2. What iscalorie?
• CALORIE - is the amount of energy
needed to raise the temperature of one
gram of water by one degree Celsius
• CALORIE = is represented by
the letterC.
2
5. Obesity
5
Obesity is defined as an excess of adipose tissue that
imparts health risk.
Etiology
genetic predisposition
diets largely derived from carbohydrates and fats
than protein rich food.
hypothyroidism, cushings syndrome, insulinoma, and
hypothalamic disorders
6. Pathophysiology
6
Obesity is associated with increased
adipose stores in the subcutaneous
tissue, skeletal muscles, internal organs
such as the kidneys, heart, liver and fatty
liver is also more common in obese
individuals. There is increase in both
sizes number of adipocytes and there is
hypertrophy as well as hyperplasia.
11. Management ofobesity
11
Nutritional therapy
Behavior modification
Support groups
MEDICAL MANAGEMENT
Drug therapy
{appetite suppressing drugs}
Phentermine, diethylpropion etc.
SURGICAL MANAGEMENT
Vertical banded gastroplasty
Adjustable gastric banding
12. Starvation
12
Starvation is a state of overall deprivation of
nutrients.
Etiology
deliberate fasting
famine conditions in a country or community.
secondary under nutrition such as chronic
wasting diseases, cancersetc.
13. Signs andsymptoms
13
Dry and scaly skin
muscular weakness
Anemia
Increased susceptibility toinfections
Loss ofappetite
Wound healing may be delayed
Brittle nails
Loss ofhair
Depression
Decreased B P ,pulse, slight cyanosis.
15. Nursing management
15
Health promotion
Acute intervention
Health education
Try to maintain an optimal body weight
TYPES OF SPECIALISED NUTRITIONAL
THERAPY
Oral feeding
Tube feeding
nasogastric and nasointestinalfeeding
gastrostomy and jejenostomy
17. KWASHIORKOR
• Growth failure
• Wasting of all tissues
including musclesand
adipose tissue
• Edema present
• No hepaticenlargement
• Serum proteinslow
• Anemia present
• Monkey-like face,
protuberant abdomen,
thin limbs
Clinical features
Occurs in children
between 6 months3
years ofage
Growth failure
Wasting muscles but
preserved adipose tissue
Edema , localized or
generalized, present
Enlarged fattyliver
Serum proteins low
Anemia present
Alternate bands oflight
and dark hair
M A RASMUS
Clinical features
17
17
24. Pathophysiology marasmus
24
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
An 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
Loss of food intake through vomiting and diarrhea
Food allergy that is not managed appropriate
Emotional problems such as disturbed mother child
relations.
25. Nursing Management of
25
marasmus
Management consists of providing a
nutritional intake that is rich in the essential
nutrients to correct the dietaryinsufficiency
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, hyperalimentation is used.
Additional vitamins and minerals and blood
transfusion may be necessary.
26. 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 range, providing for
periods of rest and appropriate activity and
stimulation, recording intake and output, daily
weighing turning and preventing infection. The
nurse carefully observes affected infants for infection
of mouth, skin and respiratory and genitourinary
tracts. These infections are appropriately treated
when they occur. The infant is protected from other
patient and care givers who have infections because
infants who have marasmus may also have emotional
deprivation, their care is like that for those who have
failure to thrive.
26
27. Prevention of marasmus
27
The prevention of marasums consists of
Parent education
Prompt treatment congenital defects
Prevention of emotional disturbance
29. Pathophysiology
29
K washiorkor
While 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 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 albumin becomeslow.
33. 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 correct any
deficiencies.
33
34. The accompanying anemia can be corrected
by administering iron and folic acid. In spite of
this management the infant or child may
initially loss weight because of the loss of
edema fluid. However improvement can
gradually be seen. Infections or infestations are
treated appropriately. The long term
management consists of feeding the child a
diet with adequate calories, especially one
high in protein of good biologic quality.
34
35. Prevention
• Prevention consists of providing a diet containing
an adequate quality of protein of high biologic quality
for all infants and children. In those areas where
kwashiorkor is endemic parents should be taught the
nutritional needs ofall family members and adequate
amounts of food should be provided to fulfill these
needs.
35
36. Anorexia nervosa
• An eating disorder in which the person
experiences hunger but refuses to eat
because of a distorted body image, leading
toa self perception offatness.
• Anorexia nervosa is a condition of self-
generated weight loss usually seen in
adolescent girls and young women, but also
in middle-aged women or men
36
37. Etiology of eatingdisorders
• Although the cause of eating disorders is not
certain, several factors are likely to contribute to
development of the disorders. Socio cultural and
environmental factors including media and peer
influences, family factors including parental discord,
and biologic factors including genetics,
neurotransmitter regulation, and hormonal
functioning have been implicated. Negative affect,
low self- esteem, and dieting behavior commonly
predate the onset ofan eating disorder.
02/11/14 37NUTRITIONAL DISORDERS
37
38. Clinical manifestationsof
38
anorexia nervosa
Clients with anorexia nervosa are usually first
introduced to the health care system when the
disordered eating behavior results in obvious
weight loss. Clients may limit themselves to 200 to
500 kcal/day-only 60% to 70% of the amount
needed for ideal body weight. Physical
manifestations include dry skin, pallor,
bradycardia, hypotension, intolerance to cold,
constipation, and amenorrhea
39. Pathophysiology
• The pathophysiologic changes associated with anorexia
nervosa are similar to those seen in starvation. When caloric
intake is severely limited, the body adapts by using the
body's fatstores and sparing nitrogen stores. With
prolonged starvation, significant shifts in fluid and electrolyte
balance can occur and can be life-threatening.
•The hypothalamus responds to the lack of
nutrient intake with changes in pituitary
function, resulting in amenorrhea and
infertility. The extent of malnutrition will
determine the pathophysiologic changes
observed.
39
41. Bulimia nervosa
• An eating disorder characterized by
uncontrollable binge eating alternating with
vomiting ordieting.
• 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 toprevent weight gain. Ithas
been suggested thatbulimia nervosa is a form of
depressive illness.
41
42. Clinical manifestations of
42
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.
44. Nursing managementof
44
eating disorders
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 forrrefractory clients with extreme
malnutrition.
45. Management co n d … … …
45
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.
46. Management co n d … … …
46
Outcomes
The client will develop a more normal image of self, as
evidenced by statements concerning increased self-esteem by
the client's ability to overcome the eating disorder.
Interventions
Recognize that clients suffering from eating
disorders typically have low self-esteem. These clients
see the regulation of food and exercise of self-control
in eating patterns and amounts as ways to prove
themselves successful. It is important that the client's
significant others help the client find other areas of
self-regard. It is expected that the client will overcome
the eating disorder with consistent and continued
treatment and that weight will return to normal.
48. Vitamin A [retinol]
48
Physiologic functionsof 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 of
specialized epithelium
Maintenance of normal cartilaginous and bone
growth.
52. Pathological changes: - Consequent to vitamin A
deficiency following pathologic changes are seen.
Ocular lesions: - Lesions in the eyes are most
obvious. Night blindness is usually the first sign of
vitamin A deficiency. As a result of replacement
metaplasia of mucus secreting cells by squamous
cells, there is dry and scaly sclera conjunctiva
(xerophthalmia). The lacrimal duct also shows
hyperkeratosis corneal ulcer may occur. Bitot's
spots may appear which are focal triangular areas
of opacities due to accumulation of keratinized
epithelium.
52
53. contd
53
If these occur on cornea, they impede transmission
of light. Ultimately, infection, scarring and
opacities lead toblindness.
Cutaneous lesion:- The skin develops popular
lesions giving toad like appearance (xeroderma).
This is due to follicular hyper kurtosis and keratin
plugging in the sebaceous gland.
54. Sources
The major sources of retinol are liver, dairy
products, eggs and carotenes are found in varying
amounts in vegetables and fruits, especially in
most of the dark green leafy and bright orange
ones. Carotenes may also be present in the foods
listed above that naturally contain retinol.
Recommended intake
The 1980 RDA for Vitamin A is (5000 IU) for
men and (4000 IU) for woman.
54
55. Management
• Mild to moderate cases of deficiency can be treated by
daily oral dose of 10,000 IU of fat soluble vitamin A for
10 days. In severe cases larger dose (50,000 IU) is
recommended for one week. A single massive dose of
50,000 IU of vitamin A every six months is prophylactic
for children below six years ofage.
55
56. Vitamin D[Calciferol]
56
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.
58. Sources
Exposure to straight, fortified foods, fish lives oil
are good sources of vitamin D natural foods are
poor sources at vitamin D although small amounts
are present in egg yolk, liver, and fish such as
herring, sardines, tuna and salmon.
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.
58
60. Tetani
• This is characterized by low serum calcium
(less than 7.5 mg per 100ml) muscle
twitching, cramps, and convulsions. It results
frominsufficient absorption of calcium or
vitamin D, or from a disturbance of the
parathyroid gland.
60
61. Osteomalacia
• as adult rickets, occurs when there is lack
of vitamin D and calcium. Itmay also
occur when there is an interference with
fatabsorption and hence also vitamin D
absorption.
61
Osteomalacia frequently called
64. Rickets
64
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.
68. Management
In case of rickets recommended
dose of vit D is 10000 to50000units
per day
68
69. Rickets heals promptly with 4,0 00 I U of oral
vitamin D per day administered for
approximately one month.. The bone
abnormalities (visible by x ray) generally
disappear gradually over a period of 3-9
months. Parents are instructed to take their
infants outdoors for 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.
69
71. Vitamin E[Tocopherol]
71
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..
73. Source
The richest source of vitamin E are the
vegetable oils that are risk in poly unsaturated
wheat germ, nuts, whole grains, legumes and
certain vegetables.
Another sources
Soybean oil, sunflower oil, mayonnaise
walnut, lima beans, sweat potatoes, spinach, fish,
liver, shell fish,eggs.
73
74. Recommended intake
Although the 1980 RDA has been set at 10 mg
tocopherol for men and 8 mg for woman this
should be considered to be a recommendation for
people consuming customary American diets.
74
75. Vitamin E deficiency
75
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 dystrophy
76. Management of Vitamin E disorders
76
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 severalreports 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.
77. 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’snatural sources. Enough
of these vitamin is produced by
intestinal flora
77
79. 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. 79
80. 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.
80
81. 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.
81
82. 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.
82
85. sources
It is freely distributed in animal and vegetable
products such as liver, egg, yolk, pork, legumes,
yeast, pericarp and germ of cereals, autolysis yeast
(marmite), and milk. Polishing the rice considerably
destroys its thiamine content
85
86. Clinical Features
86
Thiamine deficiency leads to the disease, beriberi.
It occurs usually in infants (wet beriberi) though
older infants and children may also suffer from its
chronic form (dry beriberi).
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,
abdominaldistention, flatulence, constipation/ and
insomnia.
88. 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.
The breastfeeding mother should receive thiamine
therapy simultaneously.
Prognosis is excellent provided reasonable intake of
thiamine is ensured.
Prevention
Ensuring that at least 0.4 mg of thiamine is provided in
the daily diet (thrice the quantity in case of pregnant
8802/11a/14nd lactating NwUToRImTIOeNAnLD)ISpORrDeEvRSentsberiberi. 88
89. Riboflavin
• Riboflavin (vitamin B2),another water-soluble
vitamin, is a constituent offlavoprotein enzymes vitally
concernedwith 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).
89
91. Riboflavin deficiency
91
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.
92. Treatment/management
Therapy 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.
With this regimen, response is good. Complete
recovery occurs provided that adequate intake of
vitamin B2is ensured in the weeks and months ahead.
Prevention
In 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.
92
93. Nicotinic acid
93
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.
This 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.
95. Clinical Features
95
The disease caused by nicotinic acid deficiency is
called pellagra. It usually occurs in children of school-
going age.
The characteristic lesions are seen over the exposed
areas of the skin, such as limbs, neck, ("Casal
necklace") and cheeks. It is worth noting that the
lesions are symmetrical, of desquamating pigmentary
dermatitis type and are aggravated by sunlight.
There is a widespread gastrointestinal inflammation,
leading to red and sore tongue, dysphagia, nausea,
vomiting and diarrhea.
96. C linical Features
96
Just like diarrhea, dementia is encountered
much less childhood than in adults. Most
children with pellagra are, no doubt, quite
apathetic.
Anemia as also other signs of malnutrition are
usually present.
100. Treatment/management
100
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.
101. Pyridoxin
101
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 ammilk.
103. Clinical Features of deficiency ofpyridoxin
103
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.
106. Vitamin C[ascorbicacid]
• Ascorbic acid, which structurally resembles a
monosaccharide sugar, is known to play
important role in oxidation of tyrosine and
phenylalanine, in formation of hydroxyproline, in
preventing de 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.
106
108. sources
108
Fruits and vegetables are the only
significant sources of vitaminC.
Recommended intake
For adults 60 mg daily. This level of
intake is expected to maintain a body
pool of 1500mg ascorbic acid.
109. Scurvy occurs usually in infants between the age of6
months to2 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
109
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.
110. 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 isusual.
110
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.
112. Treatment/management
112
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.
113. Folic Acid
113
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.
115. DEFICIENCY SYMPTOMS:
115
A deficiency of Folic Acid may contribute to
anemia, depression and anxiety,, and birth defects
in pregnant women, sore tongue, andfatigue.
116. Vitamin B12:Vitamin B12 is a very large
molecule 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 system.
116
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.
118. 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.
118
119. Recommended dietary allowances
About 1 mg of vitaminB12 is required to replace
the daily obligatory losses.
Treatment/management
Vitamin B12 administered in doses 250-1000mg
intramuscularly.
119
120. TRACE ELEMENTS DEFICIENCIES
120
Several minerals in trace amounts are
essential for health since they form
components of enzymes and cofactors for
metabolic function besides calcium and
phosphorus required for vitamin D
manufacture, others include iron,
copper, iodine, zinc, selenium,
manganese nickel chromium,
molybdenum, fluorine
121. 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.
121
122. 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 ofzinc.
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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123. Iodide
A regular supply of iodide is needed for the
production of the thyroid hormones, thyroxine and
triidothyronine. Lack of iodine results in endemic
goiter
Sources
Iodized salt
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124. Copper
Copper participates in many metabolic reactions
that are necessary for normal development and
maintenance of the skeleton, red blood cell
production, normal skin and hair, and other
functions.
Sources
Oysters are recognized as the leading source
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125. Chromium
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.
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