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Dr Nishant Kumar
Assistant Professor
Department of Community Medicine
Madhubani Medical College , Madhubani , Bihar
Vitamins & Minerals
 Active compound is Retinol and its Provitamin ( precursor)
carotenoids.
 It is a Fat soluble pale yellow compound
 It is stable to heat at ordinary temperature but liable to oxidation and
destruction on rancidity of fat.
 Carotenoids cannot be wholly be converted into retinol in the body and
man absorb and utilizes these pigment less efficiently (6 microgram of
β- carotene has biological activity of 1 microgram retinol(RE))
 Other carotenoids have even lesser Vitamin A activity
Vitamin A ( Retinol)
2
 Animal sources: meat, liver , kidney, milk, fish, and egg.
 It can be also be formed in intestinal mucosa from pigments know as carotenoids which is
widely distributed in plants.
 Carotenoids are found in colored fruits and vegetables. (e.g. outer green leaves of
vegetables like cabbage)
 One of the important source of Provitamin A is β- carotene and is found in abundance in
yellow – orange vegetable and fruits ( e.g. pumpkins, papaya, mango, apricots, yellow
peaches, and green leafy vegetable)
 Carrots – β- carotene, β- Crytoxanthin is in Citrus fruits.
 Food heated for long time losses Vitamin A , boiling , canning or freezing of food does not
cause loss and drying and dehydration do cause significant loss
 Vitamin E protects it from oxidation.
Vitamin A - Sources
3
 It is vital for the formation of retinal pigment rhodopsin in rods of
retina .Exposure to light results in a series of changes in its
configuration , which leads to the adaptation of vision in dark .Retinol
deficiency leads to impairment of dark adaptation or night blindness.
 It is essential for integrity of cellular structure ( epithelial tissue of
respiratory , gastrointestinal , genitourinary and skin)
 It has a role in the immune defence mechanism of the body
 It has antioxidant activity
Vitamin A - Functions
4
5
 Adult – 600 mg of retinol ( including children above 6 years and pregnant lady)
 Lactating mother- 950 mg
Deficiency
 Ocular Manifestation- Most common
a) Xeropthalmia
 Extra Ocular manifestation
a) Dry rough , itchy skin ; rash c) Loss of acuity of senses , smell and taste
b) Dry brittle hair and nails d)Loss of appetite , e) anemia , fatigue
f) low immunity g) Poor growth i) Increased risk of cancer.
Vitamin A – RDA & deficiency
 Vitamin A Deficiency(VAD) is the leading cause of preventable blindness in children.
 It also increase the risk of disease and death from severe infection.
 In pregnant women VAD causes night blindness and may increase the risk of maternal
mortality
 VAD is a public health problem in more than half the countries of Africa , and South East
Asia
 World wide 256 million people suffer from preclinical xerophthalmia and 2.6 million
develop xerophthalmia , 700,000 develop corneal ulcers and 350,000 become blind
 In India it is common in preschool children in AP, TN, Karnataka, WB & Bihar.
 The prevalence of Bitot spot is 1 to 5% in 1 to 5 years of age.
Vitamin A Deficiency -Introduction & Problem Statement
6
7
 Most common age group affected – 1 to 3 year of age
 A complex web of causation which includes , ignorance , poverty ,
infection , lack of food, malnutrition , environmental factors and social
factors.
 Weaning and infection
 Other Social factors
 Poor Environmental sanitation Practices
VAD - Etiology
8
WHO classification Clinical condition Prevalence among pre-school
children
XN Night blindness >1%
X1A Conjunctival xerosis ConjXerosis.jpg
X1B Bitot’s spot Bitot spot.jpg >0.5%
X2 Corneal Xerosis
X3A Corneal ulceration(<1/3rd of
cornea)
>0.001
X3B Corneal ulceration (>1/3rd of
cornea) corneal ulcer.jpg
>0.001
XS Corneal Scar corneal scar.jpg >0.05
XF Xeropthalmic fundus Xerophtalmia.jpg
Biochemical Plasma retinol <0.35μmol/l
VAD – Clinical feature
9
 200,000 IU(110mg) of Retinol palmitate ( oil miscible Vitamin A) is administered orally for
2 days.
 In case of vomiting waster miscible Vitamin A 100,000 IU is administered as IM injection
followed by 200,000 IU 1 to 4 weeks
 For Infants less than 8 kg of weight half of the dose is given.
 For prevention
a) Dietary modification
b) Nutritional education
c) Fortification
d) Periodic dosage – given with immunization programme.
e) Long term action.
Treatment & Prevention for Xeropthalmia
10
 Acute Hypervitaminosis can occur by a single of vitamin A more than
200mg.
 Chronic misuse of supplement more than 4000RE( retinol equivalent ;
1IU vitamin A = 0.3RE) for infants and 7000RE for adult.
 Large amount more than 100 times the requirement can overwhelm the
liver and produce intoxication
 It is characterized by skin , mucous membrane changes , dry lips,
dryness of nasal mucosa , peeling of skin , headache , nausea , it is
toxic to fetus, causing craniofacial , CNS and thymic malformation.
Toxicity – Hypervitaminosis A
11
 Vitamin D refers to two molecules – ergocalciferol ( vitamin D2) and
cholecalciferol ( vitamin D3).
 Vitamin D metabolism.jpg
 Food sources : Cod liver oil , other oily fish , milk , margarine , egg
and liver.
 Functions : It regulates the absorption and excretion of calcium from
small intestine and also plays an essential part in the mechanism of
mineralizing bone .
 Vitamin D status can be assessed by the measurement of plasma 25-
hydroxyl- cholecalciferol level.
Vitamin D ( Calciferols)
12
 Child – 100- 400IU/day ( 2.5- 10μg), adult male and female(5μg /day).
 Its deficiency rickets in children , characterized by reduced
calcification of bone epiphysis . Skeletal deformities , bone pain, and
muscle weakness. In adult it results in osteomalacia.
 Vitamin D defiency.jpg
 Rickets.jpg
 Osteomalacia.jpg
Vitamin D – RDA and Deficiency
13
 There are eight forms of vitamin E that are synthesized in the plants
they are four tocopherol (α,β,γ and δ tocopherols) and four tocotrienols
(α,β,γ and δ) . Alpha tocopherols which is synthesized commercially
has the highest biological activity , and is used as the standard against
which activity of other form is measured.
 Sources – Vegetable oil ( groundnut, sunflower, safflower, cotton seed,
corn , wheat germ , rape seed , palm and other oils). Nuts ( almond and
peanuts) are also good source. Eggs , butter whole meal cereals are
moderately good. Meat , fruits vegetable contain small amount .Food
rich in PUFA are good source.
Vitamin E ( tocopherol)
14
 It has a strong antioxidant property and protect cell membrane and
lipoprotein against the damage of free radicals. It also prevents the non
enzymatic destruction of PUFA by molecular oxygen
 It maintains the cell membrane integrity
 It has role in the DNA and prostaglandin synthesis
 RDA – 12 mg/day
 Deficiency : Interferes with normal reproduction and causes a form of
muscular dystrophy.
 Familial Isolated Vitamin E ( FIVE) deficiency is known as a genetically
inherited disease it produces, reduced tendon reflexes by age 3-4 , loss of
touch and pain sensation , unsteady gait, loss of coordination , impaired
eye movement in adolescence. ( also seen in patients with fat
malabsorption).
Vitamin E – FUNCTION , RDA and deficiency
15
 It exist in nature in two forms , Vitamin K1 ( phylloquinone) isolated from
lucerine is the only form that occur in plants. It is yellow oil , soluble in fat
solvent but only slightly in water. Vitamin K2( menaquinone) is produced by
bacteria in the lumen of large intestine.
 Food sources – Green leafy vegetables, Vegetable oil ( soya bean oil ), eggs,
meat and dairy products.
 Functions –
a) It promotes the synthesis of γ- carboxy glutamic acid (Gla)in the liver
which is essential in the formation of prothrombin( or factor –II) and also
factor ( VII, IX, and X) and helps in blood coagulation.
b) Some other proteins also contain Gla and require Vitamin K for the
synthesis ( e.g. osteocalcin , a bone protein made by osteoblast)
Vitamin K
16
 Male - 120μg and Female 90μg .
 Deficiency
a) Poor blood clotting due to low prothrombin activity
 Neonates are born with very low stores of vitamin K due to absence of
bacteria in gut flora , so neonates are given vitamin K at birth.
 Adult may manifest symptoms of vitamin K deficiency in obstructive
jaundice as lack of bile lead to poor absorption of vitamin K.
Vitamin k – RDA and Deficiency
17
 It is a water soluble ,crystalline white substance.
 It is very sensitive to oxidation which is accelerated by heat, alkaline solution light and
traces of metals, especially copper.
 It is present in all the body tissue but in high concentration in adrenal glands , pituitary
gland and intestinal gland.
 Sources: Citrus fruits, (oranges, lemons) guavas, papayas, mangoes, gooseberry, kiwifruit ,
green vegetables , root vegetables( sweet potatoes), germinating seed , pulses and grain.
 Vitamin C content of fruits and vegetables is reduced by storage and damage to plant cell by
rough handling, bruising, or cutting which result in release of ascorbic acid oxidase which
oxidises ascorbic acid.
 High pressure steaming as well as rapid frying destroys oxidase enzyme and hence causing
greater retention of ascorbic acid
Vitamin C ( ascorbic acid)
18
 It is important for the formation of collagen and is therefore important
for the formation and maintenance of normal structure of the
connective tissues, bone , tendons, skin , teeth and capillaries.
 It enhances the absorption of Iron , through the conversion of ferric to
ferrous form.
 It has antioxidant property.
 It influences the maturation of red blood cells , synthesis of bile and
metabolism of drugs and carcinogens by the liver
 RDA- 40 mg/day for adults and Lactating mother – 80mg/day.
Ascorbic acid – Functions & RDA
19
 Deficiency causes defective formation of intercellular ground
substance whose characteristic gross lesion occur in gums, bones and
capillaries.
 Wound healing is delayed
 Deficiency leads to “Scurvy” the sign and symptoms include spongy
and bleeding gums , perifollicular hemorrhage in the skin , sub
periosteal hematomas, and poor wound healing. Fatigue and muscle
weakness can also occur.
Ascorbic Acid - Deficiency
20
Vitamin RDA Deficiency Sources
B1(Thiamine) 0.5mg/1000kcal Beriberi, (dry and wet), Wernicke-
Korsakoff psychosis
Meat(pork), liver,
legume , wheat germs
B2 (Riboflavin) 0.6mg/1000kcal Cheilosis, angular stomatitis,corneal
ulcer, Magenta tounge, Ariboflavinosis
Milk meat green
vegetables
Niacin( Nicotinic
acid )
6.6mg/1000kcal Pellagra- characterized by 3D-
Dermatitis, Diarrhea, Dementia
Meat , groundnut ,
legumes, grains
B6 (Pyridoxamine) 2mg/day Anemia, neuritis, convulsions Meat, Grains, poultry,
Seeds
Folic Acid 100μg/day Megaloblastic Anemia Liver, green
vegetables, yeast and
fruits
B12(Cobalmin) 1μg/day Pernicious Anemia Liver, fish, meat,milk
Vitamin B complex Vitamin B.png
21
 Minerals can be classified into Macro minerals and micro minerals
 Those mineral which constitute at least 0.01% of body weight (5g in a
60kg man) or those mineral whose requirement are more than 100mg
per day are called macro minerals
Minerals
Macro minerals Micro minerals
Calcium, phosphorus,
magnesium, sodium,
potassium, chloride, Sulphur
Iron , Zinc Iodine, copper,
manganese, molybdenum,
selenium, chromium, and
fluroine
22
 Absorbed from duodenum and proximal jejunum.
 Transported by transferrin ,a iron binding protein.
 Stored in the reticuloendothelial system in combination with apoferritin.
 Excreted(0.8-1mg/d) through exfoliated GI cells, skin, stool, urine,sweating.
 Iron.png
Total body iron 3-4 gms
Haemoglobin 65-70%
Stores 20-25%
Myoglobin and enzymes 5-10%
Plasma iron (trasferrin bound) 0.1-0.2%
Iron - Metabolism
23
 VEGETARIAN : Green leafy vegetables, Cereals(wheat, bajra , jowar),Pulses
(Green peas, beans, ground nut) Fruits (apple, banana) ,Others (jaggery, dates)
 NON-VEG : Liver, meat
 RDA-
Male 28mg/day
Female(non pregnant) 30mg/dl
Female(pregnant) 38mg/dl
Female(lactating) 30mg/dl
Children(1-9y) 25mg/dl
Children(9-18y) 22mg/dl
Iron – Sources and RDA
24
Iron- Inhibitors and Enhancers
INHIBITORS:
 Phytates in cereals
 Tannins in tea
 Polyphenols in coffee
 Oxalates in vegetables
 Phosphates in egg
 Proteins in dals
ENHANCERS:
 Ascorbic acid :Vit C
 Citric acid,Lactic acid
 Sprouted and fermented food
 Meat and fish
25
 More than 350 Million women, twice the infant, children and equal
number adolescents are anemic.
 Anemia during pregnancy puts the women at 3 times greater risk of
delivering LBW babies & 9 times higher risk of perinatal mortality.
 contributing significantly for increased IMR & MMR. 90% of the
cases in developing countries and highest in South Asia
 In developing countries
 Half of women and young children are anemic(40-60%)
 40-80% of pregnant women are anemic.
 20-25% of maternal deaths are due to anemia
Iron deficiency Anemia- Problem Statement
26
 Low iron intake
 Haem iron is better absorbed than Non-Haem iron.
 Dietary sources poor in iron.
 Increased demand as in adolescence, pregnancy and lactation.
 Increased losses as in malaria, hook worm, excessive menstrual loss
and repeated pregnancies.
 Poor absorption and utilization.
Iron deficiency Anemia- etiology
27
 SYMPTOMS:
 Fatigue, weakness,giddiness lassitude, impaired work capacity,
dizziness, headache, insomnia,
 SIGNS:
 Pallor,edema,glossitis,stomatitis,koilonychia
 Tachycardia,haemic murmurs,basal crepts,
 Hepatospleenomegaly.
Iron deficiency Anemia-Clinical feature
28
 Mandatory: Hb%, CBC, Peripheral smear
 Others Indices Urine examination, Stool examination, Chest X-ray
Iron deficiency Anemia- Lab investigation
gms/dl MCHC
Adult males 13 34
Adult females
(non pregnant)
12 34
Adult females
(pregnant)
11 34
Children
(6m-6y)
11 34
Children(6y-14y) 12 34
29
 TREAT THE UNDERLYING CAUSE
 Modes of management.
 ORAL
 PARENTAL
 BLOOD TRANSFUSION
Iron deficiency Anemia- treatment
30
 Mild and moderate cases
 Cheap ,safe and effective
 Start with lower dose and increase if when tolerated to 2-3 times a day
 Different salts are available in market
 Tablet is to be taken with food
 Tea or coffee to be avoided
 Vitamin C helps in absorption
 Calcium salts and antacids to be avoided
Iron deficiency Anemia- oral Therapy
31
 Non compliance
 Intolerance
 Poor absorption(mal-absorption syndrome, dysentry)
 No response after 4 weeks in confirmed cases of IDA
 Moderate to severe cases seen late in pregnancy
Iron deficiency Anemia- parental
32
 Severe anaemia.
 Confirmed cases not responding to oral or parental therapy.
 Severely anaemic requiring emergency surgery.
 Refractory anaemia.
Iron deficiency Anemia- blood transfusion
33
 Individual level
Nutritional education
Personal hygiene
Contraception
Iron & folic acid supplementation
Promotion of breast feeding
 Family level
 Nutritional education
 Birth spacing/ no of pregnancies
 Control of parasites
 Improvement of sanitation
 Cooking in iron vessels
Iron deficiency Anemia- Prevention
34
 Community Level
Nutritional education .
Screening of adolescent girls in schools & iron supplementation.
Iron & folic supplements to pregnant ladies.
Deworming of school children .
Delaying marriage age & birth spacing.
Iron supplementation by fortification.
Iron deficiency Anemia- Prevention
35
 National nutritional anaemia prophylaxis programme
Children with clinical anaemia: 20mg of elemental iron and 100mcg
of folic acid,100days a year
Pregnant and lactating :100mg of elemental iron and 500mcg of
folic acid.
Treat worm infestation with mebendazole.
Drugs continued for nursing mothers and family planning acceptors
 WIFS ( Weekly Iron Folic Acid Supplementation)
Weekly Iron tablet and folic acid tablet to adolescent (10-19)at
school
Twice Yearly Deworming by Albendazole .WIFS.jpg
Iron deficiency Anemia- national Programme
36
 It is an essential trace element as it in an integral component of thyroid
hormone : thyroxine and triiodothyronine.
 Iodine deficiency is endemic in mountainous region since iodine is
washed from the soil .
 Its deficiency causes Iodine deficiency disorders that effect all ages :
abortions, still birth , cretinism , mental retardation, deaf-mutism,
dwarfism, and goiter.
 Sources
a) Food sources grown in iodine rich soil
b) Dairy products
c) Eggs
d) Cereals grain, legumes, green leafs.
IODINE- Introduction and Sources.
37
 Goitrogens
a) Certain vegetable of brassica family like cabbage , cauliflower, and
radish, contain goitrogens such as thiocyanates and cynoglycosides.
They make the iodine present in food unavailable to the body.
Goitrogens can be inactivated by heating.
 Absorption: Dietary iodine is absorbed from small intestine follows
two main pathways within the body. 30% is used by the thyroid gland
for synthesis and the remainder is excreted by the urine.
 Functions: Iodine is an integral component of thyroid hormone
thyroxine(T4) ,and tri- iodothyroxine (T3). Fetus and neonate normal
protein metabolism in the brain and CNS require iodine.
Iodine- Metabolism
38
 Daily requirement of iodine is 150μg/day for adult ;
a) Infant - 50μg/day
b) Children- 100μg/day
c) Pregnancy- 200μg/day.
 Deficiency- Iodine Deficiency Disorders(IDD)
a) Adults- hypothyroidism, raised level of TSH, resulting in hyperplasia of
thyroid gland leading to goiter. Symptoms include lethargy, poor cold
tolerance, bradycardia and myxedema. Infertility may also occur.
b) Fetus and Infant- ‘Cretinism’- symptoms include mental retardation, hearing,
speech defect, disorders of gait, and growth retardation
c) At birth- still birth, miscarriage; Neonatal hypothyroidism is a sensitive
indicator of incidence of IDD in a community
Iodine- RDA and Deficiency
39
 Fortification of salt with iodine is carried out to reduce IDD. The PFA
act has specified an iodine concentration of 30 and 15 ppm at source
and consumer end respectively thereby providing150 mg or iodine in
10 gram of salt.
 Iodized oil: Injectable and oral iodized oil are available as oral drops
(400mg/ml) and intramuscular injection (480mg/ml).Single IM
injection of iodized oil can protect a woman through pregnancy and
one year post partum; Oral supplementation is to be repeated every
months to 1 year.
 Nutritional Education
Iodine – Prevention and control
40
 Normally present in the bones and teeth and is essential for normal
mineralization of bones and formation of dental enamel.
 Sources
a) Sea food , cheese and tea are rich sources
b) Main Source for man is drinking water
 The fluoride content of drinking water in India is about 0.5mg/l;
 Deficiency of fluoride in water below 0.5mg/ml is usually associated with
dental caries
 Excess ingestion of fluorine (>2-3ppm in water ) is associated with skeletal
and dental fluorosis and is a reported health problem in rural district of AP,
Haryana, Kerala, Punjab, Rajasthan, and TN
Fluorine
41
 Changing Water sources
 Defluoridation : Removal of excess fluoride from water . Nalgonda
technique is an accepted form of defluoridation. It involves addition of
lime and alum to the water sequentially , it is then followed by
flocculation , sedimentation and filtration of water.
 Avoiding intake of excess fluoride.
Fluorine

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Vitamins and minerals

  • 1. Dr Nishant Kumar Assistant Professor Department of Community Medicine Madhubani Medical College , Madhubani , Bihar Vitamins & Minerals
  • 2.  Active compound is Retinol and its Provitamin ( precursor) carotenoids.  It is a Fat soluble pale yellow compound  It is stable to heat at ordinary temperature but liable to oxidation and destruction on rancidity of fat.  Carotenoids cannot be wholly be converted into retinol in the body and man absorb and utilizes these pigment less efficiently (6 microgram of β- carotene has biological activity of 1 microgram retinol(RE))  Other carotenoids have even lesser Vitamin A activity Vitamin A ( Retinol) 2
  • 3.  Animal sources: meat, liver , kidney, milk, fish, and egg.  It can be also be formed in intestinal mucosa from pigments know as carotenoids which is widely distributed in plants.  Carotenoids are found in colored fruits and vegetables. (e.g. outer green leaves of vegetables like cabbage)  One of the important source of Provitamin A is β- carotene and is found in abundance in yellow – orange vegetable and fruits ( e.g. pumpkins, papaya, mango, apricots, yellow peaches, and green leafy vegetable)  Carrots – β- carotene, β- Crytoxanthin is in Citrus fruits.  Food heated for long time losses Vitamin A , boiling , canning or freezing of food does not cause loss and drying and dehydration do cause significant loss  Vitamin E protects it from oxidation. Vitamin A - Sources 3
  • 4.  It is vital for the formation of retinal pigment rhodopsin in rods of retina .Exposure to light results in a series of changes in its configuration , which leads to the adaptation of vision in dark .Retinol deficiency leads to impairment of dark adaptation or night blindness.  It is essential for integrity of cellular structure ( epithelial tissue of respiratory , gastrointestinal , genitourinary and skin)  It has a role in the immune defence mechanism of the body  It has antioxidant activity Vitamin A - Functions 4
  • 5. 5  Adult – 600 mg of retinol ( including children above 6 years and pregnant lady)  Lactating mother- 950 mg Deficiency  Ocular Manifestation- Most common a) Xeropthalmia  Extra Ocular manifestation a) Dry rough , itchy skin ; rash c) Loss of acuity of senses , smell and taste b) Dry brittle hair and nails d)Loss of appetite , e) anemia , fatigue f) low immunity g) Poor growth i) Increased risk of cancer. Vitamin A – RDA & deficiency
  • 6.  Vitamin A Deficiency(VAD) is the leading cause of preventable blindness in children.  It also increase the risk of disease and death from severe infection.  In pregnant women VAD causes night blindness and may increase the risk of maternal mortality  VAD is a public health problem in more than half the countries of Africa , and South East Asia  World wide 256 million people suffer from preclinical xerophthalmia and 2.6 million develop xerophthalmia , 700,000 develop corneal ulcers and 350,000 become blind  In India it is common in preschool children in AP, TN, Karnataka, WB & Bihar.  The prevalence of Bitot spot is 1 to 5% in 1 to 5 years of age. Vitamin A Deficiency -Introduction & Problem Statement 6
  • 7. 7  Most common age group affected – 1 to 3 year of age  A complex web of causation which includes , ignorance , poverty , infection , lack of food, malnutrition , environmental factors and social factors.  Weaning and infection  Other Social factors  Poor Environmental sanitation Practices VAD - Etiology
  • 8. 8 WHO classification Clinical condition Prevalence among pre-school children XN Night blindness >1% X1A Conjunctival xerosis ConjXerosis.jpg X1B Bitot’s spot Bitot spot.jpg >0.5% X2 Corneal Xerosis X3A Corneal ulceration(<1/3rd of cornea) >0.001 X3B Corneal ulceration (>1/3rd of cornea) corneal ulcer.jpg >0.001 XS Corneal Scar corneal scar.jpg >0.05 XF Xeropthalmic fundus Xerophtalmia.jpg Biochemical Plasma retinol <0.35μmol/l VAD – Clinical feature
  • 9. 9  200,000 IU(110mg) of Retinol palmitate ( oil miscible Vitamin A) is administered orally for 2 days.  In case of vomiting waster miscible Vitamin A 100,000 IU is administered as IM injection followed by 200,000 IU 1 to 4 weeks  For Infants less than 8 kg of weight half of the dose is given.  For prevention a) Dietary modification b) Nutritional education c) Fortification d) Periodic dosage – given with immunization programme. e) Long term action. Treatment & Prevention for Xeropthalmia
  • 10. 10  Acute Hypervitaminosis can occur by a single of vitamin A more than 200mg.  Chronic misuse of supplement more than 4000RE( retinol equivalent ; 1IU vitamin A = 0.3RE) for infants and 7000RE for adult.  Large amount more than 100 times the requirement can overwhelm the liver and produce intoxication  It is characterized by skin , mucous membrane changes , dry lips, dryness of nasal mucosa , peeling of skin , headache , nausea , it is toxic to fetus, causing craniofacial , CNS and thymic malformation. Toxicity – Hypervitaminosis A
  • 11. 11  Vitamin D refers to two molecules – ergocalciferol ( vitamin D2) and cholecalciferol ( vitamin D3).  Vitamin D metabolism.jpg  Food sources : Cod liver oil , other oily fish , milk , margarine , egg and liver.  Functions : It regulates the absorption and excretion of calcium from small intestine and also plays an essential part in the mechanism of mineralizing bone .  Vitamin D status can be assessed by the measurement of plasma 25- hydroxyl- cholecalciferol level. Vitamin D ( Calciferols)
  • 12. 12  Child – 100- 400IU/day ( 2.5- 10μg), adult male and female(5μg /day).  Its deficiency rickets in children , characterized by reduced calcification of bone epiphysis . Skeletal deformities , bone pain, and muscle weakness. In adult it results in osteomalacia.  Vitamin D defiency.jpg  Rickets.jpg  Osteomalacia.jpg Vitamin D – RDA and Deficiency
  • 13. 13  There are eight forms of vitamin E that are synthesized in the plants they are four tocopherol (α,β,γ and δ tocopherols) and four tocotrienols (α,β,γ and δ) . Alpha tocopherols which is synthesized commercially has the highest biological activity , and is used as the standard against which activity of other form is measured.  Sources – Vegetable oil ( groundnut, sunflower, safflower, cotton seed, corn , wheat germ , rape seed , palm and other oils). Nuts ( almond and peanuts) are also good source. Eggs , butter whole meal cereals are moderately good. Meat , fruits vegetable contain small amount .Food rich in PUFA are good source. Vitamin E ( tocopherol)
  • 14. 14  It has a strong antioxidant property and protect cell membrane and lipoprotein against the damage of free radicals. It also prevents the non enzymatic destruction of PUFA by molecular oxygen  It maintains the cell membrane integrity  It has role in the DNA and prostaglandin synthesis  RDA – 12 mg/day  Deficiency : Interferes with normal reproduction and causes a form of muscular dystrophy.  Familial Isolated Vitamin E ( FIVE) deficiency is known as a genetically inherited disease it produces, reduced tendon reflexes by age 3-4 , loss of touch and pain sensation , unsteady gait, loss of coordination , impaired eye movement in adolescence. ( also seen in patients with fat malabsorption). Vitamin E – FUNCTION , RDA and deficiency
  • 15. 15  It exist in nature in two forms , Vitamin K1 ( phylloquinone) isolated from lucerine is the only form that occur in plants. It is yellow oil , soluble in fat solvent but only slightly in water. Vitamin K2( menaquinone) is produced by bacteria in the lumen of large intestine.  Food sources – Green leafy vegetables, Vegetable oil ( soya bean oil ), eggs, meat and dairy products.  Functions – a) It promotes the synthesis of γ- carboxy glutamic acid (Gla)in the liver which is essential in the formation of prothrombin( or factor –II) and also factor ( VII, IX, and X) and helps in blood coagulation. b) Some other proteins also contain Gla and require Vitamin K for the synthesis ( e.g. osteocalcin , a bone protein made by osteoblast) Vitamin K
  • 16. 16  Male - 120μg and Female 90μg .  Deficiency a) Poor blood clotting due to low prothrombin activity  Neonates are born with very low stores of vitamin K due to absence of bacteria in gut flora , so neonates are given vitamin K at birth.  Adult may manifest symptoms of vitamin K deficiency in obstructive jaundice as lack of bile lead to poor absorption of vitamin K. Vitamin k – RDA and Deficiency
  • 17. 17  It is a water soluble ,crystalline white substance.  It is very sensitive to oxidation which is accelerated by heat, alkaline solution light and traces of metals, especially copper.  It is present in all the body tissue but in high concentration in adrenal glands , pituitary gland and intestinal gland.  Sources: Citrus fruits, (oranges, lemons) guavas, papayas, mangoes, gooseberry, kiwifruit , green vegetables , root vegetables( sweet potatoes), germinating seed , pulses and grain.  Vitamin C content of fruits and vegetables is reduced by storage and damage to plant cell by rough handling, bruising, or cutting which result in release of ascorbic acid oxidase which oxidises ascorbic acid.  High pressure steaming as well as rapid frying destroys oxidase enzyme and hence causing greater retention of ascorbic acid Vitamin C ( ascorbic acid)
  • 18. 18  It is important for the formation of collagen and is therefore important for the formation and maintenance of normal structure of the connective tissues, bone , tendons, skin , teeth and capillaries.  It enhances the absorption of Iron , through the conversion of ferric to ferrous form.  It has antioxidant property.  It influences the maturation of red blood cells , synthesis of bile and metabolism of drugs and carcinogens by the liver  RDA- 40 mg/day for adults and Lactating mother – 80mg/day. Ascorbic acid – Functions & RDA
  • 19. 19  Deficiency causes defective formation of intercellular ground substance whose characteristic gross lesion occur in gums, bones and capillaries.  Wound healing is delayed  Deficiency leads to “Scurvy” the sign and symptoms include spongy and bleeding gums , perifollicular hemorrhage in the skin , sub periosteal hematomas, and poor wound healing. Fatigue and muscle weakness can also occur. Ascorbic Acid - Deficiency
  • 20. 20 Vitamin RDA Deficiency Sources B1(Thiamine) 0.5mg/1000kcal Beriberi, (dry and wet), Wernicke- Korsakoff psychosis Meat(pork), liver, legume , wheat germs B2 (Riboflavin) 0.6mg/1000kcal Cheilosis, angular stomatitis,corneal ulcer, Magenta tounge, Ariboflavinosis Milk meat green vegetables Niacin( Nicotinic acid ) 6.6mg/1000kcal Pellagra- characterized by 3D- Dermatitis, Diarrhea, Dementia Meat , groundnut , legumes, grains B6 (Pyridoxamine) 2mg/day Anemia, neuritis, convulsions Meat, Grains, poultry, Seeds Folic Acid 100μg/day Megaloblastic Anemia Liver, green vegetables, yeast and fruits B12(Cobalmin) 1μg/day Pernicious Anemia Liver, fish, meat,milk Vitamin B complex Vitamin B.png
  • 21. 21  Minerals can be classified into Macro minerals and micro minerals  Those mineral which constitute at least 0.01% of body weight (5g in a 60kg man) or those mineral whose requirement are more than 100mg per day are called macro minerals Minerals Macro minerals Micro minerals Calcium, phosphorus, magnesium, sodium, potassium, chloride, Sulphur Iron , Zinc Iodine, copper, manganese, molybdenum, selenium, chromium, and fluroine
  • 22. 22  Absorbed from duodenum and proximal jejunum.  Transported by transferrin ,a iron binding protein.  Stored in the reticuloendothelial system in combination with apoferritin.  Excreted(0.8-1mg/d) through exfoliated GI cells, skin, stool, urine,sweating.  Iron.png Total body iron 3-4 gms Haemoglobin 65-70% Stores 20-25% Myoglobin and enzymes 5-10% Plasma iron (trasferrin bound) 0.1-0.2% Iron - Metabolism
  • 23. 23  VEGETARIAN : Green leafy vegetables, Cereals(wheat, bajra , jowar),Pulses (Green peas, beans, ground nut) Fruits (apple, banana) ,Others (jaggery, dates)  NON-VEG : Liver, meat  RDA- Male 28mg/day Female(non pregnant) 30mg/dl Female(pregnant) 38mg/dl Female(lactating) 30mg/dl Children(1-9y) 25mg/dl Children(9-18y) 22mg/dl Iron – Sources and RDA
  • 24. 24 Iron- Inhibitors and Enhancers INHIBITORS:  Phytates in cereals  Tannins in tea  Polyphenols in coffee  Oxalates in vegetables  Phosphates in egg  Proteins in dals ENHANCERS:  Ascorbic acid :Vit C  Citric acid,Lactic acid  Sprouted and fermented food  Meat and fish
  • 25. 25  More than 350 Million women, twice the infant, children and equal number adolescents are anemic.  Anemia during pregnancy puts the women at 3 times greater risk of delivering LBW babies & 9 times higher risk of perinatal mortality.  contributing significantly for increased IMR & MMR. 90% of the cases in developing countries and highest in South Asia  In developing countries  Half of women and young children are anemic(40-60%)  40-80% of pregnant women are anemic.  20-25% of maternal deaths are due to anemia Iron deficiency Anemia- Problem Statement
  • 26. 26  Low iron intake  Haem iron is better absorbed than Non-Haem iron.  Dietary sources poor in iron.  Increased demand as in adolescence, pregnancy and lactation.  Increased losses as in malaria, hook worm, excessive menstrual loss and repeated pregnancies.  Poor absorption and utilization. Iron deficiency Anemia- etiology
  • 27. 27  SYMPTOMS:  Fatigue, weakness,giddiness lassitude, impaired work capacity, dizziness, headache, insomnia,  SIGNS:  Pallor,edema,glossitis,stomatitis,koilonychia  Tachycardia,haemic murmurs,basal crepts,  Hepatospleenomegaly. Iron deficiency Anemia-Clinical feature
  • 28. 28  Mandatory: Hb%, CBC, Peripheral smear  Others Indices Urine examination, Stool examination, Chest X-ray Iron deficiency Anemia- Lab investigation gms/dl MCHC Adult males 13 34 Adult females (non pregnant) 12 34 Adult females (pregnant) 11 34 Children (6m-6y) 11 34 Children(6y-14y) 12 34
  • 29. 29  TREAT THE UNDERLYING CAUSE  Modes of management.  ORAL  PARENTAL  BLOOD TRANSFUSION Iron deficiency Anemia- treatment
  • 30. 30  Mild and moderate cases  Cheap ,safe and effective  Start with lower dose and increase if when tolerated to 2-3 times a day  Different salts are available in market  Tablet is to be taken with food  Tea or coffee to be avoided  Vitamin C helps in absorption  Calcium salts and antacids to be avoided Iron deficiency Anemia- oral Therapy
  • 31. 31  Non compliance  Intolerance  Poor absorption(mal-absorption syndrome, dysentry)  No response after 4 weeks in confirmed cases of IDA  Moderate to severe cases seen late in pregnancy Iron deficiency Anemia- parental
  • 32. 32  Severe anaemia.  Confirmed cases not responding to oral or parental therapy.  Severely anaemic requiring emergency surgery.  Refractory anaemia. Iron deficiency Anemia- blood transfusion
  • 33. 33  Individual level Nutritional education Personal hygiene Contraception Iron & folic acid supplementation Promotion of breast feeding  Family level  Nutritional education  Birth spacing/ no of pregnancies  Control of parasites  Improvement of sanitation  Cooking in iron vessels Iron deficiency Anemia- Prevention
  • 34. 34  Community Level Nutritional education . Screening of adolescent girls in schools & iron supplementation. Iron & folic supplements to pregnant ladies. Deworming of school children . Delaying marriage age & birth spacing. Iron supplementation by fortification. Iron deficiency Anemia- Prevention
  • 35. 35  National nutritional anaemia prophylaxis programme Children with clinical anaemia: 20mg of elemental iron and 100mcg of folic acid,100days a year Pregnant and lactating :100mg of elemental iron and 500mcg of folic acid. Treat worm infestation with mebendazole. Drugs continued for nursing mothers and family planning acceptors  WIFS ( Weekly Iron Folic Acid Supplementation) Weekly Iron tablet and folic acid tablet to adolescent (10-19)at school Twice Yearly Deworming by Albendazole .WIFS.jpg Iron deficiency Anemia- national Programme
  • 36. 36  It is an essential trace element as it in an integral component of thyroid hormone : thyroxine and triiodothyronine.  Iodine deficiency is endemic in mountainous region since iodine is washed from the soil .  Its deficiency causes Iodine deficiency disorders that effect all ages : abortions, still birth , cretinism , mental retardation, deaf-mutism, dwarfism, and goiter.  Sources a) Food sources grown in iodine rich soil b) Dairy products c) Eggs d) Cereals grain, legumes, green leafs. IODINE- Introduction and Sources.
  • 37. 37  Goitrogens a) Certain vegetable of brassica family like cabbage , cauliflower, and radish, contain goitrogens such as thiocyanates and cynoglycosides. They make the iodine present in food unavailable to the body. Goitrogens can be inactivated by heating.  Absorption: Dietary iodine is absorbed from small intestine follows two main pathways within the body. 30% is used by the thyroid gland for synthesis and the remainder is excreted by the urine.  Functions: Iodine is an integral component of thyroid hormone thyroxine(T4) ,and tri- iodothyroxine (T3). Fetus and neonate normal protein metabolism in the brain and CNS require iodine. Iodine- Metabolism
  • 38. 38  Daily requirement of iodine is 150μg/day for adult ; a) Infant - 50μg/day b) Children- 100μg/day c) Pregnancy- 200μg/day.  Deficiency- Iodine Deficiency Disorders(IDD) a) Adults- hypothyroidism, raised level of TSH, resulting in hyperplasia of thyroid gland leading to goiter. Symptoms include lethargy, poor cold tolerance, bradycardia and myxedema. Infertility may also occur. b) Fetus and Infant- ‘Cretinism’- symptoms include mental retardation, hearing, speech defect, disorders of gait, and growth retardation c) At birth- still birth, miscarriage; Neonatal hypothyroidism is a sensitive indicator of incidence of IDD in a community Iodine- RDA and Deficiency
  • 39. 39  Fortification of salt with iodine is carried out to reduce IDD. The PFA act has specified an iodine concentration of 30 and 15 ppm at source and consumer end respectively thereby providing150 mg or iodine in 10 gram of salt.  Iodized oil: Injectable and oral iodized oil are available as oral drops (400mg/ml) and intramuscular injection (480mg/ml).Single IM injection of iodized oil can protect a woman through pregnancy and one year post partum; Oral supplementation is to be repeated every months to 1 year.  Nutritional Education Iodine – Prevention and control
  • 40. 40  Normally present in the bones and teeth and is essential for normal mineralization of bones and formation of dental enamel.  Sources a) Sea food , cheese and tea are rich sources b) Main Source for man is drinking water  The fluoride content of drinking water in India is about 0.5mg/l;  Deficiency of fluoride in water below 0.5mg/ml is usually associated with dental caries  Excess ingestion of fluorine (>2-3ppm in water ) is associated with skeletal and dental fluorosis and is a reported health problem in rural district of AP, Haryana, Kerala, Punjab, Rajasthan, and TN Fluorine
  • 41. 41  Changing Water sources  Defluoridation : Removal of excess fluoride from water . Nalgonda technique is an accepted form of defluoridation. It involves addition of lime and alum to the water sequentially , it is then followed by flocculation , sedimentation and filtration of water.  Avoiding intake of excess fluoride. Fluorine