8. Malnutrition
By the side of the weak….that’s where
we are…
Humble servants of the sick…that’s who
we are…
To be a vessel for the almighty’s
mercy…that’s what we hope…
& beyond the most
unachievable….that’s our destiny
………….
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8
9. Malnutrition
• There were 925 million undernourished
people in the world in 2010.
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9
10. Malnutrition
• This means an 80 million increase than
1990.
• Ironically, the world produces enough
food to feed double the actual
population (12 billion).
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11. Malnutrition is implicated in more than
half of all child deaths worldwide, a
proportion unmatched by any
infectious disease since the Black
Death.
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12. Malnutrition
• One in twelve people worldwide is
malnourished, including 160 million
children under the age of 5.
• About 183 million children weigh less
than they should for their age.
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14. Undernourished people in the world (millions)
Year
1990
1995
2005
2008
843
788
848
923
Undernourished in developing
world(%)
Year
1970 1980 1990 2005 2007
37
28
20
16
17
16. • The Indian subcontinent has nearly
half the world's hungry
people, contributing with 5.6 million
child deaths every year, more than
half the world's total.
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16
17. • Africa and the rest of Asia together have
approximately 40%.
• The remaining hungry people are found in
Latin America and other parts of the world.
19. The situation in Sudan
• More than 90% of the population suffer
from poverty and food insecurity.
• More than 35% of the population are
malnourished .
• Sudan has got one of the highest under 5
mortality (108/1000 life births) .
• Only 7.3% of the national income is spent
on health.
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19
20. Prevalence of child (%) malnutrition
timeline
Year 199 199 199 199 200 200 200 200
3
5
7
9
0
2
32. 38. 36. 38. 35. 34
8
8
5
4
5
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6
33. 31.
8
7
next
20
23. Babies born weighing less than 5 pounds, 8
ounces (2,500 grams) are considered low
birthweight.
increased risk for serious health problems
as newborns, lasting disabilities and even
death.
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23 23
24. Why are babies born with low birth weight?
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24 24
26. Risk
factors are at increased risk for
delivering prematurely:
Had a premature baby in a previous pregnancy.
Are pregnant with twins, triplets or more .
Have certain abnormalities of the uterus or cervix.
Birth defects.
Chronic health problems in the mother.
Smoking.
Alcohol and illicit drugs.
Infections in the mother.
Infections in the fetus.
Placental problems.
Inadequate maternal weight gain.
Socioeconomic factors.
26
27. What
can a woman do to reduce her risk
of having a low-birthweight baby?
See her health care provider for a
preconception checkup.
Work with her health care provider to
control chronic health conditions
Take a multivitamin containing 400
micrograms of folic acid daily
Stop smoking
Get early and regular prenatal care.
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27
28. How
is fetal growth restriction treated?
About 10 percent of fetuses are growthrestricted. A health care provider may
suspect fetal growth restriction if the
mother’s uterus is not growing at a normal
rate. This can be confirmed with a series of
ultrasounds that monitor how quickly the
fetus is growing. In some cases, fetal
growth can be improved by treating any
condition in the mother (such as high blood
pressure) that may be a contributing factor.
.
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28
28
29.
The provider closely monitors the wellbeing of a growth-restricted fetus using
ultrasound and fetal heart rate
monitoring. If these tests show that the
baby is having problems, the baby may
need to be delivered early
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29
29
30. What
medical problems are
common in low-birth weight
babies?
Low-birth weight babies are more likely than babies of
normal weight to have health problems during the
newborn period. Many of these babies require
specialized care in a newborn intensive care unit
(NICU). Serious medical problems are most common
in babies born at very low birth weight:
•
Respiratory distress syndrome
(RDS):This breathing problem is common in
babies born before the 34th week of pregnancy.
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30
30
31. •
Bleeding in the brain (called intraventricular
hemorrhage or IVH): Bleeding in the brain occurs in
some very low-birth weight premature babies, usually
in the first three days of life.
•
Patent ductus arteriosus (PDA): PDA is a
heart problem that is common in premature babies.
Before birth, a large artery called the ductus arteriosus
lets the blood bypass the baby’s nonfunctioning lungs.
The ductus normally closes after birth so that blood
can travel to the lungs and pick up oxygen. When the
ductus does not close properly, it can lead to heart
failure.
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31
32. •
Necrotizing enterocolitis (NEC):
This potentially dangerous intestinal
problem usually develops two to three
weeks after birth. It can lead to feeding
difficulties, abdominal swelling and
other complications. Babies with NEC
are treated with antibiotics and fed
intravenously (through a vein) while
the
intestine
heals.
In
some
cases, surgery is necessary to remove
damaged sections of intestine.
•
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32
32
33. •
Retinopathy of prematurity
(ROP):
ROP is an abnormal growth of blood
vessels in the eye that can lead to vision
loss. It occurs mainly in babies born
before 32 weeks of pregnancy. Most
cases heal themselves with little or no
vision loss. In severe cases, the
ophthalmologist (eye doctor) may treat
the abnormal vessels with a laser or with
cryotherapy (freezing) to preserve vision.
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33
33
35. Can
medical problems in premature, lowbirth weight newborns be prevented?
•
When a provider suspects that a woman
may deliver before 34 weeks of
pregnancy, he may suggest treating the
mother with a medicine called
corticosteroids. Corticosteroids speed
maturation of the fetal lungs and
significantly reduce the risk of
RDS, IVH, NEC and infant death. These
drugs are given by injection (a shot) and are
most effective when administered at least 24
hours before delivery.
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35
35
36.
Treatment with tocolytic drugs to delay
labor can give corticosteroids time to
work. The provider also can arrange for
delivery in a hospital with a NICU that can
give specialized care to a premature, lowbirth weight infant.
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36
36
37. Does
low birthweight contribute to adult
health problems?
Some studies suggest that individuals who
were born with low birthweight may be at
increased risk for certain chronic conditions in
adulthood. These conditions include high blood
pressure, type 2 (adult-onset) diabetes and
heart disease. When these conditions occur
together, they are called metabolic syndrome.
--One study found that men who weighed less
than 6 1/2 pounds at birth were 10 times more
likely to have metabolic syndrome than the men
who weighed more than 9 1/2 pounds at birth).
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37
37
38. It
is not yet known how low birth weight
contributes to these adult conditions.
However, it is possible that growth
restriction before birth may cause lasting
changes in certain insulin-sensitive organs
like the liver, skeletal muscles and
pancreas. Before birth, these changes
may help the malnourished fetus use all
available nutrients. However, after birth
these changes may contribute to health
problems.
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38
38
43. KWASHIORKOR
•It was identified in 1930 in Ghana,
• It is an acute form of childhood PEM, it
usually affect children age 1-4 years but can
also affect the younger children and adults.
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43
45. • the word kwash literally means the one
who is physically displaced (it is a
reference to the fact that kwash
develop commonly in children who
have just weaned off of breast milk.
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45
47. Causes:
•
•
•
Inadequate food intake both in quantity
and quality (food gap): its caused by
insufficient protein in diet.
Infections as: malaria, diarrhea, measles
and TB.
Some conditions that interfere with protein
absorption as cystic fibrosis.
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47
48. • Low level of nutritional education.
• Other contributories factors including:
• poor environmental condition
• bad food habits
• large family size
• poor maternal health.
* ….. So kwash is an outcome of several
factors……
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48
49. Symptoms and sign:
– Edema
– muscle wasting
– failure to gain weight and grow
(failure to thrive)
– fatigability and irritability
– skin pigmintary changes and
dermatitis
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49
54. the possible complications
–Frequent and recurrent infections due
to defected immune system.
–physical and mental disability
–anemia
–fatty liver
–poor wound healing
–in severe cases it may lead to shock
and trauma
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54
55. diagnosis:
• Diagnosis of kwash is mainly clinically (
i.e.: achieved through physical
examination)
• Laboratory findings:
• low total plasma proteins.
• reduced serum albumin .
• reduced K level if diarrhea developed.
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55
56. Management:
• The general treatment involves 2 phases:
• Treatment should be started as early as
possible to prevent occurrence of
complications.
– Stabilization phase: supportive management
includes treatment of acute medical conditions by
giving IV fluids and also treatment of infections
with antibiotics.
– Rehabilitation phase: its mainly by getting more
calories of protein and improvement of nutrition
in general.
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56
57. prevention and control
• The preventive measures are:
• health promotion
• specific protection: mainly regarding
the child (the child diet should contain
enough protein calories and it should
be balanced)
• immunization is mandatory
• early diagnosis and treatment:
surveillance
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61. MARASMUS
• Marasmus is a form of severe protien energy
malnutrition (PEM
• Typically, marasmic child is of low weight,severely
wasted muscles( skin on bones) and developmental
disability and stunting , due to deficiency of nearly all
nutrients, especially protein and carbohydrates
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61
62. EPIDEMIOLOGY:
Marasmus is one of leading causes of child morbidity
and mortality in developing countries, and
Approximately 9% of sub-Saharan African children
suffer from moderate to acute malnutrition.
• Incidence increases prior to st year and Case fatality
is
of all childhood deaths from malnutrition, of
which two thirds will be attributable to low
birthweight, and one third directly to malnutrition
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62
64. A study by American Society for Clinical Nutrition
in relation to Who-2004
• Of 28753 children between the ages of 6 months and
6 years were examined for manutrition every 6
months for 18 months, Two hundred thirty-two
children died during this18 months of follow-up .
• Low weight-for-height was associated with an
increased risk of mortality. Even children with better
scores were 50% more likely to die in the following 6
months.
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64
65. • Among breast-fed children, the relative
mortality associated for (weight-for-height)
was 7.3, and among not breast-fed children, it
was 26.0 . This study targeted the most
affected areas which were in Darfur-Sudan.
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65
66. Another study by American medical association
Darfur-2004
• The resulted Crude mortality rates, expressed as
deaths per 10 000, were 3.2 in Kass, 2.0 in Kalma,
and 2.3 in Muhajiria. Under 5-year mortality rates
were 5.9, 3.5, and 3.5 respectively. During the period
of displacement covered by survey Acute
malnutrition was common, affecting 14.1% of the
target population, violence was reported to be
responsible for 72% of deaths mainly in children and
young men.
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66
67. Signs and symptoms
– extensive tissue and muscle wasting
– dry skin, and loss of adipose tissue as well as skin folds
hanging over the thigh and buttocks
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67
68. Types of Marasmus
• Nutritional marasmus due to
–
–
–
–
–
Failure of breast feeding
Inadequate amount of milk formula
Starvation
Feeding difficulties (mentally retarded
Prematurity
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68
69. • Secondary Marasmus due to
–
–
–
–
–
–
Chronic infection
Chronic diarrhea and/or vomiting
Malabsorption syndrome
Metabolic disorder
Endocrine disease
Psychological disturbance of Mother affects
child health
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69
70. Investigation
• Biochemical findings
-Normal plasma protein, unless end stages
-Blood urea is low
-Blood glucose level is low
-Serum enzyme and minerals are usually within normal
range unless complicated
-Iron deficiency anemia is common
-In severe long standing cases, urine may contain
excess creatinine and ketone bodies
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70
73. Control & Prevention of PEM
1. Encourage breast feeding to last as long as
possible (at least in the 1st year).
2. Diets Education of mothers and focus on
animal proteins, milk, eggs, meat, fish .Or
vegetable proteins, Cereal, beans etc.
3. Family planning allow adequate spacing of
child birth.
4. Immunization avoiding communicable
diseases and infections.
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73
74. 5. Sanitation and fly control.
6. Getting rid of taboos and faulty traditions.
7. Last but not the least is regular check-up &
centiles.
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74
75. Marasmic kwashiorkor
– marasmic kwashiorkor is considered as
an intermediate form between
marasmus and kwash
– Its main manifestations are
• growth failure
• edema
• loss of subcutaneous fat
• marked wasting of muscles
• psychic changed
• dermatosis
• hair changes
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82. What is Obesity ?
Obesity is the heavy accumulation of fat
in the body to such a degree that it
rapidly increases the risk of diseases
that can damage health and knock years
off your life..
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82
82
83. How to know that you are obese?
There are many test and exams can be done to
see if you're obese or not. For examples:
1.Body mass index (BMI)
Is used to assess your weight relative to your
height. It is defined as
weight in kilograms divided by height in meters
squared (kg/m2)
W does B I t el l you?
hat
M
Healthy
Overweight
Obese
Morbidly
:18.5-24.9
:25.0-29.9
:30 or greater
: 40 or greater
83
84. 2. Waist circumference
central obesity (male-type or apple-type obesity) has
a much stronger correlation, particularly with
cardiovascular disease, than the BMI alone.
The absolute waist circumference
Men :> 102 cm in
Women :> 88 cm in women.
Other tests are:-
*Weight-to-height tables
*Body fat percentage
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84
84
87. Causes of obesity:
A. Genetic factors
B. life style
A. Genetic factors:*some people stay thin and some become obese.
Research shows that obesity tends to run in families
If one of your parents is obese, you are 3 times as likely to be
obese as someone with parents of healthy.
Genes cause :
• Some genes control appetite, making us less able to sense
when we are full.
• Some genes may make us more responsive to the taste, smell
or sight of food.
• Some genes may make us less likely to engage in physical
activity
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87
87
88.
B. life style
1.Physical inactivity:
is a major element in the development of obesity in
Sedentary westernized societies
2. Dietary intake:
high-fat foods or sweetened drinks.
3. Ethnicity:
increased risk of obesity in Native Americans and Hispanic
Americans compared with white Americans, although these
differences may be largely related to differences in
socioeconomic status.
4. Underlying medical disorders :
Secondary obesity may occur with medical
conditions, including:
* Hypothyroidism
* hypercortisolism
* growth hormone deficiency
* hypothalamic damage.
88
89. 5. Prescription drugs:
Some drugs may contribute to obesity. These include
1. glucocorticoids
2. antipsychotic drugs (eg. risperidone)
3. antiepileptic medications.
6.Emotions: Some people overeat because of
depression, hopelessness, anger, boredom, and many other
reasons that have nothing to do with hunger.
7.Sex: Men have more muscle than women, on average.
Because muscle burns more calories than other types of
tissue, men use more calories than women.
8.Age: People tend to lose muscle and gain fat as they age. Their
metabolism also slows somewhat. Both of these lower their
calorie requirements.
89
90. 9.Pregnancy: Women tend to weigh an average of 4-6
pounds more after a pregnancy than they did before the
pregnancy. This can compound with each pregnancy. This
weight gain may contribute to obesity in women.
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90
90
94. Heart Disease and Stroke
Overweight people are more likely to have
1.high blood pressure
2. stroke
3. Very high blood levels of cholesterol and triglycerides (blood
fats)
4.angina
5.sudden death from heart disease or stroke without any signs or
symptoms.
The good news is that losing a small amount of weight can reduce
your chances of developing heart disease or a stroke.
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94
96. Cancer
Several types of cancer are associated with obesity.
In women, these include cancer of the
uterus, gallbladder, cervix, ovary, breast, and colon
Overweight men are at greater risk of developing cancer
of the colon, rectum, and prostate.
Sleep Apnea
The apnea can cause a person to stop breathing for
short periods during sleep and to snore heavily. The
risk for sleep apnea increases with higher body
weights. Yet again, weight loss ultimately reverses
this risk.
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96
96
97. Osteoarthritis
Osteoarthritis is a common joint disorder that most often affects
the joints in your knees, hips, and lower back.
Gout
Gout is a joint disease caused by high levels of uric acid in the
blood. Uric acid sometimes forms into solid stone or crystal
masses that become deposited in the joints.
Gallbladder Disease
Gallbladder disease and gallstones are more common if you
are overweight , it may cause a consequence of changes in fat
and cholesterol handling by the body leading to
supersaturation of bile.
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97
98.
Prevention and control of Obesity:-
Most probably Is by health education.
• 1.Stay active.
• 2.Eat healthy.
• 3.Watch your weight.
4.stay out of junk food.
• 5.Only eat when you are hungry.
6.Never go all day without eating.
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98
99. Treatment of obesity
The main treatment for obesity is to reduce body fat by eating
fewer calories and exercise more.
Much more difficult than reducing body fat is keeping it off. 8095% of those who lose 10% or more of their body mass by
dieting regain all that weight back within 2-5years. The body
has systems that maintain its homeostasis at certain set
points, including body weight.
Exercise
exercise combined with diet resulted in a greater weight
reduction than diet alone".
Dieting
In general, dieting means eating less. Various dietary
approaches have been proposed"
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99
100. Drugs
Most available weight-loss medications are "appetitesuppressant" medications. Appetite-suppressant medications
promote weight loss by decreasing appetite or increasing the
feeling of being full.
· In patients with BMI > 40: referral for bariatric surgery may
be indicated. The patient needs to be aware of the potential
complications.
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100
100
102.
Bariatric surgery :bariatric surgery (or "weight loss surgery") is the use of surgical
interventions in the treatment of obesity.
it is regarded as a last resort when dietary modification and
pharmacological treatment have proven to be unsuccessful.
Weight loss surgery relies on various principles; the most
common approaches are reducing the volume of the
stomach, producing an earlier sense of satiation
while others also reduce the length of bowel that food will be
in contact with, directly reducing absorption (gastric bypass
surgery)..
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102
102
108. INTRODUCTION OF
VITAMINS
Vitamins are a class of organic compounds
categorized as essential micro nutrient.They are
required by the body in very small amounts.
Vit are divided in two groups :
Fat soluble(A-D-E-K)
Water soluble vit B+C
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108
109. HISTORY OF VITAMIN
(A)DEFICENCY
Vit (A)deficiency is a world wide Health
Problem following PEM.
Recently, data have indicated the interrelation
between vit A deficiency and child hood RTI
, diarrhea and measles .
Medical articles and reports from Sudanese
Ministry of Health were reviewed covering 4
deacades retrospectively to assess the extent of
vit A deficiency.
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109
110.
There is evidence that vit A deficiency is a
Public Health Problem in Eastern Sudan and
among communities living around Khartoum
from Western and South Sudan .
In study conducted in gezira state, involving
1265 people over 3 years old, the incidence
was found to be higher in children, especially
girls.
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110
110
111. .
In another study, conducted in a number of 69
Villages and 4 Rural Towns in Eastern
Sudan, inrolling 3461 under 5 years, the
incidence was also found to be higher in girls
than in boys.
Another survey, performed on a displaced
community around Omdurman city, employing
the Sensitive Plasma Retinol Binding Protein
Test, showed that only 3 children out of 1441
had a Protein level equal to or more than 3
mcg/dl, which is the normal level.
111
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111
112. Vitamin A
It is a fat soluble vitamin
It is found in three forms
Retinol .
A pro vitamin .
Beta carotene ,some of which is converted to
retinol in the intestinal mucosa.
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112
113. The liver has enormous capacity
forEach child in the age group at inmonth to 5
storing vitamin A mostly 6 the
years should recive mega dose of vitA every 6
form of Retinol Palmitate.
month
Free Retinol is Transported in the
blood stream in combination of
Retinal Binding Protein which is
produce by the liver.
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113
115. Daily Requirement of vit A
Group
Man
Retinol
mcg
600
B.Carotene
mcg
2400
Woman
600
2400
Pregnancy
600
2400
lactation
950
3800
infants
0-12 m
350
1200
children
1-6 yrs
7-12 yrs
400
600
1600
2400
adults
adolescent
13-19yrs
600
2400
115
116. Each child in the age group at 6 month to 5
years should recive mega dose of vitA every 6
It ismonth
indispensable for
normal vision , it
contribute
to production of
retinal pigments,
which are needed
for vision in dim light
116
117. It necessary for maintaining integrity
and the normal functioning of the
Glandular and Epithelial tissues.
It has a role in the regulation of gene
expresion and tissue differentiation
It’s important role in differentiation of
immune system cell
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117
118. It has protective functions against
some Epithelial Cancers.
Also it has functions in processes of
normal heamopoises.
Embryonic Development and
Reproduction.
Bone metabolisms.
118
119. Vit A deficiency
•The signs of vit A deficiency are
predominantly ocular but have extraocular signs.
•Night blindness.
•Conjuctival xerosis (dry, non
wetable, smooth, shiny and its appears
muddy and wrinkled .
119
122. TREATMENT
Treatment: should be urgent, nearly all of the early
stages of Xerophthalmia should be treated by
addministeration of massive doses orally
(200,000IU or 110mg) of Retinol Palmitate on two
successive days.
122
123. Prevention And Control
Nutritional education.
Improvement of people’s diet so as to ensure a
regular and adequate intake of food rich in vit
A.
Reducing the frequency and severity of cont
ributory factor ,eg;
PEM , RTI ,Diarrheoa ,and measles
123
124. The strategy is to administration single
massive dose 200,000IU of vit a orally every 6
mounth to pre school children {1y to 6y}
half of dose 100,000IU to children between
6m and one year of age.
Since vit A can be stored in the body 6-9 month
And liberated slowly.
124
125. Since 1987 WHO has advocated the administration
of vit a with measle vaccine in countries.
Great sucess has been mantained for children by
including vit A with NID.
*provides immunity by high dose to new mother soon
after delivary
*Provision of vit A supplementaion every 4 to 6
month save children life
125
126.
Each child in the age group at 6 month to 5
years should recive mega dose of vitA every 6
month
126
127. KEY MASSEGE
Children need vitA to resist illness and prevent
visual impairements
vitA can found in many fruits and vegetables
, oil, egg , breast milk
Breast milk contain adequate amount of vitA
exclusive breast feeding during first 6 month
prevent vitA deficiency among infants
Children more than 6 month should recieve
complementry feeding rich in vegatibles
&fruits
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127
128.
Each child in the age group at 6 month to 5
years should recive mega dose of vitA every 6
month
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128
131. Nutritional anemia
Nutritional anemia refers to types of anemia
that can be directly attributed to nutritional
disorders.
The most important types:Iron deficiency anemia.
pernicious anemia.
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131
132. Iron deficiency anaemia
Introduction:
-- In developing countries every second
pregnant woman and about 40% of preschool
children are estimated to be anaemic.
-- In many developing countries, iron
deficiency anaemia is aggravated by worm
infections, malaria and other infectious diseases
such as HIV and tuberculosis.
.
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133. -- Iron deficiency is the most common and
widespread nutritional disorder in the world.
--As well as affecting a large number of children
and women in developing countries, it is the
only nutrient deficiency which is also
significantly prevalent in industralized countries.
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133
134. *The numbers are staggering:
2 billion people – over 30% of the world’s
population – are anaemic, many due to iron
deficiency, and in resource-poor areas, this is
frequently exacerbated by infectious diseases.
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134
135. * The major health consequences include:-poor pregnancy outcome.
-Impaired physical and cognitive development
. -Increased risk of morbidity in children.
-Reduced work productivity in adults.
*Anaemia contributes to 20% of all maternal
deaths.
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135
136. Causes:
1. Insufficient dietary intake and absorption of iron.
2. Iron loss from intestinal bleeding ,menstruation, etc.
3. The most significant cause of iron-deficiency anemia
is parasitic worms(hookworms-whipwormsroundworms).
4.The most common cause of iron-deficiency anemia is
chronic gastrointestinal bleeding from nonparasitic
causessuch as gastric ulcers.
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143. -Serum ferritin deplete
-Serum iron decreased
- Iron binding capacity rises
-Bone marrow BM hyperplasia
-Examiation of stool and urine
for hookworm infestation and
shistosomiasis.
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143
144. Treatment
1.Treatment of the cause.
2.Iron replacement.
*for iron deficiency anemia focuses on
increasing your iron stores so they reach normal
levels.
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144
145. Treatment
*Taking iron supplement pills and getting
enough iron in food will correct most cases of
iron deficiency anemia.
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147. *Criteria for defining IDA, and the public severity
of anaemia based on prevalence estimates, are
provided.
*According to this :
Approaches to obtaining dietary
information, and guidance in designing national
iron deficiency prevention programmes.
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148. Strategies for preventing iron deficiency:
1.food-based approaches:
dietary improvement.
modification and fortification.
schedule for control and treatment IDA .
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150. 2.Attention is given to micronutrient
complementarities in programme
implementation, e.g., the particularly close link
between the improvement of iron status and
that of vitamin A.
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152. * Further recommends action:A.oriented research on the control of iron
deficiency.
B.providing guidance in undertaking
feasibility studies on iron fortification in most
countries.
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155. Definition:
Pernicious anemia is a disease in which the red
blood cells are abnormally formed, due to an
inability to absorb vitamin B12.
HISTORY:
The British physician THOMAS ADDISON first
described the disease in 1849, from which it
acquired the common name of Addison's
anemia.
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157. Epidemiology:
-The
incidence of the disease is 1:10,000 in
northern Europe. The disease occurs in all
races. The peak age is 60, although it is starting
to be recognised in younger age groups.
-The condition is more common in those :
-Scandinavian or Northern European
-A positive family history and blood group A.
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158. Causes, incidence, and risk factors:
*Pernicious anemia is a type of vitamin B12
anemia. The body needs vitamin B12 to make red
blood cells. You get this vitamin from eating foods
such as meat, eggs, and dairy products.
*A special protein, called intrinsic factor, helps your
intestines absorb vitamin B12. This protein is
released by cells in the stomach. When the
stomach does not make enough intrinsic factor, the
intestine cannot properly absorb vitamin B12.
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159. Etiology:
*Cobalamin (B12) deficiency may result from the
following:
- Inadequate dietary intake .
- Atrophy or loss of gastric mucosa .
- Functionally abnormal IF .
- Inadequate proteolysis of dietary cobalamin .
- Insufficient pancreatic protease.
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160. -Bacterial overgrowth in intestine - bacteria
compete with the body for cobalamin.
- Diphyllobothrium latum (fish tape worm)
competes with the body for cobalamin.
-Disorders of ileal mucosa.
-Disorders of plasma transport of cobalamin.
-
- Dysfunctional uptake and use of cobalamin by cells
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161. *Very rarely, pernicious anemia is passed down
through families. This is called congenital
pernicious anemia. Babies with this type of anemia
do not make enough intrinsic factor or cannot
properly absorb vitamin B12 in the small intestine.
* In adults, symptoms of pernicious anemia are
usually not seen until after age 30. The average
age of diagnosis is age 60.
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162. *Certain diseases can also raise the risk.
They include:
-Addison’s disease
-Chronic thyroditis
-Hypoparathyroidism
-Hypopituitarism
-Myasthenia gravis
-Type 1 diabetes
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163. Symptoms:
Some people do not have symptoms. Symptoms may be
mild. They can include:
-Diarrhea or constipation
-Fatigue due to lack of energy, or light-headedness
when standing up or with exertion
-loss of appetite
-Pale skin
-Problems concentrating
-Shortness of breath, mostly during exercise
-Swollen, red tongue or bleeding gums
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164. *low vitamin B12 levels for a long time, causes
nervous system damage. Symptoms can
include:
-Confusion.
-Depression.
-Loss of balance.
-Numbness and tingling in the hands and feet.
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165. Lab:
*To confirm your diagnosis :
-Complete blood count (CBC)
-schilling test
-vitamin B12 level
-Bone marrow examination (only needed if
diagnosis is unclear).
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166. Treatment:
-The goal of treatment is to increase your vitamin
B12 levels.
-Treatment involves a shots of vitamin B12 once
a month.
-Persons with severely low levels of B12 may need
more shots in the beginning.
-Some patients may also need to take vitamin B12
supplements by mouth. For some people, highdose
-Eating a well-balanced diet.
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167. Expectations (prognosis):
-Patients usually do well with treatment.
It is important to start treatment early. Nerve
damage can be permanent if treatment does not
start within 6 months of symptoms.
Complications:
-People with pernicious anemia may have gastric
polyps, and are more likely to develop gastric
cancer and gastric carcinoid tumors.
Brain and nervous system problems may continue
or be permanent if treatment is delayed.
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168. Prevention:
-There is no known way to prevent this
type of vitamin B12 anemia.
However, early detection and treatment
can help reduce complications.
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171. • Iodine deficiency
Iodine deficiency is caused by a lack of iodine, a
chemical element essential to the body's physical
and mental development, in a person's diet.
It is the single most common cause of preventable
mental retardation and brain damage in the world.
iodine
The name is from Greek word, meaning violet or
purple, due to the color of elemental iodine vapor
a nonmetallic element of the halogen group
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172. The role of iodine in the body
Iodine is an essential element for thyroid function, necessary
for the normal growth, development and functioning of the
brain and body.
It also influences a variety of metabolic processes in the body
(converting food to energy, regulating growth and
fertility, and maintaining body temperature).
Iodine is also widely available in the
following foods
Seafood's
*Plants grown in soil rich in iodine
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173. The following are the recommended daily
allowances for iodine
Infants:
:40 - 50 micrograms
one to three years
: 70 micrograms
four to six years
: 90 micrograms
seven to 10 years
: 120 micrograms
11 years:
:150 micrograms
pregnant women
: 175 micrograms
lactating women
: 200 micrograms
adult men & women : 100 - 200 microgram
173
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174. The risk factor that may lead to iodine deficiency:
* Low dietary iodine.
* Selenium deficiency
* Pregnancy
* Exposure to radiation.
* Increased intake/plasma levels of goitrogens, such as
calcium
* Sex (higher occurrence in women).
* Smoking tobacco
* Alcohol .
* Oral contraceptive.
* Perchlorates.
* Thiocyanates.
* Age.
175. Signs and symptoms :
iodine deficiency gives rise to
hypothyroidism, symptoms of which are:
*Extreme fatigue
*Goiter
*mental slowing
*Depression
*weight gain
*low basal body temperatures
Iodine deficiency is the leading cause of preventable
mental retardation, a result which occurs primarily
when babies or small children are rendered
hypothyroidic by a lack of the element.
176. • A low amount of thyroxin (one of the two thyroid
hormones) in the blood, due to lack of dietary
iodine to make it, gives rise to high levels of thyroid
stimulating hormone TSH, which stimulates the
thyroid gland to increase many biochemical
processes;
• the cellular growth and proliferation can result in
the characteristic swelling or hyperplasia of the
thyroid gland, or goiter
176
177. • GOITER
• Goiter is said to be endemic when the prevalence
in a population is > 5%, and in most cases goiter
can be treated with iodine supplementation.
• If goiter is untreated for around five
years, however, iodine supplementation or
thyroxine treatment may not reduce the size of
the thyroid gland because the thyroid is
permanently damaged
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178. Cretinism
Cretinism is a condition associated with iodine
deficiency and goiter characterized by :
1.mental deficiency.
2. deaf-mutism.
3. Squint.
4.disorders of stance and gait.
5.stunted growth.
6.hypothyroidism.
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180. IDD world wide
• WHO estimates that nearly 2 billion individuals have an
insufficient iodine
• The number of countries where iodine deficiency is a public
health problem was reduced from 110 in 1993 to 54 in
2003 , 40 are mildly iodine deficient and 14 moderately or
even severely iodine deficient.
IDD in Africa
• 67% of households in sub-Saharan Africa are using iodized
salt, but coverage varies widely from country to country . In
countries like Sudan, Mauritania, Guinea-Bissau, and
Gambia, coverage is less than 10%, whereas in
Burundi, Kenya, Nigeria, Tunisia, Uganda, and Zimbabwe it
is more than 90%.
180
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183. • salt iodization:
• the most effective way to control iodine deficiency is
through salt iodization because:
• Salt is one of few foodstuffs consumed by virtually
everyone.
• Salt intake is fairly consistent throughout the year.
• In many countries, salt production/importation is limited to
a few sources
• Iodization technology is simple and relatively inexpensive
to implement.
• The addition of iodine to salt does not affect its color or
taste.
• The quantity of iodine in salt can be simply monitored at
the production, retail, and household levels.
183
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184. •
•
•
•
•
Prevention and control
1- Health education.
2- iodizing drinking water or irrigation water
3- Iodine-containing milk
4- in animal food to increased the iodine content of
foods derived from animal sources
• 5- salt iodization
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185. Treatment
Iodine deficiency is treated by ingestion of
iodine, such as found in food supplements.
Mild cases may be treated by using iodized salt in
daily food consumption, or eating more of milk, egg
yolks, and saltwater fish.
Iodized salt offers sufficient amounts of iodine. For a
salt-restricted diet.
• In male : 150 µg/d is sufficient for normal thyroid
function.
• For female: 150-300 µg/d should be ingested
daily.
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