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Chapter 5: Nutritional Diseases
Nutritional diet
An appropriate diet should provide- Sufficient energy, in the form of carbohydrates, fats, and proteins. Amino acids and fatty acids to be used as building blocks and 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. Causes of nutritional diseases 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 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. Protein energy malnutrition (PEM): Types 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.
Marasmus
Marasmus is a form of severe protein-energy malnutrition characterized by a deficiency in calories and energy. It happens more often in developing nations or in countries where poverty, and also inadequate food supplies and contaminated water, are prevalent. A child is considered to have marasmus when Weight falls to 60% of normal for sex, height, and age. A child suffers growth retardation and loss of muscle Loss of muscle results from catabolism and depletion of the somatic protein compartment. There may be an adaptive response that provides the body with amino acids as a source of energy. Signs and Symptoms Stunted growth Voraciously hungry Extensive tissue & muscle wasting Dry skin Loss of subcutaneous fat Drastic loss of adipose tissue from buttocks and thighs Brittle hair; head appears too large for the body. Anemia and manifestations of multiple vitamin deficiencies. Pathophysiology Marasmus always results from a negative energy balance. The imbalance can result from a decreased energy intake, an increased loss of ingested calories (eg, emesis, diarrhea, burns), an increased energy expenditure, or combinations of these factors, such as, in acute or chronic diseases. The clinical features of marasmus can be considered as an evolving adaptation in a child facing an insufficient energy intake. Children adapt to an energy deficiency with a decrease in physical activity, lethargy, a decrease in basal energy metabolism, slowing of growth, and, finally, weight loss. Many of the adaptations are mediated by thyroid hormones, insulin, and growth hormone. As in any stressed state, the adrenergic response is activated. Treatment WHO guidelines (1996) highlight 10 steps for routine management of children with malnutrition, as follows:
Kwashiorkor cases occur in areas of famine or poor food supply. 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. Vitamin deficiencies are likely to be present, as are defects in immunity and secondary infections. Signs and Symptoms Growth failure Lethargy or mental apathy (lack of feeling or emotion) Muscle wasting Hair changes (bands of depigmentation and pigmentation) Depigmentation of skin Distended abdomen Enlarged fatty liver with hypoalbuminaemia Vilious atrophy of small intestine Moderate to severe anemia Pedal edema (swelling of the feet) Fatty liver Decreased immunity Anorexia, loss of appetite Ulcerating dermatosis Shock Pathophysiology Protein-deficient diet or poor intestinal absorption, chronic alcoholism, kidney disease, infections, and trauma lead to an increase need of protein and caloric intake and results in loss of protein due to the body's demand to repair. The malnutrition affects organs and impair their functions. Protein deficiency hampers cellular protein synthesis which is essential for growth and tissue repair. Lack of energy hampers the basal metabolic rate which is essential for biochemical and physiologic functions. Lack of micronutrients hampers the metabolic functions as components and cofactors in enzymatic processes. These eventually impairs physical and cognitive growth. Immune system is impaired (loss of delayed hypersensitivity, impaired lymphocyte response, fewer T lymohocytes, and impaired phagocytosis secondary to decreased cytokines and secretory immunoglobulin A (IgA). These immune changes can predispose a child to severe and chronic infections (infectious diarrhea, which leads to anorexia, decreased nutrient absorption, increased
metabolic demands, and direct nutrient loss). Fatty liver occurs from impaired hepatic synthesis of apoproteins required for the formation of lipoprotiens. Hypoalbuminaemia and sodium retention causes generalized oedema. Treatment Treatment depends on the severity of the condition. Patients who are in shock need immediate treatment to restore blood volume and maintain blood pressure. Calories are given first in the form of carbohydrates, simple sugars, and fats. Proteins are started after other sources of calories have already provided energy. Vitamin and mineral supplements are essential. Treating kwashiorkor in its late stages will improve the child's general health. However, the child may be left with permanent physical and mental problems. If treatment is not ensured or comes too late, the condition may be life-threatening. Comparison between Marasmus and Kwashiorkor Clinical Findings Marasmus Kwashiorkor Occurrence More common Less common Growth failure Present Present Wasting Present (Marked) Present Edema Absent Present Hair changes Less common Common Activity Active Apathetic Mental changes Not common Very common Dermatosis (flaky paint) Absent Present Appetite Good Poor Subcutaneous fat Absent Reduced Liver enlargement Absent Present Face Drawn in (monkey like) Edematous Infections Less prone More prone Mortality Less than Kwashiorkor High in early stage Recovery Comparatively fast Slow
Vitamin A
Vitamin A is a group of unsaturated nutritional organic compounds that includes retinol, retinal, and several provitamin A carotenoid. 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 Regulation of lipid metabolism Host resistance to infections Vitamin A deficiency states Impaired vision, particularly in reduced light (night blindness). Persistent deficiency gives rise to epithelial metaplasia and keratinization. The most devastating changes occur in the eyes and are referred to as xerophthalmia (dry eye). This is followed by erosion of the roughened corneal surface, softening and destruction of the cornea (keratomalacia) and total blindness. The epithelium lining the upper respiratory passage and urinary tract is replaced by keratinizing squamous cells (squamous metaplasia) which ultimately lead to secondary pulmonary infections (in respiratory tract) and renal and urinary bladder stones. Hyperplasia and hyperkeratinization of the epidermis with plugging of the ducts of the adnexal glands may produce follicular or papular dermatosis. Immune deficiency, which is responsible for higher mortality rates from common infections such as measles, pneumonia, and infectious diarrhea.
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 Vitamin D deficiency states
Vitamin B 3 (Niacin)
- Incorporated into nicotinamide adenine dinucleotide (NAD) and NAD phosphate. - Pellagra, dementia, dermatitis, diarrhea (three ‘D’s”) Vitamin B 5 (Pantothenic acid)
- Incorporated in coenzyme A
- Potent Antioxidant
- No nonexperimental syndrome recognized Vitamin B 6 (Pyridoxine)
- Derivatives serve as coenzymes in many intermediary reactions
- Peripheral neuropathy, glossitis, dermatiti Vitamin B 7 (Biotin)
- Cofactor in carboxylation reactions
- No clearly defined clinical syndrome Vitamin B 9 (Folate)
- Essential for transfer and use of 1 - carbon units in DNA synthesis
- Megaloblastic anemia
- Neural tube defects Vitamin B 12 (Cobalamin)
- Required for normal folate metabolism and DNA synthesis, maintenance of myelinization of spinal cord tracts
- Megaloblastic, pernicious anemia Vitamin C (Ascorbic acid)
- Serves in many oxidation- reduction reactions and hydroxylation of collagen
- Helps to protect cells and keeping them healthy, maintaining healthy skin, blood vessels, bones and cartilage
- Scurvy (internal bleeding, joint and muscle pains, gingivitis)
Minerals
Iron
Iron is present in all cells in the human body. Total body iron averages approximately 3.8 g in men and 2.3 g in women. When loss of iron is not sufficiently compensated by adequate intake of iron from the diet, it leads to iron deficiency anemia. Functions
- Carrier of oxygen to the tissues from the lungs in the form of hemoglobin
- Transport medium for electrons within the cells in the form of cytochromes
- Integral part of enzyme reactions in various tissues Iron deficiency: Causes Blood loss
- In women, long or heavy menstrual periods
Zinc
Zinc is the second most abundant trace mineral in the body after iron. It is involved in numerous aspects of cellular metabolism. It is required for the catalytic activity of approximately 100 enzymes. It plays an important role in immune function, protein synthesis, wound healing, DNA synthesis, cell division etc. Zinc also supports normal growth and development during pregnancy, childhood, and adolescence. It is required for proper sense of taste and smell. A daily intake of zinc is required to maintain a steady state because the body has no specialized zinc storage system. Zinc deficiency Zinc deficiency is characterized by:
- Growth retardation
- Loss of appetite
- Taste abnormalities
- Weight loss
- Eye & skin lesions
- Impaired immune function
- Delayed healing of wounds
- Mental lethargy
- Hair loss
- Delayed sexual maturation
- Impotence
- Hypogonadism in males
- Diarrhea etc. Zinc deficiency: Pathophysiology Zinc ions are needed by the metalloproteins because they act as catalyst and their charge maintains the structure and shape of the enzymes. So, absence of zinc from the metalloprotiens results in metabolic disorder and disease. Zinc plays an important role in the body as an antioxidant. Zinc is a co-factor for a group of metalloprotien enzymes called superoxide dismutase (SOD). Zinc is also incorporated into insulin and deficiency results in poor insulin response. It is postulated that the combined effects of zinc-related changes in multiple immune and metabolic parameters result in specific clinical features. Zinc deficiency: Treatment Zinc supplement : Supplements can contain different amounts of elemental zinc and are labeled as zinc gluconate, zinc sulfate, or zinc acetate etc. Zinc is also a common component of throat lozenges, as zinc is thought to help treat the common cold. Zinc diet: Long-term treatment for zinc deficiency may start with the diet containing oysters, red meat, baked beans, chickpeas, oatmeal, milk, yogurt, seeds etc.
