VITAMINS

1. VITAMINS By Dr Anitha

2. Vitamins May be defined as organic compounds categorized as essential nutrients since they are not synthesized at all or synthesized in insufficient amounts ,so must be supplied in the diet. Micronutrients

3. Most vitamins are obtained from the food • Some are made by bacteria in the intestine • One is made in the skin • Vitamins are non-energy producing • They dont contain calories. • They are involved in extracting energy from the macronutrients.

4. Variety is the Key Vitamins are derived from avarietyof foods.

5. Fat soluble vitamins(A,D,E,K) Fat soluble Along with lipids , requires bile salts Carrier proteins present Stored in liver Not excreted Deficiency manifests only when stores are depleted Hypervitaminosis is common Water soluble vitamins(vit C , B complex) Water soluble Simple absorption No carrier proteins No storage Excreted Manifested rapidly as there is no storage Not common Classification

6. VITAMIN A – structure • six membered ,β-ionone ring and a 11 carbon polyisoprenoid chain with a functional group

7. Chemistry • 3 Biologically active forms • Retinal • Retinol • Retinoic acid • Its heat stable and light sensitive • Provitamin form is – β carotene • Activated to vit A in the intestine .

8. Conversion to active form • β-Carotene • β -Carotene dioxygenase(intestine) • Retinal + Retinal

9. Vitamin A sources • Animal sources – fish liver oils, • Vegetable sources – carrot, papaya , peach , tomatoes (red and yellow) • Palm oil is rich in carotenoids

10. REQUIREMENT • Infants and children – 400-600μg/day • Men – 750-1000 μg/day • Women – 750 μg/day • Pregnancy – 1000 μg/day • Lactation - 1200 μg/day

11. Digestion and Absorption

12. Transport and storage

13. Biochemical functions 1. Vision- WALDS VISUAL CYCLE • rods(for vision in dim light ) and cones(colour vision) • Pigment in rods-rhodopsin(11 cis retinal +opsin) or visual purple • In cones- porphyropsin iodopsin cyanopsin

14. Walds visual cycle / rhodopsin cycle / vit A cycle

15. Dark Adaptation time: • Bright light depletes the stores of rhodopsin in rods so when a person shifts suddenly from bright to a dim light area, there is difficulty in seeing. • After a few minutes rhodopsin is resynthesized & vision is improved. • This period is called “Dark adaptation time”. • It is increased in Vit A deficiency 

17. 2. Antioxidant properties protect against cancer and heart disease 3.Maintenace of normal epithelium and skin and also prevents keratinisation. Vit A increases synthesis of glycoprotein, which is one of the constituents of membrane and mucous secretion. • 4. normal reproduction - Supports spermatogenesis, oogenesis and placental development. 5. Retinol promotes synthesis of transferrin

18. KeratinizationVitamin A deficiency symptom

19. 6. retinol and retinoic acid act as a hormone and affect the transcription of specific proteins

20. Causes of deficiency 1. malnutrition 2.Steatorrhea as in obstructive jaundice (defective absorption) and pancreatitis(indigestion of fat) 3. Cirrhosis of liver (reduced synthesis of retinol binding protein, RBP). 4. Chronic nephrosis (RBP is excreted through urine)

21. Deficiency manifestations • Night blindness/ nyctalopia – earliest symptom • Conjunctival xerosis- dryness, loss of transparency due to corneal keratinization . • Bitots spots- grey white triangular spots • All the above features are reversible

22. 4. Keratomalacia: (softening and dissolution of cornea) Degeneration of corneal epithelium leading to corneal opacities & ulceration , and total blindness. b) Effect on skin and epithelium: The skin becomes rough and dry. c) Reproductive failure and growth retardation

23. Assessment of deficiency: • Dark adaptation time prolonged. • Retinol binding protein: decreased • Vitamin A in serum: decreased

24. Hypervitaminosis – ,HAIR LOSS • BONE PAIN • HEADACHE • PEELING OF SKIN • HEPATOMEGAL • NAUSEA, VOMITING • Birth Defects Teratogenic risk resulting in abnormal fetal development and birth defects hence not recommended in the first trimester

25. Therapeutic use of vitamin A- 1. REDUCES COMLICATIONS OF MEASLES 2. PRECANCEROUS LESIONS RESPOND TO CAROTENOIDS 3. AS TOPICAL CREAMS for acne and psoriasis – tretinoin +bezoyl peroxide + antibacterials

27. VITAMIN D(CHOLECALCIFEROL) BY DR ANITHA

28. VIT D is also called CALCIFEROL due to role in Ca metabolism • Also called ANTIRACHITIC FACTOR as it prevents rickets • Also called sunshine vitamin

29. STRUCTURE • Vitamin D is a sterol derivative. • NATURALLY PRODUCED VIT D 3- CHOLECALCIFEROL • LAB SYNTHESISED VIT D 2 - ERGOCALCIFEROL

31. 7 dehydrocholesterol and ergosterol are provitamins

32. Vitamin D RDA • Adults – 5 – 10 micrograms/day • Pregnancy and lactation – 10 micrograms /day

33. ABSORPTION • Dietary vitamin D is absorbed from small intestine along with lipids aided by bile salts • In the intestine its incorporated into chylomicrons and enters into circulation • Circulated in blood bound to vitamin D binding proteins synthesized by liver • Taken to liver as chylomicron remnants and stored there.

34. ACTIVE FORM • 1:25 DIHYDROCHOLECALCIFEROL • Steps in synthesis vit D 3 MIT of liver 25 hydroxycholecalciferol 1α HYDROXYLASE (kidney) 1:25 dihydrocholecalciferol (calcitriol- plays an important role in bone formation and calcium metabolism 25 hydroxylase

35. REGULATION OF ACT VIT D • ACTIVITY OF 1α HYDROXYLASE IS REGULATED BY • PARATHYROID HORMONE • PLASMA Ca • Insulin ,GH estrogen increase syn of activated form INHIBITOR OF 1α HYDROXYLASE IS THE ACTIVE FORM OF VIT D

36. Formation of vitamin D

37. Biochemical functions

38. Hormone action of vitamin D

39. Vitamin D deficiency Causes • No exposure to sunlight • Secondary to malabsorption of vitamin • Secondary to abnormality of vitamin D activation • Secondary to abnormalities in renal absorption of phosphates

40. Clinical features Rickets – in children Bone deformities • Knock knee • Bow legs • Frontal bossing • Ricketic rossary • Pigeon chest

42. Osteomalacia -in adults • Bonepain • Bone fracture • osteoporosis Biochemical parameters • Slight decrease in calcium and phosphorus • Serum alkaline phosphatase increased

43. Different types of rickets • types of rickets • Vitamin D deficiency rickets : deficiency of vitamin D in the diet. • hypophosphatemic rickets: due to defective tubular reabsorption of phosphate and increased excretion. Seen in X linked disorder.

44. Vitamin D resistant rickets: seen in fanconi syndrome where renal tubular reabsorption of bicarbonate, phosphate, glucose and amino acids are deficient • Renal rickets: seen in chronic kidney diseases, due to decreased 1α hydroxylase activity calcitriol is not synthesised

45. Hypervitaminosis D >1500 IU for long periods Clinical features • Weakness • Confusion • Weight loss • Hypercalcemia,hypokalemia • Calcification of soft tissues – renal stones

47. VITAMIN E Also called antisterility vitamin BY DR ANITHA

48. STRUCTURE tocol ring with an isoprenoid side chain • TOCOPHEROL-αβγδ OF WHICH ALPHA IS MOST POTENT

49. Sources • Vegetable oils- RICH SOURCES- CORN AND SOYA OIL • GOOD SOURCES- PALM OIL

50. Vitamin E RDA • Males – 10mg • Females – 8mg • Pregnancy – 10mg • Lactation – 12mg • >60years – 12mg