Ricetcs cause & T/t

Introduction Rickets is defective mineralization or calcification of bones before epiphyseal closure in immature mammals due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium. Potentially leading to fractures & deformity Although it can occur in adults, the majority of cases occur in children suffering from severe malnutrition. Usually resulting from famine or starvation during the early stage of childhood. Ostesmalacia is a similar condition occurring in adults due to a deficiency of vitamin D but occurs after epiphyseral closure.  Cause o The primary cause of rickets is a vitamin D deficiency. Vitamin D is required for proper calcium absorption from the guit. o Sunlight specially ultraroslent light lets human skin cells convent vitamin D from an inactive to active state o A rave x – linked dominant form exists called vitamin D resistost or x linked pophosphatemia o The sun’s ultraroilet light was not reaching the skin due to use of strong sunblock o Mothers aroid exposure to the sun for religious or cultural reasons leading to a maternal shortage of vitamin D o People with darker skins need more sunlight to maintain vitamin D levels Types Nutritional Rickets – Due to mal nutrition This type is most common Vitamin D resistant Rickets – - Also called x-linked dominat hypophosphatemic Rickets. - It is associated with a mutation in the gene seqarence - Vitamin D – Dependent Rickets – Two distinct ereditorg degecit Type I – Deficiency of the renal 25- hydroxyl vitamin D-1 alpha hydroxyllase muscle weakness and rickets are elinical findigs type-II Consist of a spectrum of intracellubor vitamin D receptor defects. And charactenized by the early onset of rickeits and associated alopecia Signs and symptoms 1. Bone tenderness 2. Dental problems 3. Muscle weakness rickety myepathy. 4. Increased tendencyfor fracture, especially green stick graeture 5. Skeletal deformity (a) Toddlers – Boulled legs – genu varun (b) Alder children – knock knees – genu valgum (c) Skull bossing or delaged frkontanelle closure. (d) Pelvic deformity (e) Spiral deformity – such as kyphoscoliosis 6. Growth disturbance 7. Hypocalcemia – Low level of calcium in the blood. 8. Tetang- uncontrolled muscle spasm 9. Craniotabes – soft skull 10. Costochondral swelling – rickety rosary 11. Widening of wrist Diagnosis An x – ray or radiograph of an advanced sufferer from rickets tends to present in a classic usage bowed leg and a deformed chest etc. Blood test  Serum calcium may show low levels of calcium (Normal 8.8-10.8 mg /dL)  Serum phosphonus may be low (1-9 y- 145 -200 o/L (2.4-4.1 mg /dL) 10-11 y-130-560 o/L  Serum alkadine posphatase may be high Bone Bipsy Is rarely performed but will confirm rickets Epidemiology In developed countries, rickets ia a rare disease – less then1 in 2,00,000 Those at higher risk for developing rickets include :  Breast fed infants whose mother are not exposed to sunlight  Breast fed infants who are not exposed to sunlight  Breast fed babies who are exposed to little sunlight  Any child whose diet does not contain enough vitamin Treatment & prevention Vitamin D 5000-1500 IU /day for three to four weeks and then smaller dose. Diet Increasing dietary intake of calcium, phosphates and vitamin D. Cod liver oil, holibal liver oil, viosteral, butter, eggs, fortiged milk etc. are all sources of vit D. Sunlight Exposure to ultraviolet B light most easily obtained wen the sun is highest in the sky