

osteomalacia
impaired renal tubular reabsorption
of phosphate
Calcium levels normal, no
hyperparathyroidism defective of bone
mineralization
Occurs

Familial

hypophosphaetamic rickets

Commonest form, X-linked

Infancy looks normal, with genu valgum/varus
Adult heterotopic bone formation

Treatment

Phosphate (up to 3 gr/day) and large

dose of vitamin D
Bony deformities may require
bracing or osteotomy

Hyperparathyroidism
Primary : adenoma,hiperplasia
Secondary : persistent hypocalcemia
Tertiary : when secondary hyperplasia
leads to autonomous activity
Stimulating tubular absorption,intestinal
absorption,bone resorption calcinosis, stone
formation, recurrent infection, impaired
function(kidney)
Severe cases : osteoclastic hyperactivity
produces subperiosteal erosion,endosteal
cavitation,and replacementof marrow spaces
by vascular granulationand fibrous tissue
(osteitis fibrosa cistica)

1.

Primary hyperparathyroid
- Middle age, women:man = 2:1
- Clinical features : due to hypercalcemia,
chronic hypercalciuria, chondrocalcinosis
- Xray : subperiosteal cortical resorption of
middle phalanges(pathognomonic)
- Biochemical : hypercalcemia,
hypophosphatemia, serum PTH
- Diagnosis : exclusions of other causes
hypercalcemia in which PTH level
decreased
- Treatment : conservatives (adequate
hydration and dietary Ca restriction)

#parathyroidectomy indication:
- unremitting hypercalcemia, recurrent
renal calculi, progressive
nephrocalcinosis ,severe osteoporosis
#post operative hungry bone
syndrome, treated with one of the fast
acting vit D metabolites

2. Secondary hyperparathiroidisme
as response of chronic
hypocalcemia (rickets,osteomalacia)

Renal osteodistrophy
- Diffuse bone changes which are
variable combination of rickets or
osteomalacia, secondary
hyperparathyroidism,
osteoporosis, osteosclerosis
- Children clinically more severely
affected, they are stunted, pasty
faced, rachitic deformities

Xray

widened and irregular epiphyseal

plates
osteosclerosis in axial skeleton
rugger jersey in lateral xray of spine
Treatment
hemodyalisis or renal
transplatation
vit d 500.000 IU daily
1,25 DHCC in resistant cases

Scurvy
Causes failure of collagen syntesis
and osteoid formation
Clinical :
-infant irritable,
-anemic,
-gum spongy and bleeding
-subperiosteal bleeding-->pain &
tenderness near large joint

Xray : bone rarefaction, most in long bone

metaphysis

Hypervitaminosis
Hypervitaminosis

Children : excessive dosage

Clinical : bone pain, headache,
vomiting (intracranial pressure)
Xray: density in metaphysis and
subperiosteal calcification

Hypervitaminosis

PTH like effect

Ca is withdrawn from bones
Treatment :
Vit D dose regulated
Low ca diet, plentiful fluids (infants)

Fluorosis
Fluorine stimulates osteoclast activity
Clinically:
subperiosteal new bone accretion
and osteosclerosis
(vertebra,ribs,pelvis,forearm, and
leg)
Backache,bone pain,joint stiffness
Stress fracture (sometimes)

- Xray :osteosclerosis,osteophytosis,
and ossification of ligamentous and
fascial attachment

Paget disease (osteitis

deformans)
- Enlargement and thickening of bone
but internal architecture is abnormal
and the bone is unusually brittle
Clinical :
Pelvis and tibia the commonest site
Asimptomatic;pain,deformity
Limb looks bent and thick,skin
undully warm