Nutritional deficiency disorders in pediatrics represent a major public health crisis in India, responsible for approximately 55% of childhood deaths and afflicting around 60 million malnourished children. The document categorizes malnutrition into various types such as under-nutrition, over-nutrition, and specific syndromes like kwashiorkor and marasmus, emphasizing their clinical manifestations, diagnostic evaluations, and management strategies. Additionally, it outlines the importance of vitamins A, D, E, K, C, and B complex, detailing the potential deficiencies and necessary interventions for prevention and treatment.

1. Nutritional
deficiency disorders
in pediatrics
Bhavya N Kelavadiya
Nursing Tutor

3. Nutritional disease
O It is the major public health problem in
india.
O It affect the vast majority numbers of
population and responsible for approx.
55% of childhood death.
O There are about 60 million malnurished
children and every month about 1 lakh
children die due to effect of malnutrition.
O 2.5 million – threatened by blindness
O 75-80% of hospitalized children-
malnutrion

4. MALNUTRION
OIt is a pathological state that
results from relative or absolute
deficiency or excess of one or
more essential nutrients.

5. Etiological factors
1. Infections and disease
conditions

6. 2. Poor socioeconomic
condition

7. 3. Cultural influences

8. 4. Inadequate health and other
services

9. Assessment of nutritional
problems
1. Assessment of dietary intake by detailed
history of dietary pattern
2. Anthropometric examination
3. Clinical examination
4. Assessment of associate problems
5. Lab- investigation
6. Assessment of ecological factors,
morbidity and mortality pattern in
community help to detect nutritional
status

10. Classification
Malnutriti
on
Over-
nutrition
Over-
weight Obesity
Under-
nutrition
stunting wasting
SAM
MARASMU
S
KWASHIOR
KOR
MARASMIC
KWASHIOR
KOR
NUTRITION
AL
DWARFING
MAM
Under-
weight
Micronutri
ent
deficiency

11. PROTEIN ENERGY
MALNUTRION
O It is a major public health and nutritional
health problem in india.
O It can be define as a group of clinical
conditions that may results from varying
degree of protein deficiency and
energy(calorie) inadequacy.
O Previously it was also known as protein
calorie malnutrition.

12. Classification
1. Syndromal classification:
A. Kwashiorkor
B. Nutritional marasmus
C. Pre-kwashiorkor
D. Nutritional dwarfing

13. 2. Classification according to indian
academy of pediatrics
A. Grade I: between 71% to 80% of
expected weight for age.
B. Grade II: between 61% to 70% of
expected weight for age.
C. Grade III: between 51% to 60% of
expected weight for age.
D. Grade IV: 50% or less of weight
expected for that age.

14. 3. Gomez classification:
O Type equation here.Weight for age classification by
gomez,
weight for age(%)=weight of child is devided
by weight of normal child of same age X 100
A. Grade I : weight between 75 to 90% of expected
for the age.
B. Grade II : weight between 61 to 75%
of……………
C. Grade III: weight less than or equal to 60%
of…….

15. 1. Kwashiorkor
O Kwashiorkor was first described by Dr.
Cicely Williams in 1933, but the particular
term ‘kwashiorkor’ was introduced in
1935, according to local name for the
disease in ghana. The term was said to
mean ‘red boy’ due to characteristic
pigmentary changes.
O It is mainly found in preschool child but
may occur in any age.

16. CLINICAL MENIFESTATION:
O Essential features:
a) Marked growth retardation

17. b) Muscle wasting with retention of some
subcutaneous fat

18. c) Psychomotor changes
O Listless, inertness, lack o interest, lethagy
loss of appetite

19. d) Pitting edema: due to hypo-
albuminemia

20. O Non- essential features:
a) Hair changes:

21. b) Skin changes: erythma and hyper-pigmented
skin patches

22. c) Superadded infections: repeated infections

23. 2. Nutritional marasmus
O It is also term as INFANTILE ATROPHY.
O It is common in infants may found in toddlers.
O Dietary history reveals both proteins and
calories inadequacy in diet in the recent past
with predominant lack of calorie.
O The child look like old person due to lack of
buccal pads of fat.
O Initially the child is irritable, hungry and craves
for food, but in later stages may refusal to
take anything orally.

24. Clinical menifestation:
O Essential features:
a) Marked growth retardation with less then 60%
of expected weight for age.

25. b) Gross wasting of muscle and subcutaneous
tissue:

26. c) Marked stunting and absence of edema:

27. O Non-essential features:
a) Hair changes may present
b) Skin looks dry with prominent loose
folds and reduced MUAC
c) Superadded infections are common
d) Liver usually shrunk
e) Psychomotor changes
f) Features of anemia, vitamin deficiency

28. 3. Marasmic kwashiorkor
O It is condition where the child menifested
both features of marasmus and
kwashiorkor.
O The presence of edema is essential for
diagnosis and other features of
kwashiorkor may or may not be present.

29. 4. pre-kwashiorkor
O It is a condition in which the child is having
the features of kwashiorkor without
edema. If early management is initiated by
early diagnosis of the condition, the child
may be protected from full-blown
kwashiorkor.

30. 5. Nutritional dwarfing
O It is condition when the child is having
significant low weight and height for the
age without any overt features of
kwashiorkor and marasmus.
O It is usually seen when the PEM continue
over a number of years.

31. Diagnostic evaluation:
O Physical examination
O Anthropometric assessment
O Peripheral blood flim
O Stool examination
O Blood hematolog yand biochemistry
O Urine examination

32. Management
O Management of PEM can be divided in
two phases-
a) Initial phase
b) Rehabilitation phase

33. a)Initial phase(1-2weeks)
A. Treatment of comlication
B. Correction of nutritional deficiencies
C. Reversal of metabolic abnormalities
D. Beginning of feeding

34. A. Treatment of complications
O The acronym ‘shielded’ represents the
complication which may arise because of
protein-energy malnutrition. All these
complication need to be treated in the first two
day of treatment.
O S- sugar level of blood is low
H- hypothermia
I- infection
EL- electrolyte disturbances
DE- dehydration
D- deficiency of nutrients

35. • Initiation of feeding
O The feeding must be stated, after the fluid
and electrolyte balance is restored and
infection is under control. feeding must follow
the principle described by acronym ‘BEST’
a) B- beginning of feeding
b) E- energy dense feeding
c) S- stimulation of emotional and sensorial
development
d) T- transfer to home based diet before
discharge
O if oral feeding is not possible ,NG feeds are
given.

36. b) Rehabilitative phase:
O It focuses on:
O Recovery of lost weight
O Emotional and physical stimulation to the
child
O Training the mother for domiciliary care
O Preparation for discharge

37. Recovery and discharge
O Return of appetite
O Disappearance of hepato-spleenomegaly
O Gain in body weight
O Absence of edema
O Rising serum albumin level

38. Prevention of malnutrition
O Prevention at family level
O Prevention at community level
O Prevention at national level

40. VITAMIN-DEFICIENCY
DISORDERS

41. O Vitamins are organic compounds, considered
as essential nutrients required by the body in
very small amounts.
O Since the body is generally unable to
synthesize from diet, for maintenance of
normal health.
O The balanced vitamins are divided into two
categories:
a) fat-soluble vitamins :A, D, E and K
b) water-soluble vitamins : B- complex and C
 Each vitamin has specific functions to perform
and deficiency of particular vitamin may results
to specific deficiency disorders.

42. Vitamin A
O Vitamin A, also known as retinol, has
several important functions.
O These include:
O helping your body's natural defence against
illness and infection (the immune system) work
properly
O helping vision in dim light
O keeping skin and the lining of some parts of the
body, such as the nose, healthy

45. Sources:
O Good sources of vitamin A (retinol) include:
O cheese
O eggs
O oily fish
O fortified low-fat spreads
O milk and yoghurt
O liver and liver products such as liver pâté – this is a
particularly rich source of vitamin A, so you may be at risk
of having too much vitamin A if you have it more than once
a week (if you're pregnant you should avoid eating liver or
liver products)
O Good sources of beta-carotene in your diet, as the
body can convert this into retinol.
O The main food sources of beta-carotene are:
O yellow, red and green (leafy) vegetables, such as spinach,
carrots, sweet potatoes and red peppers
O yellow fruit, such as mango, papaya and apricots

46. Vitamin A deficiency
O Vitamin A deficiency can be defined clinically or
sub-clinically. Xerophthalmia is the clinical
spectrum of ocular manifestations of vitamin A
deficiency; these range from the milder stages
of night blindness and Bitot spots to the
potentially blinding stages of corneal xerosis,
ulceration and necrosis (keratomalacia).
O The various stages of xerophthalmia are
regarded both as disorders and clinical
indicators of vitamin A deficiency. Night
blindness (in which it is difficult or impossible
to see in relatively low light) is one of the
clinical signs of vitamin A deficiency, and is
common during pregnancy in developing
countries. Retinol is the main circulating form of
vitamin A in blood and plasma.

48. Clinical manifestation:
O Night blindness: poor vision in dark

49. O Xerophthalmia: eye fails to produce tears

50. O Xerosis conjunctiva: conjunctiva is dry, thickened
,wrinkled and pigmented

51. O Xerosis cornea: dryness spread to cornea.

52. O Bitot’s spot: greyish or white plaques formed of
desquamated conjunctival epithelium .

53. Other symptoms:

54. Management:
1. Supplementation:
 Mild to moderate cases should be given 10,000
𝜇g/daily
 Severe cases should be get 50,000 𝜇g/daily for
few weeks
2. Dietary consumption:
 Consumption of yellow or orange fruits and
vegetables which contains carotenoid especially
B-carotene is beneficial.

56. VITAMIN-D
O Vitamin D is a group of fat-
soluble secosteroids responsible for increasing
intestinal absorption of calcium, magnesium,
and phosphate, and many other biological
effects.
O Vitamin D is referred to as “Sunshine Vitamin”,
because it can be synthesized in body in
presence of the UV rays from sun.
O It stimulates normal mineralization of bones and
teeth.
O It is absorbed in presence of bile and fat through
lymph and is stored in liver.

58. Sources of vitamin D

59. Vitamin D deficiency
O Vitamin D deficiency can lead to a loss of bone
density, which can contribute to osteoporosis
and fractures (broken bones). Severe vitamin
D deficiency can also lead to other diseases. In
children, it can cause rickets. Rickets is a rare
disease that causes the bones to become soft
and bend.
O Vitamin D directly interacts with the cells that are
responsible for addressing infections.

60. O Clinical manifestation of vitamin D
deficiency is mainly found as
RICKETS.it is a disease of growing
bones.
O It is usually developed in children
between 6 month to 2 yr of age.
O In this the process of proliferation,
degeneration and calcification of bones
are incompleted.

61. Clinical features:

62. Management
O Specific treatment consists of administering a
single massive dose of vitamin D orally or IM.
O Gross orthopedic deformity needs surgical
correction(osteotomy).
O Associated problems like mal-absorption,
steatorrhea, should be treated.
O Diet should have adequate amount of vitamin D
from animal food.
O The child should be encouraged to play outside
for longer period for exposure to sunlight.

63. Prevention:
O Health education and promotion of
awareness
O Exposure of child to sunlight, avoidance of
overclothing and provision of proper
housing.
O Improvement of dietary habit
O Regular health supervision
O Adequate treatment of childhood disease

65. VITAMIN E
O Vitamin E is a fat-soluble vitamin with
several forms, but alpha-tocopherol is
the only one used by the human body.
O Vitamin E is found naturally in some
foods, added to others, and available as a
dietary supplement. “Vitamin E” is the
collective name for a group of fat-soluble
compounds with distinctive antioxidant
activities

68. Vitamin E Deficiency
O Vitamin E deficiency can cause nerve and
muscle damage that results in loss of feeling
in the arms and legs, loss of body movement
control, muscle weakness, and vision
problems.
O Vitamin E deficiency can cause a form of anemia
in which red blood cells rupture (hemolytic
anemia). Premature infants who have a vitamin
E deficiency are at risk of this serious disorder.
O In premature infants, bleeding (hemorrhage) may
occur within the brain, and blood vessels in the
eyes may grow abnormally (a disorder
called retinopathy of prematurity).

69. O The deficiency of vitamin E in mothers may
lead to pre-maturity.
O Children with vitamin E deficiency usually
suffer from mal-absorption states, ataxia,
cholestatic disease, muscle weakness,
dysarthria and growth impairment.

71. Management
O Treatment of vitamin E deficiency
involves taking vitamin E supplements
by mouth. Premature newborns may be
given supplements to prevent disorders
from developing. Most full-term newborns
do not need supplements, because they
get enough vitamin E in breast milk or
commercial formulas.

73. VITAMIN K
O Vitamin K is a fat-soluble vitamin that comes in two
forms. The main type is called phylloquinone,
found in green leafy vegetables like collard greens,
kale, and spinach. The other type, menaquinones,
are found in some animal foods and fermented
foods.
O Vitamin K helps to make various proteins that are
needed for blood clotting and the building of bones.
Prothrombin is a vitamin K-dependent protein
directly involved with blood clotting.

74. Functions of Vitamin K

76. VITAMIN K DEFICIENCY
O Vitamin K deficiency can contribute
to significant bleeding, poor bone
development, osteoporosis, and
increased risk of cardiovascular
disease.
O Vitamin K Deficiency Bleeding (VKDB) in
newborns can be separated into three
categories based on the timing of the
presentation.

78. Management

79. O VKDB is easily prevented by giving babies
a vitamin K shot into a muscle in the thigh.
One shot given just after birth will protect
your baby from VKDB.
O In order to provide for immediate bonding
and contact between the newborn and
mother, giving the vitamin K shot can be
delayed up to 6 hours after birth.

81. VITAMIN C
O Vitamin C also known as ascorbic
acid and ascorbate .
O It is a water-soluble vitamin found in citrus
and other fruits and vegetables, also sold
as a dietary supplement and as
a topical 'serum' ingredient to
treat melasma (dark pigment spots) and
wrinkles on the face.
O It absorbed from intestines and passed on
through portal to general circulation. liver
and other organs and tissues have an
optimum level of vitamin C.

85. Vitamin C Deficiency
O Scurvy is a clinical syndrome that results from
vitamin C deficiency.
O Vitamin C deficiency manifests symptomatically
after 8 to 12 weeks of inadequate intake and
presents as irritability and anorexia.
O It is also called as ‘Bleeding Gums’.
O Deficiency of vitamin C usually present between 6
month to 7 years of age.

87. Management
O Scurvy is generally easy to treat by increasing
vitamin C levels. In mild cases, scurvy can be
treated simply with vitamin C–rich foods.
O “The ‘five servings of fruits and vegetables per day’
rule will provide the recommended daily intake of
vitamin C and will treat mild cases, and prevent
future cases, of scurvy.”
O The only medication to treat scurvy is vitamin C–rich
foods and vitamin C supplementation (pill form,
intravenous, or injected).
O Infants are given ascorbic acid in a dose of 50mg, IM
twice daily for 1 week. Therafter a dose of
100mg/day is given for 1 month.

90. VITAMIN B1 (THIAMINE)
O Vitamin B1 or thiamin is essential for glucose
metabolism and nerve, muscle, and heart
function.
O Thiamine is essential coenzyme for utilization
and metabolism of carbohydrate and proteins.
O Vitamin B1 has vital role in nutrition of heart and
peripheral nerve.
O It is required for the synthesis of acetylcholine
and it’s deficiency results in impaired nerve
conduction.

92. Beri-beri
O Deficiency of thiamine B1 containing food,
mal-absorption states and prolonged illness.
O The deficiency condition is mainly mainly beri-
beri.
O Wernicke-korsakoff syndrome and subacute
necrotizing encephalopathy may also occur
due to deficiency of vit. B1.
O Beri beri may occur in blow given forms:
a) Dry beri beri
b) Wet beri beri
c) Cerebral beri beri

93. O Dry beri-beri:
 Loss of appetite
 Diminished abdominal reflexes
 Tingling and numbness of legs and hands
 Wasting of muscle, muscle pain
 Main feature is “burning feet syndrome”
 Difficulty in walking due to weakness
 Sever deficiency can experience seizures

94. O Wet beri beri:
 Generalized oedema
 Cardiac enlargement
 Palpitation
 Difficulty in breathing
 Congestive heart failure

95. O Cerebral beri beri:
 Foot drop
 Wrist drop
 Ataxia of gait
 Derrangement of mental functions
 Confusion

96. Management
O Thiamine supplement is required.
O Infant: 5 mg/week IM
5 mg/daily, orally for a month
 Adult: 25 mg/day IM for 1 week
then 10 mg orally thrice daily for 1-2
month

97. VITAMIN B2(RIBOFLAVIN)
O Vitamin B2 is a coenzyme in metabolism
of protein, fatty acid and carbohydrate. It
helps in cellular oxidation.
O Rich source of vitamin B2 in natural food
are milk, eggs, liver, green leafy veg. etc.
O Meat and fish contain small amounts.
O Cereals and pulses are relatively poor
sources.

98. Deficiency
O Deficiency of riboflavin is manifested as angular
stomatitis, cheilosis, magenta tongue, glossitis,
nasolabial seborrhea, seborrheic dermatitis,
desquamation etc.
O It may cause keratitis, watering of eyes,
photophobia, blurring of vision, burning and
itching of eye.
O This may occur due to restricted protein intakes
and mal-absorption of protein. It may also occur
in neonates under phototherapy and following
administration of protein.
O MANAGEMENT: child: orally 5mg for 1 month

100. VITAMIN B5(NIACIN)
O Niacin or nicotinic acid is essential for
carbohydrate, fat and protein metabolism.
O It helps in normal functions of skin, GI,
nervous and hemopoietic system.
O Sources of vitamin B5 are the natural
foods like milk, liver, chees, cereals,
pulses, groundnuts, fish etc.

101. Deficiency
O Deficiency of vitaminB5 results in “PELLAGRA”
O It is characterized by three Ds,
I. Diarrhea
II. Dermatitis
III. Dementia
• Other features include glossitis, stomatitis,
dysphagia, nausea, vomiting, loss of appetite,
anemia and mental changes like depression,
irritability and delirium.
• It found in malnutrition and in jowar and maize
eater.
• Management: adm. Of niacin 50mg IM
2sweek followed by 100mg orally 2sday for 2-3
week.

102. VITAMIN B6(PYRIDOXINE)
O It helps in metabolism of carbohydrate,
proteins and fatty acid.
O It is essential for normal function of brain and
nervous system.
O It has also role in blood formation and
maturation of polymorphonuclear cells.
O Sources of vitamin B6 are natural foods like
egg, meat, wheat germ, soya bean, peas,
pulses, cereals etc.

103. Deficiency
O Deficiency of pyridoxine is manifested as
convulsion, peripheral neuritis, irritability,
anemia as seborrheic dermatitis around the
nose and eyes, GI upset as loss of appetite,
abdominal discomfort and diarrhea.
O This deficiency is rare in the child, especially for
nutritional origin, but can occur in association
with INH therapy in TB.
O Management: vitamin B6 rich food and
supplement should initiate.

104. VITAMIN B12
(CYNOCOBALAMIN)
O Vitamin B12 cooperates with folate for
synthesis of DNA.
O Separately it is essential for the synthesis of of
fatty acid in myelin.
O It may have some role in carbohydrate and fat
metabolism, growth of lactobacilli in intestine
and for maturation of RBCs.
O Source of vit B12 are only animal foods.

105. Deficiency
O Deficiency of vitamin B12 is associated
with juvenile pernicious anemia, a
megaloblastic anemia due to lack of
intrinsic factors in stomach and
achlorhydria.
O Gastrectomy, surgical removal of ileum,
intestinal tuberculosis and long-term
therapy with PAS or neomycin and mal-
absorption state may also result to vitamin
B12 deficiency.
O It can found who are strictly vegetarian.

106. O Management: vitamin B12 is
supplemented in forms of oral pills,
sublingual, liquid or intranasal spray.
O Transdermal patch supplements in form of
cyanocobalamin, hydroxycobalamin and
methycobalamin may be prescribed.
O 1000 𝜇g, two times in a week

108. CALCIUM
O Calcium is an important mineral element
in body, mainly utilized in formation of
bones and teeth.
O It is also involved in bloodcoagulation,
cardiac function, nerve conduction,
muscle contraction and metabolism of
enzymes and hormones.
O Sources of calcium are mostly milk and
milk products, egg and fish, cheapest
sources are green leafy vegetables,
cereals, and millets(ragi).

109. Calcium Deficiency
O Hypocalcemia, also known as calcium deficiency
disease, occurs when the blood has low levels of
calcium.
O A long-term calcium deficiency can lead to dental
changes, cataracts, alterations in the brain,
and osteoporosis, which causes the bones to
become brittle.
O Deficiency of calcium may produce rickets and
hypocalcemic tetany with muscle cramp, numbness,
tingling sensation of limb etc.
O It may also result in growth retardation, dental
caries, osteoporosis, osteomalacia, insomnia, skin
problems, joint pain and palpatation.

110. Prevention
O To be done by increased dietary intake of
calcium containing food, promoting
calcium absorption by avoiding excess
dietary intake of phytic acid, increasing
dietary protein and treating chronic
diarrhea.

111. PHOSPHORUS
O It plays a vital role in in metabolism of protein,
fat and carbohydrates.
O It is essential for bone and teeth, synthesis of
phospholipid and regulation of acid-base
equilibrium.
O Significant dietary sources are milk, meat,
fish, egg yolk, cereals and pulses.
Phosphorus is widely available foodstuff, so
its deficiency occurs rarely.

112. Phosphorus Deficiency
O Deficiency of phosphorus may lead to
rickets in growing children.
O Hyperphosphatemia results in renal
failure.

113. SODIUM
O Sodium is an important electrolyte,
present in all body fluids.
O It is essential for maintenance of osmotic
pressure, irritability of muscle and nerve
for acid-base balance.
O It is available in salt, drinking water,
vegetable, milk, egg, meat etc.

114. Sodium Deficiency
O Deficiency of sodium results in
hyponatremia due to excess loss through
secretion, vomiting, gastric aspiration,
diarrhea, diuresis etc.
O The clinical features of low sodium are
dehydration, weakness, dizziness, N/V,
anorexia, hypotension and convulsion.
O Hypernatremia may results in edema and
CNS symptoms.

115. POTASSIUM
O Potassium is an important element of
muscular contraction, conduction of nerve
impulses, cell membrane permeability and
enzyme action.
O It is essential for osmotic pressure, fluid
electrolyte balance and integrity of cardiac
muscle and rhythm.
O All food contains potassium but meats,
milk, cereals, vegetable, legumes, dried
fruits and fruit juice.

116. Potassium Deficiency
O Deficiency does not occurs in healthy
normal child.
O Hypokalemia develop in starvation,
malnutrition, gastroenteritis steroids and
diuretics therapy.
O It is manifested by tachycardia, ECG
changes, marked muscle weakness,
hypotonia, abdominal distension and
drawsiness.

117. O Hyperkalemia results from increased
extra cellular potassium, most often due to
renal failure and excess potassium
therapy.
O The C/F may shows muscle weakness,
abdominal distension, restlessness,
diarrhea, abnormal cardiac reaction and
ventricular fibrillation.

118. MAGNESIUM
O It is present in all body cells.it is essential
for formation of bones and teeth,
enzymatic action, carbohydrate
metabolism, synthesis of FA and proteins.
O It helps in metabolism of calcium and
potassium.
O It obtains from banana, milk, cereals, nuts,
meats and green leafy veggies.

119. Magnesium Deficiency
O It is usually associated with PEM, mal-
absorption syndrome, chronic renal failure,
diarrhea, persisting vomiting, gastric
aspiration.
O Its C/F are CNS symptoms like irritability,
convulsion, ataxia, muscular weakness and
tetany.
O Hyper-magnesemia may occur in diminished
urinary excretion and manifested as muscular
weakness, low BP, sedation, extreme thirst.

120. IRON
 It has great significance as nutritional
element.
 It is plays an important role in formation of
hemoglobin and myoglobin.
 It helps in the development and function of
brain, regulation of body temperature,
muscular activity.
 It is essential for production of antibodies
enzymes and cytochromes.
 The most important in oxygen transport
and cell respiration.

121. O There are two forms of iron:
a) Heme-iron
b) Nonheme- iron
 Best sources of heme-iron are liver, meat,
egg and fish which also promote the
absorption non-heme.
 Best source of non- heme iron is green
leafy vegetables.

122. Iron Deficiency
O Deficiency of iron leads to nutritional
anemia.
O Other condition which may lead to
impaired cell mediated immunity,
susceptibility of infections.
O Excess of iron and deposition of abnormal
iron pigment in tissue may occur in iron
poisoning, breakdown of RBCs in
hemolytic anemia.

123. IODINE
O It is significant micronutrient essential for
synthesis of thyroid hormones-
thyroxin(T4) and triiodothyronine(T3).
O Important sources of iodine are sea foods,
and veg. grown in soil rich in iodine.
O Smaller amount is available from milk,
meat and cereals.

124. Iodine Deficiency
O Iodine deficiency disorders(IDD) include
goiter, hypothyrodism, dwarfism, deaf-
mutism, subnormal intelligence, impaired
physical and mental growth.
O Prevention: it include improvement of
dietary intake of iodine containing food in
balanced diet, compulsory use of iodized
salt.

125. ZINC
O Zinc is trace element and essential
component of many enzymes.
O It is required for a synthesis of insulin in
pancreas and for development of cell
immunity.
O It promotes wound healing process.
O It also need for VIT.A metabolism by
promoting mobilization from liver.

126. O It is available from vegetable and animal
foods like meat, milk, fish, cheese, nuts,
whole wheat, etc.
O Zinc deficiency leads to growth failure,
delayed wound healing, liver diseases,
anorexia, alopecia and behavior changes.
O Balanced diet provides normal
requirement for the prevention of the
deficiency states.
O Growing children, antenatal and lactating
mother require more amount of zinc.

127. COPPER
O It is required for connective tissue
formation, iron metabolism, myelin
production, melanin synthesis, cell
respiration and energy utilization.
O Dietary sources of copper are sea food,
meats, legumes, nuts, milk, sugar, cereals
etc.

128. Copper Deficiency
O Deficiency of copper results in anemia,
neutropenia, hypopigmentation of hair and
skin, osteoporosis, fracture and defective
immune system.
O Genetic defects of copper metabolism
may give rise to Wilson’s diseseand
menkes kinky hair syndrome.
O Wilson’s disease may present as hepatic
dysfunction and neurological involvement.

129. O Hyporcupremia occurs in patients with
nephrosis.
O Hypercupremia may be found in
excessive intake of copper which may
results from eating food prepared in
copper made cooking vessels or may be
associate with acute/ chronic infections.