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  3. 3. 3it is also called SUNSHINE is available in 2 formsD3 – cholecalciferolD2 - calciferol
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  5. 5. Cholecalciferol (vitamin D3)is made from 7-dehydrocholesterol in the skinof animals and humans.calciferol - D2obtained artificially by irradiation of ergo-sterol and is called ergocalciferol
  6. 6. It is a steroid hormone.Biologically active formis CalcitriolSOURCES Fish liver oil Egg yolk Milk Butter Cheese MargarineRDA: 100 IU/day in adultspregnancy, lactation, infant and children ( 220 IU)
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  9. 9. 10 Sunshine Fish liver oils Oily fish Margarine
  10. 10. 11 The kidney, as well as liver furtherconverts this precursor into 1,25-hydroxyvitamin D, the mostphysiological active vitamin-Dmetabolite, which is also calledcalcitrol.
  11. 11.  Traditionally, calcitrol is understood as ahormone that, together with parathyroidhormone, regulates blood calcium levels and,in turn, bone density., calcitrol targets the intestine, where itpromotes calcium absorption; and bone, whereit catalyzes calcium deposition.
  12. 12. 13 Sunlight causes an opening of the sterol ringstructure, leading to formation of pre-vitaminD3. A slow process (1-2 days) converts pre-vitamin D3 to cholecalciferol. Daily exposureto sunshine is not necessary.
  13. 13.  Continued exposure to sunshine causes thereversible formation of inactivecomponents. There can be nooverproduction (hence no toxicity) ofnaturally-produced cholecalciferol since anyexcess is converted to these inactivecompounds.
  14. 14.  Ability to form cholecalciferol dependsupon availability in skin of 7-dehydrocholesterol. Although thismolecule is generally plentiful in skin,reduction with aging can diminishcholecalciferol production, necessitatingvitamin D supplementation in the elderly.
  15. 15.  Since vitamin D from foods is transported tothe liver in chylomicrons. All free vitamin Dmetabolites are transported in the blood, asD-binding protein (DBP). In the mitochorndriaof the renal proximal tubular cells, 1,25-(OH)2-D reaches its target organs throughthe bloodstream where it circulates bound toproteins.
  16. 16.  Hydroxylation in the liver at C25 yieldsthe intermediate 25-hydroxy-cholecalciferol. This is transformed intothe active form of the vitamin byfurther hydroxylation at C1 to 1,25-dihydroxy-cholecalciferol (1,25-(OH)2-D-3), a steroid hormone. Additionally, amultitude of synthetic vitamin Danalogues exist that are used for thetreatment of disturbances in a Ca
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  18. 18. 20 Precursors of vitamin D are found in bothyeast and animal tissues. In yeast, a sterolprecursor (ergosterol) is converted to vitaminD2 (ergocalciferol). Ergocalciferol is thecompound most commonly found as theadditive to fortify milk.
  19. 19.  In the dermal tissue of animals, the precursor is7-dehydrocholesterol which is converted first to apre-vitamin D3, then to vitamin D3(cholecalciferol). Vitamin D2 and vitamin D3 are both converted tosimilar active compounds (calcidiol andcalcitriol) in the liver and kidney. D2 and D3 aresometimes referred to as vitamers.
  20. 20.  circulating calcitrol enters cells andcomplexes with the genes in the cell nucleus. This affects DNA expression and, in turn,overall cell functioning and growth. Because calcitrol maintains normal cellproliferation, it inhibits cancerous growth.
  21. 21. 23 In addition, calcitrol influences immune-cell activity, helping to explain vitaminD’s seemingly beneficial role ininfectious disease and immune-relateddisorders, such as multiple sclerosis,rheumatoid arthritis, and diabetes.
  22. 22.  How is vitamin D transported andstored?This depends upon the source of the vitamin D.Vitamin D that is taken into the gut (vitamin D-containing foods or nutritional supplements) areabsorbed by intestinal mucosal cells in theduodenum and jejunum and packaged, alongwith dietary fat, into lipoproteins calledchylomicrons (CM).
  23. 23. 25 These CM are first put into the lymph, thendeposited into the blood stream. The CM carrythe vitamin to the liver or adipose for storageand eventual use. Vitamin D synthesized in skin through theaction of sunlight is bound to a blood proteincalled (vitamin) D binding protein (DBP),which transports it to the liver.
  24. 24. 1. Vitamin-D promotes absorption of Ca++and P by the intestine. It stimulatesthe synthesis of a specific Ca++binding protein by intestinalepithelium.
  25. 25. 1. Vitamin-D induces the synthesis ofspecific Ca++binding protein inbones2. Vitamin-D regulates the Ca++level byreabsorbing Ca++through the kidney
  26. 26. 4. Vitamin-D promotes mineralization ofbones through deposition of Ca++andP in growing bones.5. Vitamin-D increases the reabsorptionof PO4 through renal tubules.
  27. 27. 4. Vitamin-D acts as coenzyme foralkaline phosphatase5. Vitamin-D is responsible forenameling of the teeth. Itsdeficiency leads to irregular andrough teeth
  28. 28. 8. Vitamin-D promotes growth in generaland is essential for normal health.BMR is decreased in vitamin-Ddeficiency. The deficiency of vitamin-D leads to the repeated attacks ofrespiratory diseases.
  29. 29. 33 Men and women- 0.01 mg. Pregnancy and lactation – 0.01 mg Infants & Children –0.01 mg
  30. 30. DEFICIENCYRicketsOsteomalacia
  31. 31. 36 Rickets was once considered an extremelycommon disorder of childhood. The termitself is derived from the old English wordfor "twist,”
  32. 32.  Rickets is caused by a deficiency in vitaminD. During growth, human bone is made andmaintained by the interaction of calcium,phosphorus, and vitamin D. Calcium isdeposited in immature bone (osteoid) in aprocess called calcification, which transformsimmature bone into its mature and familiarform.
  33. 33.  in order to absorb and use the calciumavailable in food, the body needs vitamin D. Inrickets, the lack of this important vitamin leadsto low calcium, poor calcification, anddeformed bones.
  34. 34. 39Bow LegsFrontal & Parietal BossingPigeon ChestSoft & fragile bonesProminence of sternumDEFICIENCYRICKETSHarrison’s groove
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  36. 36. 42Frontal bossingHarrisons sulcusand pot belly
  37. 37. 43Rib beadingrickety rosaryBowleg deformity
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  39. 39. 45ScoliosisWrist enlargement
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  41. 41. 47Knock knee deformityWrist enlargementRib beading(rachitic rosaryHarrisons sulcusand pot belly Chest deformity Frontal bossingScoliosisX-ray in rickets
  42. 42. 48Rickets can be caused by lack ofsunlight, but also frominsufficient calcium. Vitamin Dlinked to calcium absorption.
  43. 43. 50Osteomalacia it is also known as adult rickets and flat bonesand diaphysis of long bones are affected it is most commonly seen in post menopausefemale with history of low dietary calciumintake. The majority of patient have bone pain&muscle weakness..
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  45. 45. 52 Teeth – developmental abnormalities ofdentine & enamel. Caries – higher risk of caries Enamel – there may be hypoplasia of enamel,may be mottled, yellow gray in color Pulp – high pulp horns, large pulp chamber,delayed closure of root apices
  46. 46. 53 Dietary enrichment of vitamin D in the form ofmilk Curative treatment includes 2000 to 4000 IU ofcalcium daily for 6 to 12 weeks. Patient with osteomalacia due to intestinalmalabsorption require larger dose of vitamin D &calcium i.e. 40,000 to 1,00,000 IU of vitamin D&15 to 20 gms of calcium lactate.
  47. 47. 54Before treatment After treatment
  48. 48. Effects are mainly due to hypercalcaemiaIMMEDIATE DELAYEDAnorexia Urinary lithiasis. ThirstMetastatic calcification LassitudeConstipationPolyuria
  49. 49. Toxicity: Malaise, drowsiness, nausea, abdominalpain, thirst, constipation and loss ofappetite. Long term effect – ectopic calcificationanywhere in the body, renal damage,renal calculi. Prolonged use in infants can causemental and physical retardation, kidneyfailure and death.
  50. 50.  Dangerous to exceed 10,000units daily vit D in an adult morethan 12 weeks. Vit D supplements should beavoided in individuals especiallyinfants and children. Should not exceed 400 units aday.