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1. Vitamin
Vitamins are defined as "small organic molecules present in diet which are required in small
amounts." Most of the vitamins are not synthesized in the body and hence they must be
supplied in the diet. However few vitamins are synthesized in the body. Vitamins are
essential for growth, maintenance and reproduction. However, they are not used for energy
production.
Classification of Vitamins
Vitamins are divided into two groups.
1. Fat soluble vitamins (vitamin A, D, E, K)
2. Water soluble vitamins (vitamin B, C)
Vitamin A
Vitamin A (retinol) is a fat soluble vitamin found in vitamin retinol and a pro-vitamin beta
carotene form. The active forms of vitamin A are the oxidation products of retinol, all-trans-
retinal and all-trans-retinoic acid. The recommended daily allowance of vitamin A is as
follows: (i) infants 300- 400 μg; (ii) children 400-600 μg; (iii) adolescents 750 μg.
Sources
● In animal source, found as pre-formed vitamin A (retinol) and in plants as pro-
vitamins (carotene).
● Animal sources: food rich in retinol are liver, eggs, butter, cheese, whole milk, and
meat. Fish liver oils are the richest natural sources of retinol.
● Plant sources: green leafy vegetables such as spinach and yellow fruits and vegetables
and some roots like carrot.
Functions
Vitamin A participates in many bodily functions:
1) It is indispensable for normal vision. It contributes to the production of retinal
pigments which are needed for vision in dim light.
2) It is necessary for maintaining the integrity & the normal functioning of glandular &
epithelial tissue which lines intestinal, respiratory & urinary tracts as well as the skin
& eyes.
3) It supports growth especially skeletal growth.
4) It is anti-infective there is increased susceptibility to infection and lowered immune
response in vitamin A deficiency.
5) It may protect against some epithelial cancers such as bronchial cancers, but the data
are not fully consistent.
Causes of vitamin A deficiency
● Dietary deficiency of vitamin A
● Malabsorption of vitamin A due to repeated diarrhea, worm infestation and obstructed
jaundice.
● Increased demand of vitamin A due to respiratory infection and measles.
● Age between 1-3 years as is often related to weaning.
Deficiency
The signs of vitamin A deficiency are predominantly ocular. They include night blindness,
conjunctival xerosis, bitot's spots, corneal xerosis & keratomalacia. The term

2. "xerophthalmia" (dry eye) comprises all the ocular manifestations of vitamin A deficiency
ranging from night blindness to keratomalacia.
Vitamin A deficiency still remains to be a public health problem among school-aged children
& women. Rates of night blindness increase with age in both children & women.
Furthermore, rates are higher in rural areas. Among preschool children, no cases of night
blindness are reported in urban areas. The highest rate of night blindness is seen in the eastern
& central Terai.
1) Night blindness: Lack of vitamin A, first causes night blindness or inability to see in
dim light. The mother herself can detect this condition when her child cannot see in
late evenings or find her in a darkened room. Night blindness is due to impairment in
dark adaptation. Unless vitamin A intake is increased, the condition may get worse,
especially when children also suffer from diarrhoea & other infections.
2) Conjunctival xerosis: This is the first clinical sign of vitamin A deficiency. The
conjunctiva becomes dry & non wettable. Instead of looking smooth & shiny, it
appears muddy & wrinkled. It has been well described as "emerging like sand banks
at receding tide" when the child ceases to cry.
3) Bitot's spots: Bitot's spots are triangular, pearly-white or yellowish, foamy spots on
the bulbar conjunctiva on either side of the cornea. They are frequently bilateral.
Bitot's spots in young children usually indicate vitamin A deficiency. In order
individuals these spots are often inactive sequelae of earlier disease.
4) Corneal xerosis: This stage is particularly serious. The cornea appears dull, dry, non-
wettable & eventually opaque. It does not have a moist appearance. In more severe
deficiency there may be corneal ulceration. The ulcer may heal leaving a corneal scar
which can affect vision.
5) Keratomalacia: Keratomalacia or liquefaction of the cornea is a grave medical
emergency. The cornea (a part or the whole) may become soft & may burst open the
process is a rapid one. If the eye collapses, vision is lost. Keratomalacia is one of the
major causes of blindness & is frequently associated with protein energy malnutrition.
OR
Xerophthalmia
It is characterized by a bilateral dry, lusterless condition of the conjunctiva and cornea.
WHO classification of xerophthalmia (1982) and its clinical features:
i. XN: Night blindness: earliest symptoms of xerophthalmia in children in which child
is unable to see in the darkness.
ii. X1A: Conjunctival xerosis: one or more patients of dry lusterless, none wet table,
wrinkled conjunctivitis emerging like sand bags, patches involve the inter palpebral
area.
iii. X1B: Bitot's spot: patients notice the presence of triangular, foamy, white patches on
the inner and outer side of cornea.
iv. X2 : Corneal xerosis: cornea appears dull, dry and lusterless.

3. v. X3A: Keratomalacia: corneal meeting or ulcer over less than or equal to 1/3 rd the
corneal surface.
vi. X3B: Keratomalacia corneal meting or ulcer over more than 1/3 rd of the corneal
surface.
vii. XS: Corneal scar due to healing of keratomalacia resulting in blindness.
viii. XF: Xerosis of fundus: Typically seed-like, raised whitish lesions, scattered,
uniformly over the parts of fundus at the level of the optic disc.
TREATMENT
i. Immediately of diagnosis : Give vitamin A
- Child age < months: 5,0000 IU
- 6-12 months: 1 lakhs IU
- > 12 months: 2 lakhs IU
Repeat same dose on the following days and 4 weeks later. If the children has diarrhea or
gets sick and unable to tolerate vit.A (orally) then give intramuscular vit.A 25000 IU in child
less than 6 months, 50,000 IU in children 6-12 months of age and 1 lakhs IU in above 1 years
of children.
ii. Treatment of underlying causes such as PEM, measles and dehydration.
iii. Treat the general condition of children:-
- diet should be improved to induce food rich in vit. A as well as proteins.
- follow the measures to prevent diarrhea.
- immunized against common childhood diseases.
iv. Treatment of local condition of eyes.
PREVENTION OR CONTROL OF VITAMIN A DEFICIENCY IN NEPAL
 Dietary modification: The foods include dark green leafy vegetables, deep or bright
coloured fruits (e.g. papayas, oranges), carrots, and yellow vegetables (e.g. squash,
pumpkin), liver, beef, chicken, eggs, fish liver oil, whole milk, mangoes, sweet
potatoes, spinach, etc. are the Vitamin A rich food.
 Nutritional education: It is an important tool to increase awareness and consumption
of Vitamin A foods and supplementations.
 Food fortification: Fortification or enrichment of widely consumed foods with
Vitamin A is another strategy to prevent and control Vitamin A deficiency.
 Supplementation of Vitamin A: Prophylactic supplements of Vitamin A 200,000 IU
every 6 months are advised for all children between 1 and 5 years of age. Infants < 6
months can be given a one – time dose of 50,000 IU, and those aged 6 to 12 months
can be given a one – time dose of 100,000 IU.
Distribute the dose vit.A capsules to children between 6 and 59 months in community.
Supplementation of vit.A capsule (2,00,000 IU)to postpartum mothers through health
care facilities.

4. Strengthen the use of vit.A treatment protocol.
Conduct mini survey to assess the outreach supplementation programme.
 Prevention of childhood illness: PEM and infections like measles, diarrhoea,
respiratory tract infections and worm infestations
VITAMIN D
The nutritionally important forms of vitamin D are vitamin D2 (calciferol) and vitamin D3
(cholecalciferol). Calciferol may be derived by irradiation of the plant sterol, ergosterol.
Cholecalciferol is the naturally occurring (performed) vitamin D which is found in animal
fats and fish liver oils. It is also derived from exposure to UV rays of the sunlight which
convert the cholesterol in the skin to vitamin D. Vitamin D is stored largely in the fat depots.
The daily recommended dose for infant is 5 micrograms (200 IU) and for children 10
microgram (400 IU). Human milk is deficient in vitamin D and contains only 30-40 IU per
liter, mostly from 25(0H) D3. Breastfed infants must therefore receive an additional source of
vitamin D
Functions
1) Intestine: Promotes intestinal absorption of calcium and phosphorus.
2) Bone:
- Stimulates normal mineralization.
- Enhances bone reabsorption.
- Affects collagen maturation.
3) Kidney:
- Increases tubular reabsorption of phosphate
- Variable effect on reabsorption of calcium
4) Other: Permits normal growth
The traditional practice of giving an oil massage in sunlight to new born infants &
lactating mothers has been good source of vitamin D.
Deficiency
Rickets
Softening and weakening of bones in children due to deficiency of vitamin D is known as
rickets. Vitamin D deficiency leads to rickets, which is usually observed in young children
between the age of 6 months to 2 years. It is caused by a failure of osteoid to calcify in
growing bones where proliferation, degeneration and calcification of bone are incomplete. It
is a disease of rapid growing period. There is reduced calcification of growing bones.
Vitamin D deficiency is not as common as vitamin A deficiency in Nepal.
Causes
1. Decreased dietary intake and/or absorption.
Certain malabsorption syndromes such as celiac disease, short bowel syndrome, gastric
bypass, inflammatory bowel disease, chronic pancreatic insufficiency, and cystic fibrosis may
lead to vitamin D deficiency. Lower vitamin D intake orally is more prevalent in the
elderly population.

5. 2. Decreased sun exposure.
About 50% to 90% of vitamin D is absorbed through the skin via sunlight while the rest
comes from the diet. Twenty minutes of sunshine daily with over 40% of skin exposed is
required to prevent vitamin D deficiency. Cutaneous synthesis of vitamin D declines with
aging. Dark-skinned people have less cutaneous vitamin D synthesis. Decreased exposure to
the sun as seen in individuals who are institutionalized, or have prolonged hospitalizations
can also lead to vitamin D deficiency. Effective sun exposure is decreased in individuals who
use sunscreens consistently.
3. Decreased endogenous synthesis.
Individuals with chronic liver disease such as cirrhosis can have defective 25-hydroxylation
leading to deficiency of active vitamin D. Defect in 1-alpha 25-hydroxylation can be seen in
hyperparathyroidism, renal failure and 1-alpha hydroxylase deficiency.
4. Increased hepatic catabolism.
Medications such as Phenobarbital, carbamazepine, dexamethasone, nifedipine,
spironolactone, clotrimazole, and rifampin induce hepatic p450 enzymes which activate
degradation of vitamin D.
5. End organ resistance.
End organ resistance to vitamin D can be seen in hereditary vitamin D resistant rickets.
Signs & symptoms
1) Head: frontal bossing, increased size & delayed closure of fontanelle.
2) Teeth: delayed dentition.
3) Thorax:
Pigeon: chest deformity.
4) Spine: Scoliosis, kyphosis.
5) Limbs: Widening of wrist, ankle & other epiphysis, Genu Vulgum (knock knee),
Genu Varum (bowlegs)
6) Other features: Delayed milestones of development such as walking delayed, flat feet,
pot belly, constipation, growth failure, tetany & convulsions due to hypo-calcemia.
7) Mineral content (calcium low, phosphate elevated) of the bones, causing them to
break or curve easily.
Treatment
1) Give a single massive dose of vitamin D3 3,00,000 unit up to 1 year of age &
6,00,000 units for later age orally or intramuscularly together with supplementary
calcium & phosphorus. If healing does not occur after 3-4 weeks, repeat the same
dose of vitamin D3. If response to this therapy, further 400 unit per day for 3-4
months should be given.
2) Gross orthopaedic deformities, especially in adolescents, may occasionally need
surgical correction.
Prevention
1) Educate parents to expose their children regularly to sunshine.
2) Supplement of vitamin D containing food to young children with vitamin D.
3) Vitamin D fortification of foods, especially milk.
4) Making sure women have good vit.D level during pregnancy.
5) Identifying babies who are at risk of low vit. D.

6. 6) Timely complementary feeding.
7) Exposure to sun.
8) Include enough calcium and phosphate in the children in the children's diet.
Vitamin E
Vitamin E is a group of eight fat soluble compounds that includes 4 tocopherols and 4
tocotrienols. It is a fat soluble anti-oxidants protecting cell membranes from reactive oxygen
species. Vitamin E requirement of normal infants is approximately 0.4 μg/kg body weight/
day. For premature infants, 15 to 20 mg/day is required. The RDA for infants increases from
3 to 6 mg tocopherol from birth to 2 yr of age. One mg of tocopherol provides 1.5 IU activity
of vitamin E. a) 1-3 years: 6 mg/day b) 4-8 years: 7 mg/day c) 9-13 years: 11 mg/day.
Women who are breastfeeding should get 10 mg/day.
SOURCES
- Plant sources: flower seeds, almonds, spinach, avocados, squash, kiwi fruit, trout, olive oil,
wheat germ oil and broccoli.
- Animal sources: fish, egg, butter, cheese, chicken, pork, milk.
DEFICIENCY
Vitamin E deficiency is rare in humans, occurring as consequences of abnormalities in
dietary fat absorption or metabolism rather than from a diet low in vit.E.
- Peripheral neuropathy
- Myopathies
- Retinopathy
- Impairment of immune responses
Vitamin E deficiency results from a rare genetic condition known as ataxia .This condition is
neurologically based and affects muscle control and co-ordination.
VITAMIN K
Vitamin K refers to a group of fat soluble vitamins that plays a role in blood clotting, bone
metabolism and regulating blood calcium level. The body need vit.K to produce prothrombin,
a protein and clotting factors that is important in blood clotting and bone metabolism.
SOURCES
- Plants: green leafy vegetables such as kale spinach, turnip greens, mustard greens, green
leafy lettuce, broccoli, cauliflower and cabbage.
- Animals: fish, liver, meat, eggs.
DEFICIENCY
Deficiency is rare but in severe cases; it can increase clotting time, leading to hemorrhage and
excessive bleeding.
Vitamin C (Ascorbic acid)
Vitamin C (Ascorbic acid) is a water soluble vitamin. It is the most sensitive of all vitamins
to heat. Man, monkey & guinea pig are perhaps the only species known to require vitamin C
in their diet.
Function

7. Vitamin C has an important role to play in tissue oxidation.
It is needed for the formation of the collagen, which accounts 25% of total body protein.
Collagen provides a supporting matrix for the blood vessels and connective tissue and for
bones and cartilage.
Sources
The main sources of vitamin C are fresh fruits & green leafy vegetables. Germinating pulses
contain good amounts. Amala is one of the richest sources of vitamin C both in the fresh as
well as in the dry condition.
Deficiency
Scurvy: Deficiency of vitamin C result in scurvy. It occurs in people who have eaten no fruits
or vegetables, or taken no vitamin supplements for 2-3 months. Breast feed infants are
protected as the breast contains adequate amount of vitamin except when the mother is
deficient in vitamin.
Signs & symptoms
(i) Swollen & spongy gums (become swollen) particularly the papillae between the teeth
(scurvy buds) these bleed easily.
(ii) Subcutaneous patechial bruising, haemorrhage into joints or into gastrointestinal tract.
(iii)Loss of appetite & weakness.
(iv)Tenderness of bones & joints.
(v) Delayed wound healing.
(vi)There may also be emotional changes.
Treatment
Vitamin C (Ascorbic acid) 250 mg 8 hourly for 30 days
Prevention
(i) Daily use of vitamin C containing foods such as fresh fruits, vegetables, amala (water
berry), guava etc.
(ii) Heat destroys this vitamin, so such food should be eaten raw & eaten as soon after harvest
as possible.
VITAMIN ‘B’ COMPLEX DEFICIENCIES
Vitamin B is a water soluble compound. Vitamin B complex group includes B1, B2, B3,
B6, B12.
Vitamin B1 (Thiamine)
Vitamin B1 is a water soluble compound. It is essential co-enzyme for utilization and
metabolism of carbohydrate and proteins. Thiamine occurs in all natural foods, although in
small amounts. Milk is an important source of thiamine for infants, provided the thiamine
status of their mothers is satisfactory. It is available in all natural foods i.e. whole grain
cereals, wheat, gram, pulses and nuts. The requirement of thiamine is 0.2 - 0.3mg in infants
and 0.5-1.2 mg in child.
Thiamine losses
1. Thiamine is readily lost from rice during the process of milling.

8. 2. Being a water- soluble vitamin, further losses take place during washing and cooking of
rice.
3. Much of thiamine in fruits and vegetable is generally lost during prolonged storage.
4. Thiamine is also destroyed in fruits and vegetable is generally lost during prolonged
storage.
5. Thiamine is also destroyed in toast and in cereals cooked with baking soda.
Deficiency
Beriberi
a) Dry beriberi: The dry form characterized by anorexia, indigestion, weight loss,
weakness, diarrhea, constipation, edema, drowsiness, vocal cord paralysis.
b) Wet beriberi: The wet form is characterized by congestive cardiac failure with
dyspnea, cyanosis, tachycardia, edema and hepatomegaly.
c) Infantile beriberi: may found between 2-4 months of age of breast-fed baby of a
thiamine deficient mother with peripheral neuropathy.
Treatment
 Inj. Thiamine 50-100 mg/day IM or IV for 3days then 5-10 mg/ day.
 Give thiamine containing food.
Prevention
1. Give nutrition education to community related to eat well balanced, mixed diets
containing thiamine-rich foods.
2. Educate people to stop all alcohol.
3. Advise people to eschew highly polished rice & eat parboiled or under-milled rice.
4. Do not wash the rice before cooking.
5. Direct supplementation of high-risk groups (e.g. lactating mothers) is another
approach.
6. Patients on regular haemodialysis should routinely be given supplements of thiamine.
Thiamine should also be given prophylactically to people with persistent vomiting or
prolonged gastric aspiration & those who go one long fast.
Vitamin B2 (Riboflavin)
Riboflavin (vitamin B2) is a member of the B-group vitamins. It has a fundamental role in
cellular oxidation. It is a co-factor in a number of enzymes involved with energy metabolism.
Its richest natural sources are milk, eggs, liver, kidney & green leafy vegetables. Germination
increases the riboflavin content of pulses & cereals. Its requirement for infant - 0.3 - 0.4mg
per day and child - 0.5 - 1.3mg per day.
Deficiency
Angular stomatitis: The most common lesion associated with riboflavin deficiency is angular
stomatitis, which occurs frequently in malnourished children
Causes
1. Decrease dietary intake
2. Malabsorption
3. It may also occur in neonates under phototherapy.
Signs & symptoms
1. Cracking at the angle of mouth (cheiolosis)

9. 2. Glossitis: Sore and fissures at the corners of the mouth.
3. The tongue becomes swollen & purple
4. Scaly dermatitis, pruritus seborrhoea.
5. Photophobia, dry eyes, burning sensation of eyes.
6. This deficiency is usually seen just before & at the start of monsoon when fresh
vegetables become scarce.
Treatment
 Riboflavin 20mg/day in divided doses initially & followed by smaller doses once healing
has begin.
 Give riboflavin containing foods
Prevention
Nutrition education: Eat a variety of foods rich in riboflavin such as milk, green leafy
vegetables, eggs, liver, kidney etc to prevent deficiency.
VitaminB3 (Niacin)
Niacin or nicotinic acid normal is essential for the metabolism of carbohydrate, fat and
protein. It is also essential for the normal functioning of the skin, intestinal and nervous
system.
It is supplied by whole cereal grains, pulses, groundnuts, liver, and other organ meats of eggs.
This vitamin differs from the other vitamins of the B-complex group in that an essential
amino acid, tryptophan serves as its precursor. Another characteristic of niacin is that it is not
excreted in urine as such, but is metabolized to at least 2 major methylated derivatives: N-
methyl-nicotinamide & N-methylpridones. So the recommended daily allowance is 6.6
mg/1000 kcal of energy intake.
Deficiency
Pellagra: Pellagra is a nutritional disease due to deficiency of niacin, form endemic among
the poor who subsisted chiefly on maize.
Signs & symptoms
It has been called the disease of the three Ds; Dermatitis, diarrhoea & dementia.
(i) The dermatitis is bilaterally symmetrical & is found over the parts of the body exposed to
sunlight & especially on the neck, face, back of the hands & legs.
(ii) It is erythematic resembling severe sunburn & the lesion may progress to vesiculation,
cracking, exudation & crusting with ulceration & sometimes secondary infection.
(iii)The diarrhoea is often associated with nausea, glossitis & dysphasia.
(iv)Mental changes may occur in severe form which includes depression, irritability &
delirium.
(v) Pellagra is also associated with riboflavin deficiency & there may be fissures at the
corners of the mouth as well.
Treatment
Nicotinamide is given in a dose of 100 mg 8 hourly by mouth for 14 days.
Prevention
 Pellagra is a preventable disease.
 A good mixed diet containing milk &/or meat is universally regarded as an essential part
of prevention & treatment.

10.  Avoidance of total dependence on maize or sorghum is an important preventive measure
because pellagra is a disease of poverty.
Vitamin B6 (Pyridoxine)
Vitamin B6 (pyridoxine) exists in three forms, pyridoxine, pyrodoxal and pyridoxamine. It
plays an important role in the metabolism of amino acids, fats and carbohydrate. It is widely
distributed in foods, e.g. milk, liver, meat, egg yolk, fish, whole grain, cereals, legumes and
vegetables. It helps in metabolism of carbohydrate, protein and fatty acid. It is essential for
normal function of brain and nervous system. Its requirements for infants are 0.1- 0.3mg and
child is 1.5-1.3mg.
Deficiency
Peripheral neuritis: Pyridoxine deficiency is associated with peripheral neuritis. Riboflavin
deficiency impairs the optimal utilization of pyridoxine. INH, an anti tuberculosis drug is a
recognized antagonist and patients receiving INH are often provided with a supplement of
pyridoxine (10 mg/day)
Causes
 Decrease dietary intake
 Taking some dietary drugs-e.g. Isoniazide (INH), penicillamine hydralazine, oral
contraceptive.
Signs & symptoms
 Tingling sensation of limbs.
 Impairment of the nervous system, hyper anaesthesia
 Muscular cramp
 Convulsion in neonate.
 Impairment of the immune system
Treatment
Pyridoxine 20-50 mg/day for 14 days
Prevention
 Nutritional education should be provided
 Daily use of food rich in pyridoxine, such as meat, legumes, nuts & unrefined grains.
 Provide 10 mg pyridoxine supplement daily to the patient receiving INH.
Vitamin B12 (Preparation-cyanocobalamine)
Vitamin B12 is complex organo-metallic compound with a cobalt atom. The preparation
which is therapeutically used is cyanocobalamine, which is relatively cheap. Vitamin B12 co-
operates with folate in the synthesis of DNA, so deficiency of either leads to megaloblastosis.
Vitamin B12 has a separate biochemical role, unrelated to folate, in synthesis of fatty acids in
myelin. The physiological mechanism for its absorption requires intrinsic factor from the
stomach & the complex is absorbed only at a special site in the terminal ileum. It has role in
growth of lactobacilli in intestine and for maturation of RBCS. Its requirement foe infant is
0.3microgrsm per day and children is 0.5-1.5 microgram per day.
Sources

11. Good sources are liver, kidney, meat, fish, eggs, milk and cheese. Vitamin B12 is not founds
in foods of vegetable origin. It is also synthesized by bacteria in colon. Unlike folic acid,
vitamin B12 is relatively heat stable. Liver is the main storage site of vitamin B12.
Deficiency
Megaloblastic anaemia: Vitamin B12 deficiency is associated with Megaloblastic anaemia
(pernicious anaemia), demyelinating neurological lesions in the spinal cord and infertility (in
animal species).
Causes
(i) Nutritional deficiency of vitamin B12 may arise in subjects who are strict vegetarians &
eat no animal products.
(ii) There are fewer red blood cells & they do not contain much haemoglobin. The number of
platelets & white blood cells also decreases.
(iii)Pregnant & lactating women, infants & adolescents are prone to this disease because they
need additional amount of their vitamins & often do not get enough of the supply in the
diet.
Signs & symptoms
 Pallor of the skin, mucous membrane, palms of hands, conjunctiva.
 Tachycardia
 Cardiac dilation
 Oedema
 Lassitude, fatigue, breathlessness on exertion
 Palpitation throbbing in head & ears
 Dizziness, tinnitus, headache, dimness of vision
 Insomnia
Treatment
 Find out the cause & treat it.
 Blood transfusion if severe anaemia
 Supplement vitamin B12 & folate.
 Advise to take vitamin B12 containing food such as liver, kidney, meat, fish, eggs,
milk & cheesiest.
Prevention
 Supplement of iron, folic acid & vitamin B12 to pregnant women.
 Early find out the causes of anaemia & treat it
 Nutrition education
Mineral
Mineral is an inorganic element needed by the body for the following functions
 Build tissues
 Regulate body fluids
 Assist in body functions
 Help form body structures
 Remains as ash when food is burned

12. Classification of Minerals
 Major minerals –It is required in amounts greater than 100mg a day. It is also known
as “macrominerals" e.g sodium, potassium, calcium, etc
 Trace minerals - It is required in the diet in amounts lesser than 100mg a day .It is
also known as “microminerals” e.g iron, iodine, etc.
Calcium
Calcium is the most abundant mineral in the body and is located primarily (98%) in bone.
Calcium is essential for the coagulation cascade, nerve conduction and muscle stimulation.
Intestinal absorption of calcium varies inversely with intake and is regulated by 1,25(0H)D3,
which controls the synthesis of calcium-binding protein at the brush border. In the presence
of vitamin D, calcium absorption can adapt to a wide range of dietary calcium intakes. The
main sources of calcium for infants are milk and dairy products, with smaller amounts
derived from grains and fruits once solid foods are introduced. Children consuming strict
vegetarian diets may develop calcium deficiency, either alone or in combination with vitamin
D deficiency. Strict vegetarian diets may provide as little as 250 mg of calcium per day and
include generous amounts of substances that inhibit calcium absorption, such as fiber and
phytates. Children aged 1 to 10 yr require an intake of 500 to800 mg per day. During the
pubertal growth spurt calcium requirements are as high as 1000 to 1200 mg per day.
Pregnant and lactating women require 400 mg per day.
Deficiency
1. Rickets
2. Hypocalcaemia, tetany with muscle cramps
3. Numbness
4. Tingling sensation of limbs
5. Growth retardation
6. Dental carries
7. Palpitation
Phosphorus
It is mineral which help in formation of bones and teeth, metabolism of proteins, fat &
carbohydrates, energy production. Its sources are milk, fish, egg yolk, cereals & pulses. Its
daily requirements are:-
1. 0 – 6 months: 100 mg/day
2. 7 – 12 months: 275 mg/day
3. 1 – 3 years: 460 mg/day
4. 4 – 8 years: 500 mg/day
5. 9 – 18 years: 1250 mg/day
Deficiency
1. Rickets in growing children
2. Fatigue
3. Anorexia
4. Bone pain
5. Muscular weakness.
Potassium

13. It is a mineral which help muscular contraction, osmotic balance, and fluid electrolyte
balance, conduction of nerve impulses cardiac contractility & rhythm. It sources are meat,
fish, milk, cereals, banana, sweet potato, broccoli, fruit juices, etc. The daily requirements
are:-
1. 1 – 3 years : 3000 mg/day
2. 4 – 8 years : 3800 mg/day
3. 9 – 13 years : 4500 mg/day
4. 14 years and older : 4700 mg/day
Deficiency
1. Tachycardia
2. ECG changes , abnormal heartbeat
3. Marked muscle weakness
4. Hypotonia
5. Drowsiness.
Sodium
It is a mineral which maintenance of osmotic pressure, irritability of muscle and nerves for
acid - base balance. The sources of sodium are common salt, drinking water, vegetables,
milk, egg, meat etc. The daily requirements of sodium are:-
1. Up to 12 months : < 0.4 g/day
2. 1 – 3 years : 0.8 g/day
3. 4 – 6 years : 1.2 g/day
4. 7 – 10 years : 2 g/day
5. 11 years & over : 2.4 g/day
Deficiency
1. Hyponatremia
2. Muscular cramps
3. Nerve impulses do not get transmitted.
Magnesium
Magnesium is essential for bioenergetics reactions controlling fuel oxidation, membrane
transport and signal transmission contributing to the action of more than 300 enzymes. Over
80% of the total body magnesium is in bone and skeletal muscle. Rich sources of magnesium
include legumes, nuts, bananas and whole grains. Magnesium is absorbed efficiently by the
intestine and regulation of its balance depends on renal tubular reabsorption.
Deficiency of Magnesium
1. PEM
2. Malabsorption syndrome
3. Chronic renal failure
4. Diarrhea
5. Persistent vomiting
6. Hypocalcaemia
7. Irritability
8. Convulsions

14. 9. Ataxia
10. Muscular weakness and tetany.
Iodine
Iodine is an essential mineral commonly found in seafood. It is essentials for synthesis of
thyroid hormones. [Thyroxin (T4) & Triiodothyronine (T3)]. Its sources are seafood's (sea
fish, sea salt), vegetables grown in soil rich in iodine, milk, meat, cereals, etc. The daily
requirements are:-
1. 0 – 6 months : 90 microgram/day
2. 7 – 12 months : 110 microgram/day
3. 1 – 8 years : 90 microgram/day
4. 9 – 13 years : 120 microgram/day
5. 14 – 18 years : 150 microgram/day
Deficiency
1. Goiter
2. Hypothyroidism
3. Cretinism
4. Dwarfism
5. Impaired physical and mental growth
6. Delayed motor milestones.
Zinc
Zinc is a component of over 100 metalloenzymes and participates in many biological
processes. As a component of zinc finger proteins, zinc regulates gene transcription and
participates in nucleic acid metabolism, protein synthesis and thereby, cellular growth.
Thyrnidine kinase, DNA polymerase and RNA polymerase are reported to be zinc dependent
enzymes. The sources of zinc are vegetables, animal foods like meat, milk, fish, cheese, nuts,
whole wheat and egg yolks. The daily requirements are:-
1. 7 months – 3 years: 3 mg/day
2. 4 – 8 years: 5 mg/day
3. 9 – 13 years: 8 mg/day
4. 14 – 18 years: 9 mg/day
Deficiency
1. Growth failure
2. Delayed wound healing
3. Liver disease
4. Hypogonadism
5. Anorexia
6. Alopecia
7. Behaviour changes.
Copper
Copper is a component of several metalloenzymes required for oxidative metabolism.
Ceruloplasrnin, a glycoprotein that contains eight copper atoms per molecule, accounts for
95% of the ion in blood. The richest sources are meats, liver, seafood, nuts and seeds.
Additional copper may enter the food chain through pesticides and contamination of water by
pipes and cooking utensils.

15. Deficiency
1. Anemia
2. Neutropenia
3. Hypopigmentation of hair and skin
4. Osteoporosis
5. Fracture
6. Defective immune system
Selenium
Selenium is a constituent of glutathione peroxidase, an antioxidant in red blood cells and
other tissues. It play vital role in reducing cellular damage and support immune response. The
sources of selenium are fish, eggs, pork, whole grains, dairy products, milk (human milk). Its
daily requirement is:-
1. 1 – 3 years : 20 mcg/day
2. 4 – 8 years : 30 mcg/day
3. 9 – 13 years : 40 mcg/day
4. > 14 years : 55 mcg/day
Deficiency
1. PEM
2. Refusal to eat
3. Poor body weight gain
4. Keshan disease (Juvenile cardiomyopathy)
5. Kaschin – Beck disease (Chondrodystrophy).
Iron
Iron is a mineral that is naturally present in many foods, added to some food products, and
available as a dietary supplement. Iron is an essential component of hemoglobin, an
erythrocyte (red blood cell) protein that transfers oxygen from the lungs to the tissues. Iron is
also necessary for physical growth, neurological development, cellular functioning, and
synthesis of some hormones The sources of iron in the diet include lean meat, seafood, nuts,
beans, vegetables, and fortified grain product, etc.
Age Male Female Pregnancy Lactation
7-12 months 11mg 11mg
1- 3 yr 7mg 7mg
4-8 yr 10 mg 10mg
9-13 yr 8mg 8mg
14-18 yr 11mg 15mg 27mg 10mg
19-50 yr 8mg 18mg 27mg 9mg
Above 51 yr 8mg 8mg
Deficiency
• Nutritional anemia
• Susceptibility to infection
• Weakness
• Poor growth.
Prevention
 Nutrition education/ counselling.
 Giving iron fortified milk formula & iron fortified cereals to infants.

16.  Deworming, change in dietary habits, wearing of shoes are important measures.
 Addition of meat & animal products to children's diet as well as foods high in iron.
 Recognizing the severe consequences of iron deficiency & its effects on health,
learning capacity, productivity & maternal & neonatal survival Ministry of Health &
Population has approved five year anaemia Plan of Action (plan of action developed
by Child Health Division, DoHS.
 Iron supplementation during pregnancy has been a key initiative in Nepal since 1980.
According to the government policy all pregnant women are supplied with iron tablet
containing 60mg of elemental iron, free of cost. It is provided to all pregnant women
since the beginning of second trimester of pregnancy & continued up to 45 days
postpartum (225 days in total)
 There have been extensive efforts to increase awareness about anaemia & need for
iron supplementation during pregnancy.
 Awareness raising activities mainly include advocacy, information through public
media & training of health workers/volunteers at all levels. IEC materials such as flip
chart & posters are also being distributed for this purpose.
Reference of vitamin and mineral
 Dahal k, Community Health Nursing, 5th
edition, Makalu publication house,
Dillibazar, Kathmandu, Page no179 to186
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3936686/
 https://www.who.int/nutrition/publications/vad_consequences.pdf
 Paul VK, Bagga A, Ghai Essential Pediatrics, eight edition, CBS Publisher and
Distributors Pvt Ltd page 110 to 117
 WilsonD, Rodgers CC, Hockenberry M, Wongs Essential of pediatric Nursing 10 th
edition, ELSEVIER, page no Page 638-639