NUTRITIONAL DISEASES

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.

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

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/m2 is considered malnutrition (normal range 18.5 to 25 kg/m2). 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.

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

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.

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.)

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.

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.)

NUTRITIONAL DISEASES(PART 2)

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.

Vitamin deficiencies

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

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

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.

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

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

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.

NUTRITIONAL DISEASES(PART 3)

3. Thiamine (vitamin B1) 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

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

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.)

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.)