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  LESIONS IN VITAMIN D DEFICIENCY.  Deficiency of vitamin D may result from: i) reduced endogenous synthesis due to inadequate exposure to sunlight; ii) dietary deficiency of vitamin D; iii) malabsorption of lipids due to lack of bile salts such as in intrahepatic biliary obstruction, pancreatic insufficiency and malabsorption syndrome; iv) derangements of vitamin D metabolism as occur in kidney disorders (chronic renal failure, nephrotic syndrome, uraemia), liver disorders (diffuse liver disease) and genetic disorders; and v) resistance of end-organ to respond to vitamin D. Deficiency of vitamin D from any of the above mechanisms results in 3 types of lesions: 1. rickets in growing children; 2. osteomalacia in adults; and 3. hypocalcaemic tetany due to neuromuscular dysfunction. RICKETS .  The primary defects in rickets are: interference with mineralisation of bone; and deranged endochondral and intramembranous bone growth. The pathogenesis of lesions in rickets is bette...

  LESIONS IN VITAMIN D DEFICIENCY.  Deficiency of vitamin D may result from: i) reduced endogenous synthesis due to inadequate exposure to sunlight; ii) dietary deficiency of vitamin D; iii) malabsorption of lipids due to lack of bile salts such as in intrahepatic biliary obstruction, pancreatic insufficiency and malabsorption syndrome; iv) derangements of vitamin D metabolism as occur in kidney disorders (chronic renal failure, nephrotic syndrome, uraemia), liver disorders (diffuse liver disease) and genetic disorders; and v) resistance of end-organ to respond to vitamin D. Deficiency of vitamin D from any of the above mechanisms results in 3 types of lesions: 1. rickets in growing children; 2. osteomalacia in adults; and 3. hypocalcaemic tetany due to neuromuscular dysfunction. RICKETS .  The primary defects in rickets are: interference with mineralisation of bone; and deranged endochondral and intramembranous bone growth. The pathogenesis of lesions in r...