fat soluble vitamins


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fat soluble vitamins

  1. 1. DONE BY MANOJ 1
  2. 2. The word "vitamin" comes from the Latin word vita, means "life".Vitamins are chemicals found in very small amounts in many different foods. “vitamins have been defined as organic compounds which are required in minute amounts to maintain normal health of organisms’. 2
  3. 3. 3
  4. 4. A Short History From about 1500 BC it was of Vitamins known that various diseases could be treated with specific foods. . In 1880 Christian Eijkman dutch physician and professor of physiology produced vitamin-deficiency conditions in animals on an experimental basis and then reversed the condition with an appropriate feeding regimen.  4
  5. 5.  Frederick Hopkins, English biochemist said in 1906 that foods contain a small amount of "growth factors" needed to sustain growth and life itself. The general category of "vitamins" was defined as (1) substances found to be absolutely necessary for life (i.e., vital) and which (2) the body cannot synthesize on its own. 5
  6. 6.  In 1912 Kaziemirz funk Polish-British-American biochemist named these growth factors “vitamines” vit + amine Funks original term "vitamine" was changed to "vitamin" when many scientists identified, purified, and synthesized all of the vitamins and discovered they did not all contain nitrogen. 6
  7. 7.  In the 1930s a scientific discovery demonstrated the biochemical functions of the vitamins and established the bodys requirements for them. From then on, they have been commercially produced. 7
  8. 8. Classification of VitaminsFAT SOLUBLE WATER SOLUBLE A  B1- Thiamine D  B2 - Riboflavin E  B3 – Niacin K  B5 – pantothenic acid  B6 –Pyridoxine  B8 – biotin  B 9-Folic acid  B12 -CyanoCobalamin  C vitamin (ascorbic acid) 8
  9. 9. Fat soluble Vitamins They are soluble in fat. Bile salts are essential for there absorption. They are generally stored in liver. They are not excreted in urine. 9
  10. 10. Vitamin AIt is recorded in the history that Hippocrates(about 500 B.C.) cured night blindness.He prescribed to the patients ox liver (in honey),which is now known to contain high quantity of vitamin A. 10
  11. 11. VITAMIN A :- Is widely distributed in animal and plant foods animals –pre-formed – Retinol. plants – pro-formed - carotene 11
  12. 12. CHEMISTRYRetinol (vitamin A alcohol) : 12
  13. 13. Retinal (vitamin A aldehyde) :This is an aldehyde form obtained by the oxidation of retinol. Retinal and retinol are interconvertible. 13
  14. 14. Retinoic acid (vitamin A acid) :produced by the oxidation of retinal.However,retinoic acid cannot give rise to the formation of retinal or retinol. 14
  15. 15. Beta-Carotene (provitamin A) : Found in plant foods. lt is cleaved in the intestine to produce two moles of retinal.ln humans, this conversion is inefficient, hence beta- carotene possesses about one-sixth vitamin A activity compared to that of retinol. 15
  16. 16. Dietary Sources of Vitamin APlant sources Animal sourcesSweet potatoes Chicken liver Carrots Cod liver oil Pumpkin Fish oil Winter squash Canned beef stew Cantaloupe EggsPink Grapefruit Fish Mangoes Shellfish Apricots Butter Oranges Fortified margarine Spinach Cheese Kale Whole milk Beet greens Fortified skim milk Broccoli Fortified low fat dairyDark green leafy products vegetables 16
  17. 17. DAILY REQUIRMENT Men and women – 600 mcg. Pregnancy and lactation – 950 mcg. Infants – 350mcg. Children – 600mcg. 17
  18. 18. ABSORPTION & STORAGE The liver has enoromous capacity to store – in the form of retinol palmitate. Free retinol is highly active but toxic & therefore transported in blood stream in combination with retinol binding protein (liver) 18
  19. 19. Physiological Functions of Vitamin A Vision Epithelial cell "integrity’ Reproduction Resistance to infectious disease Bone remodeling Growth 20
  20. 20. Vision Retinal is a necessary structural component of rhodopsin , the light sensitive pigment within rod and cone cells of the retina.Rods are involved in dim light visionCones are responsible for bright light & colour vision 21
  21. 21. Walds visual cycle 22
  22. 22. 23
  23. 23. colour visionThe colour vision is governed by colour sensitive pigments porphyropsin (red), iodopsin (green) and cyanopsin (blue).All these pigments are retinalopsin complexes.When bright light strikes the retina, one or more of these pigments are bleached,depending on the particular colour of light.The pigments dissociate to all-trans-retinal and opsin.And this reaction passes on a nerve impulse to brain 24
  24. 24. Epithelial cell "integrity Many epithelial cells appear to require vitamin A for proper differentiation and maintenance. Lack of vitamin A leads to dysfunction of many epithelia The skin becomes keratinized and scaly, and mucus secretion is suppressed 25
  25. 25. Reproduction: Normal levels of vitamin A is required for sperm production, Normal reproductive cycles in females require adequate availability of vitamin A. Bone remodeling: Normal functioning of osteoblasts and osteoclasts is dependent upon vitamin A. 26
  26. 26. Resistance to infectious disease vitamin A deficiency has been shown to increase the frequency and severity of disease. Several large trials with malnourished children have demonstrated dramatic reductions in mortality from diseases such as measles by the simple and inexpensive procedure of providing vitamin A supplementation. 27
  27. 27. 28
  28. 28. Deficiency symptoms 29
  29. 29. Deficiency of Vitamin AMost susceptible populations: Preschool children with decreased intake Poor persons Older adults Alcoholism Liver disease (limits storage) Fat malabsorption
  30. 30. The signs of vitamin A deficiency Ocular Extra ocular Night blindness.  Retarded growth Conjunctival xerosis  Skin disorders bitot’s spot  Effect on reproductive Corneal xerosis organs. keratomalacia  Effect on bone 31
  31. 31. Xerophthalmia WHO classificationNight blindness (XN)Conjunctival xerosis (X1A)Bitot‘s spot (X1B)Corneal xerosis (X2)Corneal ulceration/keratomalacia (X3A) <1/3 of corneal surfaceCorneal ulceration/keratomalacia (X3B) ≥1/3 of corneal surfaceCorneal scar (XS)Xerophthalmic fundus (XF) 32
  32. 32. Night blindnessLack of vitamin A causes night blindness or inability to see in dim light as a result of inadequate pigment in the retina.Earliest symptom 33
  33. 33. Conjunctival xerosis Conjunctiva becomes dry, lustureless and non wettable. Described as “emerging like sand banks at receding tide” Commonly involves the interpalpebral area of temporal quadrants Advanced cases > entire bulbar conjunctiva involved Conjunctival thickening, wrinkling & pigmentation. 34
  34. 34. Bitots spots Raised, silvery white, foamy, triangular patch of keratinised epithelium. Usually bilateral and temporal aspect. 35
  35. 35. Corneal xerosisEarliest change is punctate keratopathy followed by haziness and/or granular pebbly drynessLower nasal quadrant 36
  36. 36. keratomalacia Stromal defects occurs due to colliquative necrosis Small ulcers occurs peripherally Circular, steep margins & are sharply demarcated 37
  37. 37. Corneal scarsHealing of stromal defects results in corneal scars of different densities & sizes which may or may not cover the pupilarry area. 38
  38. 38. Xerophthalmic fundusSeed like, raised, whitish lesions scattered uniformly over part of fundus at level of optic disc 39
  39. 39. SKIN CHANGESDry, lustureless appearance occursPhrynoderma results: occurs due to plugging of hair follicles by keratotic plugs , which consist of keratinised epithelium projecting outwards from follicles.Skin -> scaly & toad like.Seen on outer side of legs, buttocks, elbow & back of forearm 40
  40. 40. phr ynoder ma 41
  41. 41. RESPIRATORY TRACT: squamous metaplasia of respiratory mucosa & ciliary damageGASTROINTESTINAL SYSTEM: reccurent diarrhoeaREPRODUCTIVE SYSTEM: atrophy of germinal epitheliumGROWTH: retardation occursIMMUNOLOGICAL SYSTEM: decreased immune response 42
  42. 42. TREATMENT LOCAL OCULAR THERAPHY VITAMIN AArtificial tears Oral administration is (0.7% hydroxypropyl methyl recommended cellulose or 0.3 % hypromellose) In case of side effects, IM• Should be instilled every 3-4 injections of water miscible hours preparations prefered 43
  43. 43. Aboveage of 1yearUnderage of 1yearWomenofreproductiveage 44
  44. 44. PROPHYLAXIS 45
  45. 45. SHORT TERM APPROACH Infants 6-12 months old & any older 1,oo,ooo IU orally every 3-6 months children who weigh less than 8 kgChildren over 1 yr & under 6 yrs of age 2,00,000 IU every 6 months Lactating mothers 20,000 IU at deliveryInfants less than 6 months not being 50,000 IU orally- should be given breast fed before they attain 6 months of age 46
  46. 46. A revised schedule being followed in india since 1992, under the programme named as “CHILD SURVIVAL AND SAFE MOTHERHOOD” is as follows AT 9 MONTHS OF AGE FIRST DOSE (1 LAKH IU) ALONG WITH MEASLES VACCINE AT 18 MONTHS OF AGE SECOND DOSE(2 LAKH ALONG WITH BOOSTER IU) DOSE OF DPT/OPV THIRD DOSE(2 LAKH IU) AT 2 YEARS OF AGE 47
  47. 47. MEDIUM TERM APPROACH: food fortification with vitamin A• LONG TERM APPROACH: promotion of adequate intake of vit A rich foods. nutritional health education 48
  48. 48. HYPERVITAMINOSIS A: ACUTE TOXICITY CHRONIC TOXICITYHeadache & dizziness  Anorexia  Dry skinNausea  PruritisVomiting  Sparse hairAbdominal pain  Bone pain  Weight lossPseudotumour cerebri{bulginganterior fontanel}  Benign intracranial hypertension  hepatosplenomegaly 49
  49. 49. 50
  50. 50. VITAMIN D it is also called SUNSHINE VITAMIN. it is available in 2 forms D3 – cholecalciferol D2 - ergocalciferolCholecalciferol (vitamin D3)is made from 7-dehydrocholesterol in the skin ofanimals and humans. Ergocalciferol - D2 obtained artificially by irradiation of ergo- sterol 51
  51. 51. chemical origins of vitamin D Precursors of vitamin D are found in both yeast and animal tissues. In yeast, a sterol precursor (ergosterol) is converted to vitamin D2 (ergocalciferol). In the dermal 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. 52
  52. 52. Dietary Sources of Vitamin D 53
  53. 53. DAILY REQUIRMENTMen and women-100 IUPregnancy and lactation – 400IUInfants & Children –200IU 54
  54. 54. Vitamin-D Production and Metabolism 55
  55. 55. Press F5 to view as aslide show. skin 7-dehydrocholesterol D3 (Cholecalciferol) blood DBP-D3 DBP (vit. D binding protein) Ca++ transport Ca++ resorption (intestine) (bone) D3liver kidney 25-OH D3 1, 25-OH D3 (active) (calcidiol) (calcitriol) 25-OH D3 DBP-calcidiol 24, 25-OH D3 (inactive) (tight binding) 56
  56. 56. FUNCTIONS Calcium Balance Cell Differentiation Immunity Blood Pressure Regulation Development of Bones & Teeth 57
  57. 57. Endocrine, paracrine and intracrinefunctions of Vitamin D
  58. 58. vitamin D - deficiency RICKETS  ChildrensOSTEOMALACIA  Adults Increase the risk of Osteoporosis 59
  59. 59. Rickets Rickets derived from the old English word for "twist," or "wrick,“ Rickets is caused 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. In order to 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. 60
  60. 60. DEFICIENCYRICKETS Frontal & Parietal Bossing Pigeon Chest Prominence of sternum Harrison’s groove Bow Legs Soft & fragile bones 61
  61. 61. X-ray in rickets Knock knee deformity Bowleg deformity Wrist enlargement ScoliosisRib beading Harrisons sulcus(rachitic rosary and pot belly Chest deformity Frontal bossing 62
  62. 62. Osteomalacia it is also known as adult rickets 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.. 63
  63. 63. Oral manifestation Teeth – developmental abnormalities of dentine & enamel. Caries – higher risk of caries Enamel – there may be hypoplasia, may be mottled, yellow gray in color 64
  64. 64. MANAGEMENTDietary enrichment of vitamin D in the form of milkCurative treatment includes 2000 to 4000 IU of calcium daily for 6 to 12 weeks.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 . 65
  65. 65. Before treatment After treatment 66
  66. 66. HYPERVITAMINOSIS DAnorexia, nausea & vomitingConstipationHypertensionDrowsiness, irritability & hypotoniaPolyuria & polydipsiaRenal damageHyperkalaemia CLOUDING OF CORNEA 67
  67. 67. TREATMENTDecrease the intake of vitamin dOral aluminium hydroxideCortisone 68
  68. 68. 69
  69. 69. Tocopherol or vitamin E It is also called anti-aging factor. The word tocopherol is derived from the word toco meaning child birth and pheros meaning to bear. It is yellow oily liquid freely soluble in fat solvent. Tocopherol alpha,beta,gamma,lambda have been obtained from the natural sources 70
  70. 70. SOURCES EGG, FISH, BUTTER ,LIVERPalm oil  Nuts sunflower  sunflower seeds corn  green leafy soybean vegetables olive  whole grain 71
  71. 71. DAILY RECOMMENDED DOSE  men - 8 – 10mg  women – 5- 8mg  Children – 8.3mg   Infants – 4- 5mg 72
  72. 72. ABSORPTION ,STORAGE, EXCRETION ABSORPTION small intestine it is incorporated into lipoproteins [VLDL & LDL] & transported through the blood stream via the lymph.STORAGE  liver & fatty tissue 73
  73. 73. FUNCTIONS  REPRODUCTIVE FUNCTION it has got protective effect on reproduction and prevention of sterility. BLOOD FLOW AND CLOTTING MECHANISM it dilates the capillaries & enables the blood to flow freely.  ELECTRON TRANSPORT SYSTEM - it functions as co factor in electron transport system 74
  74. 74. Protects liver from being damaged by toxic compounds such as carbon tetrachloride.Prevents the oxidation of vitamin A and carotenes. 75
  75. 75. DEFICIENCY REPRODUCTIVE – abortion of fetus in females & atrophy of spermatogenic structure in males leading to permanent sterility. HEART - there is necrosis & fibrosis of heart muscle. BLOOD CAPILLARIES – may lead to degenerative changes in the blood capillaries 76
  76. 76. ORAL MANIFESTATION – loss of pigmentation , atrophic degenerative changes in enamel OCULAR MANIFESTATION PTOSIS, OPHTHALMOPLEGIA AND PIGMENTED RETINOPATHY 77
  77. 77. MANAGEMENT – vitamin E is given in the doses of100 to 400mg. 78
  78. 78. 79
  79. 79. VITAMIN K (PHYLOQUINONE) It is essential for production prothrombin & other factor involve in blood clotting mechanism. Hence it is known as anti – hemorrhagic vitamin. it is also known as PHYLOQUINONE 80
  80. 80. Forms It is available in 3 forms - NAPHTHOQUINONE K1 – it is the form occurs in plant origin. K2 –is synthesized by intestinal bacteria. K3 - synthetic form 81
  82. 82. DAILY REQUIRMENT  men and women – 70 – 140 mcg.  children – 35 – 75mcg 83
  83. 83. ABSORPTION ,STORAGE, EXCRETION ABSORPTION small intestine STORAGE  liver adipose tissue 84
  84. 84. FUNCTIONS it is essential for the hepatic synthesis of coagulation factor II, V, VII, IX, X. CLOTTING – it prevents hemorrhage only in cases when there is defective production of prothrombinServes as a essential cofactor in carboxylation of glutamic acid residues in vit k dependent proteins 85
  85. 85. 86
  86. 86. DEFICIENCY Causes Decrease synthesis of factor 2,7,9,10 Increase clotting timeAfter antibacterial Prolong bleedingtherapy,Surgical operations- Cholecystectomy HemorrhagicConditions like Malabsorption conditions Obstructivejaundice 87
  87. 87. SYMPTOMS OF VIT K DEFICIENCYBruising from bleeding into the skinNose bleedsBleeding gumsBleeding in stomachBlood in stoolBlack tarry stoolExtremly heavy menstrual bleedingIntracranial bleedingNEWBORNS: . HEMORRHAGIC DISEASE OF NEWBORN . HYPOPROTHROMBINEMIA 88
  88. 88. MANAGEMENTVit k can be given orallyIn case of someone who improperly absorbs fat or at risk of excessive bleeding, can be given imIn case of associated liver disorder, vit k is insufficient , blood transfusion may be neccesaryAll newborns are recommended to give vit k IM to prevent intracranial bleed after delivery 89
  89. 89. 90