micronutrients and macronutrients, deficiency and excess

Deficiency and excess of micronutrients and macronutrients

1. MICRONUTRIENTS AND MACRONUTRIENTS AVMC

2. objectives Vitamin A its functions and deficiency Hypervitaminosis A Vitamin D its functions and deficiency Hypervitaminosis D Vitamin E its functions and deficiency Hypervitaminosis E Vitamin K and deficiency

3. INTRODUCTION Fat Soluble Vitamins are: A, D, E and K Absorbed from intestine and dissolved in fat globules Require bile acids for emulsification and micelle formation to get absorbed into enterocytes Excess fat soluble vitamins are stored in liver and adipose tissue in the body. So their deficiencies take months to manifest

4. VITAMIN A Vitamin A deficiency: most common cause of preventable blindness in Indian children WHO recommends: serum retinol levels <20 micrograms/dl- indicator to assess subclinical vitamin A deficiency in community National Nutritional Monitoring Bureau (NNMB) survey estimates 62% of Indian Preschool children are having Vitamin A deficiency

5. FORMS OF VITAMIN A In our body: Retinol Retinal Retinoic acid : most bioactive form Retinyl palmitate

6. In food and commercial preparations: Preformed Vitamin A: animal sources: liver, milk, egg, cheese and fish liver oil Provitamin A (carotenoids): plant sources: orange yellow fruits like carrot, papaya, ripe mangoes, melons and green leafy vegetables Synthetic retinal palmitate

7. ROLE OF VITAMIN A IN HEALTH & DISEASE 1. In vision 2. Regulation of gene expression and tissue differentiation 3. To sustain normal epithelial morphology and function 4. It influences proliferation and differentiation of T-cells 5.Embryogenesis: acts as a signaling molecule in determining morphogenesis 6.Hematopoiesis 7. Anti-tumor effects 8. Growth

8. R ECOMMENDED DIETARY ALLOWANCE AGE GROUP RDA 0 – 12 months 350 mcg 1 – 6 years 400mcg 7 – 9 years 600mcg Adolescents and adults 600mcg Pregnant women 800mcg Lactating women 950mcg

9. Groups at risk of Vitamin A deficiency: Poor intake: inadequate breast feeding, vegetarians Defective absorption: chronic or persistent diarrhoea, malabsorptive states Defective metabolism: impaired synthesis of retinol transport protein Increased requirements: preterm babies, during infections such as measles.

10. CLINICAL FEATURES Increased risk of infections: recurrent respiratory tract infections, UTI Phyrnoderma (toad skin) Hyperostosis due to reduced osteoclastic and increased osteoblastic activities Poor growth Recurrent and persistent diarrhea Ophthalmic manifestations

11. WHO classification of Ophthalmic manifestations: NOMENCLATURE PATTERN OF DISEASE SPECIAL POINT X1A Conjunctival xerosis Affected areas appear as “sandbank at receding tides” as tears drain off X1B Bitot’s spots Conjunctival xerosis first appears in the temporal quadrant as a triangular patch Keratin and saprophytic bacilli accumulate in the xerotic surface giving it a foamy or cheesy appearance X2 Corneal xerosis Corneal epithelium becomes hazy, lusterless and dry

12. NOMENCLATURE PATTERN OF DISEASE SPECIAL POINT X3A Corneal ulcer involving less than 1/3 rd of corneal surface At this stage it is not reversible even with vitamin A therapy, hence usually resulting in scarring Also, cornea can undergo perforation and result in blindness X3B Corneal ulcer involving more than 1/3 rd of corneal surface XN Night blindness Earliest and best clinical indicator of vitamin A deficiency Affected children aren’t able to move around the house after dusk XF Xerophthalmic fundus XS Corneal scar May result in corneal blindness

13. Bitot spot Bilateral keratomalacia

14. BITOT SPOT CONUNCTIVAL XEROSIS CORNEAL XEROSIS CORNEAL ULCERATION CORNEAL SCARRING XEROPHTHALMIC FUNDUS

15. T REATMENT AGE DOSE NUMBER OF DOSES < 6 MONTHS 50,000 IU 3 doses 1 st dose STAT 2 nd dose on the next day 3 rd dose after 2 weeks 6 -12 MONTHS 1 LAKH IU > 1 YEAR 2 LAKH IU

16. P REVENTION Vitamin A prophylaxis program > at 9 months along with MR vaccine: 1lakh IU > at 16months along with MR2, DPT and OPV: 2lakh IU > then every 6months until completion of 5 years of age: 2lakh IU 2. Children who are diagnosed with measles should get two age appropriate doses 3. Children with severe anaemia, persistent diarrhoea, SAM should get 1 age appropriate dose 4. Encouraging consumption of Vitamin A rich diet 5. Fortification of commonly used local food items with vit A

17. HYPERVITAMINOSIS A A cute vitamin A toxicity Occurs from ingestion of 25000 IU/kg or more Clinical features: Nausea, vomiting, diarrhoea Altered sensorium Pseudotumor cerebri Skin changes: erythema, pruritis and desquamation Peeling of skin around mouth initially which spreads to rest of the body later.

18. VITAMIN D Also known as calciferol Is a prohormone Different forms: Natural sources: Ergocalciferol (D2) in plants Cholecalciferol (D3) in animals Present in our body: 25 hydroxy vitamin D or Calcidiol : storage and circulating form 1,25 hydroxy vitamin D or Calcitriol : biologically active form

19. Sources: Sunlight is the most important source: exposure of 40% of the body to one-forth of Minimal Erythma dose will produce 1000 IU of vitamin D ( i.e , about 30min exposure of face and arms between 11am to 2pm daily.) Dietary sources: tuna, salmon, fish liver oil, cheese, egg yolk and foods fortified with vitamin D like dairy products RDA: 400IU for infants and 600IU for children >1years of age

20. M ETABOLISM OF VITAMIN D

21. F UNCTIONS OF VITAMIN D Related to calcium, phosphate and bone metabolism: GIT & Kidney: increases absorption of calcium and phosphate Bone: promotes mineralization at low levels and facilitates parathormone action on bone at high levels On PTH: high calcitriol inhibits PTH and vice versa

22. Extra skeletal effects: Potent antioxidant Regulates cell proliferation and differentiation Mediates apoptosis in cancer cell lines Modulates T-cell responses and has anti-inflammatory action Suppresses renin production, hence preventing development of hypertension In children with CKD, suppresses proteinuria and retards disease progression Increases insulin secretion and decreases insulin resistance Is a potent inhibitor of keratinocytes so can be used for psoriasis

23. NUTRITIONAL RICKETS Vitamin D deficiency: In children causes rickets In adults causes osteomalacia There are other causes of rickets like calcium deficiency, phosphorous deficiency and renal disorders.

24. NUTRITIONAL RICKETS Stage 1: Deficiency of vitamin D Decreased intestinal absorption of calcium and phosphorous Parathyroid hormone secretion Upregulation of 1-alpha hydroxylase in kidney Increased calcitriol production

25. Stage 2: Serum calcium normalised but phosphorous remains low Rachitic changes become apparent in X-ray Stage 3: Calcitriol levels can no longer be maintained due to limited stores of 25- OH-vitamin D Florid clinical and radiographic pictures of rickets

26. Rachitic Rosary

27. Evaluation Serum levels of calcium maybe normal or low Serum phosphate will be low Serum alkaline phosphatase will be high Serum 25OHD3 is best indicator for vitamin D status: >20ng/ml- normal 10-20ng/ml- insufficient <10ng/ml- deficiency

28. Radiological findings: Thickening of the growth plate Cupping at the end of metaphysis Splaying: widening at the end of metaphysis Fraying at the end of metaphysis Severe deficiency leads to looser zones and pathological fractures

29. 5 year old boy showing rickets with mild frontal bossing, wide wrist and bow legs X-ray wrist: widening, cupping and fraying at the metaphyseal ends of forearm bones .

30. Treatment of Nutritional Rickets: Dosage Schedule for vit D administration: Daily regimen for 3months: 1000IU for preterm neonates 2000IU for term neonates and infants 2000-6000 IU for children >1year of age Weekly regimen for 6 weeks: 60000IU weekly for 6 weeks for infants beyond 3 months of age Stoss regimen- mega single dose, not used now

31. Calcium supplementation along with any of the above regimen: 175-200mg/kg/day for premature neonates 500mg/kg/day for infants 600-800mg/kg/day for children more than 1 year of age Maintenance RDA dose of Vit D should be given following any of the above regimen If seizures are present in neonates then calcium levels should be corrected using 2ml/kg of calcium gluconate in slow IV infusion and calcitriol in dose of 25-50ng/kg/day orally. Once the neonate is stable, oral Cholecalciferol (1000IU/day) is given for 3 months, alongside additional calcium as discussed above

32. Response to Treatment: With treatment, calcium and phosphorous level normalize within 6-10days First radiological sign of response is appearance of zone of provisional calcification, the healing line of rickets, occurs by 2 weeks of therapy By three months all radiological and biochemical changes go back to normal , though severe bony deformities may persist. If zone or provisional calcification cannot be seen by 6 weeks of treatment then the child should be considered a case of refractory rickets and evaluated for the same

33. Healing of growth plate after vitamin D therapy

34. Prevention of Nutritional Rickets All new-borns should be supplemented with 400IU of vitamin D starting from few days of life till one year of age Pregnant mothers should receive 600IU daily and should continue during lactation Additional vit D should be supplemented to children with malabsorption, liver and renal insufficiency.

35. Hypervitaminosis d Caused by accidental or intentional ingestion of extremely high dose of Vitamin D It can cause neuropsychiatric symptoms like: apathy, confusion, drowsiness, depression, psychosis and even coma Recurrent vomiting, polydipsia, anorexia, pancreatitis Hypertension, shortened QT interval, ST segment elevation, bradyarrhythmia with 1 st degree heart block Nephrocalcinosis, hearing loss, renal failure

36. Treatment IV hydration with NS @1.5-2.5 maintenance to increase GFR and calcium excretion Loop diuretics If no response then glucocorticoids, bisphosphonates, calcitonin and haemodialysis can be done.

37. Vitamin e Belongs to group of compounds called as the tocopherols Alpha tocopherol is the most potent compound and is the major form present in humans Functions as a potent antioxidant: scavenges free radicals to protect cell membranes and lipoproteins form oxidative damage It also modulates immune response Regulates signal transduction and gene response Inhibits platelet adhesion and aggregation

38. Dietary sources: vegetable oils, seeds, nuts, whole grains and green leafy vegetables Groups at risk of deficiency: Preterms SAM children Defective absorptive states Defective transport: ataxia with isolated vitamin E deficiency, autosomal recessive condition Children receiving aggressive iron therapy

39. AGE RDA (mg/day) 0-6 months 4 7 months to 3 years 5 4-8 years 6 >9 years girls 8 9-13 years boys 9 >13 years boys 10

40. Clinical Manifestation: Loss of DTR, decreased proprioception and vibratory sense Intentional tremor, nystagmus Retinitis pigmentosa, limitation of upward gaze, strabismus, visual field constriction Muscle weakness Dementia, behaviour disturbances In preterms presents as, hemolytic anaemia in 2 nd month of life along with thrombocytosis and oedema. It can even lead to intraventricular haemorrhage.

41. Diagnosis Best indicator: ratio of serum vitamin E and serum lipid of <0.6mg/g in infants and <o.8mg/g in older children and adults is diagnostic Peripheral smear may show acanthocytosis Treatment 15-20IU/ day can be given in cases of malabsorption and cholestasis Hypervitaminosis E May lead to necrosing enterocolitis in newborns .

42. Vitamin k Forms of vitamin K: Phylloquinone (K1): green leafy vegetables, plant oils and legumes Menaquinone (K2): produced by bacteria in large intestine Menadione (K3): synthetic form, water soluble Functions: Acts as co-factor in post translational carboxylation of glutamic acid to form gamma-carboxyglutamates in liver Activation of factor 2,7,9,10 and protein C and S

43. Dietary sources Spinach, lettuce, cabbage, broccoli, soya bean Groups at risk of deficiency Newborns Children taking long duration of broad spectrum antibiotics Fat malabsorptive state Prolonged diarrhoea

44. Clinical Manifestation In neonates and young infants there are three forms of Vitamin K deficiency bleeding (VKDB) also known as the haemorrhagic disease of the newborn .

45. Diagnosis Prolongation of prothrombin time more than 4times the normal value and also INR more than or equal to 4 according to age specific normal values with normal platelet and fibrinogen level

46. Treatment 1 dose of parenteral vitamin K, 1mg for infants and 2.5 – 10mg for young children and adolescents In life threatening VKDB, FFP is to be given in addition to parenteral Vit K In children with malabsorption, after the correction, regular vitamin K supplementation and periodic monitoring of PT to be done

47. Water Soluble Vitamins THIAMINE ( VIT B1) Daily Requirement: 0.4 mg/ 1000 k cal. Dietary Sources: unrefined or fortified cereal grains, enriched bakery products, organ meats (liver, kidney) and legumes. DEFICIENCY occurs in Severely malnourished states, during critical illness Malignancy and following surgery. Diet consisting largely of polished rice (oriental beriberi), In alcoholics In food faddists (occidental beriberi)

48. Thiamin deficiency leads to disease BERI-BERI. Three forms 1) In infants – Wet Beri-Beri ( Acute cardiac form) 2) Older infants and Children – Dry Beri-Beri (Chronic neurologic form) 3) Meningitic form. ACUTE CARDIAC FORM (Wet beri-beri ) - Infant may develop congestive cardiac failure in the form of Tachycardia , Dyspnea , Cyanosis, Hepatomegaly , Cardiomegaly , Pulmonary edema CLINICAL MANIFESTATIONS

49. CHRONIC NEUROLOGIC FORM ( D ry beri - beri) : May manifest with ataxia, anorexia, weight loss, weakness, diarrhea, constipation and edema. Child will be drowsy and apathetic and may present with peripheral neuritis and various palsies including vocal cord palsy Deep tendon reflexes are usually absent. MENINGITIC FORM : Bulging anterior fontanel, dilated pupils, head retraction ,convulsions and coma. WERNICKE ENCEPHALOPATHY : classic clinical triad of mental retardation, occular changes and ataxia(occurs in chronic alcoholics)

50. DIAGNOSIS The biochemical diagnostic criteria of thiamine deficiency consist of low erythrocyte transketolase activity and high thiamine pyrophosphate effect (normal range: 0-14%). Urinary excretion of thiamine or its metabolites ( thiazole or pyrimidine ) after an oral loading dose of thiamine may also be measured

51. Children with cardiac failure, convulsions, or coma should be given 10 mg of thiamine i.m or i.v daily for the 1st wk followed by 3-5 mg of thiamine per day orally for at least 6 wk. The response dramatic in infants and in those having predominantly cardiovascular manifestations, whereas the neurologic response is slow and often incomplete. PREVENTION: parboiling of rice TREATMENT

52. RIBOFLAVIN (Vit B2) : DAILY REQUIREMENT : 0.6 mg/ 1000 k cal DIETARY SOURCES : It is found in both animal and vegetable foods such as meat, beans, yeast, green leafy vegetables, cereals, legumes, groundnut and milk

53. Cheilosis . glossitis Keratitis , conjunctivitis photophobia lacrimation , corneal vascularization seborrheic dermatitis Normochromic , normocytic anemia CLINICAL FEATURES

54. DIAGNOSIS: 1. Urinay excretion of riboflavin less than 30 μg/24 hrs. 2. Increased erythrocyte glutathione reductase activity after the addition of flavin adenine dinucleotide (FAD). TREATMENT Therapy consists in administering riboflavin, 3 to 10mg orally or 2 mg intramuscularly daily for a few days. This should be followed by 10 mg orally daily for about three weeks.

55. NICOTINIC ACID ( VIT B3 ) DAILY REQUIREMENT : 6.6 mg/1000kcal. DIETARY SOURCES: Endogenously – from Tryptophan Natural Foods- milk,liver , pork, cheese, yeast, cereals, etc

56. CLINICAL FEATURES: The disease, PELLAGRA , usually occurs in school going children. Disease of 4 D’s Dermatosis,Diarrhea,Dementia,Death The characteristic lesions are seen over the exposed areas of the skin, such as limbs, neck, (“ Casal necklace”, pellagra glove, pellagra boot) and cheeks. Lesions are symmetrical, of desquamating pigmentary dermatitis type and are aggravated by sunlight.

57. CASAL NECKLACE

58. TREATMENT : Nicotinamide , 50 - 300 mg daily in divided doses orally, given for two weeks followed by adequate supply of B-complex vitamins in diet brings about complete recovery.

59. PANTHOTHENIC ACID( VIT B5) DAILY REQUIREMENT : Infants - 1.5 – 5 mg Children- 5 – 8 mg Adults - 10 mg DIETARY SOURCES : Germinated wheat , liver ,dried yeast , egg yolk , fish DEFICIENCY : Burning feet syndrome, GI upset , Insomnia, Headache and muscle cramps, hair loss, seborrhea, premature graying of hair , obesity , multiple sclerosis.

60. BIOTIN DAILY REQUIREMENTS : 0.15 mg . DIETARY SOURCES : Meat (especially liver), egg, milk and yeast extract. MC cause of deficiency is consumption of raw eggs.( The avidin in egg white binds to biotin and hinders biotin absorption.)

61. DEFICIENCY Clinical features: Anorexia,vomiting,pre -mature hair fall, hyperkeratotic skin, glossitis , muscle pains, hyperesthesia, anemia, hyperlipidemia and rarely dysmorphism in maternal deficiency. TREATMENT Mild Deficiency – 2-5 mg/d / po / 2-3 weeks Severe deficiency- 200 microgms /d parenterally 2-5 days.

62. PYRIDOXINE( VIT B6) DAILY REQUIREMENT: 1-1.5 mg DIETARY SOURCES : - Liver, egg yolk, meat, wheat, soyabeans , yeast, peas, pulses and cereals. Small quantity in most vegetables and milk. FUNCTIONS : Plays vital role in metabolism of proteins and fatty acids. Claimed to have role in blood formation Proper functioning of Nervous system.

63. DEFICIENCY ETIOLOGY : Pyridoxine deficiency of nutritional origin is rare in childhood. But deficiency risk increases in prolonged isoniazid or cycloserine therapy in tuberculosis. Penicilamine therapy in Wilson disease. Use of contraceptives. Pyridoxine –Responsive Convulsions and Anemia have been described Pyridoxine –Dependent inborn errors of metabolism Eg - Homocystinuria,hyperoxaluria,xanthurenic aciduria etc.

64. CLINICAL FEATURES : Convulsions refractory to usual therapy. Microcytic - hypochromic anemia refractory to iron therapy. Growth retardation. GI symptoms like diarrhea. Seborrheic dermatitis around nose and eyes. Sensory neuropathy( uncommon in children). Cheliosis and glossitis (infrequent in childhood).

65. TREATMENT In infant with Vit B6 deficiency or dependent seizures and refractory anemia, should receive 50 to 100 mg of pyridoxine intravenously. The confirmation of deficiency may be done by the tryptophan loading test. Administration of 5 mg of pyridoxine intramuscularly followed by 0.5 mg daily orally for two weeks causes complete recovery in B6 deficiency

66. FOLIC ACID Dietary requirements – infancy- 40 µg Children- 100 µg DIETARY SOURCES : meat ( liver,kidney ), egg,yeast,green leafy vegetables(spinach, cabbage, turnipgreens ), asparagus, mushrooms, beans,peas , sunflower seeds, whole grains. FUNCTIONS : Essential for maturation of RBCs Assists in protecting DNA and ensuring its replication when under attack by free radicals.

67. CLINICAL FEATURES : Megaloblastic anemia Neural tube defects, Cleft lip / palate Nonhematologic manifestations include glossitis , listlessness, and growth retardation

68. TREATMENT 0.5-1 mg of folic acid daily PREVENTION : For prevention of NTDs, periconceptional folic acid therapy one month before and 2-3 months after conception. Primary prevention:0.4 mg Secondary prevention:4 mg

69. VITAMIN B12 Also known as Extrinsic Factor of Castle. DAILY REQUIREMENT : Infants - 0.3µg. Children-1 µg. Adolescents- 1.5-2 µg. DIETARY SOURCES: Animal origin foods such as meat, fish, eggs , fresh milk and cheese milk powders.

70. DEFICIENCY ETIOLOGY : Strict vegetarianism Deficiency of Intrinsic factor(Pernicious anemia) Malabsorption syndrome Infantile tremor syndrome Drugs like Neomycin, Colchicine ,Para amino salicylic acid(PAS).

71. CLINICAL FEATURES : Megaloblastic anemia Pallor with Pigmentation Smooth,red and painful tongue Neurological manifestations Ataxia Paresthesias Hyporeflexia Tremors Peripheral neuropathy Sub Acute Combined Degeneration Depression.

72. DIAGNOSIS Macrocytic/ Megaloblastic erythropoiesis. Serum B12 < 100µg/ml with increased serum LDH Methyl malonic aciduria is a sensitive and reliable index Schilling test. TREATMENT : For Megaloblastic anemia – Vit B12 1 mg(1000µg) IM leads to prompt hematological response in 2-4 days. For Neurologic involvement -1 mg IM dose daily 2 weeks followed by monthly maintenance dose 1 mg IM throughout life.

73. VITAMIN C(Ascorbic Acid) DAILY REQUIREMENT : Infants and Children-30-40 mg Pregnancy and Lactation – 60 mg. DIETARY SOURCES: Citrus fruit- Indiangooseberry ( amla ), guava,lemon,orange,grapes,green leafy vegetables,soaked cereals.

74. FUNCTIONS : Play important role in oxidation of tyrosine and phenylalanine Formation of hydroxyproline, Preventing depolymerization of collagen Maintaining integrity of ground substance, In hemopoiesis.

75. CLINICAL FEATURES : Infant lowers limbs adopt FROG – POSITION due to pseudo paralysis and palpable subperiosteal hemorrahges prevent further movement of legs. Hemorrhages in skin and corkscrew hair can be seen. Hemorrhages into mucus membranes, gums,conjunctiva and intestinal tract Follicular hemorrhages with development of minute hemorhages at root of hair follicles Anorexia, diarrhoea, pallor, irritability, increased susceptibility to infections and delayed wound healing

76. DIAGNOSIS Ascorbic acid level in serum, white cells or buffy coat, i.e. platelet layer, is usually less than 0.1 mg%. Excretion of ascorbic acid in urine below 1.5 mg after a loading dose of 20 mg/kg by intravenous route 4 hours earlier. X RAY changes

77. TREATMENT It consists in giving a loading dose of 500 mg of vitC followed by a daily dose of 100 to 300 mg for several weeks orally Clinical response occurs rapidly—within 24 to 48 hrs. Improvement in the radiological picture takes a week or two. Subperiosteal hemorrhages are likely to take months to disappear.

78. CALCIUM 99% of body calcium-found in bones and teeth. 1% is involved in clotting cascade, nerve conduction, muscle stimulation, vitamin D metabolism and parathyroid function. Its metabolism is regulated by vitamin D, calcitonin and parathyroid hormone In order that calcium performs its function well, adequate magnesium, phosphorus and vitamin A, C, D and E should be available in the body. Sources-milk and its products, millets and fruits Daily requirement :500-1000mg/day.

79. CALCIUM DEFICIENCY Clinical Features 1. Tetany , Muscle cramps, numbness, tingling 2. Impaired growth 3. Calcium-deficiency rickets 4. Osteoporosis 5. Nonspecific: Arthralgia , palpitations

80. HYPERCALCEMIA Anorexia, irritability, constipation, nausea, vomiting, soft-tissue swellings and neuropsychiatric symptoms. It may result from Vitamin D excess, milk alkali syndrome, prolonged immobilization, hyper parathyroidsm , etc Idiopathic hypercalcemia ( William syndrome ) is characterized by elfin facies and supravalvular aortic stenosis

81. MAGNESIUM DEFICIENCY Next to potassium, it is the most abundant mineral cation in cells. Sources : plant foods and meat. Requirements are: • First 6 months 40 mg/day • Second 6 months 60 mg/day • Later 200-300 mg/day Clinical Features 1. Irritabilty 2. Tetany 3. Increased or decreased reflexes

82. TREATMENT Mild: oral magnesium 6mg tablet; 2-3 times daily Severe: oral magnesium 12 mg 3-4times daily Acute severe hypomagnesemia : IV infusion of MgSO4 (50% solution), 25-50mg/kg slowly 6 hourly, 2-3 doses In renal insufficiency, dose needs to be reduced Toxicity /excess cause respiratory depression, drowsiness and coma. Antidote is calcium

83. IRON Human body contains just 3-4g iron; 75% in hemoglobin, 20% in stores and 5% in myoglobin Storage as ferritin and hemosiderin is in bone marrow, liver and spleen. Functions : hemoglobin formation, normal growth and maintenance of normal immune function and in brain development.

84. DIETARY SOURCES OF IRON Green leafy vegetables (amaranth richest around 30mg/100g), pulses, beans, dried fruits, nuts, cereals, molasses, meat, eggyolk and fish Milk is poor source of iron , providing just 0.2mg/ dL Daily requirements (10-20mg/day) Preterm and LBW infants require 1.5-2 mg/kg for the whole first year

85. IRON DEFICIENCY Major nutritional problem Iron deficiency anemia (IDA) with overt manifestaitons such as pallor, poor growth and development, reduced learning capacity, cognitive function and work capacity. Preterm and LBW are at high risk of developing iron deficiency since iron requirement is enhanced on account of rapid postnatal growth.

86. Iodine Functions: synthesis of thyroid hormones which eventually influence the physical and mental growth and development Regulation of metabolism of nutrients of the body,functioning of nerves and muscles Sources : water, iodized salt, seafoods , fish Daily requirements : 90-150 mg/day depending on age Less than 6 year: 90 mg 6-12 years: 120mg 12 years : 150mg Excess: goiter, iodism ptyalism , coryza , forntal headache, emaciation, and skin eruptions

87. IODINE DEFICIENCY DISORDER (IDD) Enlargement of the thyroid gland as a result of iodine deficiency is endemic in sub-Himalayan belt Intrauterine life : abortion, still birth, congenital defects, perinatal mortality; congenital hypothyroidism (cretinism) Newborns: mental retardation, goiter and neonatal hypothyroidism Infants, children and adolescents: goiter, growth retardation , poor cognition and subclinical hypothyroidism

88. PREVENTION OF IDD Usage of iodized salt (common salt fortified with sodium or potassium iodate in a ratio of 1 in 40,000) or iodized oil capsules at 6-10months interval, iodized oil given as an intramuscular injection once in three years, lugols iodine periodically and iodization of water supply. Double fortified salts iodine plus iron are also available

89. ZINC Next to iron, zinc is the most abundant trace element in the human body Its concentration in hair is deemed to reflect the zinc status of a subject. It is also present in erythrocytes, prostate, eye, bone and endocrine glands. Dietary sources : meat,liver , fish, nuts, grains, dry beans and legumes Daily requirements :5-15 mg/day 1-2mg/kg in preterm infants

90. FUNCTIONS OF ZINC Zinc is a component of over 100 metalloenzymes and participates in many biological processes. zinc regulates gene transcription and participates in nucleic acid metabolism, protein synthesis and thereby, cellular growth. Thymidine kinase , DNA polymerase and RNA polymerase are zinc dependent enzymes. Zinc deficiency may occur in PEM, malabsorption,prolonged parenteral nutrition,consumption of fibres and phytates in excess hampers zinc absorption.

91. Oral administration of Zn in diarrhoea acts by Early regeneration of brush border enzymes leading to increased absorption of water and electrolytes Inhibition of basolateral potassium channels Improved immune response Zinc is required for brain development, intelligence, normal functioning of growth hormone Also found to be helpful in treatment of ADHD, PEM, Wilson disease

92. ZINC DEFICIENCY Gastrointestinal manifestations : protracted diarrhea, delayed wound healing, anorexia, failure to thrive, pica, impaired taste perception ( hypogeusia ) Dermatological manifestations : hyperkeratotic skin Acrodermatitis enteropathica Infantile tremor syndrome (ITS) In pre-school and school-age children: growth retardation, delayed sexual maturation, hypogonadism , anemia and hepatospleenomegaly .

93. Diagnosis of zinc deficiency plasma zinc level of below 70mcg/ dL or hair zinc level of below 70mcg/g dry weight

94. TREATMENT Zinc sulfate : 0.2 – 1 mg elemental zinc or 1-5mg of the salt/kg/day orally In very severe deficiency states, as high dose as 20-40 mg/day of elemental zinc may be given In all infants and children with diarrhea, zinc supplementation is given for 14 days. 10mg daily-< 6months 20mg daily ->6 months Zinc excess: may cause copper deficiency if given for longer periods.

95. COPPER Copper- also called the “iron twin”, It is distributed in all tissues of body, including kidney, liver, brain, heart, bone marrow and bones. copper stores of an infant are sufficient for the first six months of life. In the liver, copper is incorporated into a protein complex, “ ceruloplasmin ”. Daily requirement 1-2mg. In preterm infants 30mcg is enough for maintian normal growth though some recommend 120-150mcg

96. CLINICAL FEATURES OF COPPER DEFICIENCY Failure to thrive Anemia ( microcytic-hypochromic that is refractory to iron therapy) neutropenia , vascular abnormalities Hypopigmental hair and skin Osteoporosis, metaphyseal fraying and fractures Deficient immune function. Excess of copper , usually genetic in origin, is associated with: – Wilson disease – Menke’s kinky hair disease – Indian childhood cirrhosis.

97. KAYSER FLEISCHER RING MENKE KINKY HAIR DISEASE

98. SELENIUM Selenium is an integral part of glutathione peroxidase and is linked to vitamin E and is an important antioxidant , it protects cells and membrane against oxidative damage. Selenium and Vitamin C both antioxidants are known to spare each other. Selenium is found in soil, over cultiavation leads to depletiion of selenium content in the crops Cardioprotective as well as liver protective

99. SELENIUM Dietary sources : meat, cheese, milk ; cashew nuts, brazilnuts ; grains,sunflower seeds, garlic and onion Daily requirement: children : 20-30mcg Selenium excess causes dental caries, alopecia and garlic odor in breath Etiology : malnutriton , TPN, low soil content Clinical features : growth retardation, myalgia , myopathy , cardiomyopathy and liver necrosis

100. ENDEMIC DCM/ KESHAN DISEASE It is a preventable cardiomyopathy , but once DCM sets in, total reversal to normality is not possible even with selenium supplementation.

101. FLUORINE Mainly a component of bone and teeth where in it is found as calcium and salt Only upto 1 ppm in drinking water is desirable; more than 2 ppm in water may cause fluorosis Function : protection of dental enamel and inhibition of dental caries,Calcification of bones Antibacterial against streptococcus mutans , known for causing dental decay Dietary sources: drinking water, seafoods (fish), cheese and tea

102. Daily requirement : children: 0.7-1mg/day, Adolescents : 2-3mg/day Deficiency : dental caries manifesting as loss of luster of enamel, yellow brownish staining and even pitting Excess: fluorosis, both dental (chalky white mottled with brownish staining) and skeletal (fluorine deposits in vertebral column, spine, pelvis, lower limbs; eventually neurologic signs and symptoms, deformities and crippling develop

103. CHROMIUM Important role in glucose tolerance and in facilitating insulin action Daily requirement : 10-70mg/day Deficiency : malnutrition and TPN Clinical features: hyperglycemia, glycosuria , peripheral neuritis, poor glucose tolerance complicating malnutrition and total parenteral nutrition and neuropathy. Excess : dermatitis and renal failure

104. MANGANESE Enzyme cofactor in superoxide dismutase, oxidative phosphorylation and bone mineralization Daily requirement : 1-5 mg Deficiency: growth retardation, weight loss, red hair, hypercholesterolemia, increased prothrombin time. Deficiency usually associated with PEM, TPN. Excess: cholestasis , encephalopathy, basal ganglia disorder, goiter and cardiomyopathy

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