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Unit 5:Nutritional deficiency

(malnutrition)

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Common Nutritional Problems of Public Heath
Importance in Ethiopia
Ethiopia, as many other developing countries, is
affected by several nutritional deficiencies.
Common
Protein-energy malnutrition (PEM)
Iron deficiency anemia (IDA)
Iodine deficiency disorders (IDD)
Vitamin A deficiency (VAD)
Others
Vitamin D deficiency (Rickets)
Fluorine excess (fluorosis)
Zinc deficiency
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Causes of Malnutrition
Multi-factorial
Having a number of interwoven factors operating
simultaneously
Three causes:
Basic causes
Underlying causes
Immediate causes

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Cont
Immediate causes
Inadequate nutrient intake
Inappropriate breastfeeding practices
Inappropriate complementary foods and feeding practices
Harmful traditional practices (food prejudices omission
from family diet, age bias during feeding, sex bias during
feeding, etc)
Infections (diarrhea, measles, tuberculosis, pertusis, etc)
The requirement for nutrients increases
Increased loss of nutrients due to diarrhea
Genesis of fever and other acute phase proteins is at
the expense of nutrients
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Cont
Underlying causes
Inadequate access to food (food)
Inadequate care to mothers and children (care)
Vulnerable segments of the population need someone
to:-
Care for them
Feed them
Take them to the nearby health institution for
preventive and therapeutic care
Give them psychosocial support
Inadequate health services and unhealthy environment

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Cont
Basic causes
Related to the amount, quality, control and use of various
resources.
Availability and control of human, economic and
organizational resources at different levels of society.
Divided into four groups
1. Ecological/technical conditions of production
Including the environment (soil and climate), level of
technology used, population resource ratio, level of
peoples skill.

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Cont
2. Social conditions of production
Including ownership of the means of production,
division of labor, power relationships.
3. Political factors
Including policies on employment, prices, incomes,
health, education and agriculture, food and nutrition
polices, and the legal system as a whole.
4. Ideological factors/socio-cultural factors
Including habits, beliefs, cultural preferences and all
ideas that legitimize actions in society.

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Cont
The UNICEF Conceptual Framework

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Intergenerational linkage of malnutrition

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Who is at risk for malnutrition?

Infants and children.


Women of reproductive age especially pregnant and
lactating.
People with eating disorders.
People with certain diseases such as cystic fibrosis
(hereditary disorder which affects the exocrine glands),
liver disease, kidney disease and cancer.
People with a low income (poor socioeconomic status).

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Protein Energy Malnutrition
Other terms are
Multi-deficiency syndrome
Failure to thrive
The term PEM has been used to describe
A range of disorders primarily characterized by growth
failure or retardation in children.
PEM is mostly common in children under five years of age.
Marasmus is common in children less than 2 years of age.
Kwashiorkor is prevalent in children less than 5 years.

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PEM
PEM can be
Clinical forms
Marasmus
Retarded growth with wasting of subcutaneous fat.
Kwashiorkor
Growth failure with wasting of muscles and
preservation of subcutaneous fat and pitting type
edema.
Mixed: Marasmus-Kwashiorkor (MK)
Edema with wasting

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PEM
PEM can be
Clinical (acute) forms
Kwashiorkor
Characterized by symmetric edema is evident especially in the lower
limbs
Hair is sparse
Flaky paint rash on the buttocks, legs and arms
Marasmus
Generally thought to be the result of cumulative, usually slow,
inadequate energy and protein intake
Shows a characteristic muscle wasting particularly evident in the
buttocks, the pinched face and anxious behavior
Mixed
Commonly coexist
Simple unified approach to clinical management of both conditions

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Marasmus
Progressive wasting of the body
and is associated with insufficient
intake or malabsorption of nutrients.
Characteristics
Occurs in children < 2 yrs of age
Severe deprivation
Develops slowly
Severe weight loss
Low growth (<60%), Low WAZ
No edema, no fatty liver
Anxiety, apathy
Sunken eye balls
Possible good appetite
Hair thin, dry; skin dry
Old Man face, wrinkled
appearance
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Kwashiorkor
Caused by lack of nutrients including
protein in the diet
Characteristics
1st to 3rd yrs of life
Pitting edema, enlarged fatty liver
Low protein, infections
Rapid onset
Some weight loss
Some muscle wasting
Growth: 60-80%
Low WAZ
Apathy, unhappy, irritable
Moon face
Loss of appetite
Hair dry
Dermatosis (skin lesions)

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PEM
Marasmic kwashiorkor can have the clinical features of
both Marasmus kwashiorkor.
Milder forms
Wasting
Thinness using weight for height (W/H)
Stunting
Linear growth retardation using height for age
(H/A)
Underweight
A result of wasting and/or stunting
Using weight for age (W/A)

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PEM
Ethiopia
Milder forms are rampant in children
Ethiopia Mini EDHS 2014 report
Stunting (short for their age) = 40%
Under weight (low weight for age) =25.7%
Wasting (thin for their height) = 9%

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Trend in nutritional status of under 5 children in Ethiopia

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Diagnosis of Protein Energy Malnutrition
The diagnosis of PEM rests mainly on meticulous
clinical examination for the symptoms and signs of
the syndrome plus anthropometric assessments
using different methods.
Additionally one may need laboratory investigation
for the assessment of complications and other health
problems associated with malnutrition.
Epidemiological considerations also contribute to the
diagnosis of malnutrition.

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Classification of PEM in Under Five Children

1. Gomez classification (weight-for-age), 1956


Percentage (%) of NCHS reference Level of malnutrition
90-109 Normal
75-89 Mild (Grade I)
60-74 Moderate (Grade II)
< 60 Severe (Grade III)
Disadvantages are:
Too high cut off point (90%)
Edema is ignored and yet it contributes to weight
Age is difficult to know in developing countries

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2. Welcome classification (weight-for-age), 1970
Percentage (%) of NCHS Level of malnutrition
Edema No edema
60-79% Kwashiorkor Undernourished
< 60% Marasmic- kwashiorkor Marasmus
Disadvantage: it does not differentiate acute from chronic
malnutrition.
In general, in the clinical setups it is preferable to use
welcome classification in order to clearly distinguish the
different clinical forms like Marasmus, kwashiorkor,
Marasmic-kwashiorkor or undernourished.
However, in the field (community) set ups the milder forms of
malnutrition like stunting and wasting are very widespread.

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3. Water low-classification (Height for age and weight for height), 1972
Index % of NCHS ref. Degree Duration of malnutrition
HFA 90-94% mild stunting(chronic)
85-89% moderate
<85% severe
WFH 80-89% mild wasting(acute)
70-79% moderate
<70% severe

It is preferable to use Water low classification in the field set up to


distinguish the acute and chronic forms of malnutrition.

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Management of PEM

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Classification of PEM in Adults

Grades of Chronic Energy Body mass index (BMI)


Deficiency

Normal 18.5 kg/m2-25kg/m2


I 17.0 -18.4kg/m2
II 16.0 -16.9kg/m2
III <16.0 kg/m2

which one is appropriate for Pregnant women BMI/MUAC?


Why?

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Management of PEM
Focuses on
The correction of specific nutrient deficiencies, treatment of
complications and superimposed infections.
The treatment approach is classified into three phases
Acute stabilization (phase I)
The main focus is treatment of infections and other
complications such as dehydration, hypothermia, hypoglycemia
and other electrolyte imbalances.
F75 milk
Transition phase: F100 milk and others
Rehabilitation (phase II): focuses on the restoration of the lost
tissue and promotion of catch up growth.
Plumpynut
Read on how to admit, treat, follow and discharge case of
malnutrition (protocols).
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Prevention PEM
1. Nutrition education
Focuses on educating mothers/care givers on the
importance of having a balanced diet through
diversification of food.
2. Dietary diversification
Production of food stuffs at the back yard garden and
intensification of horticultural activities.
3. Economic approach
Aims at improving the incomes of the target community
as a solution to their nutritional problems
Different methods in this approach
Food for work, food subsidy, income generating
projects
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Prevention of PEM.
4. Dietary modification
Focuses on modifying the energy, protein and
micronutrient content of the complementary foods.
In order to reduce dilution of the energy and protein
contents of the complementary foods and their level of
contamination, we need to educate mothers and
demonstrate to them the benefits of germination and
fermentation.
5. Supplementation
Could also be considered based on the local needs.
6. Fortification

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Micronutrient Deficiencies of Public Health
Significance in Ethiopia
The micronutrient deficiencies of public health
importance in Ethiopia are:-
Vitamin A Deficiency Disorders
Iron Deficiency Anemia
Iodine Deficiency Disorders
Zinc Deficiency

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Vitamin A Deficiency Disorders

Ever wonder why


carrots are orange?
Its because of beta-
carotene!
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Vitamin A Deficiency Disorders
Vitamin A deficiency is a serious nutritional problem that
affects children aged from 6-59 months.
According to WHO Xerophthalmia is classified in to the
following stages:
1. Night Blindness (XN)
Is the inability to see in low levels of light (eg. dusk,
moonlight, darkened room).
It is the rods within the retina, which are primarily
responsible for vision, as they are more sensitive to light
than the cones.
Retinal is an essential component of rhodopsin, the main
visual pigment in the rods.
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2. Conjunctival Xerosis (Conjunctival dryness) (X1A)
3. Bitots spots (X1B)
Are frothy or cheesy white lesions within the
conjunctiva of the eye.
Bitots spots are made up of clumps of squamous cells,
and are most often seen in the lower lateral quadrant of
the bulbar conjunctiva.
4. Corneal xerosis (X2) is seen as a wrinkling of the cornea.
5. A Corneal ulcer (X3A and X3B) is self-explanatory.
6. A corneal scar (XS) is seen as a white spot on the cornea and
is due to a healed corneal ulcer.

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Cont

Active corneal xerophthalmia (i.e. corneal xerosis and/or ulcers) is


extremely rare below 6 months and above 5 years of age. However,
corneal scars (inactive corneal xerophthalmia) are permanent sequelae
among survivors of full-thickness corneal ulcers, and Bitots spots can
sometimes persist even if the VAD is reversed.
INDICATOR LEVEL PREVALENCE THRESHOLD (%)
Night blindness (XN) 1.0
Xerophthalmia Bitots spot (XIB) 0.5
Corneal xerosis or ulcer
(X2/3A/3B) 0.01
Corneal scars 0.05

Biochemical deficiency
(Serum retinol) < 0.70 mol/L 5.0
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Causes of Vitamin A deficiency
Inadequate intake
Poor bioavailability
Reduced fat intake
Infections
Anorexia
Mal absorption
HIV, Measles, parasitic infections
Increased needs
Age
Physiologic status
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Treatment
Doses of oral vitamin A (as retinal palmitate in oil) for
treatment.
0-5 months 50, 000 IU per dose.
6-11 months 100,000 IU per dose.
12 months and above 200,000 IU per dose.
Time for Rx:1st day, 2nd day and 15th day.

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Prevention and Control Strategies
I. Supplementation
. Diseases targeted supplementation of at risk children.
. Universal (blanket) supplementation for at risk groups (6-
59months) every 4-6 months and lactating women within 6
weeks after delivery.
II. Dietary Diversification: sustainable
III. Breast feeding
IV. Food fortification: e.g. vitA in oil
V. Nutritional education

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Toxicity symptoms
Too much retinol can, in severe cases, lead to birth
defects (teratogenic) and spontaneous abortions if
pregnant women consume excess vit A.
Symptoms: headache, vomiting, double vision, hair loss,
joint pain.

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Iron Deficiency anemia

Nutritional anemia may develop due to:


Increased demand as in the case of pregnancy, lactation,
rapid growth etc.
Decreased intake of a nutrient.
Decreased absorption of a nutrient from food.
Chronic blood loss resulting in iron deficiency (e.g. in
hook worm and schistosoma infection).
Vitamin A deficiency
Malaria infection
Chronic infections: TB, HIV
Others
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Iron deficiency in Ethiopia
According to EDHS 2011 in Ethiopia
17% of women in reproductive age have anemia (any anemia).
22% of pregnant women were anemic.
44% of children between 6-59months have anemia (any anemia).
Principal types of nutritional anemia involve macrocytic anemia and
microcytic anemia.
Deficiencies of the following nutrients causes the development of
nutritional anemia.
Iron
Cyanocobalamin (vitaminB12), Folic acid (folate), Pyridoxine,
Vitamin C
Copper
Protein
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Hemoglobin and hematocrit cutoffs used to define
anemia in people living at sea level (WHO, 1997)

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Relationship between iron deficiency, iron deficiency
anemia and anemia in a population

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Daily iron requirements and daily dietary iron
absorption in pregnancy

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Deficiency Signs

Glossitis

Spoon Nails

Angular Stomatitis
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Public Health Significance of anaemia
Prevalence:
5-19% mild
20-39% Moderate
> 40% Severe
Consequences of Iron Deficiency and iron deficiency anemia
Decreased work capacity
Prematurity and low birth weight
Perinatal mortality
Maternal mortality
Child mortality
Impaired neuro-cognitive function in children
etc.

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Effective control of anemia through combination of strategies

Increased iron intake


Iron supplementation
Fortification of foods with iron (especially weaning
foods)
Dietary diversification
Control of parasitic infections (diagnosis and treatment,
chemoprophylaxis, preventing transmission)
Increased intake of other vitamins such as vitamin A, folic
acid through
Supplementation, Fortification, Nutrition Education etc.

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Cont.
For Pregnant women
Supplementation of 60 mg/day of Iron and 400 mcg/day Folic
acid should continue for at least Six months during pregnancy to
continue after delivery.
Deworming of children under five years and pregnant women in
the 3rd trimester.

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Zinc Deficiency
Causes of excess zinc losses
Fever/catabolism increases muscle breakdown
and urinary zinc losses.
Diarrhea causes excess losses.
Factors Suggesting Zinc Deficiency
High phytates staple foods
Low intake of flesh food
Prevalent stunting
High rate of diarrhea
Nutritional iron deficiency
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Effects of zinc deficiency on immune function
Reduced nonspecific immunity function and complement
activity.
Reduced T and B lymphocytes.
Suppressed delayed hypersensitivity, cytotoxic activity and
antibody production.
88% of diarrhea deaths are preventable with widespread use
of ORS and zinc supplementation for diarrhea treatment.

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Clinical spectrum of human zinc deficiency
Adolescent nutritional:
Hepatosplenomegaly, hypogonadism, dwarfism
Severe zinc deficiency:
Hypogonadism, growth retardation, dermatitis,
alopecia, mental disturbances, infections, death
Mild-moderate zinc deficiency:
Hypogonadism, growth retardation, decreased
immune function, infections.

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Prevention of zinc deficiency

Nutritional education
Diet diversification
Supplementation (ORS with zinc during diarrhea
treatment)

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Iodine Deficiency Disorders (IDD)
Endemic Goiter and cretinism (IDD) In Ethiopia
In Ethiopia, one out of every 1000 is a cretin, and about
50,000 peri-natal deaths are occurring annually due to
iodine deficiency disorders.
In some pocket areas of the country the prevalence of
goiter is found to be 50-95 %.
WHO considers that if the goiter rate is above 5% in the
population it is a public health problem.

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2008 Thomson - Wadsworth
Iodine Deficiency Disorderscont
It is common in Ethiopia because of high plateau areas.
Sex - More females are affected
Age - School children, pregnant and lactating mothers are
vulnerable to the problem .
Causes of IDD
Soil devoid of iodine
Erosion of the land owing to the mountainous topography
especially in Ethiopia
Crops growing in this type of soil are deficient in iodine
Animal products from animals grazing grass growing in
this soils are deficient in iodine
Water will also be deficient
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Iodine Deficiency Disorderscont
Cause.cont
Poor consumption of sea foods
Deficiency of other micronutrients (Iron, selenium, etc)
Goiterogenic Factors
These are factors in the food that interfere with iodine
uptake by the thyroid gland.
e.g. cassava, cabbage
An area is said to be endemic if 10% or more of child
population has goiter.

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Iodine Deficiency Disorderscont
Risk factors for IDDs in Ethiopia
Marine foods are rarely consumed
Staple diets are of plant origin
Soils in the highlands are believed to be low in
iodine as it is leached out of the soil due to its
solubility in water
If soil is deficient in iodine, so are the plants
grown in it, including the grains and vegetables
consumed by people and animals.

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Iodine Deficiency Disorderscont
Interaction with other nutrients
Deficiencies of selenium, iron and vitamin A have been
implicated in exacerbating iodine deficiency.
Accumulated peroxides may damage the thyroid gland
during selenium deficiency due to impaired production of
the selenium-dependent gluthathione peroxidase.
Moreover, selenium deficiency impairs thyroid hormone
metabolism as T4 into T3 is catalyzed by selenium-
dependent enzymes called iodothyronine deiodinases.

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Iodine Deficiency Disorderscont

Vitamin A deficiency activates thyroid stimulating hormone


(TSH) and increases risk for goiter through decreased
vitamin A mediated suppression of the pituitary TSH gene.
PEM
Iodine is essential for the synthesis of thyroid hormones.
Thyroid hormones are made up of the amino acid called
tyrosine.
Deficiency of proteins will lead to deficiency of tyrosine
and hence impaired synthesis of thyroid hormones
resulting in IDD.

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Health consequences of iodine deficiency

The term IDD encompasses all


consequences of IDD which can be
prevented by optimal iodine
nutrition.
The most damaging effect of
inadequate intake of iodine is on the
developing brain.
Cretinism is an extreme form of
neurological damage due to severe
iodine deficiency or fetal
hypothyroidism.
Cretinism is a congenital disease
characterized by mental and
physical retardation and
commonly caused by maternal
iodine deficiency during pregnancy.
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An adult male
from the Congo,
with three women
of the same age
(17-20 years), all
of whom are
cretins.

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Measuring thyroid size(WHO)
STAGE O No Goiter
STAGE IA Goiter detectable by palpation and not
visible when neck distended
STAGE IB Goiter palpable and visible when neck
is extended
STAGE II Goiter visible with the neck in normal
position
STAGE III Goiter visible at a distant
STAGE IV Huge Goiter

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Intervention strategies

One or a combination of strategies may be decided to


eradicate iodine deficiency
Strategies decided depend upon
The severity of IDD
The accessibility of the target population
The resources available
Programs may include one or both of the following
strategies
Food based approaches
Fortification(salt, oil)
Nutrition education
supplementation
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Treatment options: depends on the size of the enlargement,
signs , symptoms and the underlying cause.
Observation
Medications
Surgery
Radioactive iodine

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Vit.D deficiency: Reading assignment
Prevalence in Ethiopia
Causes
Consequences
Treatment
Prevention and control

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ASSIGNMENT

Assessment and Result\Assignment\I&


G Assignment for PH(R) year II.docx

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Thank You !!!
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