VITAMINS

Dr. Babiker Mohamed Ali Rahamtalla

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 What are vitamins ?
 An organic compounds.
 Must be supplied exogenously.
 Essential nutrients for normal growth & development and
body functioning.
 Play a role in enzymatic systems.
 Either fat-soluble: Vit. A, D, E & K. Or;
 Water-soluble:
 Vit. B-complex include: Thiamine(B1), Riboflavin(B2),
Pantothenic acid , Niacin(B3), Pyridoxine(B6), Biotin(B7),
Folate & Vit. B12.
 Vit. C.
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 What are vitamins ?

 What is the difference between fat-soluble and water-soluble

vitamins?
 Fat-soluble are stored in the liver and fatty tissues. These
are not readily excreted from the body.
 Water-soluble vitamins travel in the blood and are stored
in limited amounts. These are readily excreted from the
body through urine.
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Fat-soluble Vitamins
 Vitamin A (Retinol)
 Fat soluble.

 Heat stable.

 Stored in the liver.

 Sources are: Liver, meat,

milk, eggs, green vegetables,
fruits & butter.

 It`s major role is in vision.

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 Vitamin A (Retinol)

 Very important for night vision.

 Is essential for :

 Cell differentiation .

 Membrane stability .

 Maintenance of epithelia.

 Activation of retinoic-acid responsive genes.

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 Vitamin A deficiency
 Causes:
 A deficient diet.
 Low dietary intake of fat.
 Inadequate intestinal absorption.
 Clinical Manifestations:
 A main cause of blindness in
developing countries.
 Ocular lesions: Night blindness,
Xerosis conjunctivae, Xerosis
corneae, Bitot spots. Cloudiness of
cornea, Photophobia,
Keratomalacia, Blindness.
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 Vitamin A deficiency
 Clinical Manifestations:
 Growth & mental retardation.
 Anemia ± hepatosplenomegaly.
 Skin: Dry & scaly follicular
hyperkeratosis.
 Increased intracranial
pressure.
 Pyuria & hematuria.
 Bronchopneumonia .
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 Diagnosis of Vitamin A deficiency
 Initial assessment may be made based on clinical signs.
 Dark adaptation tests:
 Abnormalities of dark adaptation are strongly suggestive of
vitamin A deficiency.
 Conjunctival impression cytology can be used to assess the
presence of xerophthalmia.
 Vitamin A level in plasma:
 Serum levels below the normal range of 30–65 mg/dL are
commonly seen in advanced deficiency. 9
 Treatment of Vitamin A deficiency

 Treatment:

 Latent Vit. A deficiency: Give 5000 iu of Vit. A daily.

 Xerophthalmia (eye changes): Give 5000 iu per kg orally for

5 days, followed by 25000 iu of Vit. A in oil IM daily until

recovery.

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 Prevention of Vitamin A deficiency
 Prevention:
 Provision of Vit. A to infants, older children & postpartum
mothers.
 Provision of Vit. A to children with malnutrition.
 Provision of Vit. A in cases of severe diarrhea & measles.
 Measles: Give 5000-10000 iu daily.
 Water-miscible preparation of Vit. A in cases of poor
absorption & to preterm.
 Supplement low-fat diets with Vit. A.
 By giving carotene.
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 Vitamin D (Calciferol)
 It is a fat soluble.
 Vit. D2 & D3, both of which are produced synthetically.
 Vit. D3 is also present naturally in human skin.
 D2 & D3 are hydroxylated in liver to 25-OH- cholecalciferol, then in
renal cortex to 1,25- dihydroxycholecalciferol, which act as a hormone.
 Role of 1,25- dihydroxycholecalciferol.
 Facilitate intestinal absorption of ca & ph.
 Renal reabsorption of ph.
 Affect bone deposition & reabsorption of ca & ph.
 Bile is necessary for absorption.
 Breast milk content of Vit. D is low but adequate, of bovine milk is even
lower. 12
 Vitamin D (Calciferol)
 Good sources are : Vit. D-
fortified milk, fish liver oils &
margarine.
 Cereals, vegetables & fruits
contain negligible amounts .
 Food & sunshine
 Synthesized in the skin due to
ultraviolet rays. 13
 Vitamin D deficiency: Rickets
 A disease caused by Vit. D deficiency.
 It means failure to mineralize growing bone or osteoid tissue .
 Causes:
 Inadequate exposure of babies to sunlight.
 Inadequate Vit. D intake.
 Breast-fed infants of Vit. D-deficient mothers.
 Get a deficiency of ca & ph. in the serum.
 Normal epiphyseal cartilage growth & calcification is suppressed.
 Get a frayed, irregular epiphyseal line at the end of bone shaft .
 Parathormone is secreted .
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 Vitamin D deficiency: Clinical manifestations
 The head: A box-like appearance,
asymmetry, flattening, craniotabes
& large anterior fontanel.
 Enlargement of the wrists &
ankles.
 Chest: Rachitic rosary, pigeon
breast deformity & Harrison
groove.

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 Vitamin D deficiency: Clinical manifestations
 Delayed eruption of teeth.
 Deformity of the pelvis.
 Bowlegs or knock-knees.
 Greenstick fractures in long
bones.
 Poorly developed muscles with
hypotonia.
 Relaxation of ligaments.
 Short stature.
 Delayed standing or walking
 Liable to intercurrent infections.
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 Vitamin D deficiency: Diagnosis
 History.
 Clinical signs.
 Radiology findings.

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Vitamin D deficiency: Diagnosis

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 Vitamin D deficiency: Diagnosis
 Chemistry:
 Serum calcium: Normal or low.
 “phosphorus: Low ( < 4 mg/dl )
 “Alkaline phosphatase: High.
 “25- Hydroxycholecalciferol: Low.
 Urine: Contain amino acids, phosphate & glucose.

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 Vitamin D deficiency: Treatment & Prevention
 Treatment:
 Both natural & artificial light.
 Oral administration of 50-150 ug of vit. D3.
 May give a single dose of 15000 ug vit D.
 Or o.5-2 ug of 1,25 dihydroxycholecalciferol.
 Prevention:
 By exposure to ultraviolet light.
 Oral administration of Vit. D.
 Vit. D to pregnant & lactating mothers. 20
 Vitamin E (Tocopherol)
 Active form is alpha tocopherol.
 Good antioxidant.
 Antioxidants used to prevent oxidation of lipids (mainly
phospholipids).
 Requirement is tied to selenium deficiency (Se is cofactor in
glutathione peroxidase).
 Deficiency in fish = muscular dystrophy, reduced fertility
 Requirement: 50-100 mg/kg
 Sources: alfalfa meal, fish meal, rice bran, wheat middlings,
barley grains 21
 Vitamin E (Tocopherol)
 Protects cell membranes and other fat-soluble parts of the body
from oxidation.
 May reduce the risk of heart disease.
 May also discourage development of some types of cancer.
 Promotes normal growth and development.
 Promotes normal red blood cell formation.
 Also been known to aid the process of wound healing.
 Vitamin E act as enzyme co-factor.
 Impairment of fertility in men (vitality).
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 Vitamin K (Menadione)
 Originally identified as a fat-soluble factor required for normal blood
clotting
 Menadione is the most active form
 Actually works by activating blood-clotting proteins
 Dietary sources: alfalfa meal, liver meal.
 Vitamin K1 (phylloquinon) – plant origin
 Vitamin K2 (menaquinon) – normally produced by bacteria in the large
intestine.
 K1 a K2 are used differently in the body:
 K1 – used mainly for blood clothing
 K2 – important in non-coagulation actions - as in metabolism and
bone mineralization, in cell growth, metabolism of blood vessel walls
cells. 23
 Vitamin K (Menadione)
 Deficiency is caused by fat malabsorption or by the liver
failure.
 Blood clotting disorders – dangerous in newborns, life-
threatening bleeding (hemorrhagic disease of the newborn)
 Under normal circumstances there is not a shortage, vit. K is
abundant in the diet.

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Water-soluble Vitamins
 Vitamin B1 (Thiamine)
 Water soluble.
 Destroyed by heat.
 Functions as a coenzyme in
carbohydrate metabolism .
 Required for synthesis of
acetylcholine.
 Good sources are: Milk, vegetables,
fruits, cereals & eggs.
 Polishing of cereals reduces its
availability.
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 Vitamin (B1) Thiamine Deficiency (Beri-Beri)
 Causes:
 Polishing of cereals.
 Cooking food.
 Breast-fed infants of thiamine-
deficient mothers.
 Gastrointestinal or liver diseases.
 Clinical manifestations:
 Early: Fatigue, apathy, irritability,
drowsiness & anorexia.
 Peripheral neuritis.
 Congestive heart failure.
 Psychic disturbances. 27
 Vitamin (B1) Thiamine Deficiency (Beri-Beri)
 Clinical manifestations (cont.):
 Hoarseness or aphonia.
 Ptosis of eyelids.
 Muscle atrophy.
 Ataxia & loss of deep sensation.
 Effusions in serous cavities.
 Brain hemorrhage, ↑ intracranial pressure & coma.
 Full-blown picture is called “beriberi”.
 Wet type: Malnourished, pale, edema, waxy skin, vomiting, dyspnea
& tachycardia.
 Dry type: Plump, pale, flappy, hepatomegaly, dyspnea &
tachycardia.
 Death is due to cardiac involvement. 28
 Vitamin Thiamine (B1) Deficiency (Beri-Beri)
 Diagnosis:
 The clinical picture .
 Urinary thiamine excretion after a loading dose.
 Clinical response to administration of thiamine.
 Treatment:
 Thiamine orally: Children 10 mg daily & adults 50 mg daily. If
there is cardiac failure it is given IM or IV.
 Other B-complex vitamins.
 Prevention:
 A varied, good diet .
 Infant formulas with adequate thiamine.
 Sufficient amounts of thiamine in maternal diets.
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 Vitamin B2 (riboflavin)
 Yellow to orange-yellow natural dye slightly soluble in water.
 Has a central role in energy-yielding metabolism.
 Provides the reactive moieties of the coenzymes flavin mononucleotide
(FMN) and flavin adenine dinucleotid (FAD).
 Flavin coenzymes are electron carries in oxidoreduction reaction.
 Important in:
 Energy production.
 Carbohydrate, fat, and protein metabolism.
 Formation of antibodies and red blood cells.
 Cell respiration.
 Maintenance of good vision, skin, nails, and hair.
 Alleviating eye fatigue.
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 Vitamin B2 Deficiency
 Causes:
 Lack of dietary vitamin B.
 A result of conditions that affect absorption in the intestine.
 The body not being able to use the vitamin.
 An increase in the excretion of the vitamin from the body.
 Symptoms and signs:
 Cracked and red lips.
 Inflammation of the lining of mouth and tongue.
 Dry and scaling skin- keratitis, dermatitis and iron-deficiency
anemia.

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 Vitamin B3 (Niacin)
 Called Nicotinic acid & is water
soluble.
 It forms part of two cofactors (NAD &
NADP) that are important in electron
transfer & glycolysis.
 Dietary Tryptophan can partially
substitute for it.
 Good sources: Liver, salmon, poultry,
red meat & green vegetables.
 Milk & eggs contain little, but are good
sources of Tryptophan.
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 Vitamin (B3) Niacin Deficiency: Pellagra
 Result from Niacin deficiency.
 Occurs mainly in countries where corn “maize”, a poor
source of Tryptophan, is a basic food stuff.

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 Vitamin (B3) Niacin Deficiency: Pellagra
 Clinical manifestations:
 Early symptoms of Anorexia & weakness.
 Later: The classic triad of Dermatitis, Diarrhea & Dementia.
 Vomiting, stomatitis & ulceration of tongue.
 Disorientation & delirium.
 Secondary anemia.
 Dermatitis:
• May be elicited by intense sunlight.
• Symmetric in nature.
• Pellagrous glove & boot.
• Around the neck : casal necklace.
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Vitamin (B3) Niacin Deficiency: Pellagra

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 Vitamin (B3) Niacin Deficiency: Pellagra
 Diagnosis:
 Clinical picture.
 Rapid response to Niacin.
 Treatment:
 A liberal & well-balanced diet.
 Niacin: 50-300 mg daily. In severe cases
give 100 mg IV.
 Other B-complex vitamins.
 Sun exposure should be avoided.
 Soothing applications for skin lesions. 36
 Vitamin (B3) Niacin Deficiency: Pellagra

 Prevention:

 A well-balanced diet.

 Supplements of niacin ?

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 Vitamin B5 (Panthotenic Acid)
 Co-enzyme A assists the following reactions:
 Formation of sterols (cholesterol and 7-dehydrocholesterol).
 Formation of fatty acids.
 Formation of keto acids such as pyruvic acid.
 Other reactions are acylation, acetylation, signal transduction
deamination.
 Sources:
 Meat, foods of animal origin.
 Yeast.
 Wholemeal bread.
 Broccoli, avocado.
 Royal gelly. 38
 Vitamin B6 (Pyridoxine)
 Vitamin B6 is needed for more than 100 enzymes involved in
protein metabolism.
 It is also essential for red blood cell metabolism and
hemoglobin formation.
 The nervous and immune systems need vitamin B6 to function
efficiently.
 It is also needed for the conversion of tryptophan to niacin
(vitamin B3).
 Vitamin B6 also helps maintain blood glucose within a normal
range. When caloric intake is low, vitamin B6 helps to convert
stored carbohydrate or other nutrients to glucose to maintain
normal blood sugar levels. 39
 Vitamin B6 (Pyridoxine)
 Important in:
 Production of red blood cells.
 Conversion of tryptophan to niacin (B-3).
 Immunity.
 Nervous system functions.
 Reducing muscle spasms, cramps, and numbness.
 Maintaining proper balance of sodium and phosphorous in
the body. 40
 Vitamin B6 deficiency
 Signs of vitamin B6 deficiency include:
 Skin: dermatitis (skin inflammation), stomatitis (inflammation of the
mucous lining of any of the structures in the mouth), glossitis
(inflammation or infection of the tongue).
 Neurological abnormalities: depression, confusion, and convulsions.
 Vitamin b6 deficiency also can cause anemia.
 Nervousness.
 Loss of muscle control, muscle weakness.
 Arm and leg cramps.
 Water retention.
 Narural sources:
 cereals, beans, meat, liver, fish, yeast, nuts and some fruits as banana, potatoes.
 It is also produced by bacterial flora in the colon.
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 Vitamin B7 (Biotin)
 Prosthetic group of pyruvate carboxylase, acetyl-coa carboxylase
and other atp-dependent carboxylases.
 Natural source:
 Liver
 Meat
 Kidney
 Yeast
 Egg yolk
 Mushrooms
 Milk and diary products.
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 Vitamin B9 (Folic Acid)
 Recently shown as very important for pregnant females to avoid birth
defects.
 Function: synthesis of purines, pyrimidines, nucleic acids (single carbon
metabolism), DNA synthesis(cell division).
 Sources: yeast, alfalfa meal, full-fat soybeans.
 Deficiencies: anemia, large erythrocytes, pale gills.
 Requirements: 1-4 mg/kg (fish, shrimp).
 Deficiency:
 Results in elevated levels of homocysteine.
 Megaloblastic anemia.
 Deficiency in pregnant women can lead to birth defect.
 Sources of vitamin B9: sources of animal origin, milk and milk products,
yeast, greens.
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 Vitamin B12 (Cyanocobalamin)
 Chemically complex, cobalt nucleus.
 Function: coenzyme in metabolic reactions, maturation of erythrocytes.
 Deficiency: pernicious anemia, nerve disorders.
 Requirement: very low 0.015 mg/kg or not at all.
 In man there are two metabolically active forms: methylcarbylamine and
adenosylcobalamin.
 Important in:
 Proper nerve function.
 Production of red blood cells.
 Metabolizing fats and proteins.
 Prevention of anemia.
 DNA reproduction.
 Energy production?
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 Vitamin B12 (Cyanocobalamin)
 Sources: fish and shellfish, meat (especially liver), poultry, eggs,
milk, and milk products
 Deficiency:
 Pernicious anemia.
 Nerve damage.
 Hypersensitive skin.
 Progressive degeneration to death.
 Concern among the elderly.
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 Vitamin C (Ascorbic acid)
 A potent reducing agent i.e. an antioxidant.
 Functions in a number of enzyme systems.
 Major role in the formation of normal collagen.
 Plays a role in iron metabolism.
 Necessary for conversion of folic acid.
 Water soluble.
 Cooking has destructive effect.
 Good sources are: Fresh fruits (especially citrus fruits),
vegetables e.g. tomato & cabbage.
 Bovine milk contains very little.
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 Vitamin C deficiency: Scurvy
 Formation of collagen & chondroitin sulfate is impaired, lead to:
 Tendency to hemorrhage & defective tooth with it`s
loosening.
 Endochondral bone formation can not proceed.
 Bone marrow depression.
 Causes:
 A low breast milk content due to low maternal vit. C intake .
 Infants fed bovine & evaporated milk.
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 Vitamin C deficiency: Clinical manifestations
 Usual age at onset is between 6 & 24
months.
 Vague symptoms: Irritability, tachypnea
& loss of appetite.
 Generalized tenderness.
 Pseudo paralysis (from pain).
 Edematous legs.
 Low grade fever.
 Subperiosteal hemorrhage.
 Gums are swollen & spongy with bluish
purple discoloration.
 Anemia. 48
 Vitamin C deficiency: Clinical manifestations
 Scorbutic rosary.
 Depression of the sternum.
 Petechial hemorrhages in the skin
& m. membranes.
 Wound healing is slow.
 Orbital or subdural hemorrhages.
 Hematuria & melena .
 Follicular hyperkeratosis.
 Swollen joints .
 Growth is affected .
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 Vitamin C deficiency: Diagnosis
 History of poor Vit. C intake.
 Characteristic clinical picture.
 Radiographic changes :
 Ground-glass appearance of bone with
thin cortex.
 Epiphyseal ends are sharply outlined.
 Epiphyseal centers are surrounded by a
white ring.
 Epiphyseal separation may occur.
 Zones of destruction or rarefaction .
 Subperiosteal calcification .
Vit. C concentration of the white
cell/platelet layer. 50
 Treatment & Prevention of Vitamin C deficiency

 3-4 oz of orange or tomato juice daily.

 Ascorbic acid: 100-200 mg orally or by injection daily.

 Adequate intake of Vit. C.

 Lactating mothers should consume about 100 mg of Vit. C

daily.

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Thank you