Rickets

Question 1

What is rickets?

Answer 1

A disorder of defective mineralization of growing bone and cartilage due to deficiency of vitamin D, calcium, or phosphate. Occurs only in children with open growth plates.

Question 2

How does rickets differ from osteomalacia?

Answer 2

Rickets occurs in children with open growth plates, affecting cartilage mineralization, while osteomalacia occurs in adults, affecting bone matrix mineralization.

Question 3

What are the main types of rickets?

Answer 3

1. Calcipenic rickets – due to vitamin D or calcium deficiency. 2. Phosphopenic rickets – due to renal phosphate wasting or inherited defects.

Question 4

Describe the pathophysiology of rickets.

Answer 4

Defective mineralization of growth plate cartilage → disorganized proliferation → thickened metaphysis → soft, deformed bones.

Question 5

Why do bone deformities occur in rickets?

Answer 5

Unmineralized osteoid bends under mechanical stress, causing bow legs, knock knees, and widened metaphyses.

Question 6

Which hormone is elevated in calcipenic rickets and why?

Answer 6

Parathyroid hormone increases due to low calcium, enhancing bone resorption and phosphate loss (secondary hyperparathyroidism).

Question 7

List the general clinical features of rickets.

Answer 7

Failure to thrive, delayed milestones, irritability, muscle weakness, and skeletal deformities; severe cases may show tetany or seizures.

Question 8

List cranial manifestations of rickets.

Answer 8

Craniotabes (soft skull bones), frontal/parietal bossing, delayed fontanelle closure, and delayed dentition.

Question 9

What are the chest deformities seen in rickets?

Answer 9

Rachitic rosary (beading of costochondral junctions), Harrison’s sulcus (diaphragm pull groove), and pigeon chest (pectus carinatum).

Question 10

Describe the limb changes in rickets.

Answer 10

Widened wrists and ankles, bow legs (genu varum), knock knees (genu valgum), and windswept deformity.

Question 11

What neurological symptoms can occur in rickets?

Answer 11

Hypocalcaemia may cause carpopedal spasm, laryngospasm, tetany, and seizures.

Question 12

What are the classical radiographic features of rickets?

Answer 12

Cupping, fraying, and widening of the metaphysis with generalized demineralization, best seen at distal radius and ulna.

Question 13

Which bones are commonly affected radiologically in rickets?

Answer 13

Metaphyseal ends of long bones such as distal radius, ulna, femur, and tibia — most active growth areas.

Question 14

Summarize the biochemical findings in calcipenic rickets.

Answer 14

↓ Calcium, ↓ Phosphate, ↑ Alkaline phosphatase, ↑ PTH, and ↓ 25-hydroxyvitamin D.

Question 15

Summarize the biochemical findings in phosphopenic rickets.

Answer 15

Normal calcium, ↓ phosphate, ↑ alkaline phosphatase, normal or mildly low vitamin D levels.

Question 16

Which biochemical marker correlates best with disease activity in rickets?

Answer 16

Alkaline phosphatase level, reflecting osteoblastic activity and severity of disease.

Question 17

Outline treatment for nutritional (vitamin D deficiency) rickets.

Answer 17

Vitamin D 2,000–5,000 IU daily for 4–6 weeks or a single Stoss dose (300,000–600,000 IU) + calcium supplementation and sunlight exposure.

Question 18

How is acute hypocalcaemia managed in rickets?

Answer 18

Administer IV calcium gluconate (100 mg/kg) followed by oral calcium and vitamin D maintenance.

Question 19

How is rickets prevented?

Answer 19

Daily vitamin D 400 IU for term infants, 800 IU for preterms/twins, maternal supplementation, adequate calcium, and sunlight exposure.

Question 20

What indicates radiologic healing in rickets?

Answer 20

Formation of a dense line of provisional calcification at metaphyses and disappearance of cupping and fraying.