Nutritional diseases

Nutritional diseases , causes and their remedies.

1. NUTRITIONAL
DISEASES

2. Nutritional diseases
An appropriate diet should provide-
(1) Sufficient energy, in the form of carbohydrates, fats, and proteins
(2) Amino acids and fatty acids to be used as building blocks and
(3) Vitamins and minerals, which function as coenzymes or
hormones or as in the case of calcium and phosphate, as important
structural components.
In primary malnutrition, one or all of these components are missing
from the diet.
In secondary malnutrition, the supply of nutrients is adequate, but
malnutrition results from insufficient intake, malabsorption, impaired
utilization or storage, excess loss, or increased need for nutrients.

3. There are several conditions that may lead to
malnutrition-
Poverty
Infections: infections have a negative effect on
nutrition
Acute and chronic illnesses: PEM in advanced cancers
Chronic alcoholism: sometimes suffer PEM but more
frequently have deficiency of several vitamins
Ignorance and failure of diet supplementation: infants,
adolescents, and pregnant women have increased
nutritional needs
Self-imposed dietary restriction: anorexia in person
obsessed with body weight
Causes of nutritional diseases

4. Protein energy malnutrition (PEM)
Severe PEM is a serious, often lethal disease
affecting children. It is common in low-income
countries, where up to 25% of children may be
affected, and where it is a major factor in the high
death rates among children younger than 5 years.
Malnutrition is determined according to the body
mass index (BMI, weight in kilograms divided by
height in meters squared). A BMI less than 16 kg/m
2

is considered malnutrition (normal range 18.5 to 25
kg/m
2
). In malnourished children, PEM presents as a
range of clinical syndromes, all characterized by a
dietary intake of protein and calories inadequate to
meet the body's needs.

5. The two ends of the spectrum of PEM
syndromes are known as marasmus and
kwashiorkor. From a functional standpoint,
there are two differentially regulated protein
compartments in the body: the somatic
compartment, represented by proteins in
skeletal muscles, and the visceral
compartment, represented by protein stores in
the visceral organs, primarily the liver. As we
shall see, the somatic compartment is affected
more severely in marasmus, and the visceral
compartment is depleted more severely in
kwashiorkor.
Protein energy malnutrition (PEM):
types

6. 1. Marasmus
A child is considered to have marasmus when
weight falls to 60% of normal for sex, height, and age.
A marasmic child suffers growth retardation and loss of muscle
loss of muscle, resulting from catabolism and depletion of the
somatic protein compartment.
This seems to be an adaptive response that provides the body
with amino acids as a source of energy.
The visceral protein compartment, which is presumably more
precious and critical for survival, is only marginally depleted, and
hence serum albumin levels are either normal or only slightly
reduced.

7. In addition to muscle proteins, subcutaneous fat is also
mobilized and used as fuel. With such losses of muscle
and subcutaneous fat, the extremities (external body
parts) are emaciated; by comparison, the head appears
too large for the body.
Anemia and manifestations of multiple vitamin
deficiencies are present, and there is evidence of
immune deficiency, particularly T cell–mediated
immunity. Hence, concurrent infections are usually
present, which impose additional nutritional demands.
Marasmus (contd.)

8. 2. Kwashiorkor
Kwashiorkor occurs when protein deprivation is
relatively greater than the reduction in total calories.
Less severe forms may occur worldwide in persons
with chronic diarrheal states in which protein is not
absorbed or in those with chronic protein loss (the
nephrotic syndrome), or after extensive burns.
In kwashiorkor, marked protein deprivation is
associated with severe loss of the visceral protein
compartment, and the resultant hypoalbuminemia
gives rise to edema.

9. The loss of weight in these patients is masked by the
increased fluid retention.
In contrast to marasmus, there is relative sparing of
subcutaneous fat and muscle mass.
Children with kwashiorkor have characteristic skin
lesions, with alternating zones of hyperpigmentation,
areas of desquamation, and hypopigmentation, giving a
“flaky paint” appearance. Hair changes include overall
loss of color or alternating bands of pale and darker hair.
Other features that differentiate kwashiorkor from
marasmus include an enlarged, fatty liver and the
development of apathy, listlessness, and loss of appetite.
Vitamin deficiencies are likely to be present, as are
defects in immunity and secondary infections.
2. Kwashiorkor (contd.)

10. NUTRITIONAL
DISEASES
(PART 2)

11. 3. Cachexia
PEM is a common complication in patients with AIDS or
advanced cancers, and in these settings it is known as
cachexia.
Cachexia occurs in about 50% of cancer patients, most
commonly in individuals with gastrointestinal, pancreatic,
and lung cancers
is responsible for about 30% of cancer deaths
is characterized by
extreme weight loss
fatigue
muscle atrophy
anemia
anorexia, and
edema
Mortality is generally the consequence of atrophy of the
diaphragm and other respiratory muscles.

12. Vitamin deficiencies
Thirteen vitamins are necessary for health;
vitamins A, D, E, and K are fat-soluble, and all
others are water-soluble.

13. 1. Vitamin A
The important dietary sources of vitamin A are
liver, fish, eggs, milk and butter. Yellow and
leafy green vegetables such as carrots,
squash, and spinach supply large amounts of
carotenoids.
Function
Maintenance of normal vision
Cell growth and differentiation
Metabolic effects of retinoids
Host resistance to infections

14. Vitamin A deficiency states
1.One of the earliest manifestations of vitamin
A deficiency is impaired vision, particularly in
reduced light (night blindness). 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
softening and destruction of the cornea
(keratomalacia) and total blindness.

15. 2.The epithelium lining the upper respiratory passage
and urinary tract is replaced by keratinizing squamous
cells (squamous metaplasia). Loss of the mucociliary
epithelium of the airways predisposes to secondary
pulmonary infections, and desquamation of keratin
debris in the urinary tract predisposes to renal and
urinary bladder stones.
3.Hyperplasia and hyperkeratinization of the epidermis
with plugging of the ducts of the adnexal glands may
produce follicular or papular dermatitis.
4.Immune deficiency, which is responsible for higher
mortality rates from common infections such as
measles, pneumonia, and infectious diarrhea.
Vitamin A deficiency states

16. 2. Vitamin D
The major function of vitamin D is the maintenance of
adequate plasma levels of calcium and phosphorus to
support metabolic functions, bone mineralization, and
neuromuscular transmission. Vitamin D is required for
the prevention of bone diseases.
Functions
Stimulation of intestinal calcium absorption
Stimulation of calcium reabsorption in the kidney
Interaction with parathyroid hormone (PTH) in the
regulation of blood calcium
Mineralization of bone

17. Deficiency States
Rickets in growing children and osteomalacia
in adults are skeletal diseases with worldwide
distribution. They may result from diets
deficient in calcium and vitamin D, but an
equally important cause of vitamin D deficiency
is limited exposure to sunlight.
Other, less common causes of rickets include
renal disorders causing decreased synthesis of
1, 25-dihydroxyvitamin D, phosphate depletion,
malabsorption disorders, and some rare
inherited disorders.

18. NUTRITIONAL
DISEASES
(PART 3)

19. 3. Thiamine (vitamin B
1
)
The major targets of the thiamine deficiency
are the peripheral nerves, the heart and the
brain. So persistent thiamine deficiency give
rise to three distinctive syndromes:
A polyneuropathy (dry beriberi)
A cardiovascular syndrome (wet beriberi)
Wernicke-Korsakoff’s syndrome

20. Dry beriberi: Dry beriberi is usually a peripheral
neuropathy with myelin degeneration and disruption
of axons involving motor, sensory and reflex arcs.
So these patients present with toe drop, foot drop
and wrist drop. The progressive sensory loss is
accompanied by muscle weakness and
hyporeflexia.
Thiamine deficiency states

21. Wet beriberi: Wet beriberi is associated with
peripheral vasodilatation, leading to more rapid
arteriovenous shunting of blood, cardiac failure
and eventually peripheral edema. The heart
may be markedly enlarge and globular with
pale, flabby myocardium. The dilation thins the
ventricular walls.
Thiamine deficiency states
(contd.)

22. Wernicke-Korsakoff’s syndrome: In severe
deficiency state, in chronic alcoholism,
Korsakoff syndrome may appear.
Wernicke encephalopathy is marked by
ophthalmoplegia, nystagmus, ataxia of gait and
derangement of mental function characterized
by global confusion, apathy, listlessness and
disorientation.
Korsakoff psychosis takes the form of serious
retrograde amnesia, inability to acquire new
information and confabulation.
Thiamine deficiency states
(contd.)