NUTRITIONAL DISORDERS
C. MRUCHE
Nutritional Disorders
• An adequate diet should provide:–
• Sufficient energy in the form of carbohydrates,
fats and
proteins.
MAIN NUTRITIONAL DISORDERS
Obesity
Kwashiorkor
Marasmus
Vitamin deficiency
Trace element
deficiency
MALNUTRITION
Malnutrition, from a worldwide
perspective, is one of the
leading causes of morbidity
and mortality in childhood
improper and / or inadequate inadequate absorption
food intake of food
food faddism MALNUTRITION poor dietary habits
Deficient supply of food diseases
emotional factors metabolic abnormalities
MALNUTRITION
The World Health Organization defines
malnutrition as "the cellular imbalance between
supply of nutrients and energy and the body's
demand for them to ensure growth,
maintenance, and specific functions.“
Primary: related to diet.
Secondary: related to:
⚫ –Nutrient malabsorption.
⚫ –Impaired nutrient utilization or storage.
⚫ –Excess nutrient losses.
⚫ –Increased need for nutrients.
Diseases
Diarrhea or digestive system
diseases
Upper Respiratory Infection and
Pneumonia
Malformations
PROTEIN-ENERGY
MALNUTRITION
Inadequate intake of protein and calories.
Two main clinical syndromes:
⚫ Marasmus
* starvation in infant with overall
lack of calories.
* somatic protein compartment
(skeletal
muscles) affected
⚫ Kwashiorkor.
* protein deprivation more severe than
deficit in calories
* visceral compartment (protein stores in
liver ) affected
Marasmus Kwashiorkor
:
KWASHIORKO
R MARASMUS
⚫ Clinical features Clinical features
⚫ Occurs in children ⚫ Common in infants
between 6 months 3 under 1 year of age
years of age
⚫ Growth failure ⚫ Growth failure
⚫ Wasting muscles but ⚫ Wasting of all
preserved adipose tissues including
muscles and
tissue adipose tissue
⚫ Edema , localized or
⚫ Edema absent
generalized, present
⚫ Enlarged fatty liver
⚫ No hepatic
⚫ Serum proteins low
enlargement
⚫ Anemia present ⚫ Serum proteins
⚫ Alternate bands of normal
light and dark hair – ⚫ limb
Anemia present 11
FLAG sign ⚫ s
Monkey-like face,
KWASHIORKO
MARASMUS
R
Morphology Morphology
Enlarged fatty liver No fatty liver
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Atrophy of different Atrophy of different
tissues and organs tissues and organs
but subcutaneous including
DISORDERS
NUTRITIONAL
fat preserved subcutaneous fat
Small bowel – Rarely seen
mucosal atrophy &
loss of villi and micro
villi
Hypoplasia
Seen
Bone marrow
Less marked
hypoplasia
Cerebral atrophy
Thymic & lymphoid
12
atrophy
KWASHIORKOR AND MARASMUS
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1
DIS
ETIOLOGY
deficient intake of protein of good biologic
value
impaired absorption of protein, as in
chronic diarrheal states
abnormal losses of protein in proteinuria
Infection
hemorrhage or burns
failure of protein synthesis, as in chronic
liver diseases
INDICATORS
FOR EVALUATION OF MALNUTRITION
an accurate dietary history
evaluation of present deviations from
average height, weight, head
circumference, and past rates of growth
comparative measurements of mid arm
circumference and skinfold thickness
chemical and other tests
CLINICAL MANIFESTATIONS
Failure to gain weight or loss
of weight
Thin, subcutaneous fat reduced or despaired
( orderly abdomen, buttocks, limb and finally face )
Disturbulence of functions of organs
CLINICAL MANIFESTATIONS
MARASMUS
(Infantile Atrophy, energy-deficiency
or energy-protein deficiency)
MARASMUS
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1
ONA
L
DIS
MARASMUS
Marasmus is a consequence of protein energy
deficiency
characterized by:–
⚫ Wasting of muscles and fat tissue (“skin and
bone”).
growth retardation
Serum protein is normal, and there is no edema.
It can occur at any age and can be easily
compensated by normalizing nutritional supply of
proteins and other nutrients.
C/F :
⚫ Weight is less than 60%of normal.
⚫ Loss of muscle mass and subcutaneous fat
emaciation of extremities and head
appears too large for body
⚫ Usually there is associated anemia,
multivitamin deficiencies and immune
deficiency (T-cell mediated immunity)
concurrent infections
Failure to gain weight followed by
loss of weight until emaciation
results
Loss of turgor in skin which
becomes wrinkled and loose as
subcutaneous fat disappears
Low temperature and slow pulse
Reduced basal metabolic rate
Fretful or listless
Diminished appetite and constipation
followed by the so-called starvation
type of diarrhea, with frequent, small
stools containing mucus
Emaciation
Skin wrinkled
Subcutaneous fat disappears from
abdomen first, then extremities, and
finally face
KWASHIORKOR
a clinical syndrome resulted from a severe
deficiency of protein & inadequate caloric intake
the most serious and prevalent form in
industrially underdeveloped areas
“deposed child” may become evident from early
infancy to 5 yr of age, usually after weaning
height and weight are accelerated with treatment
but never equal those of consistently well-
nourished children.
CLINICAL MANIFESTATIONS
Early clinical evidence----vague, including
lethargy, apathy, and irritability
Inadequate growth, lack of stamina, loss
of muscular tissue, increased
susceptibility to infections, and edema
Dermatitis and dyspigmentation
Secondary immunodeficiency
Anorexia, flabbiness of subcutaneous
tissues, and loss of muscle tone
Lethargy, apathy
Inadequate growth, loss of muscular tissue
Infections, and edema and dermatitis
Flabbiness of subcutaneous tissues, and loss of
muscle tone
Liver enlargement early or late
Fatty infiltration
Edema usually develops early (failure to gain
weight may be masked by edema, which is
often present in internal organs before it can
be recognized in the face and limbs)
Renal plasma flow, glomerular filtration rate,
and renal tubular function are decreased
The heart may be small in the early stages
and enlarged later
LABORATORY DATA
Concentration of serum albumin decreased
Aminoaciduria
Ketonuria in the early stage
Low blood glucose values
Potassium and magnesium deficiencies
Amylase, esterase, transaminase, lipase,
alkaline phosphatase, pancreatic enzymes
decreased
normocytic, microcytic, or macrocytic Anemia
Bone growth delayed and GH increased
Diagnosis
The feeding history
Low body weight, loss of muscular
tissue and disturbances of system
functions
Laboratory data
Excluding other diseases
Comparing with children in the same
age group (or height) and sex:
Underweight: weight for age is lower than -2SD
Stunting: height for age is lower than -2SD
Wasting: weight for height is lower than -2SD
One or two or three may present to
one child. Having any one of the three,
the child can be diagnosed
malnutrition.
PREVENTION
Diet containing an adequate
quantity of protein of good biologic
quality
Adequate dietary instruction and
food distribution
Treatment of diseases
OBESITY
Obesity is defined as an accumulation of
excess of adipose tissue that imparts health
risk.
A body wt of 20% excess over ideal wt for age,
sex and height is considered as health risk
Etiology
Obesity results when calorie intake exceeds
utilisation like in
⚫ Over eating
⚫ Inactivity and sedentary life style
OBESITY
⚫ genetic predisposition to develop obesity
Loss of function mutation in leptin
Mutation of melanocortin receptor 4(MC4R)
Haploinsufficiency of BDNF (brain
derived neurotrophic factor) a/w obesity
in WAGR syndrome (wilms tumor ,
aniridia, genitourinary defects, mental
retardation)
⚫ diets largely derived from
carbohydrates and fatsthan protein
rich food.
⚫ Secondary obesiy d/t hypothyroidism,
OBESITY
How to measure fat accumulation:
⚫ Body mass index (BMI: kg/m2):.
Normal BMI 18.5 to 25
25-30 overweight
>30 obese
⚫ Skin fold measurements.
⚫ Various body circumferences particularly the ratio of
the waist-to-hip circumference.
Distribution of fat has also an effect: central or
visceral obesity is associated with more risk
than excess accumulation of fat in
subcutaneous tissue.
OBESITY
Two basic types of obesity:
A. Life-long obesity:
Also called hyperplastic obesity.
Begins in childhood and is characterized by
an increased number of adipocytes on
peripheral parts of the body.
B. Adult onset obesity:
Also called hypertrophic obesity.
It is characterized by an increased size of fat
cells and central obesity. Fat accumulates on
the trunk.
HOW DOES THE BODY PREVENT THE
DEVELOPMENT OF OBESITY?
o Balance between calorie intake and
expenditure.
o The critical role in this regulation is played
by
Leptin.
o Neurohumoral mechanism regulating energy
balance – 3 components
1. Peripheral or afferent system genertes
signals from various sites . Componenets are:
Leptin & adiponectin produced by fat cells
ghrelin from the stomach,
peptide YY (PYY) from the ileum and colon, and
insulin from the pancreas.
ADVERSE CONSEQUENCES OF
OBESITY
1. Hyper insulinaemia and insulin resistance
Non- Insulin dependant diabetes (type 2
DM)
2. Hypertension
3. Hyper triglyceridemia and lowHDL
Atherosclerosis Coronary artery disease
4. Cholelithiasis
5. Non aloholic fatty liver disease
6. Hypoventilation syndrome / pickwickian
syndrome
⚫ c/c by Hypersomnolence, both at night and
during the day,
⚫ is often associated with apneic pauses during
sleep
(sleep apnea),
⚫ polycythemia, and
⚫ right-sided heart failure (cor pulmonale).
7. Cancer
8. Osteoarthritis
CHILD MANUTRITION —— Multiple choices
What are the factors contributing to malnutrition?
Deficient supply of food
Poor dietary habits
Food faddism and emotional factors
Certain metabolic abnormalities
The indicators for evaluation of nutritional status are:
Weight for age
Height for age
Weight for height
24hr creatinine excretion
CHILD MANUTRITION —— Multiple choices
The lower weight for height indicates:
The child has acute malnutrition
The child is stunted
The child is wasted
The child is normal
Protein reserves in malnourished child are assessed from:
Serum albumin
Transferring
Hemoglobin
Prealbumin
High density lipid protein