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VITAMINS
MNR MEDICAL COLLEGE & HOSPITAL
Dr Anurag Yadav
MBBS, MD
Assistant Professor
Department of Biochemistry
Instagram page –biochem365
YouTube – Dr Biochem365
Email: dranurag.y.m@gmail.com
Vitamins
May be defined as organic compounds
required in small quantities necessary for
growth and maintenance of good health in
human beings
Classification
Fat soluble vitamins
 Fat soluble
 Along with lipids ,
requires bile salts
 Carrier proteins present
 Stored in liver
 Not excreted
 Deficiency manifests
only when stores are
depleted
Water soluble vitamins
 Water soluble
 Simple absorption
 No carrier proteins
 No storage
 Excreted
 Manifested rapidly as
there is no storage
 Hypervitaminosis may
result
 Unlikely since vitamins
are excreted
VITAMIN A
VITAMIN A – structure
 Six membered ring with 11 carbon
containing side chain
Chemistry
 Provitamin form is – beta carotene (HAS
2 MOLECULES OF RETINAL )
 Biologically active forms
 Retinal
 Retinol
 Retinoic acid
 Its heat stable and light sensitive
Vitamin A
 Sources
 Animal sources – fish
liver oils,
 Vegetable and animal
sources – carrot,
papaya , peach ,
tomatoes (red and
yellow)
 Palm oil is rich in
carotenoids
ABSORPTION
 BETA CAROTENE is cleaved in the lumen
of intestine to retinal (beta carotene
dioxygenase)
 Retinal is reduced to retinol by retinal
aldehyde dehydrogenase
 This is then incorporated in to
chylomicrons and stored in liver
 Retinol is transported from liver to other
sites by (RBP)retinol binding protein
 in other tissues its bound to CRBP
Biochemical functions
1. Vision- WALDS VISUAL CYCLE
 rods(for vision in dim light ) and
cones(colour vision)
 Pigment in rods-rhodopsin or visual purple
 In cones- porphyropsin
iodopsin
cyanopsin
2. Antioxidant properties protect against
cancer and heart disease
3.Maintenace of normal epithelium and skin
4. Metabollic role-Glycoprotein synthesis for
mucous secretions
 Biosynthesis of cholestrol
 Controls gluconeogenesis in liver
5. normal reproduction
6. retinoic acid for Growth and
differentiation
REQUIREMENT
 1000 μg/day
 1 RE= 1MICROGRAM OF RETINOL
Causes of deficiency
 Impaired absorption of lipids
 Impaired storage in liver disease
 Failure to synthesize RBP
 Deficiency of particular enzymes
 Decreased intake
Deficiency manifestations
Manifestations
Early symptoms
 Night blindness
 Xerophthalmia
Later as disease progresses
 Bitot’s spots
 Keratomalacia –affects retina
 Conjunctival xerosis
 Skin and mucous membrane lesions
 Failure of skeletal growth
 Skin diseases
 Abnormalities of reproduction
 Hypervitaminosis – ,HAIR LOSS
 BONE PAIN
 HEADACHE
 PEELING OF SKIN
 HEPATOMEGALY
 NAUSEA, VOMITING
 Therapeutic use of vitamin A-
1. REDUCES COMLICATIONS OF MEASLES
2. PRECANCEROUS LESIONS RESPOND TO
CAROTENOIDS
3. AS TOPICAL CREAMS
VITAMIN D
(CHOLECALCIFEROL)
 VIT D is also called CALCIFEROL due to
role in Ca metabolism
 Also called ANTIRACHITIC FACTOR as it
prevents rickets
 Also called sunshine vitamin
STRUCTURE
 NATURALLY PRODUCED VIT D 3-
CHOLECALCIFEROL
 LAB SYNTHESISED VIT D 2 -
ERGOCALCIFEROL
cholesterol
7 -
dehydrocholesterol
Cholecaiciferol
Vit D3
Ergosterol
From plant
Ergocalciferol
Vit D2
Vitamin D
Sources
 Exposure to sunlight
 Fish liver oil, fish, egg yolk
RDA
 Pre-school children – 400 IU
 Children and adults – 200 IU
 Pregnancy and lactation – 400 IU
 Old age – 600 IU
ABSORPTION
 Skin liver
 Circulated in blood bound to vit d binding
proteins synthesized by liver
 Dietary vit d is absorbed from duodenum
along with lipids
 Carried by plasma as a constituent of
chylomicrons
 Taken to liver as chylomicron remnants
 Cholecalciferol- PROHORMONE
ACTIVE FORM
 1:25 DIHYDROCHOLECALCIFEROL
 Steps in synthesis
vit D 3
MIT of liver
25 hydroxycholecalciferol kidney
1α HYDROXYLASE 24 HYDROXYLASE
1:25 dihydrocholecalciferol 24:25
dihydrocholecalciferol
REGULATION OF ACT VIT D
 ACTIVITY OF 1α HYDROXYLASE IS
REGULATED BY
1. PARATHYROID HORMONE
2. PLASMA Ca
3. Insulin ,GH estrogen increase syn of activated
form
INHIBITOR OF 1α HYDROXYLASE IS THE
ACTIVE FORM OF VIT D
Formation of vitamin D
Biochemical functions
CALCITRIOL
INTESTINE BONES KIDNEY
↑CALCIUM AND
PHOSPHORUS
ABSORPTION
INCREASES
MINERALISATION
OF BONES
↑ CALCIUM AND
PHOSPHORUS
REABSORPTION
OTHER FUNCTIONS
CELL GROWTH AND DIFFERENTIATION
OF
 IMMUNOREGULATORY CELLS
 EPIDERMAL CELLS
 MALIGNANT TUMOUR CELLS
 ACTIVE FORM OF VIT D DEPRESSES
IMMUNE SYSTEM
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
Clinical features
Rickets – in
children
Bone deformities
 Knock knee
 Bow legs
 Frontal bossing
 Ricketic rossary
 Harissons sulcus
 Pigeon chest
Osteomalacia -in adults
 Bone pain
 Bone fracture
 osteoporosis
Biochemical parameters
 Slight decrease in calcium and phosphorus
 Serum alkaline phosphatase increased
Different types of rickets
 Vitamin D deficiency rickets-
 Vitamin D resistant rickets
 Hypophosphatemic rickets
 Renal rickets
Hypervitaminosis D
>1500 IU for long periods
Clinical features
 Weakness
 Polyuria
 Polydipsia
 Difficulty in speaking
 Confusion
 Weight loss
 Hypercalcemia,hypokalemia,metabolic alkalosis
 Calcification of soft tissues in vascular and renal
tissues
VITAMIN E
STRUCTURE
Chromane ring /
tocol with an
isoprenoid side
chain
 TOCOPHEROL-αβγδ
OF WHICH ALPHA IS
MOST POTENT
Sources
 Vegetable oils-
RICH SOURCES-
CORN AND SOYA
OIL
 GOOD SOURCES-
PALM OIL
 OLIVE AND
COCONUT OIL ARE
RELATIVELY POOR
Vitamin E
RDA
 Males – 10mg
 Females – 8mg
 Pregnancy – 10mg
 Lactation – 12mg
 >60years – 12mg
ABSORPTION
 Absorbed from the
small intestine
along with lipids
 Incorporated into
chylomicrons and
delivered to tissues
 Then taken to liver
in the form of
chylomicron
remnants
 From liver
exported to target
tissues in the form
of VLDL
Biochemical role
 Most powerful antioxidant
 Reduces the risk of MI by reducing
oxidation of LDL
 Slows progression in Alzheimer’s disease
 Boosts immune response
 Protects erythrocyte membrane from
oxidants
Hypervitaminosis > 1000 IU
 Tendency to haemorrhage
DEFICIENCY
 ITS RARE
FEATURES
1. HAEMOLYTIC ANAEMIA
2. Neuropathy
premature infants with low birth weight are
most commonly deficient.
VITAMIN K
STRUCTURE
1. VITAMIN K 1(PHYLLOQUINONE) from
plants
2. VITAMIN K 2(MENAQUINONE) syn by
microorganisms
3. VITAMIN K 3(MENADIONE)-
SYNTHESIZED FORM
Vitamin K
Sources
 Green leafy
vegetables
 Intestinal bacterial
synthesis
RDA
 50-100mg/day
Chemistry
 Naphthoquinone derivatives,with a long
isoprenoid side chain.
Absorption and storage
 Bile salts are required for normal
absorption and are stored in liver.
Biochemical
functions
 Coagulation –
required for the
activation of
clotting factors
II,VII,IX,X.They
undergo post
translational
modification.
Functional activity of
C reactive protein,
osteocalcin and
structural proteins of
kidney ,lung,spleen
Vitamin K deficiency
Causes
 Malabsorption of lipids
 Prolonged antibiotic therapy and GI
infections
C/F
 Haemorrhagic disease of the new born
 In children and adults – bruising
tendency,echymotic patches,mucous
membrane haemorrhage,post traumatic
bleeding,internal bleeding
 Prolonged prothrombin time and delayed
clotting time
 Warfarin and dicoumarol will competitively
inhibit vitamin K
Hypervitaminosis K
 Administration of large quantities of
vitamin K
 Hemolysis,Hyperbilirubinemia,Kernicterus
and brain damage
Vitamins A, D, E, K by Dr. Anurag Yadav

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Vitamins A, D, E, K by Dr. Anurag Yadav

  • 1. VITAMINS MNR MEDICAL COLLEGE & HOSPITAL Dr Anurag Yadav MBBS, MD Assistant Professor Department of Biochemistry Instagram page –biochem365 YouTube – Dr Biochem365 Email: dranurag.y.m@gmail.com
  • 2. Vitamins May be defined as organic compounds required in small quantities necessary for growth and maintenance of good health in human beings
  • 3. Classification Fat soluble vitamins  Fat soluble  Along with lipids , requires bile salts  Carrier proteins present  Stored in liver  Not excreted  Deficiency manifests only when stores are depleted Water soluble vitamins  Water soluble  Simple absorption  No carrier proteins  No storage  Excreted  Manifested rapidly as there is no storage
  • 4.  Hypervitaminosis may result  Unlikely since vitamins are excreted
  • 6. VITAMIN A – structure  Six membered ring with 11 carbon containing side chain
  • 7. Chemistry  Provitamin form is – beta carotene (HAS 2 MOLECULES OF RETINAL )  Biologically active forms  Retinal  Retinol  Retinoic acid  Its heat stable and light sensitive
  • 8. Vitamin A  Sources  Animal sources – fish liver oils,  Vegetable and animal sources – carrot, papaya , peach , tomatoes (red and yellow)  Palm oil is rich in carotenoids
  • 9. ABSORPTION  BETA CAROTENE is cleaved in the lumen of intestine to retinal (beta carotene dioxygenase)  Retinal is reduced to retinol by retinal aldehyde dehydrogenase  This is then incorporated in to chylomicrons and stored in liver  Retinol is transported from liver to other sites by (RBP)retinol binding protein  in other tissues its bound to CRBP
  • 10. Biochemical functions 1. Vision- WALDS VISUAL CYCLE  rods(for vision in dim light ) and cones(colour vision)  Pigment in rods-rhodopsin or visual purple  In cones- porphyropsin iodopsin cyanopsin
  • 11.
  • 12. 2. Antioxidant properties protect against cancer and heart disease 3.Maintenace of normal epithelium and skin 4. Metabollic role-Glycoprotein synthesis for mucous secretions  Biosynthesis of cholestrol  Controls gluconeogenesis in liver 5. normal reproduction 6. retinoic acid for Growth and differentiation
  • 13.
  • 14. REQUIREMENT  1000 μg/day  1 RE= 1MICROGRAM OF RETINOL
  • 15. Causes of deficiency  Impaired absorption of lipids  Impaired storage in liver disease  Failure to synthesize RBP  Deficiency of particular enzymes  Decreased intake
  • 16. Deficiency manifestations Manifestations Early symptoms  Night blindness  Xerophthalmia Later as disease progresses  Bitot’s spots  Keratomalacia –affects retina  Conjunctival xerosis  Skin and mucous membrane lesions  Failure of skeletal growth
  • 17.  Skin diseases  Abnormalities of reproduction
  • 18.  Hypervitaminosis – ,HAIR LOSS  BONE PAIN  HEADACHE  PEELING OF SKIN  HEPATOMEGALY  NAUSEA, VOMITING
  • 19.  Therapeutic use of vitamin A- 1. REDUCES COMLICATIONS OF MEASLES 2. PRECANCEROUS LESIONS RESPOND TO CAROTENOIDS 3. AS TOPICAL CREAMS
  • 21.  VIT D is also called CALCIFEROL due to role in Ca metabolism  Also called ANTIRACHITIC FACTOR as it prevents rickets  Also called sunshine vitamin
  • 22. STRUCTURE  NATURALLY PRODUCED VIT D 3- CHOLECALCIFEROL  LAB SYNTHESISED VIT D 2 - ERGOCALCIFEROL
  • 24.
  • 25. Vitamin D Sources  Exposure to sunlight  Fish liver oil, fish, egg yolk RDA  Pre-school children – 400 IU  Children and adults – 200 IU  Pregnancy and lactation – 400 IU  Old age – 600 IU
  • 26. ABSORPTION  Skin liver  Circulated in blood bound to vit d binding proteins synthesized by liver  Dietary vit d is absorbed from duodenum along with lipids  Carried by plasma as a constituent of chylomicrons  Taken to liver as chylomicron remnants  Cholecalciferol- PROHORMONE
  • 27. ACTIVE FORM  1:25 DIHYDROCHOLECALCIFEROL  Steps in synthesis vit D 3 MIT of liver 25 hydroxycholecalciferol kidney 1α HYDROXYLASE 24 HYDROXYLASE 1:25 dihydrocholecalciferol 24:25 dihydrocholecalciferol
  • 28. REGULATION OF ACT VIT D  ACTIVITY OF 1α HYDROXYLASE IS REGULATED BY 1. PARATHYROID HORMONE 2. PLASMA Ca 3. Insulin ,GH estrogen increase syn of activated form INHIBITOR OF 1α HYDROXYLASE IS THE ACTIVE FORM OF VIT D
  • 30. Biochemical functions CALCITRIOL INTESTINE BONES KIDNEY ↑CALCIUM AND PHOSPHORUS ABSORPTION INCREASES MINERALISATION OF BONES ↑ CALCIUM AND PHOSPHORUS REABSORPTION
  • 31. OTHER FUNCTIONS CELL GROWTH AND DIFFERENTIATION OF  IMMUNOREGULATORY CELLS  EPIDERMAL CELLS  MALIGNANT TUMOUR CELLS  ACTIVE FORM OF VIT D DEPRESSES IMMUNE SYSTEM
  • 32. 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
  • 33. Clinical features Rickets – in children Bone deformities  Knock knee  Bow legs  Frontal bossing  Ricketic rossary  Harissons sulcus  Pigeon chest
  • 34.
  • 35. Osteomalacia -in adults  Bone pain  Bone fracture  osteoporosis Biochemical parameters  Slight decrease in calcium and phosphorus  Serum alkaline phosphatase increased
  • 36. Different types of rickets  Vitamin D deficiency rickets-  Vitamin D resistant rickets  Hypophosphatemic rickets  Renal rickets
  • 37. Hypervitaminosis D >1500 IU for long periods Clinical features  Weakness  Polyuria  Polydipsia  Difficulty in speaking  Confusion  Weight loss  Hypercalcemia,hypokalemia,metabolic alkalosis  Calcification of soft tissues in vascular and renal tissues
  • 39. STRUCTURE Chromane ring / tocol with an isoprenoid side chain  TOCOPHEROL-αβγδ OF WHICH ALPHA IS MOST POTENT
  • 40. Sources  Vegetable oils- RICH SOURCES- CORN AND SOYA OIL  GOOD SOURCES- PALM OIL  OLIVE AND COCONUT OIL ARE RELATIVELY POOR
  • 41. Vitamin E RDA  Males – 10mg  Females – 8mg  Pregnancy – 10mg  Lactation – 12mg  >60years – 12mg
  • 42. ABSORPTION  Absorbed from the small intestine along with lipids  Incorporated into chylomicrons and delivered to tissues  Then taken to liver in the form of chylomicron remnants  From liver exported to target tissues in the form of VLDL
  • 43. Biochemical role  Most powerful antioxidant  Reduces the risk of MI by reducing oxidation of LDL  Slows progression in Alzheimer’s disease  Boosts immune response  Protects erythrocyte membrane from oxidants Hypervitaminosis > 1000 IU  Tendency to haemorrhage
  • 44.
  • 45. DEFICIENCY  ITS RARE FEATURES 1. HAEMOLYTIC ANAEMIA 2. Neuropathy premature infants with low birth weight are most commonly deficient.
  • 47. STRUCTURE 1. VITAMIN K 1(PHYLLOQUINONE) from plants 2. VITAMIN K 2(MENAQUINONE) syn by microorganisms 3. VITAMIN K 3(MENADIONE)- SYNTHESIZED FORM
  • 48. Vitamin K Sources  Green leafy vegetables  Intestinal bacterial synthesis RDA  50-100mg/day
  • 49. Chemistry  Naphthoquinone derivatives,with a long isoprenoid side chain. Absorption and storage  Bile salts are required for normal absorption and are stored in liver.
  • 50. Biochemical functions  Coagulation – required for the activation of clotting factors II,VII,IX,X.They undergo post translational modification. Functional activity of C reactive protein, osteocalcin and structural proteins of kidney ,lung,spleen
  • 51. Vitamin K deficiency Causes  Malabsorption of lipids  Prolonged antibiotic therapy and GI infections C/F  Haemorrhagic disease of the new born  In children and adults – bruising tendency,echymotic patches,mucous membrane haemorrhage,post traumatic bleeding,internal bleeding
  • 52.  Prolonged prothrombin time and delayed clotting time  Warfarin and dicoumarol will competitively inhibit vitamin K Hypervitaminosis K  Administration of large quantities of vitamin K  Hemolysis,Hyperbilirubinemia,Kernicterus and brain damage