Micronutrient deficinecy disorders .pptx

Micronutrient deficinecy disorders

1. Micronutrient Deficiency Disorders

2. 1. Micronutrients play a central part in metabolism and in maintenance of tissue function. 2. Vitamins and minerals

3. What are vitamins? Vitamins are organic molecules that are essential for normal health and growth. They are required in trace amounts and must be obtained from the diet because they are not synthesized in the body. Organic molecules with a wide variety of functions Cofactors for enzymatic reactions Acts as hormones (vitamin D) Acts as antioxidant (vitamin E) Acts as mediators of cell signalling and regulators of cell and tissue growth and differentiation(vitamin A) •Essential, supplied in the diet • Two distinct types: Fat soluble (A, D, E, K) • Water soluble (B – complex, C)

4. Dark leafy green vegetables have the most vitamins & minerals in them!

5. Vitamin deficiency A deficiency of vitamins may be primary (dietary in origin) or secondary because of disturbances in intestinal absorption, transport in the blood, tissue storage, or metabolic conversion

6. Vitamin A Beta-carotenes are converted by liver enzymes to vitamin A (retinol). Function : Promote good vision, normal growth, and healthy nerve function Sources : Liver, yellow & orange fruits and vegetables, egg yolks, dairy products, pears, and broccoli TOXICITY can cause liver damage and severe birth defects.

7. Sources of Vitamin A Vitamins & Minerals Carrots Pumpkin Leafy Vegetables Fish Mangoes Papaya Melon Milk

8. Vitamin A deficiency The most devastating changes occur in the eyes and are referred to as xerophthalmia (dry eye). First, xerosis conjunctivae Buildup of keratin debris in small opaque plaques ( Bitot spots) and, eventually, Erosion of the roughened corneal surface with softening and destruction of the cornea ( keratomalacia ) and total blindness.

9. Night Blindness nyctalopia : inability to see clearly in dim light; due to a deficiency of vitamin A or to a retinal disorder

10. Changes in Co njunctiva

11. Clouding and Melting of Cornea

12. BITOT SPOT KERATOMALACIA BILATERAL BLINDNESS V A D

13. Non ocular manifestations Epithelium lining the upper respiratory passage and urinary tract is replaced by keratinizing squamous cells ( squamous metaplasia ) Another very serious consequence is immune deficiency Vitamin A deficiency increases the severity of mortality from measles and diarrhea

14. HYPERVITAMINOSIS A SIGNS Birth defects Liver damage Osteoporosis Hair loss Dry skin Hemorrhage Coma SYMPTOMS Anorexia Nausea Vomiting Blurred vision Headache Abdominal pain Altered mentality

15. PREVALENCE OF DEFICIENCY Clinical deficiency : India, most of central and south Africa, Middle East, Sri Lanka, parts of Indonesia. (WORLD)

16. PREVALENCE - INDIA < 1 % 1 - 3 % 3 - 6 % > 6 % 0 – 6 years (National Survey 1986-89)

17. CAUSES OF DEFICIENCY Early weaning PEM Faulty feeding practices Infections – Diarrhoea, Measles Consumption of Skimmed Milk Most common in children aged 1-3 yrs.

18. ASSESSMENT OF DEFICIENCY (WHO) CRITERIA PREVALENCE IN POPULATION AT RISK Night blindness More than 1 % Bitot’s spots More than 0.5 % Corneal xerosis/ Keratomalacia More than 0.01 % Corneal ulcer More than 0.05 % Serum retinol < 10 mcg/dl More than 5 %

19. Vitamin A Prophylaxis Programme One of the components of National Programs for Control of Blindness. This includes administration of 200,000 I.U of vitamin A orally to all preschool children every six months The programme was launched in 1970 by the ministry of health and family welfare MCH centres in urban areas, PHC in rural areas and ICDS projects are engaged in the implementation of the program .

20. Short term strategy Administration of supplemental dose of Vit . A. 6-11months-1 dose of 1 lac IU. 1-5 years- 2 lac IU biannually. Long term strategy Promotion of regular intake of Vit A- rich food. Feeding locally available food. Kitchen gardening of Vit A-rich food. Treatment of Vit A defciency Immediately after diagnosis-2 lac IU followed by another dose of 2 lac IU 1-4 weeks later

21. Vitamin D Major function of the fat-soluble vitamin D is the maintenance of adequate plasma levels of calcium and phosphorus Metabolic functions, Bone mineralization, and Neuromuscular function Calciferols (vitamin D₂) - the sun vitamin (UV rays) Sources : Dairy Products, seafood, eggs, mushrooms, cereal, pork, sunshine

22. Sources of Vitamin D Vitamins & Minerals Egg Yolk Mushrooms Fatty Fish Cheese Sunlight Fortified Milk

23. Vitamin D deficiency Normal reference range for circulating 25-(OH)-D is 20 to 100 ng / mL ; Concentrations of less than 20 ng / mL constitute vitamin D deficiency Causes Diet deficiency Limited exposure to sunlight Renal disorder

24. Rickets (in children whose epiphyses have not already closed) Osteomalacia (in adults), and Hypocalcemic tetany [Extracellular concentration of ionized calcium, which is required for normal neural excitation and the relaxation of muscles]

25. Rickets A deficiency disease resulting from a lack of Vitamin D or from insufficient exposure to sunlight. Characterized by softening of developing bone, bow legs, growth failure, muscular hypotonia , tetany and convulsions. Most common during the first year of life.

26. Rickets During the nonambulatory stage of infancy, the head and chest sustain the greatest stresses. Frontal bossing and a squared appearance to the head Rachitic rosary Pigeon chest deformity K yphoscoliosis

27. TOXICITY Hypervitaminosis D – infants-2,000-3,000 IU/day, adults-10,000 IU/day for several months. causes hypercalcemia,hyperphosphatemia , hypertension which manifest as: Nausea & vomiting Excessive thirst & polyuria Severe itching Joint & muscle pains Azotemia , nephrolithiasis, ectopic calcification. Disorientation & coma.

28. Vitamin E Anti oxidant Free radical scavanger Antineoplastic effect and may raise the concentration of high density lipoprotein cholesterol. Transported in the body by lipoprotein. sources - nuts, seeds, whole wheat grain. Recommended daily allowance -15-25 IU/day- 6wks(preterm),infants-3mg alfa-tocopherol , adults- 10mg/day.

29. Deficiency Observed in low birth weight infants. Anemia , reticulocytosis , thrombocytopenia, and abnormal erythrocyte metabolism. Low levels of vitamin e in premature infants is associated with hemolytic anemia , hyperbilirubinemia and intraventricular hemorrhage . Prophylaxis reduces retinopathy of prematurity. Clinical menifestation - loss of reflexes, ataxia of trunks and limbs, dimnished priopioception , muscle weakness, ptosis, pes cavus , scoliosis and dysarthria.

30. Vitamin K It is a cofactor of the enzyme that catalyzes one step in the formation of prothrombin . Needed for the generation of several clotting factors in the liver. Source - green leafy vegetables. Deficiency- coagulation defect due to hypoprothrombinemia and deficiency of factor VII resulting in hemorrhagic disease of the newborn . 1mg IM – newborn . In severe deficiency-2.5 to 5 mg parenterally

31. The B Vitamins B-1, B-2, B-3, B-6, B-12

32. B-1 Thiamin Important in: Producing energy from carbohydrates proper nerve function stabilizing the appetite promoting growth and good muscle tone ATP production B-1 is nontoxic even at high dosages

33. B-1 Deficiency( beri beri ) Occurs in adults when the intake drops below 1mg/day. Three forms-dry, wet, acute Dry-no edema , severe muscle wasting, and cardiomegaly. Wet-peripheral edema , ocular paralysis, ataxia and mental impairment. Infantile beriberi more subtle than adults o ccurs in breastfed infants of thiamine deficient mothers. Cardiac involvement with cardiomegaly , cyanosis, dyspnea , and aphonia if untreated results in death.

34. Riboflavin Deficiency Deficiency is rare and often occurs with other B vitamin deficiencies Several months for symptoms to occur Burning, itching of eyes Angular stomatitis Cheilosis Swelling and shallow ulcerations of lips Glossitis

35. Riboflav i n defi c ien c y Angular stomatitis Glossitis

36. Niacin – Vitamin B3 Essential for healthy skin, tongue, digestive tract tissues, and RBC formation Processing of grains removes most of their niacin content so flour is enriched with the vitamin

37. Pellagra – Signs & Symptoms ‘Three Ds’: diarrhea, dermatitis and dementia Reddish skin rash on the face, hands and feet which becomes rough and dark when exposed to sunlight (pellagrous dermatosis) acute: red, swollen with itching, cracking, burning, and exudate chronic: dry, rough, thickened and scaly with brown pigmentation dementia, tremors, irritability, anxiety, confusion and depression

38. Pellagra Dermatitis

39. SCURVY (VIT. C DEFICIENCY) Prolonged vitamin c deficiency results in scurvy. Usually occurs in those who are deprived of citrus fruit, fresh vegetables, or vitamins. IN INFANCY- clinical features- Anorexia, diarrhea , pallor, irritability and increased susceptibility to infections, sub-periosteal hemorrhages and long bone tenderness can occur. OLDER CHILDREN- hemorrhagic sign predominate. Bleeding of gums, conjunctiva and the intestinal tract

40. Diagnosis By characteristric physical findings and history of inadequate dietary intake. X-ray of long bones -infantile scurvy TREATMENT Supplimentation of vitamin c resolves symptoms in 24- 48hrs. RDA-30-40 mg /day-infants 40-70 mg/day- children.

41. Iron Deficiency Anemia “ a condition in which the haemoglobin content of blood is lower than normal as a result of a deficiency of one or more essential nutrients” Iron-deficiency anemia is usually due to : blood loss poor diet an inability to absorb enough iron from food.

42. Anemia- Signs & Symptoms Symptoms Tiredness/ Fatigue/ Headache/Breathlessness Signs Pallor: Pale conjunctivae, palms, tongue, lips, skin, Spoon shaped nails. Tachycardia, Systolic murmur If Hb<3, check for signs of CHF

43. Sources of Iron Vitamins & Minerals

44. Clinical Presentation Iron-deficiency anemia can cause: brittle nails cracks in the sides of the mouth

45. Extreme fatigue (tiredness) chest pain

46. Pale skin Dizziness or lightheadedness

47. Fast heart rate Headache

48. Anaemia in children Classification of Anaemia mild anaemia (10.0-10.9 grams/ decilitre ), moderate anaemia (7.0-9.9 g/dl), and severe anaemia (less than 7.0 g/dl)

49. Treatment- iron replacement

50. National Nutritional A naemia Prophylaxis Programme The program envisages distribution of iron and folic acid to young children(less than 12 years), lactating and expectant mothers through MCH centres in urban areas PHC/SC in rural areas and. The commercial production of iron fortified common salt was started in1985.

51. National Iron Plus Initiative:

52. Weekly Iron and Folic acid supplementation (WIFS) programme for adolescents Also known as WIFS-Blue campaign . Nodal agency- Ministry of H&FW Beneficiaries- Adolescent girls/boys enrolled in school, 6th- 12th std. (Min of Education) Adolescent girls not enrolled in schools (Min of Social Welfare) Services IFA tablet to target population on weekly basis on a fixed day (Monday) for 52 weeks. Biannual deworming (February and August)

53. Zinc Deficiency Zinc essential for the function of many enzymes and metabolic processes Zinc deficiency is common in developing countries with high mortality Zinc commonly the most deficient nutrient in complementary food mixtures fed to infants during weaning

54. Zinc Deficiency- Signs & Symptoms S kin lesions Immune impairment D iarrhea Poor growth Acrodermatitis enteropathica : AR disorder (defect of Zn absorption) Begins within 2-4 weeks of weaning Perioral/ Perianal dermatitis/ Failure to thrive

55. Zinc Deficiency- Treatment Regular zinc supplements can greatly reduce common infant morbidities in developing countries Adjunct treatment of diarrhea -10 mg/day for infants below 6 months, -20mg/day of zinc for 10-14 days(>6months)  Zinc deficiency commonly coexists with other micronutrient deficiencies including iron, making single supplements inappropriate  Emperical trial of Zinc supplementation(1ug/kg/day) is safe and reasonable

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