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vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
vitamin A deficiency and protein energy malnutriton
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vitamin A deficiency and protein energy malnutriton

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  • 1. Prevalence , etiology, biochemical and metabolic changes in VAD and PEM
  • 2. WHAT IS VITAMIN A DEFICIENCY
  • 3. WHO defines it as tissue concentrations of vitamin A low enough to have adverse health consequences even if there is no evidence of clinical xerophthalmia . In addition to the specific signs and symptoms of xerophthalmia and the risk of irreversible blindness, nonspecific symptoms include increased morbidity and mortality, poor reproductive health, increased risk of anaemia, and contributions to slowed growth and development.
  • 4. Prevalence of vitamin A deficiency
  • 5. In 1987, WHO estimated that vitamin A deficiency was endemic in 39 countries based on the ocular manifestations of xerophthalmia or deficient serum (plasma) retinol concentrations (<0.35 µmol/l). Globally, night blindness is estimated to affect 5.2 million preschoolage children and 9.8 million pregnant women which corresponds to 0.9% and 7.8% of the population at risk of VAD, respectively.  Low serum retinol concentration (<0.70 µmol/l) affects an estimated 190 million preschool-age children and 19.1 million pregnant women globally. This corresponds to 33.3% of the preschool-age population and 15.3% of pregnant women in populations at risk of VAD, globally.
  • 6.  Xeropthalmia reportedly affects 5 million Asian children and causes a total and partial blindness among 1,60,000 to 1,85,000 Indian children .  Over one million children die by vitamin A deficiency and about 3,50,000 others go blind, every year worldwide.
  • 7. The WHO Regions of Africa and South-East Asia were found to be the most affected by vitamin A deficiency for both population groups. Despite a marked increase in submitted data, there are still numerous countries lacking national prevalence data. There is a need to inform and motivate governments and agencies to collect, and report to WHO, national data on the prevalence of deficiency and, whenever possible, vitamin A programme coverage conditions prevailing at the time that population assessment data were collected.
  • 8. Etiology of VAD
  • 9. Vitamin A deficiency can have two different causes. •The first cause of vitamin A deficiency is called a primary deficiency which is when not enough vitamin A is consumed by the individual. •A secondary deficiency in vitamin A is when the individual consumes enough vitamin A, but the vitamin A is either not absorbed correctly or utilized correctly.
  • 10. PRIMARY CAUSE OF VITAMIN A DEFICIENCY •The primary source of vitamin A deficiency is not enough vitamin A or beta carotene in the diet. Vitamin A rich foods can be both from animal and plant sources. •Liver, eggs, cheese are all animal sources of vitamin A while carrots, broccoli and leafy vegetables such as spinach provide large amounts of beta carotene, which is converted by the body into vitamin A. • A lack of proper daily intake of vitamin A will result in symptoms of vitamin A deficiency.
  • 11. SECONDARY CAUSE OF VITAMIN A DEFICIENCY A secondary cause of vitamin A deficiency and its symptoms is when the ingested vitamin A is not absorbed by the small intestines or when it is not released by the liver when needed. Because vitamin A is fat soluble, it can be stored by the liver, but certain diseases, especially damage to the liver from alcoholism can reduce the ability of the liver to release vitamin A properly. There are a large number of conditions that can cause vitamin A to not be absorbed from food sources in the small intestines.
  • 12.    Infection with the nematode roundworm parasite Ascaris lumbricoides lowers serum retinol concentrations. Zinc is needed by the small intestines to absorb vitamin A, therefore a deficiency in zinc will often lead to a deficiency in vitamin A. Because vitamin A is transported into the body along with fats, any condition that impairs fat absorption can lead to vitamin A deficiency. The most common of these is liver disease that results in poor bile quality.
  • 13. BIOCHEMICAL AND METABOLIC CHANGES IN VAD
  • 14. Vitamin A functions at two levels in the body. The first is in the visual cycle in the retina of the eye; the second is in all body tissues systemically to maintain growth and the soundness of cells.
  • 15. In the visual system, carrier-bound retinol is transported to ocular tissue and to the retina by intracellular binding and transport proteins. Rhodopsin, the visual pigment critical to dim-light vision, is formed in rod cells after conversion of all-trans retinol to retinaldehyde, isomerization to the 11-cis-form, and binding to opsin. Alteration of rhodopsin through a cascade of photochemical reactions results in ability to see objects in dim light . The speed at which rhodopsin is regenerated relates to the availability of retinol. Night blindness is usually an indicator of inadequate available retinol, but it can also be due to a deficit of other nutrients, which are critical to the regeneration of rhodopsin, such as protein and zinc.
  • 16. The growth and differentiation of epithelial cells throughout the body are especially affected by vitamin A deficiency (VAD). Goblet cell numbers are reduced in epithelial tissues.  The consequence is that mucous secretions with their antimicrobial components diminish. Cells lining protective tissue surfaces fail to regenerate and differentiate, hence flatten and accumulate keratin.  Both factors - the decline in mucous secretions and loss of cellular integrity - diminish resistance to invasion by potentially pathogenic organisms. The immune system is also compromised by direct interference with production of some types of protective secretions and cells . Classical symptoms of xerosis (drying or non wetability) and desquamation of dead surface cells as seen in ocular tissue (i.e., xerophthalmia) are the external evidence of the changes also occurring to various degrees in internal epithelial tissues.
  • 17. WHAT IS PROTEIN ENERGY MALNUTRITION
  • 18. Protein-Energy-Malnutrition is a clinical syndrome present in infants and children as a result of deficient intake and/or utilization of food.
  • 19. PREVALENCE OF PEM
  • 20.  Approximately 70.0% of the world's malnourished children live in Asia, resulting in the region having the highest concentration of childhood malnutrition.  About half of the preschool children are malnourished ranging from 16.0% in the People's Republic of China to 64.0% in Bangladesh.  Prevalence of stunting and underweight are high especially in South Asia where one in every two preschool children is stunted.
  • 21.  The World Bank estimates that India is ranked 2nd in the world of the number of children suffering from malnutrition, after Bangladesh (in 1998), where 47% of the children exhibit a degree of malnutrition.  The prevalence of underweight children in India is among the highest in the world, and is nearly double that of Sub-Saharan Africa with dire consequences for morbidity, mortality, productivity and economic growth.  The UN estimates that 2.1 million Indian children die before reaching the age of 5 every year – four every minute – mostly from preventable illnesses such as diarrhoea, typhoid, malaria, measles and pneumonia.
  • 22. ETIOLOGY OF PEM
  • 23. The causes of PEM can either be direct or indirect.
  • 24. DIRECT CAUSES The direct factors, which are commonly referred to as immediate factors include: (i) Inadequate food intake (ii) Diseases (i) Inadequate food intake Inadequate food intake is the result of limited access to food in terms of quality and quantity. (ii) Diseases Diseases notably malaria and measles lead to loss of appetite, increased rate of metabolism due to fevers thereby increasing the body’s nutrient demands. Diarrhoea reduces the absorption of food nutrients, whereas vomiting decreases food intake. Intestinal parasites compete for nutrients with the body e.g. hookworm competes for iron.
  • 25. INDIRECT CAUSES Indirect causes of PEM include: (i) Food insecurity and limited access to foodstuffs • Families cannot acquire or produce enough food to cater for energy needs. • Lack of or limited access to land or agriculture inputs, marketing and distribution of foods. • Poor farming practices often due to lack of knowledge, money, time or equipment. • Poor weather conditions like failure of rains, floods etc. • Lack of time to gather food, prepare it properly and provide special dishes for young children. Among the time consuming and energy expending activities of the rural African housewife are the fetching of water from long distances. • Urbanization and rapid migration to the larger towns resulting in unemployment and low incomes.
  • 26. (ii) Poor water / sanitation and inadequate health services. • Health services may be of low quality, expensive, non-existent or unfriendly. • Lack of pre-natal and child health care. • Inadequate management of sick children. • Inadequate water and sanitation facilities. (iii) Inadequate maternal and childcare practice. • Families do not give adequate time and resources for women and children’s health, dietary and emotional needs. • Poor caring practices, including the inappropriate care of sick children. • Not utilizing health care facilities for special needs of pregnant mothers or adolescent girls. • Not supporting mothers to breastfeed adequately. • Inadequate diets for women including food taboos during and after pregnancy.
  • 27. BIOCHEMICAL AND METABOLIC CHANGES IN PEM
  • 28. PEM ADAPTATIONS Various body systems adapt as much as possible to the decreased nutrient availability • Insulin levels low – Leads to hormonal changes that ultimately affect thyroxin and lowers thermogenesis and oxygen consumption (lowers basal metabolic rate) • Non-vital hormonal secretion decrease – i.e. sex hormones
  • 29. •Red blood cell production decreases due to decreased oxygen demands due to lowered amount of lean body mass. • Cardiac muscle atrophies in parallel with loss of lean body mass Cardiovascular reflexes are altered – can lead to postural hypotension and decreased venous return – In severe PEM can get peripheral circulation failure comparable to hypovolemic shock
  • 30. RESPIRATORY ADJUSTMENTS IN PEM Lowered basal metabolic rates leads to •decreased ventilatory response to hypoxia and increased carbon dioxide • Deterioration of function and emphysema like changes have been Seen.
  • 31. CARDIAC AND RENAL FUNCTION  Decreased renal plasma flow and glomerular filtration rate are due to decreased cardiac output  Water clearance and ability to concentrate and acidify urine are not impaired
  • 32. PEM – IMMUNE SYSTEM CHANGES Marked depletion of lymphocytes from the thymus and atrophy of the thymus gland. • Cells from the t-lymphocyte regions of the spleen and lymph nodes are depleted.
  • 33. PEM - ELECTROLYTES • Total body potassium is reduced in PEM – Due to decreased muscle proteins and loss of intracellular potassium • Decreased amounts of ATP, due to decreased energy substrates ,alters cellular exchange of sodium and Potassium.
  • 34. Na-K-ATP pump actively pumps potassium into and sodium out of cells – when this is not working, results in potassium loss and increased intracellular sodium – Water goes with sodium, so there may be intracellular overhydration.
  • 35. PEM – GASTROINTESTINAL FUNCTION • Severe protein deficiency results in – impaired intestinal absorption of lipids and disaccharides – a decreased rate of glucose absorption • The greater the protein deficit, the great the functional impairment
  • 36. •Also a decrease in gastric, pancreatic and bile production with normal to low enzyme and conjugated bile acid concentration – Diarrhoea when fed due to these alterations and perhaps also irregular GI motility and GI bacterial overgrowth.
  • 37. • Hypoproteinemia leads to intestinal edema which decreases luminal absorption which lead to diarrhoea • Diarrhea aggrevates the malabsorption and can further decrease nutritional status • Diarrhea disappears with nutritional Recovery.
  • 38. PEM – CENTRAL AND PERIPHERAL NERVOUS SYSTEM ADJUSTMENTS • Early life PEM leads to decreased – brain growth (cell number and size) – Nerve mylenation – Neurotransmitter production – Velocity of nervous conduction
  • 39. CONCLUSION

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