Uploaded byDr Muhammad Mustansar
VITAMIN D MUHAMMAD MUSTANSAR
Vitamin D is an essential nutrient that promotes calcium absorption in the intestines and maintains adequate serum calcium and phosphate concentrations to enable normal mineralization of bone. It exists in two main forms, D2 (ergocalciferol) and D3 (cholecalciferol), and is obtained through exposure to sunlight, dietary intake of oily fish, eggs, and vitamin D fortified foods. The liver converts vitamin D to calcidiol which is then converted by the kidneys to calcitriol, the biologically active form, which regulates calcium and phosphate levels. Deficiencies can lead to rickets in children and osteomalacia in adults, characterized by soft, deformed bones and muscle weakness.
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VITAMIN D MUHAMMAD MUSTANSAR
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- 3. 3 it is alsocalled SUNSHINE VITAMIN. it is available in 2 forms D3 – cholecalciferol D2 - calciferol
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- 5. Cholecalciferol (vitamin D3) ismade from 7-dehydrocholesterol in the skin of animals and humans. calciferol - D2 obtained artificially by irradiation of ergo- sterol and is called ergocalciferol
- 6. It is asteroid hormone. Biologically active form is Calcitriol SOURCES Fish liver oil Egg yolk Milk Butter Cheese Margarine RDA: 100 IU/day in adults pregnancy, lactation, infant and children ( 220 IU)
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- 10. 10 Sunshine Fishliver oils Oily fish Margarine
- 11. 11 The kidney,as well as liver further converts this precursor into 1,25- hydroxyvitamin D, the most physiological active vitamin-D metabolite, which is also called calcitrol.
- 12. Traditionally, calcitrolis understood as a hormone that, together with parathyroid hormone, regulates blood calcium levels and, in turn, bone density., calcitrol targets the intestine, where it promotes calcium absorption; and bone, where it catalyzes calcium deposition.
- 13. 13 Sunlight causesan opening of the sterol ring structure, leading to formation of pre-vitamin D3. A slow process (1-2 days) converts pre- vitamin D3 to cholecalciferol. Daily exposure to sunshine is not necessary.
- 14. Continued exposureto sunshine causes the reversible formation of inactive components. There can be no overproduction (hence no toxicity) of naturally-produced cholecalciferol since any excess is converted to these inactive compounds.
- 15. Ability toform cholecalciferol depends upon availability in skin of 7- dehydrocholesterol. Although this molecule is generally plentiful in skin, reduction with aging can diminish cholecalciferol production, necessitating vitamin D supplementation in the elderly.
- 16. Since vitaminD from foods is transported to the liver in chylomicrons. All free vitamin D metabolites are transported in the blood, as D-binding protein (DBP). In the mitochorndria of the renal proximal tubular cells, 1,25- (OH)2-D reaches its target organs through the bloodstream where it circulates bound to proteins.
- 17. Hydroxylation inthe liver at C25 yields the intermediate 25-hydroxy- cholecalciferol. This is transformed into the active form of the vitamin by further hydroxylation at C1 to 1,25- dihydroxy-cholecalciferol (1,25-(OH)2- D-3), a steroid hormone. Additionally, a multitude of synthetic vitamin D analogues exist that are used for the treatment of disturbances in a Ca
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- 20. 20 Precursors ofvitamin D are found in both yeast and animal tissues. In yeast, a sterol precursor (ergosterol) is converted to vitamin D2 (ergocalciferol). Ergocalciferol is the compound most commonly found as the additive to fortify milk.
- 21. In thedermal tissue of animals, the precursor is 7-dehydrocholesterol which is converted first to a pre-vitamin D3, then to vitamin D3 (cholecalciferol). Vitamin D2 and vitamin D3 are both converted to similar active compounds (calcidiol and calcitriol) in the liver and kidney. D2 and D3 are sometimes referred to as vitamers.
- 22. circulating calcitrolenters cells and complexes with the genes in the cell nucleus. This affects DNA expression and, in turn, overall cell functioning and growth. Because calcitrol maintains normal cell proliferation, it inhibits cancerous growth.
- 23. 23 In addition,calcitrol influences immune- cell activity, helping to explain vitamin D’s seemingly beneficial role in infectious disease and immune-related disorders, such as multiple sclerosis, rheumatoid arthritis, and diabetes.
- 24. How isvitamin D transported and stored? This depends upon the source of the vitamin D. Vitamin D that is taken into the gut (vitamin D- containing foods or nutritional supplements) are absorbed by intestinal mucosal cells in the duodenum and jejunum and packaged, along with dietary fat, into lipoproteins called chylomicrons (CM).
- 25. 25 These CMare first put into the lymph, then deposited into the blood stream. The CM carry the vitamin to the liver or adipose for storage and eventual use. Vitamin D synthesized in skin through the action of sunlight is bound to a blood protein called (vitamin) D binding protein (DBP), which transports it to the liver.
- 27. 1. Vitamin-D promotesabsorption of Ca++ and P by the intestine. It stimulates the synthesis of a specific Ca++ binding protein by intestinal epithelium.
- 28. 1. Vitamin-D inducesthe synthesis of specific Ca++ binding protein in bones 2. Vitamin-D regulates the Ca++ level by reabsorbing Ca++ through the kidney
- 29. 4. Vitamin-D promotesmineralization of bones through deposition of Ca++ and P in growing bones. 5. Vitamin-D increases the reabsorption of PO4 through renal tubules.
- 30. 4. Vitamin-D actsas coenzyme for alkaline phosphatase 5. Vitamin-D is responsible for enameling of the teeth. Its deficiency leads to irregular and rough teeth
- 31. 8. Vitamin-D promotesgrowth in general and is essential for normal health. BMR is decreased in vitamin-D deficiency. The deficiency of vitamin- D leads to the repeated attacks of respiratory diseases.
- 33. 33 Men andwomen- 0.01 mg. Pregnancy and lactation – 0.01 mg Infants & Children –0.01 mg
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- 36. 36 Rickets wasonce considered an extremely common disorder of childhood. The term itself is derived from the old English word for "twist,”
- 37. Rickets iscaused by a deficiency in vitamin D. During growth, human bone is made and maintained by the interaction of calcium, phosphorus, and vitamin D. Calcium is deposited in immature bone (osteoid) in a process called calcification, which transforms immature bone into its mature and familiar form.
- 38. in orderto absorb and use the calcium available in food, the body needs vitamin D. In rickets, the lack of this important vitamin leads to low calcium, poor calcification, and deformed bones.
- 39. 39 Bow Legs Frontal &Parietal Bossing Pigeon Chest Soft & fragile bones Prominence of sternum DEFICIENCY RICKETS Harrison’s groove
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- 43. 43 Rib beading rickety rosary Bowlegdeformity
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- 47. 47 Knock knee deformity Wristenlargement Rib beading (rachitic rosary Harrison's sulcus and pot belly Chest deformity Frontal bossing Scoliosis X-ray in rickets
- 48. 48 Rickets can becaused by lack of sunlight, but also from insufficient calcium. Vitamin D linked to calcium absorption.
- 50. 50 Osteomalacia it isalso known as adult rickets and flat bones and diaphysis of long bones are affected it is most commonly seen in post menopause female with history of low dietary calcium intake. The majority of patient have bone pain &muscle weakness..
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- 52. 52 Teeth –developmental abnormalities of dentine & 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
- 53. 53 Dietary enrichmentof vitamin D in the form of milk Curative treatment includes 2000 to 4000 IU of calcium daily for 6 to 12 weeks. Patient with osteomalacia due to intestinal malabsorption 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.
- 54. 54 Before treatment Aftertreatment
- 55. Effects are mainlydue to hypercalcaemia IMMEDIATE DELAYED Anorexia Urinary lithiasis. Thirst Metastatic calcification Lassitude Constipation Polyuria
- 56. Toxicity: Malaise, drowsiness,nausea, abdominal pain, thirst, constipation and loss of appetite. Long term effect – ectopic calcification anywhere in the body, renal damage, renal calculi. Prolonged use in infants can cause mental and physical retardation, kidney failure and death.
- 57. Dangerous toexceed 10,000 units daily vit D in an adult more than 12 weeks. Vit D supplements should be avoided in individuals especially infants and children. Should not exceed 400 units a day.