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By
Dr KHALED ALGARIRI
International Medicine School – MSU
January 2018
INTRODUCTION
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
INTRODUCTION
VITAMINS
FAT SOLUBLE
VITAMINS
Vitamin A, D, E and
K
WATER SOLUBLE
VITAMINS
Vitamins of B-complex
group and Vit C
VITAMIN A CHEMISTRY
Vitamin A occurs in two forms in food
1. Active vitamin A-
The Active form of vitamin is retinol, an alcohol
which can be converted to other forms
2. Provitamin A-, substances that are transformed
into vitamins in the body
 Beta-carotene is the most abundant and
widespread provitamin A.
 One need to eat approximately six times as much
beta-carotene to get the same amount of vitamin
A as in retinol.
 Carotenoids are not toxic even at high doses for
long times.
VITAMIN A
SOURCES OF VITAMIN A
Liver, fish, and eggs are excellent
food sources for preformed vitamin A;
• Vegetable sources of provitamin A
carotenoids include dark green and
deeply colored fruits and vegetables.
• Moderate cooking of vegetables
enhances carotenoid release for
uptake in the gut.
• Carotenoid absorption is also aided
by some fat in a meal
DIGESTION AND ABSORPTION
 Dietary Vitamin A, from animal sources is available
in the form of retinyl esters, which is hydrolyzed to
retinol and fatty acid by pancreatic hydrolases .
 The absorption of retinol requires the presence of
bile salts
 In the intestinal cells, retinol is esterified back and
secreted with chylomicrons
β-Carotene is cleaved in the intestinal mucosa by carotene
dioxygenase, yielding retinaldehyde,which is reduced to
retinol,esterified and secreted in chylomicrons together with
esters formed from dietary retinol.
The intestinal activity of carotene dioxygenase is low, so that
are latively large proportion of ingested β -carotene may
appear in the circulation unchanged.
FATE OF CAROTENES
Transport from liver to tissue
The vitamin A from the liver is transported to peripheral tissue as
Trans retinal by RBP(retinol binding protein)
FUNCTIONS OF VITAMIN A
 Vitamin A is essential for vision (especially dark
adaptation)
 Immune response
 Bone growth
 Reproduction
 Maintenance of the surface linings of the eyes, epithelial
cell growth and repair, andthe epithelial integrity of the
respiratory,urinary, and intestinal tracts.
 Vitamin A is also important for embryonic development
and the regulation of adult genes.
 Antioxidants :β -carotenes
VITAMIN A DEFECIENCY
CAUSES
• Inadequate intake
• Impaired absorption
• Impaired storage & transport
• Increased excretion [RBP]
• Alcoholism
CLINICAL MANIFESTATIONS
Nightblindness : due to retinal injury -Vitamin A has a
major role in photo transduction. Vitamin A deficiency
leads to alack of visual pigments; this reduces the
absorption of various wavelengths of light, resulting in
blindness
Bitot spots :Areas of abnormal squamous cell
proliferation and keratinization of the conjunctiva can
be seen in young children with vitamin A deficiency .
CLINICAL MANIFESTATIONS
 Keratomalacia: In advanced deficiency; the cornea becomes
hazy and can develop erosions, which can lead to its
destruction.
 Xerophthalmia : results from keratinization of the
conjunctiva.
 Infections
 Hyperkeratosis of skin
 Growth retardation
LABORATORY BIOCHEMICAL
INVESTIGATIONS
 Serum retinol level-Normal range is 28 to 86 μg/dL (1 to 3 μmol/L). The level
decreases in vitamin A deficiency.
 Serum RBP level
 Serum zinc level is useful because zinc deficiency interferes with RBP
production.
 An iron panel is useful because iron deficiency can affect the metabolism of
vitamin A.
 Albumin levels are indirect measures of vitamin A levels.
 Complete blood count (CBC) with differential if anemia, infection, or sepsis is
a possibility.
 An electrolyte evaluation and liver function studies should be performed to
evaluate for nutritional and volume status.
VITAMIN D
Vitamin-D is a fat soluble vitamin
Vitamin – D is a sterol, it contains steroid nucleus
(Cyclopentanoperhydrophenanthrene ring)
Vitamin – D function like a hormone
Forms of vitamin D:
Vitamin D in the diet occurs in two forms
Vitamin D2 (Ergocalciferol)
Vitamin D3 (Cholecalciferol)
Sunlight
Ergosterol
(in plants)
7-Dehydrocholesterol
Vitamin D3
Cholecalciferol)
Sunlight
dermal tissue of animals
Vitamin D2
(Ergocalciferol)
Vitamin D3
Cholecalciferol
1,25-dihydroxyvitamin D3
25-hydroxyvitamin D3
In the liver cholecalciferol is
hydroxylated at the 25 position
by a specific enzyme 25-
hydroxylase to form 25-
hydroxy-cholecalciferol ,requires
cyt. p450 & NADPH .
In the kidney it is further
hydroxylated at 1st position by 1-
hydroxylase present in the proximal
convoluted tubules. it requires Cyt
P450, O2 and NADPH
24-25 dihydroxy cholecalciferol may
be formed by hydroxylation of 25-
HCC at 24th position.
ACTIVATION OF VITAMIN-D
24,25 – DHCC is another metabolite of vitamin D
It is synthesized in kidney by 24 - hydroxylase
Calcitriol concentration is adequate, 24 – hydroxylase acts
leading to the synthesis of a less important compound 24,25
– DHCC
To maintain calcium homeostasis, synthesis of 24,25 –
DHCC is important
24,25 - Dihydroxycholecalciferol
Calcitriol (1,25 – DHCC) acts at three different levels to
maintain plasma calcium
Action on intestine:
Calcitriol increases the intestinal absorption of calcium and
phosphate
In the intestinal cells, calcitriol leads to the synthesis of a
specific calcium binding protein
This protein increases calcium uptake by intestine
VITAMIN D FUNCTIONS
Action on bone:
Calcitriol is essential for bone formation.
Calcitriol along with parathyroid hormone increases the mobilization
of calcium and phosphate from the bone causes elevation in the
plasma calcium and phosphate
Action on kidney:
Calcitriol is also involved in minimizing the excretion of calcium and
phosphate through the kidney by decreasing their excretion and
enhancing reabsorption
Children - 10 μgm/day
Adults - 5 μgm/day
Pregnency,lactation -1200 μ gm/day
Recommended dietary allowance (RDA)
Sources of vitamin D
Absorption : vitamin D2 and D3 form mixed micelles
by combining with bile salts & through the mucosal
cells of small intestine they are absorbed by passive
transport
Transport: vitamin D is transported from intestine to
the liver by binding to vitamin D binding globulin
Storage: 25 – hydroxycholecalciferol is the major
storage and circulatory form of vitamin D
ABSORPTION & TRANSPORT
RICKETTS in CHILDREN OSTEOMALACIA IN ADULTS
Deficiency of vitamin-D
LABORATORY BIOCHEMICAL
INVESTIGATIONS
 Serum Calcium level
 Serum Phosphate level
 Thyroid hormones Tests
 Serum Alkaline phosphatase
 Serum Acid phosphatase
 Vitamin D is stored mainly in liver .
 Vitamin D is most toxic in overdoses .
 Toxic effects include demineralization of bones and increased calcium
absorption from intestine, leading increased plasma calcium
(hypercalcemia).
 Hypercalcemia is associated with deposition of calcium in many soft
tissues such as kidney and arteries
 It leads to formation of stones (renal calculi)
 High consumption is associated with loss of appetite, nausea,
increased thirst, and loss of weight .
VITAMIN D TOXICITY
FAT SOLUBLE VITAMINS  A & D

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FAT SOLUBLE VITAMINS A & D

  • 1. By Dr KHALED ALGARIRI International Medicine School – MSU January 2018
  • 2. INTRODUCTION 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
  • 3. INTRODUCTION VITAMINS FAT SOLUBLE VITAMINS Vitamin A, D, E and K WATER SOLUBLE VITAMINS Vitamins of B-complex group and Vit C
  • 4. VITAMIN A CHEMISTRY Vitamin A occurs in two forms in food
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  • 7. 1. Active vitamin A- The Active form of vitamin is retinol, an alcohol which can be converted to other forms 2. Provitamin A-, substances that are transformed into vitamins in the body  Beta-carotene is the most abundant and widespread provitamin A.  One need to eat approximately six times as much beta-carotene to get the same amount of vitamin A as in retinol.  Carotenoids are not toxic even at high doses for long times. VITAMIN A
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  • 9. SOURCES OF VITAMIN A Liver, fish, and eggs are excellent food sources for preformed vitamin A; • Vegetable sources of provitamin A carotenoids include dark green and deeply colored fruits and vegetables. • Moderate cooking of vegetables enhances carotenoid release for uptake in the gut. • Carotenoid absorption is also aided by some fat in a meal
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  • 14. DIGESTION AND ABSORPTION  Dietary Vitamin A, from animal sources is available in the form of retinyl esters, which is hydrolyzed to retinol and fatty acid by pancreatic hydrolases .  The absorption of retinol requires the presence of bile salts  In the intestinal cells, retinol is esterified back and secreted with chylomicrons
  • 15. β-Carotene is cleaved in the intestinal mucosa by carotene dioxygenase, yielding retinaldehyde,which is reduced to retinol,esterified and secreted in chylomicrons together with esters formed from dietary retinol. The intestinal activity of carotene dioxygenase is low, so that are latively large proportion of ingested β -carotene may appear in the circulation unchanged. FATE OF CAROTENES Transport from liver to tissue The vitamin A from the liver is transported to peripheral tissue as Trans retinal by RBP(retinol binding protein)
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  • 17. FUNCTIONS OF VITAMIN A  Vitamin A is essential for vision (especially dark adaptation)  Immune response  Bone growth  Reproduction  Maintenance of the surface linings of the eyes, epithelial cell growth and repair, andthe epithelial integrity of the respiratory,urinary, and intestinal tracts.  Vitamin A is also important for embryonic development and the regulation of adult genes.  Antioxidants :β -carotenes
  • 18. VITAMIN A DEFECIENCY CAUSES • Inadequate intake • Impaired absorption • Impaired storage & transport • Increased excretion [RBP] • Alcoholism
  • 19. CLINICAL MANIFESTATIONS Nightblindness : due to retinal injury -Vitamin A has a major role in photo transduction. Vitamin A deficiency leads to alack of visual pigments; this reduces the absorption of various wavelengths of light, resulting in blindness Bitot spots :Areas of abnormal squamous cell proliferation and keratinization of the conjunctiva can be seen in young children with vitamin A deficiency .
  • 20. CLINICAL MANIFESTATIONS  Keratomalacia: In advanced deficiency; the cornea becomes hazy and can develop erosions, which can lead to its destruction.  Xerophthalmia : results from keratinization of the conjunctiva.  Infections  Hyperkeratosis of skin  Growth retardation
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  • 22. LABORATORY BIOCHEMICAL INVESTIGATIONS  Serum retinol level-Normal range is 28 to 86 μg/dL (1 to 3 μmol/L). The level decreases in vitamin A deficiency.  Serum RBP level  Serum zinc level is useful because zinc deficiency interferes with RBP production.  An iron panel is useful because iron deficiency can affect the metabolism of vitamin A.  Albumin levels are indirect measures of vitamin A levels.  Complete blood count (CBC) with differential if anemia, infection, or sepsis is a possibility.  An electrolyte evaluation and liver function studies should be performed to evaluate for nutritional and volume status.
  • 23. VITAMIN D Vitamin-D is a fat soluble vitamin Vitamin – D is a sterol, it contains steroid nucleus (Cyclopentanoperhydrophenanthrene ring) Vitamin – D function like a hormone Forms of vitamin D: Vitamin D in the diet occurs in two forms Vitamin D2 (Ergocalciferol) Vitamin D3 (Cholecalciferol)
  • 26. 1,25-dihydroxyvitamin D3 25-hydroxyvitamin D3 In the liver cholecalciferol is hydroxylated at the 25 position by a specific enzyme 25- hydroxylase to form 25- hydroxy-cholecalciferol ,requires cyt. p450 & NADPH . In the kidney it is further hydroxylated at 1st position by 1- hydroxylase present in the proximal convoluted tubules. it requires Cyt P450, O2 and NADPH 24-25 dihydroxy cholecalciferol may be formed by hydroxylation of 25- HCC at 24th position. ACTIVATION OF VITAMIN-D
  • 27. 24,25 – DHCC is another metabolite of vitamin D It is synthesized in kidney by 24 - hydroxylase Calcitriol concentration is adequate, 24 – hydroxylase acts leading to the synthesis of a less important compound 24,25 – DHCC To maintain calcium homeostasis, synthesis of 24,25 – DHCC is important 24,25 - Dihydroxycholecalciferol
  • 28. Calcitriol (1,25 – DHCC) acts at three different levels to maintain plasma calcium Action on intestine: Calcitriol increases the intestinal absorption of calcium and phosphate In the intestinal cells, calcitriol leads to the synthesis of a specific calcium binding protein This protein increases calcium uptake by intestine VITAMIN D FUNCTIONS
  • 29. Action on bone: Calcitriol is essential for bone formation. Calcitriol along with parathyroid hormone increases the mobilization of calcium and phosphate from the bone causes elevation in the plasma calcium and phosphate Action on kidney: Calcitriol is also involved in minimizing the excretion of calcium and phosphate through the kidney by decreasing their excretion and enhancing reabsorption
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  • 31. Children - 10 μgm/day Adults - 5 μgm/day Pregnency,lactation -1200 μ gm/day Recommended dietary allowance (RDA) Sources of vitamin D
  • 32. Absorption : vitamin D2 and D3 form mixed micelles by combining with bile salts & through the mucosal cells of small intestine they are absorbed by passive transport Transport: vitamin D is transported from intestine to the liver by binding to vitamin D binding globulin Storage: 25 – hydroxycholecalciferol is the major storage and circulatory form of vitamin D ABSORPTION & TRANSPORT
  • 33. RICKETTS in CHILDREN OSTEOMALACIA IN ADULTS Deficiency of vitamin-D
  • 34. LABORATORY BIOCHEMICAL INVESTIGATIONS  Serum Calcium level  Serum Phosphate level  Thyroid hormones Tests  Serum Alkaline phosphatase  Serum Acid phosphatase
  • 35.  Vitamin D is stored mainly in liver .  Vitamin D is most toxic in overdoses .  Toxic effects include demineralization of bones and increased calcium absorption from intestine, leading increased plasma calcium (hypercalcemia).  Hypercalcemia is associated with deposition of calcium in many soft tissues such as kidney and arteries  It leads to formation of stones (renal calculi)  High consumption is associated with loss of appetite, nausea, increased thirst, and loss of weight . VITAMIN D TOXICITY