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Nutrients:
The constituents of the food which are essential for
the body are called nutrients.

Nutritional Disorders
Types of nutrients:
Carbohydrates - Provide energy
Proteins - Help in growth
Fats - Provide energy
Vitamins - Help in physiological activities
Minerals - Act as regulators in physiological activities
Dr Perugu Shyam Water - Transports food, regulates body temperature
Assistant Professor

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• Common causes of undernutrition:

• An adequate diet should contain:
1- Energy in the form of carbohydrates , fats , proteins
2- Essential aminoacids and fatty acids to be used as building
blocks for synthesis of structural and functional proteins and
lipids.
3- Vitamins and minerals- as coenzymes or hormones in vital
metabolic pathways
1- Ignorance and poverty
2- Chronic alcoholism
3- Acute and chronic illnesses
4- Self- imposed dietary restriction
Other less common causes are malabsorption
syndromes, genetic diseases, specific drug
therapies and total parenteral nutrition .

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What is calorie?
Essential nutrients
• CALORIE - is the amount of energy  Proteins
needed to raise the temperature of one  Fats
gram of water by one degree Celsius
 Carbohydrates
 Vitamins
 Minerals
CALORIE = is represented by the  water
letter C.
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Main nutritional disorders Obesity

 Obesity  Obesity is defined as an excess of adipose tissue thatimparts
 Starvation health risk.

 Kwashiorkor
 Marasmus Etiology
 genetic predisposition
 Anorexia nervosa
 diets largely derived from carbohydrates and fatsthan protein
 Bulimia nervosa rich food.
 Vitamin deficiency  hypothyroidism, cushings syndrome, insulinoma, and
hypothalamic disorders
 Trac e element deficiency
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Pathophysiology
Metabolic changes
 H yper insulinaemia
Obesity is associated with increased adipose  N o n - Insulin dependant diabetes
stores in the subcutaneous tissue, skeletal muscles,  Hypertension
internal organs such as the kidneys, heart, liver and  Hyper lipoproteinaemia
fatty liver is also more common in obese individuals.
 Atherosclerosis
 Coronary artery disease
There is increase in both sizes number of
adipocytes and there is hypertrophy as well as  Cholelithiasis
hyperplasia.  Cancer
 Osteoarthritis

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Serious health hazards of obesity

Stroke
Coronary artery diseases
Hypertension
F a t t y liver
Diabetes
Atherosclerosis
Hyperlipidaemia
Osteoarthritis

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Management of obesity
Starvation
Nutritional therapy
Behavior modification  Starvation is a state of overall deprivation of
Support groups nutrients.

MEDICAL MANAGEMENT
Drug therapy {appetite suppressing drugs}
Etiology
Phentermine, diethylpropion etc. deliberate fasting
famine conditions in a country or community.
SURGICAL MANAGEMENT secondary under nutrition such as chronic
Vertical banded gastroplasty Adjustable wasting diseases, cancers etc.
gastric banding
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Starvation
Signs and symptoms
 D r y and scaly skin
 muscular weakness
 Anemia
 Increased susceptibility to infections
 L o s s of appetite
 W o u n d healing may be delayed
 Brittle nails
 L o s s of hair
 Depression
 Decreased B P,pulse, slight cyanosis.
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Nursing management
Protein deficiency malnutrition
Health promotion
Ac u t e intervention
Health education
 Kwashiorkor- Which is related to protein
T r y to maintain an optimal body weight
deficiency through calorie intake may be
sufficient.
TYPES OF SPECIALISED NUTRITIONAL
THERAPY
Oral feeding Tube
feeding  Marasmus- is starvation in infants occurring due
nasogastric and nasointestinal feeding to overall lack of calories.
gastrostomy and jejenostomy

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KWASHIORKOR
Clinical features
•  Gro wth failure
•  Wasting of all tissues
including muscles and
adipose tissue
•  E d e m a present
•  N o hepatic enlargement
•  S e r u m proteins low
•  Anemia present
•  Monkey-like face,
protuberant abdomen, thin
limbs
MARASMUS
 Clinical features
 Occurs in children
between 6 months 3
years of age
 G rowth failure
 Wasting muscles but
preserved adipose tissue
 E d e m a , localized or
generalized, present
 Enlarged fatty liver
 S e r u m proteins low
 Anemia present
 Alternate bands of lightand
dark hair

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Morphology
KWASHIORKOR MARASMUS
 Morphology  Morphology
 Enlarged fatty liver  N o fatty liver
 Atrophy of different  Atrophy of different
tissues and organs but tissues and organs
subcutaneous fat including
preserved subcutaneous fat

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Marasmus
Diagnostic Evaluation
Severe hypo chromic anemia is generally
diagnosed. The plasma proteins level is
usually lowered unless hemo concentration is
present.

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Pathophysiology marasmus Nursing Management of

When adequate calories are not ingested to fulfill the metabolic
needs of the body, reserve food elements such as protein and fat in
the tissues are used to sustain life.
This process may be caused by:
A n inadequate diet or faulty eating habits
Congenital anomalies that present the infant taking an
adequate diet
Disease condition that interfere with the assimilation of food
 Infections that produce anorexia and decrease the infants ability to
digest food
L o s s of food intake through vomiting and diarrhea
F o o d allergy that is not managed appropriate
Emotional problems such as disturbed mother child
relations.
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marasmus
Management consists of providing a nutritional intake
that is rich in the essential nutrients to correct the
dietary insufficiency and to promote normal growth and
development.
Parenteral fluid therapy may initially be necessary to
correct the electrolyte imbalance and dehydration and
to restore kidney if oral feedings are not tolerated,
hyper alimentation is used.
Additional vitamins and minerals and blood
transfusion may be necessary.
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In addition to assisting with administering parenteral fluids

and giving oral feedings, the nurse is also responsible for
maintaining the infant’s body temperature within a normal Prevention of marasmus
range, providing for periods of rest and appropriate activity
and stimulation, recording intake and output, daily weighing
turning and preventing infection. The prevention of marasums consists of

The nurse carefully observes affected infants for infection of

 Parent education
mouth, skin and respiratory and genitourinary tracts. These  Prompt treatment congenital defects
infections are appropriately treated when they occur. The
infant is protected from other patient and care givers who  Prevention of emotional disturbance
have infections because infants who have marasmus may
also have emotional deprivation, their care is like that for
those who have failure to thrive.

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Pathophysiology Kwashiorkor
Wh i l e growth is occurring, sufficient nitrogenous food
must be consumed to maintain a positive nitrogen balance.
When inadequate amounts of the essential aminoacids are
not provided, not absorbed or abnormally lost, protein
KWASHIORKOR under nutrition results.

The impaired absorption or loss of protein may occur in

infants and children who have chronic diarrhea, nephrosis,
hemorrhage, burns or infection. Nutritional edema, results
when the body, lacking sufficient intake or sustaining a
loss of high quality protein, burns its own tissues and
destroys the plasma protein so that the level of plasma
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kwashiorkor
PROTEIN CONTENT FOODS
Eggs
 C o w ’ s milk
 Cheese
 M e a t cooked
 F i s h cooked
 R i c e cooked
 S o y beans
 W h i t e potato
 w h e a t germ
Nuts

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Nursing Management
The management of infants and children who have
kwashiorkor includes replacement of the missing
nutrients and treatment for any acute problems such as
diarrhea, renal failure and shock.

The dietary intake of protein and calorie in

increased gradually, skin milk, synthetic amino acid
mixtures or case in hydrolysates may be given to
supplement the usual diet.

Vitamins and minerals, especially vitamin 4,

magnesium and potassium are added to the intake to
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T h e accompanying anemia can be corrected by

administering iron and folic acid. In spite of this
Prevention
management the infant or child may initially loss Prevention consists of providing a diet containing an
weight because of the loss of edema fluid. However adequate quality of protein of high biologic quality for all
infants and children. In those areas where kwashiorkor is
improvement can gradually be seen. Infections or
endemic parents should be taught the nutritional needs of
infestations are treated appropriately.
all family members and adequate amounts of food should
be provided to fulfill these needs.
The long term management consists of feeding the child
a diet with adequate calories, especially one high in
protein of good biologic quality.

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Anorexia nervosa Etiology of eating disorders

Although the cause of eating disorders is not certain, several
• A n eating disorder in which the person factors are likely to contribute to development of the disorders.
experiences hunger but refuses to eat because
Socio cultural and environmental factors including media and
of a distorted body image, leading to a self peer influences, family factors including parental discord, and
perception of fatness. biologic factors including genetics, neurotransmitter regulation,
and hormonal functioning have been implicated.

• Anorexia nervosa is a condition of self- Negative affect, low self- esteem, and dieting behavior
generated weight loss usually seen in commonly predate the onset of an eating disorder.
adolescent girls and young women, but also in
middle-aged women or men
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Clinical manifestations of Pathophysiology

anorexia nervosa
 The pathophysiologic changes associated with anorexia
• Clients with anorexia nervosa are usually first nervosa are similar to those seen in starvation. When caloric
introduced to the health care system when the disordered intake is severely limited, the body adapts by using the body's
eating behavior results in obvious weight loss. Clients may fat stores and sparing nitrogen stores. With prolonged
limit themselves to 200 to 500 kcal/day-only 60% to 70% starvation, significant shifts in fluid and electrolyte balance can
of the amount needed for ideal body weight. occur and can be life-threatening.

• Physical manifestations include dry skin, pallor, The hypothalamus responds to the lack of nutrient intake
bradycardia, hypotension, intolerance to cold, constipation, with changes in pituitary function, resulting in amenorrhea
and amenorrhea and infertility. The extent of malnutrition will determine the
pathophysiologic changes observed.

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Bulimia nervosa
 An eating disorder characterized by uncontrollable
binge eating alternating with vomiting or dieting.

Bulimia nervosa is a less serious and entirely

separate illness. Clients with bulimia nervosa tend to
maintain a relatively normal weight, but go through
periods of eating excessively (binging) and vomiting
(purging) gastric contents to prevent weight gain. It has
been suggested that bulimia nervosa is a form of
depressive illness.

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Clinical manifestations of bulimia nervosa

 Clinical manifestations of bulimia nervosa include episodes of

binge eating followed by self-induced vomiting. The eating and
vomiting episodes occur most often in the late afternoon and
evening and are done in secret. Some clients may abuse
laxatives and diuretics as well. Personality characteristics
typical of clients with bulimia are related to depression.

 Physical manifestations may not be as obvious, because the

client with bulimia may be of normal weight without any
depletion of fat stores. Less obvious clinical manifestations are
erosion of tooth enamel from frequent vomiting and esophageal
and throat irritation.

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Nursing management of eating disorders Management cond………

Outcomes:
 The client will be able to resume normal earning behaviors. In clients with severe
nutritional depletion, the client will be able to regain weight at a safe rare (1 to 2
pounds/week).
 Interventions: When caring for a client with anorexia nervosa, help the
client select foods from the Food Guide Pyramid for a nutritionally
balanced diet. The client is usually allowed to refuse a specific number of
foods (such as two or three) so that some sense of control is felt.
 Observe the client during mealtimes. Be supportive during mealtimes and,
if needed, stay with the client after he or she eats to prevent him or her
from purging. Education related to nutrition must include the client's
family, care-givers, or co-residents.
 An accurate calorie count and regular monitoring of weight are other
important interven-tions. Parenteral or enteral nutrition may be needed forr
refractory clients with extreme malnutrition.
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Outcomes
 The client will lose 1 to 2 pounds per week until
ideal body weight is achieved and maintain ideal body
weight thereafter
 Interventions
Teach the client how to use the Food Guide Pyramid
to select a healthy diet with portions of appropri-ate size.
Encourage the client to eat slowly and develop a regular
exercise pattern. Encourage the client to approach food,
eating, and self-image in a new way. Provide emotional
support and supervision for the client to overcome
stressful periods and break the binge-and-purge cycle.
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Management cond……… Vitamins

Outcomes
 F a t soluble vitamins
The client will develop a more normal image of self, as evidenced
by statements concerning increased self-esteem by the client's ability to a) vit A
overcome the eating disorder.
b) vit D
Interventions
Recognize that clients suffering from eating c) vit E
disorders typically have low self-esteem. These clients see the d) vit K
regulation of food and exercise of self-control in eating  water soluble vitamins
patterns and amounts as ways to prove themselves successful.
It is important that the client's significant others help the client a) vit C
find other areas of self-regard. It is expected that the client will b) vit B complex
overcome the eating disorder with consistent and continued
treatment and that weight will return to normal.

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Vitamin A [retinol]
Physiologic functions of retinol
Maintenance of normal vision in reduced light.
This involves synthesis of rhodopsin, a light sensitive pigment in
the rods and cones of retina, by oxidation of retinol. This pigment
then transforms the radiant energy in to nerve impulses.

Maintenance of structure and function specialized

epithelium

Maintenance of normal cartilaginous and bonegrowth.

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Deficiencies of vit A Bitot’s spot

 Nig ht blindness
 Ocular lesions
 Cutaneous lesions
 B i t o t spot
 Xerophthalmia

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 Pathological changes: - Consequent to vitamin A

deficiency following pathologic changes are seen.
contd
 Ocular lesions: - Lesions in the eyes are most  I f these occur on cornea, they impede transmission
obvious. Night blindness is usually the first sign of of light. Ultimately, infection, scarring and
vitamin A deficiency. As a result of replacement opacities lead to blindness.
metaplasia of mucus secreting cells by squamous
cells, there is dry and scaly sclera conjunctiva
 Cutaneous lesion:- The skin develops popular
(xerophthalmia). The lacrimal duct also shows
lesions giving toad like appearance (xeroderma).
hyperkeratosis corneal ulcer may occur. Bitot's
This is due to follicular hyper kurtosis and keratin
spots may appear which are focal triangular areas
plugging in the sebaceous gland.
of opacities due to accumulation of keratinized
epithelium.

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 Sources
The major sources of retinol are liver, dairy
Management
products, eggs and carotenes are found in varying
amounts in vegetables and fruits, especially in Mild to moderate cases of deficiency can be
most of the dark green leafy and bright orange treated by daily oral dose of 10,000 IU of fat
ones. Carotenes may also be present in the foods soluble vitamin A for 10 days. In severe cases
listed above that naturally contain retinol. larger dose (50,000 IU) is recommended for one
week. A single massive dose of 50,000 IU of
 Recommended intake vitamin A every six months is prophylactic for
children below six years of age.
The 1980 RDA for Vitamin A is (5000 IU) for
men and (4000 IU) for woman.

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Vitamin D[Calciferol]
 Functions
Vitamin D is of almost importance in the
regulation of calcium and phosphorous
metabolism in the body. It serves to maintain
proper blood levels of calcium and phosphorous
by promoting their intestinal absorption and by
mobilizing these minerals from the skeleton when
needed. Mineralization of the skeleton and teeth
requires an adequate supply of vitamin D.

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 Sources Vitamin D deficiencies

Exposure to straight, fortified foods, fish lives oil
are good sources of vitamin D natural foods are  Tetani
poor sources at vitamin D although small amounts
are present in egg yolk, liver, and fish such as  Rickets
herring, sardines, tuna and salmon.
Osteomalacia
 Recommended dietary allowances
Vitamin D is now considered more as a pro
hormone than a vitamin. Exposure to sunlight even
for 5 minutes per day. A specific recommendation
of a daily supplement of 400 IU is made.
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Tetani
• T h i s is characterized by low serum calcium
(less than 7.5 mg per 100ml) muscle twitching,
cramps, and convulsions. It results from
insufficient absorption of calcium or vitamin D,
or from a disturbance of the parathyroid gland.
Osteomalacia
 Osteomalacia frequently called
• as adult rickets, occurs when there is lack
of vitamin D and calcium. It may also occur
when there is an interference with fat
absorption and hence also vitamin D
absorption.

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Osteomalacia
Rickets
 Etiology
Poor exposure to sunlight may also be related
to the inactivity of the malnourished children.
Disturbed metabolism and poor synthesis of vit
D from the skin ,malabsorption state , diarrheal
diseases and excessive phylate with low
calcium and low phosphate content of the food
may well be some causes of rickets in
malnourished children.

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Rickets Rickets clinical features

H e a d - Increased size and delayed

closure of fontanels , craniotabes
 Teeth-delayed dentition
Thorax- rachitic rosary, pigeon chest
Spine-scoliosis , kyphosis
Limbs-widening of wrists, ankles andother
epiphysis, genu valgum

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Rickets heals promptly with 4,000 IU of oral vitamin D

per day administered for approximately one month.. The
bone abnormalities (visible by x ray) generally disappear
Management gradually over a period of 3-9 months.
 I n case of rickets recommended dose
Parents are instructed to take their infants outdoors for
of vit D is 10000 to 50000units per day approximately 20 minutes per day with their faces
exposed. Children should also be encouraged to play
outside.

Foods that are good sources of vitamin D include cod liver

oil, egg yolks, butter, and oily fish. Some foods, including
milk and breakfast cereals, are also fortified with synthetic
vitamin D.
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Vitamin E[Tocopherol]
 Functions
Vitamin E is needed for normal stability of red
blood cells. In animals it has been shown to be
essential for normal reproduction and for integrity
and muscle and for nerves.

There is no sound scientific basis for claims in

the lay literature that vitamin E promotes fertility
and sexual performance..

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 Source
The richest source of vitamin E are the
vegetable oils that are risk in poly unsaturated  Recommended intake
wheat germ, nuts, whole grains, legumes and
certain vegetables.
Although the 1980 RDA has been set at 10 mg
tocopherol for men and 8 mg for woman this
 Another sources
should be considered to be a recommendation
Soybean oil, sunflower oil, mayonnaise for people consuming customary American
walnut, lima beans, sweat potatoes, spinach, fish, diets.
liver, shell fish, eggs.

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 Vitamin E deficiency
 Vitamin E deficiency is extremely rare in
humans. It is limited to those individuals with
fat malabsorption, or patients on total
parenteral nutrition, or in formula fed
premature infants.
Changes occurring in severe deficiency
include, increased hemolysis of red blood
cells, creatinuria deposition of brandish
ceroid pigments in smooth muscles and , in
some cases, development of a form of
muscular dystrophyShyam perugu
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Vitamin K
Vitamin K is concerned with
synthesis of coagulation factors
2,7,9,and 10 in the liver. Green leafy
vegetables, soybeans and fish are
it’s natural sources. Enough of these
vitamin is produced by intestinal
flora
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 Management of Vitamin E disorders
 Vitamin E has been used in daily doses of 400 to
800 mg for the treatment of diverse conditions such as
habitual abortion, sterility muscular dystrophy
diabetes ischemic heart disease, skin disorders and
anemia in infants. Benefit has been reported in some of
these cases but none has been established in clinical
trails.
 Administration of 3 to 4 g of tocopherol daily over long
periods has not produced any toxic effects in human
beings. However several reports of adverse effects
such as elevation of serum lipids, impaired blood
coagulation and reduction of serum thyroid hormones
suggest that indiscriminate ingestion of excessive
amounts over long periods should be avoided.
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 Function
Vitamin K is essential for the hepatic synthesis of
prothrombin and certain others factors involved in
blood clotting. For this reason it is sometimes called the
antihemorrhagic it also appears to have a role in some
metabolism.
 Sources
Green leafy vegetables, cauliflower, broccoli and
liver all the richest dietary sources of vitamin K. However,
bacterial synthesis of vitamin K in the gut accounts for a
large proportion of a persons daily supply initially a new
born infant has a sterile gastro intestinal tract and thus
cannot synthesize significant amounts of vitamin K for a
few days since milk is low in vitamin K the vitamin is
routinely administered to new borne.
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 Malabsorption syndrome:- Patients suffering
from malabsorption of fat develops vitamin K
deficiency e.g. coelic disease, sprue, pancreatic
disease, hyper motility of bowel etc.
 Diffuse liver disease:- Patients with diffuse liver
disease (e.g. cirrhosis, omyloidosis of liver
hepatocellular carcinoma, hepatoblastoma) have
hypoprothrombinaemia due to impaired synthesis
of prothrombin administration of vitamin K to such
patients is of no avail since liver, where
prothrombin synthesis utilizing vitamin K takes
place, is diseased.
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DEFICIENCY DISORDERS
 Hemorrhagic disease of new born:- The new
born infants are deficient in vitamin K because of
minimal stores of vitamin K of birth, lack of
established intestinal flora for endogenous
synthesis and limited dietary intake since breast
milk is a poor source of vitamin K.
 Biliary obstruction:- Bile is prevented from
entering the bowel due to biliary obstruction so
that this fat soluble vitamin cannot be absorbed.
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 Deficiency of vitamin K
Deficiency of vitamin K causes defective blood
coagulation
 Recommended dietary allowances
Because of variation is the intestinal synthesis of
vitamin K no special recommendation for
allowance has been made. The food and nutrition
board has established 1-2mg of vitamin K per kg
body weight to be safe and adequate intake.
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Thiamine

 Thiamine (vitamin B1), a water-soluble vitamin,

is an essential coenzyme for metabolism of
carbohydrates

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Clinical Features
sources
 Thiamine deficiency leads to the disease, beriberi.
 It is freely distributed in animal and vegetable It occurs usually in infants (wet beriberi) though
products such as liver, egg, yolk, pork, legumes, older infants and children may also suffer from its
yeast, pericarp and germ of cereals, autolysis chronic form (dry beriberi).
yeast (marmite), and milk. Polishing the rice
considerably destroys its thiamine content
The earliest symptoms, occurring in early
infancy (especially if the mother is providing
thiamine-deficient breast milk), include
restlessness, bouts of excessive crying (as if the
infant is having an abdominal colic), vomiting,
abdominal distention, flatulence, constipation/ and
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insomnia.
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Treatment/management
 As soon as the diagnosis is convincingly made,

The child must receive 10 mg of thiamine intravenously. In the

subsequent three days, he should be given 10 mg of the vitamin
intramuscularly twice daily. Over the next six weeks, 10 mg daily
should be administered orally.
• T h e breastfeeding mother should receive thiaminetherapy simultaneously.
• Prognosis is excellent provided reasonable intake ofthiamine is ensured.
• Prevention
• Ensuring that at least 0.4 mg of thiamine is provided inthe daily diet (thrice the
quantity in case of pregnant and lactating women) prevents beri beri.

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Riboflavin

 Riboflavin (vitamin B2), another water-soluble

vitamin, is a constituent of flavoprotein enzymes
vitally concerned with the intermediary
metabolism of carbohydrates.

 It is found in both animal and vegetable foods

such as liver, fish, egg, kidney, meat, beans,
yeast, green leafy vege- tables, cereals,
legumes, groundnut and milk (5 times more in
cow milk than in human milk).
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Riboflavin deficiency Treatment/management

 Clinical Features
Manifestations include angular stomatitis,
cheilosis (fissuring of lips), nasolabial
seborrhea and, occasionally magenta
(purplish-red, smooth) tongue. There may
occur corneal injection (vascularization) at the
limbus, leading; to excessive lacrimation,
photophobia, eye pain and later interstitial
keratitis.
Th erap y consists in administering riboflavin, 3 to 10 mg orally or 2 mg
intramuscularly daily for a few days. This / should be followed by 10 mg
orally daily for about three weeks.
W i t h this regimen, response is good. Complete recovery occurs
provided that adequate intake of vitamin B2 is ensured in the weeks and
months ahead.
Prevention
I n order to prevent riboflavin deficiency, it should be ensured that the
daily diet provides at least 0.6 mg riboflavin per 1,000 kcal. It is advisable
to administer supplements of riboflavin (the whole B-complex may . be
still better) to the infants and children belonging to vulnerable categories.

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Nicotinic acid
 Nicotinic acid (niacin) is also involved in the
carbohydrate metabolism and plays vital role
in the functioning of the skin, gastrointestinal
tract, central nervous system and hemopoietic
system.
 T h i s vitamin may be obtained either from the
natural food sources or from the tryptophan
endogenously. The natural food sources
include milk, liver, pork, cheese, yeast,
cereals, etc.
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Clinical Features
 T h e disease caused by nicotinic acid deficiency is Clinical Features
called pellagra. It usually occurs in children of school-
going age.
 J u s t like diarrhea, dementia is encountered
 T h e characteristic lesions are seen over the exposed
areas of the skin, such as limbs, neck, ("Casal much less childhood than in adults. Most
necklace") and cheeks. It is worth noting that the children with pellagra are, no doubt, quite
lesions are symmetrical, of desquamating pigmentary apathetic.
dermatitis type and are aggravated by sunlight.  Anemia as also other signs of malnutrition are
 T h e r e is a widespread gastrointestinal inflammation,
usually present.
leading to red and sore tongue, dysphagia, nausea,
vomiting and diarrhea.

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Pellagra Treatment/management
 Nicotinamide, 50 to 300 mg daily in
divided doses orally, given for two
weeks followed by adequate supply of B-
complex vitamins in diet brings about
complete recovery.
 Prevention
 The disease may be prevented by
providing a balanced diet containing 5 to
10 mg daily supply of nicotinamide.
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Pyridoxin
 Pyridoxine (vitamin B6) plays a vital role in the
metabolism of proteins and fatty acids. It is
claimed to have a role in blood formation, in
proper functioning of the nervous system and in
conversion of tryptophan into nicotinic acid.

 Its natural sources include liver, egg yolk,

meat, wheat] germ, soybeans, yeast, peas, pulses
and cereals. It ii found in only small quantity in
most vegetables am milk.

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Clinical Features of deficiency of pyridoxin Growth retardation

The manifestations include convulsions and microcytic, hypo
chromic anemia refractory to iron therapy. Growth retardation
and gastrointestinal symptoms like diarrhea may occur.
Seborrheic dermatitis around nose and eyes, and sensory
neuropathy occur only uncommonly in children.
Cheilosis and glossitis are infrequent in childhood.

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Vitamin C[ascorbic acid]

Treatment/management • Ascorbic acid, which structurally resembles a

monosaccharide sugar, is known to play important role
 Administration of 5 mg of pyridoxine in oxidation of tyrosine and phenylalanine, in
intramuscularly followed by 0.5 mg daily orally for formation of hydroxyproline, in preventing de
two weeks causes complete recovery. polymerization of collagen and in hemopoiesis.

Deficiency of vitamin C, though quite common in its

subclinical form, has virtually disappeared in its overt
form from the affluent countries. But, its frank cases still
continue to be seen from time to time in some parts of the
developing regions.
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sources
Fruits and vegetables are the onlysignificant sources of
vitamin C.

Recommended intake

For adults 60 mg daily. This level of intake is expected

to maintain a body pool of 1500mg ascorbic acid.

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Scu rvy occurs usually in infants between the age of 6
months to 2 years. No age is a bar, however.
• Infantile scurvy is characterized by gross irritability,
excessive crying and tenderness to touch, more so in the lower
limbs. The infant adopts the so-called "frog- position”. The
posture of the lower limbs gives an impression as though these
are paralyzed
The palpable sub periosteal hemorrhage into the lower third
of the femur may contribute to pain, thus preventing
movements of the leg further and strengthening the
impression that the limb may be paralyzed.
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Scurvy :
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 Hemorrhages may occur into the skin and mucous
membranes. Hemorrhages into the gums may
result in spongy, swollen, bluish purple gums,
especially about the erupted teeth. Hemorrhages
in the internal organs may cause hematuria,
melena, proptosis and subdural swellings. Mild to
moderate anemia is usual.
Scorbutic rosarymay result from posterior
displacement of the sternum. Unlike rachitic
rosary, it is tender,-sharp and angular and has a
"step-shaped" configuration the sternum, being
depressed.
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Treatment/management:
It consists in giving a dose of 500 mg of vitamin C
followed by a daily dose of 100 to 300 mg for
several weeks. Oral administration is good
enough.
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Folica c i d :
functions
Folic Acid is needed for energy production,
protein metabolism, the formation of red blood
cells and it is vital for normal growth and
development

 Sources
Found in beans, beef, bran, barley, brown rice,
cheese, chicken, dates, green leafy vegetables,
lamb, lentils, liver, milk, oranges, organ meats (like
liver), split peas, pork, root vegetables (like carrots),
salmon, tuna, whole grains, whole wheat and yeast.
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Vitamin B12:Vitamin B12 is a very largemolecule

 DEFICIENCY SYMPTOMS: and requires a special mechanism of absorption. Vitamin
B12 functions in all the cells but especially those of the
gastrointestinal tract and bone marrow and the nervous
A deficiency of Folic Acid may contribute to system.
anemia, depression and anxiety,, and birth defects
in pregnant women, sore tongue, and fatigue.
Sources : Found in beef, blue cheese, cheese, clams,
crab, fish, eggs, herring, kidney, liver, mackerel, milk
and milk products, pork, seafood and tofu. It is not
found in vegetables - only in animal sources.

BODY PARTS AFFECTED:

liver, nerves, red blood cells, gastrointestinal tract.
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DEFICIENCY SYMPTOMS:

Appetite loss, diminished reflex responses, fatigue,

irritability, memory impairment, mental depression and
confusion, nervousness, pernicious anemia, unpleasant
body odor, walking and speaking difficulties, weakness in
arms and legs.

A deficiency can cause problems with digestion,

absorption of food, metabolism of carbohydrates and fats,
nerves, fertility, growth and development. There can also
be hallucinations, memory loss, eye disorders, and anemia.

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 Recommended dietary allowances  T R ACE ELEMENTS DEFICIENCIES

About 1 mg of vitaminB12 is required to replace
the daily obligatory losses. Several minerals in trace amounts are essential
for health since they form components of enzymes
Treatment/management and cofactors for metabolic function besides calcium
Vitamin B12 administered in doses 250-1000mg and phosphorus required for vitamin D manufacture,
intramuscularly. others include iron, copper, iodine, zinc, selenium,
manganese nickel chromium, molybdenum, fluorine

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Iron
Iron is best known for being an active part of hemoglobin in
red blood cells but it is also a constituent of the muscle
protein myoglobin and of a variety of protein that speed up
chemical reactions within the body.
Sources
Rating foods as sources of iron requires consideration of the
bioavailability of the iron they contain in general flesh foods are
the best sources because they contain heam iron. Some plant
foods appear to be much better source of iron than they actually
are.
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Zinc
Recognition of the importance of zinc as a nutrient is
steadily increasing. growth ,sexual development, wound
healing , ability to fight infections sense of taste, night
vision, healthy epithelial tissue, and other vital functions
depend upon an adequate supply of zinc.
Sources
 Flesh foods are the most reliable sources of zinc because
they contain reasonably high amount of zinc. Red meats
especially beef are higher in zinc. among plant foods sun
flower seeds are good sources of zinc. Whole grains
,legumes and vegetables are richer in zinc.
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 Iodide
Copper
 A regular supply of iodide is needed for the
Copper participates in many metabolic reactions
production of the thyroid hormones, thyroxine and that are necessary for normal development and
triidothyronine. Lack of iodine results in endemic maintenance of the skeleton, red blood cell
goiter production, normal skin and hair, and other
functions.
 Sources
 Iodized salt Sources
Oysters are recognized as the leading source

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Deficiency disorders of trace elements

 Chromium Iron: - Microcytic ,hypochronic anemia

 Chromium is essential for normal utilization of
glucose. Chromium is active in the body only in
the form of a complex molecule called glucose
tolerance actor. Meat, cheese, and whole grains
are also reported to be good sources.
Copper:- Muscle weakness, neurologic defect
Iodine:- Goiter and hyperthyroidism
Zinc: - Growth retardation, infertility
Selenium:- Myopathy, cardiomyopathy

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Goiter Growth retardation

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