Vitamin D

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Vitamin D

  1. 1.         Introduction Sources of dietary vitamin d Formation of vitamin d Biochemical effects of vitamin d Vitamin d related diseases rickets osteomalacia Toxicity hypervitaminosis D Requirements RDA References
  2. 2.      Sunshine vitamin. Vitamin D are a group of sterols that have hormone like function. Production of vitamin D is directly proportional to sunlight and inversely proportional to melanin pigmentation of skin. Commercially vitamin is derived from the fungus ergot. Two forms D2 ergocalciferol D3 cholecalciferol
  3. 3.       Not found naturally in many foods Synthesized in body Natural sources including cod-liver oil. Fatty fish species like eel catfish, salmon, tuna. Egg yolk also contains vit D Milk contains moderate quantity of the vitamin. Mushrooms also gives greater amounts of vitamin D when exposed to sunlight immediately after harvesting fungi and yeast which possess vitamin D precursor ergo sterol Vitamin D is also available from fortified food when supplemented with required nutrients such as bread cereal, margarine oil, milk pastries, yogurt etc.
  4. 4. The major biologic function of vitamin D is to maintain normal blood levels of calcium and phosphorus. Vitamin D aids in the intestinal absorption of calcium and phosphorous It promotes bone mineralization in concern with a number of other vitamins, minerals, and hormones. It maintains normal cellular growth and function. Stimulates renal tubular transport of Ca and P
  5. 5.    Although the body can obtain vit d from the diet the major source of this prohormone is its production in the skin from 7-dehydrocholestrol. It is located primarily in the malpighian layer of the skin. Upon exposure to UV light it is photo chemically converted to previtamin D, which then isomerizes to vitamin D over a period of several days. Once formed vitamin D is preferentially removed from the skin into the circulatory system by the blood transport protein for vitamin D, the vitamin Dbinding protein (DBP)
  6. 6.     In liver:- Cholecalciferol is first transported to liver –hydroxylation at 25th position-25 hydroxy cholecalciferol-by the enzyme 25 hydroxylase Note:- 25 hrdroxy cholecalciferol is the major transport form in plasma In kidney:-hydroxylated at 1st position-by 1 alpha hydroxylase-1,25dihydroxy cholecalciferol is generated. Since it has 3 hydroxyl groups its also called calcitriol-active form of vitamin d
  7. 7.    Vitamin D is best absorbed when ingested with lipids. Vitamin D will be incorporated into micelles and these will be absorbed by the intestine by passive diffusion. In the intestinal cells, chylomicrons will be formed, and these will enter the lymphatic system and enter the plasma. Vitamin D will then be transported to the liver by chylomicron remnants and to specific target with the help of carrier vitamin D binding protein (DBP) or transcalciferin.
  8. 8.  Vitamin D and intestinal absorption of calcium  Effect of vitamin D in bone  Effect of vitamin D in renal tubules
  9. 9.     Calcitriol promotes the absorption of calcium and phosphorous from the intestine. In the brush bordered surface ca is absorbed passively. From the intestinal cell to blood, absorption of calcium needs energy. Calcitriol enters the target cell and binds to a cytoplasmic receptor. The hormone-receptor complex interacts with DNA and causes derepession and consequent transcription of specific genes that code for calbindin. Due to the increased availability of calcium binding protein, the absorption of calicum is increased.
  10. 10.    Mineralization of bone is increased by increasing the activity of osteoblasts. Calcitriol stimulates osteoblasts which secrete alkaline phosphatase. Due to this enzyme the local concentration of phosphate is increased. The ionic product of calcium and phosphorous increases, leading to mineralization.
  11. 11.  Calcitriol increases the reabsorption of calcium and phosphorous from renal tubules, therefore both minerals are conserved.
  12. 12. Causes  Inadequate supply  Impaired absorption as in obstructive jaundice and steatorrhea. High phytate content in diet may also reduce the absorption of vitamin.  Secondary to abnormality of vitamin D activation. Liver and renal diseases may retard the hydroxylation reactions.  Secondary to abnormalities in renal absorption of phosphates.  Secondary to end organ resistance
  13. 13. Seen in children. Insufficient mineralization of bone. Bones become soft and pliable. Features  Delayed milestones  Delayed closure of anterior fontanellae  Delayed dentition  Deformities of bones  Decreased serum calcium
  14. 14. Bone deformities        Frontal bossing Weight bearing bones are bent Rachitic rosary Pigeon chest Knock-knee Bowed legs Harrison’s sulcus- transverse depression passing outwards from the costal cartilage to axilla. This is due to the indentation of lower ribs at the site of the attachment of diaphragm
  15. 15.    Classical vitamin D deficiency rickets- cured by giving vitamin d in the diet Hypophosphatemic rickets-result from defective renal tubular reabsorption of phosphate. Supplementation of vitamin D or its active form along with phosphate is found to be useful. Vitamin d resistant rickets-found to be associated with fanconi syndrome where the renal tubular reabsorption of bicarbonate, phosphate, glucose, and amino acids are also deficient. Metabolic acidosis is associated. Supplementation of vitamin D, phosphate and bicarbonate are beneficial.
  16. 16.   Renal rickets-in kidney diseases even if vit D is available calcitriol is not synthesized. These cases will respond to administration of calcitriol. End organ refractoriness to 1,25-DHCC will also lead to rickets. Either a decrease in the number of cytosolic receptor or a structurally abnormal receptor is noticed. The bone diseases has been found to respond to mega doses of calcitriol (35mg/day)
  17. 17.    Seen in adults Bones are softened due to insufficient mineralization and increased osteoporosis. Involves generalized reductions in bone density and the presence of pseudo fractures especially of the spine, femur and humerus Clinical features  Muscular weakness and bone tenderness  Increased softness of bones  Greater risk of fractures particularly of the wrist and pelvis  Bowing of long bones
  18. 18.    Excessive exposure to sunlight does not lead to overproduction of vitamin D. Toxicity is inevitably the result of overdosing on vitamin D supplements. Doses above 1500 I.U/ day for a very long periods may cause toxicity Excessive formation of vitamin D metabolites enhances the calcification of various tissues along with bones
  19. 19.          Intense thirst Difficulty in speaking Confusion Weight loss Hypokalemia Metabolic alkalosis Arterosclerosis or hardening of arteries occurs due to calcification of blood vessels Nephrocalcinosis deposition of ca in kidneys Nephrolithiasis deposition of ca in renal tubules
  20. 20.      Preschool children =10 microgram (400 I .U/ day) Older children and adults=5 to 10 microgram (200 I.U)/ day Pregnancy and lactation=10 microgram (400 I. U)/ day Persons between ages 50-60 =400 I.U/ day Senior citizens above the age of 60= 600 I.U /day

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