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• An adequate diet should provide:–
• Sufficient energy in the form of carbohydrates, fats and
• Vitamins and minerals, which function as co-enzymes or
hormones in vital metabolic pathways or, as for the case
of Ca &P, as important structural components.
MAIN NUTRITIONAL DISORDERS
Trace element deficiency
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:
–Impaired nutrient utilization or storage.
–Excess nutrient losses.
–Increased need for nutrients.
Inadequate intake of protein and calories.
Two main clinical syndromes:
* starvation in infant with overall lack of
* somatic protein compartment (skeletal
* protein deprivation more severe than deficit
* visceral compartment (protein stores in liver )
Marasmus is a consequence of protein energy deficiency
Wasting of muscles and fat tissue (“skin and bone”).
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
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
Kwashiorkor is a childhood protein energy deficiency that
occurs when protein deprivation is greater than reduction
in total calories.
Typically occurs in children who have been weaned of
the mother’s breast when the second child was born
c/c by hypoalbuminemia and generalized or
Loss of weight masked by edema
Usually there is sparing of muscle and subcutaneous fat.
Weight is between 60% -80% of normal.
Other clinical features include:
FLAKY PAINT appearance of skin (alternating zones of
hyperpigmentation, areas of desquamation and
Alternating bands of pale and dark hair – FLAG sign
Enlarged FATTY LIVER
atrophy and loss of small intestinal villi, leading to
concurrent loss of small intestinal enzymes
Devp of apathy and listlessness,
Loss of appetite
other vitamin deficiencies, and defects in immunity
Occurs in children
between 6 months 3 years
Wasting muscles but
preserved adipose tissue
Edema , localized or
Enlarged fatty liver
Serum proteins low
Alternate bands of light
and dark hair – FLAG sign
Common in infants under
1 year of age
Wasting of all tissues
including muscles and
No hepatic enlargement
Serum proteins normal
protuberant abdomen, thin
Enlarged fatty liver
Atrophy of different
tissues and organs but
Small bowel – mucosal
atrophy & loss of villi and
Bone marrow hypoplastic
Thymic & lymphoid
No fatty liver
Atrophy of different
tissues and organs
KWASHIORKOR AND MARASMUS
PEM IN DEVELOPED WORLD
Develops in chronically ill, older and bed ridden
Obvious Signs of secondary PEM include:
Depletion of subcutaneous fat in arms, chest wall,
shoulders or metacarpal regions
Wasting of quadriceps and deltoid muscles
Ankle or sacral edema
PEM in patients with AIDS or advanced CANCERS
is k/a cachexia
c/c by extreme wt loss, fatigue, muscle atrophy,
anemia, anorexia, and edema
Exact cause not known
Mediators secreted by tumors contribute to
Proteolysis inducing factor
lipid- mobilizing factor
Self induced starvation resulting in marked wt loss
C/F similar to severe PEM
In addition effects on endocrine system are:
AMENORRHEA (GnRH secretion decreases)
Symptoms of HYPOTHYROIDISM
BONE DENSITY decreased
Dehydration & electrolyte abnormalities
Major complication: CARDIAC ARRHYTHMIA &
SUDDEN DEATH d/t hypokalemia
Pt binges on food and then induces vomiting
More common than anorexia nervosa
No specific signs or symptoms
Diagnosis depend on psychological assessment
Major complications occur d/t frequent vomiting &
chronic use of laxatives n diuretics:
Electrolyte imbalance (hypokalemia) cardiac
Pulmonary aspiration of gastric contents
Esophageal and gastric rupture
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
Obesity results when calorie intake exceeds utilisation
Inactivity and sedentary life style
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
fats than protein rich food.
Secondary obesiy d/t hypothyroidism, cushings
d/s, insulinoma, and hypothalamic disorders
How to measure fat accumulation:
Body mass index (BMI: kg/m2):.
Normal BMI 18.5 to 25
Skin fold measurements.
Various body circumferences particularly the ratio of the
Distribution of fat has also an effect: central or
visceral obesity is associated with more risk than
excess accumulation of fat in subcutaneous tissue.
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
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
o Neurohumoral mechanism regulating energy balance – 3
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.
2. Arcuate nucleus in hypothalamus processes the
signals and generate efferent signals. Consists of two
subsets of firstorder neurons:
(1) POMC (pro-opiomelanocortin) and CART (cocaine and
amphetamine-regulated transcripts) neurons
POMC/CART neurons enhance energy expenditure and
weight loss through the production of the anorexigenic α-
melanocyte-stimulating hormone (MSH), and
the activation of the melanocortin receptors 3 and 4
(MC3/4R) in second-order neurons.
These second order neurons are in turn responsible for
producing factors such as thyroid releasing hormone (TSH)
and corticotropin releasing hormone (CRH) that increase
the basal metabolic rate and anabolic metabolism, thus
favoring weight loss
(2) neurons containing NPY (neuropeptideY) and AgRP
the NPY/AgRP neurons promote food intake (orexigenic
effect) and weight gain, through the activation of Y1/5
receptors in secondary neurons.
These secondary neurons then release factors such as
melanin-concentrating hormone (MCH) and orexin,
which stimulate appetite.
These first-orderneurons communicate with second-
order neurons in thehypothalmus.
3. Efferent system 2 pathways anabolic and
catabolic pathway which controls food intake and
energy expenditure respectively
Leptin binds to leptin receptors in the hypothalamus,
increases energy consumption by
stimulating POMC/CART neurons produe anorexigenic
neuropeptide( MSH) and
inhibiting NPY/AgRP neurons produce orexigenic np
thus suppressing food intake and increasing expenditure
Thermogenesis, an important catabolic effect mediated
by leptin, is controlled in part by hypothalamic signals
that increase the release of norepinephrine from
sympathetic nerve endings in adipose tissue.
In addition to these effects, leptin can function as a
proinflammatory cytokine and participates in the
regulation of hematopoiesis and lymphopoiesis.
called as “fat-burning molecule” and the
“guardian angel against obesity,” directs fatty
acids to muscle for their oxidation.
It decreases the influx of fatty acids to the liver and
the total hepatic triglyceride content
decreases the glucose production in the liver,
increase in insulin sensitivity and
protecting against the metabolic syndrome
Gut peptides act as short-term meal initiators and
They include ghrelin, PYY, pancreatic polypeptide,
insulin, and amylin among others.
Ghrelin is produced in the stomach and in the arcuate
nucleus of the hypothalamus.
It is the only known gut hormone that increases food
intake (orexigenic effect).
stimulates NPY/AgRP neurons to increase food intake.
Ghrelin levels rise before meals and fall between 1 and
2 hours after eating.
In obese individuals the postprandial suppression of
ghrelin is attenuated and may contribute to overeating
PYY is secreted from endocrine cells in the ileum
Plasma levels of PYY are low during fasting and
increase shortly after food intake.
levels of PYY generally decrease in individuals
with the Prader-Willi syndrome (caused by loss of
imprinted genes on chromosome 15q11-q13), a
disorder marked by hyperphagia and obesity.
These observations have led to ongoing work to
produce PYYs for the treatment of obesity.
peptide secreted with insulin from pancreatic β-cells
reduces food intake and weight gain, is also being
for the treatment of obesity and diabetes.
Both PYY and amylin act centrally by stimulating
POMC/CART neurons in the hypothalamus,
causing a decrease in food intake.
ADVERSE CONSEQUENCES OF
1. Hyper insulinaemia and insulin resistance Non-
Insulin dependant diabetes (type 2 DM)
3. Hyper triglyceridemia and lowHDL
Atherosclerosis Coronary artery disease
5. Non aloholic fatty liver disease
6. Hypoventilation syndrome / pickwickian syndrome
c/c by Hypersomnolence, both at night and during the
is often associated with apneic pauses during sleep
right-sided heart failure (cor pulmonale).
VITAMIN DEFICIENCY STATES
Dietary sources Consequence of
β-carotenes in carrots etc Vit. A
in fish, eggs, liver, margarine
infctns mainly measles
(calcitriol) Milk, fish, eggs, liver
Rickets ( children)
Osteomalacia ( adults)
Cereals, eggs, vegetable oils Neuropathy,
cell life span)
The major functions of vitamin A are
maintenance of normal vision, regulation of cell
growth and differentiation, and regulation of
Vitamin A is the name given to a group of
compounds that include retinol , retinal ,and
retinoic acid , which have similar biologic activities.
Retinol is the chemical name given to vitamin A. It
isthe transport form and, as retinol ester, also
Vitamin A is a fat-soluble vitamin, and its absorption
requires bile, pancreatic enzymes, and some level of
antioxidant activity in the food.
Retinol (generally ingested as retinol ester) and β-
carotene are absorbed in the intestine,where β-carotene
is also converted to retinol .
Retinol is then transported in chylomicrons to the liver for
esterification and storage.
Uptake in liver cells takes place through the
apolipoprotein E receptor.
More than 90% of the body’s vitamin A reserves are
stored in the liver, predominantly in the perisinusoidal
stellate (Ito) cells
Retinol esters stored in the liver can be mobilized;
before release, retinol binds to a specific retinol
binding protein (RBP), synthesized in the liver.
The uptake of retinol/RBP in peripheral tissues is
dependent on cell surface receptors specific for
After uptake, retinol binds to a cellular RBP, and the
RBP is released back into the blood.
Retinol may also be stored in peripheral tissues as
retinol ester or may be oxidized to form retinoic
FUNCTIONS OF VITAMIN A
Maintenance of normal vision.
Cell growth and differentiation. Vitamin A maintains
differentiation of mucus-secreting epithelium;
when a deficiency state exists, the epithelium
undergoes squamous metaplasia, differentiating into a
Metabolic effects of retinoids
key regulators of fatty acid metabolism, including fatty
acid oxidation , adipogenesis, and lipoprotein
Host resistance to infections.
Vitamin A supplementation can reduce morbidity and
mortality from some forms of diarrhea, and in preschool
children with measles, and improve the clinical outcome.
The beneficial effect of vitamin A in diarrheal diseases
may be related to the maintenance and restoration of
the integrity of the epithelium of the gut.
ability to stimulate the immune system,
photoprotective and antioxidant property
VITAMIN A DEFICIENCY
earliest manifestations is impaired vision, particularly in reduced
light (night blindness).
Persistent deficiency gives rise to epithelial metaplasia and
The most devastating changes occur in the eyes and are referred
to as xerophthalmia (dry eye).
First, there is dryness of the conjunctiva (xerosis conjunctivae)
as the normal lacrimal and mucus-secreting epithelium is replaced
by keratinized epithelium.
This is followed by a buildup of keratin debris in small opaque
plaques (Bitot spots)
Progresses to erosion of the roughened corneal surface, softening
and destruction of the cornea (keratomalacia)
Squamous metaplasia in respiratory and urinary
tract predisposing to infections and renal stones
Hyperplasia and hyperkeratinization of the
epidermis with plugging of the ducts of the adnexal
gland produce follicular or papular dermatosis.
Another very serious consequence is immune
deficiency, which is responsible for higher mortality
rates from common infections such as measles,
pneumonia, and infectious diarrhea.
VITAMIN A TOXICITY
The symptoms of acute vitamin A toxicity include
symptoms may be confused with those of a brain tumor
Chronic toxicity is associated with weight loss, anorexia,
nausea, vomiting, and bone and joint pain.
Retinoic acid stimulates osteoclast production and
activity, leading to increased bone resorption and high
risk of fractures.
The major function of the fat-soluble vitamin D
maintenance of adequate plasma levels of
calcium and phosphorus to support metabolic
functions, bone mineralization, and
Vitamin D is a key regulator of calcium and
The major source of vitaminD for humans is its
endogenous synthesis from a precursor,7-
dehydrocholesterol, in a photochemical
reaction that requires solar or artificial UV light
in the range of 290 to 315 nm (UVB radiation).
This reaction results in the synthesis of
cholecalciferol, known as vitamin D3.
Vitamin D is produced from 7-dehydrocholesterol in
the skin or is ingested in the diet.
It is converted in the liver into 25(OH)D, and in
kidney into 1,25(OH)2D (1,25-dihydroxyvitamin D),
the active form of the vitamin.
1,25(OH)2D stimulates the expression of RANKL,
an important regulator of osteoclast maturation and
function, on osteoblasts, and enhances the
intestinal absorption of calcium and phosphorus in
VITAMIN D DEFICIENCY
lack of dietary vit D
inadequate exposure to sunlight
intestinal malabsorption of fat
impaired hydroxylation due to hepatic and renal diseases
lack of vit D impairs mineralisaton of the growing skeleton
Signs of deficiency
• Rickets (children)
• Osteomalacia (adults)
• Hypocalcemic etany
SIGNS OF RICKETS
Skeletal deformities –
bow legs & lumbar
THORACIC CHANGES IN RICKETS
Deformation of the chest results from overgrowth of
cartilage or osteoid tissue at the costochondral
junction, producing the “rachitic rosary.”
The weakened metaphyseal areas of the ribs are
subject to the pull of the respiratory muscles and
thus bend inward, creating anterior protrusion of the
sternum (pigeon breast deformity).
Harrisons sulcus (horizontal groove along lower
border of thorax)
During the nonambulatory stage of infancy, the
head and chest sustain the greatest stresses.
The softened occipital bones may become
flattened, and the parietal bones can be buckled
inward by pressure; with the release of the
pressure, elastic recoil snaps the bones back into
their original positions (craniotabes).
An excess of osteoid produces frontal bossing
and a squared appearance to the head.
MORPHOLOGY OF RICKETS
Vitamin D deficiency in both rickets and osteomalacia
results in an excess of unmineralized matrix. The
following sequence occurs in rickets:
Overgrowth of epiphyseal cartilage due to
inadequate provisional calcification and failure of
the cartilage cells to mature and disintegrate
Persistence of distorted, irregular masses of
cartilage, which project into the marrow cavity
Deposition of osteoid matrix on inadequately
mineralized cartilaginous remnants
Disruption of the orderly replacement of cartilage by
osteoid matrix, with enlargement and lateral
expansion of the osteochondral Junction
Abnormal overgrowth of capillaries and fibroblasts
in the disorganized zone resulting from
microfractures and stresses on the inadequately
mineralized, weak, poorly formed bone
Deformation of the skeleton due to the loss of
structural rigidity of the developing bones
a. normal costochondral junction of a young child illustrating formation of cartilage
palisades and orderly transition from cartilage to new
b. detail of a rachitic costochondral junction in which the palisades of
cartilage is lost. darker trabeculae are well-formed bone; paler trabeculae
consist of uncalcified osteoid.
VITAMIN C DEFICIENCY
Causes: Dietary lack of fresh fruits and vegetables.
Mechanism: impaired collagen synthesis ( Vitamin C is
needed for collagen synthesis and collagen cross-linking
and tensile strength.)
Vit c def l/t to dev of SCURVY c/c by bonedisease in
growing children and by hemorrhages and healing
defects in both children and adults.
Vascular pattern –gingival bleeding, petechiae and
Skeletal changes –soft bones, growth retardation
Delayed wound healing
LIST OF DEFICIENCES OF
Iron - microcytic hypochromic anemia.
Iodine- hypothyroidism, goiter, growth retardation.
Copper- neuromuscular disorders.
Zinc- acrodermatitis enteropathica (rash around
eye mouth nose and anus), infertility, growth
retardation, anorexia and diarrhoea
Fluoride- dental caries.
Selenium – keshan disease congestive
cardiomyopathy d/t combination of dietary
deficiency of Se and presence of mutated strain of