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    Add as FriendVitamin a deficiency HYPERVITAMINOSIS A

    by: pankaj

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    2 : Introduction Vitamin A deficiency (VAD) is a major nutritional concern in poor societies, especially in lower income countries like INDIA. Vitamin A is an essential nutrient needed in small amounts for the normal functioning of the visual system, and maintenance of cell function for growth, epithelial integrity, red blood cell production, immunity and reproduction.
    3 : Active forms are retinol, retinaldehyde, and retinoic acid Plants synthesize the more complex carotenoids which are cleaved to retinol by most animals and stored in the liver as retinyl palmitate N retinol plasma values: 15-30 mcg/dl in infants & 30-90 mcg/dl in adults Retinal is the prosthetic group of photosensitive pigment in both rods (rhodopsin) & cones (iodopsin), major difference lies in the nature of protein bound Needed in lysosomal membrane stability Plays a role in keratinization, cornification, bone development & cell growth & reproduction
    4 : Absorption of Vitamin A Retinoids Retinyl esters broken down to free retinol in small intestine - requires bile, digestive enzymes, integration into micelles Once absorbed, retinyl esters reformed in intestinal cells 90% of retinoids can be absorbed Carotenoids Absorbed intact, absorption rate much lower Intestinal cells can convert carotenoids to retinoids
    5 : Transport and Storage of Vitamin A Liver stores 90% of vitamin A in the body Reserve is adequate for several months Transported via chylomicrons from intestinal cells to the liver Transported from the liver to target tissue as retinol via retinol-binding protein, which is bound to transthyretin
    6 : Excretion of Vitamin A Not readily excreted Some lost in urine Kidney disease and aging increase risk of toxicity because excretion is impaired
    7 : Functions of vitamin A Vision (night, day, colour) Epithelial cell integrity against infections Immune response Haematopoiesis Skeletal growth Fertility (male and female) Embryogenesis
    8 : Functions of Vitamin A: Growth and Differentiation of Cells Retinoic acid is necessary for cellular differentiation Important for embryo development, gene expression Retinoic acid influences production, structure, and function of epithelial cells that line the outside (skin) and external passages (mucus forming cells) within the body
    9 : Functions of Vitamin A: Immunity Deficiency leads to decreased resistance to infections Supplementation may decrease severity of infections in deficient person
    10 : The Visual Cycle
    11 : Prevention of cardiovascular disease Antioxidant capabilities =5 servings/day of fruits and vegetables Cancer prevention Antioxidant capabilities Lung, oral, and prostate cancers Studies indicate that vitamin A-containing foods are more protective than supplements Age-related macular degeneration Cataracts Acne AML
    12 : Source of vitamin A Colostrum foods containing either preformed vitamin A esters - liver, milk,cheese,eggs or food products fortified with vitamin A or carotenoid precursors (mainly beta-carotene), such as green leaves, carrots, ripe mangoes,eggs, and other orange-yellow vegetables and fruits.
    13 : Source of vitamin A fruit carotenoid sources(micrograms/100gm) Mango (golden) 307 Papaya (solo) 124 Cucurbita (mature pulp) 862 Buriti palm (pulp) 3,000 Red palm oil 30,000 Carrot 2,000 Dark green leafy vegetables 685 Tomato 100 Apricot 250 Sweet potato, red and yellow 670 Animal (micrograms/100gm) Fatty fish liver oils Halibut 900,000 Cod 18,000 Shark 180,000 Dairy produce Butter 830 Margarine, vitaminized 900 Eggs 140 Milk 40 Cheese, fatty type 320 Liver of sheep and ox 15,000 Beef, mutton, pork 0–4
    14 : Vitamin A requirement
    15 : Units of measuring vitamin A Each µg RAE corresponds to 1 µg retinol, 2 µg of ß-carotene in oil, 12 µg of "dietary" beta-carotene, One International Unit (I.U.)  = 0.3 mcg. of retinol   = 0.6 mcg. of beta-carotene   = 1.2 mcg. of other total mixed carotenoids
    16 : Prevalence of vitamin A deficiency in South Asia (%) Country sub clinical clinical VAD (%) VAD (%) Afghanistan 53 - Bangladesh 28 0.7 Bhutan 32 0.7 INDIA 57 0.7 Nepal 33 1 Pakistan 35
    17 : High risk group Infancy Childhood Pregnancy Lactation Urban poor Older adults Alcoholism Liver disease (limits storage) Fat malabsorption Increased excretion as in cancer & UTI Low protein intake resulting in deficient carriers
    18 : Usually, VAD develops in an environment of ecological social and economical deprivation Synergism between deficient dietary intake of vitamin A coexists with severe infections, such as measles, and frequent infections causing diarrhoea and respiratory diseases that can lower intake through depressed appetite and absorption, and deplete body stores of vitamin A through excessive metabolism and excretion
    19 : Health consequences Xerophthalmia is the most specific VADD,and is the leading preventable cause of blindness in children throughout the world Night blindness Anaemia can result from VAD in children and women,likely due to multiple apparent roles of vitamin A in supporting iron mobilization and transport, and hematopoiesis
    21 : Assessing vitamin A status and deficiency Two sets of indicators of VAD are commonly used for population surveys: 1 clinically assessed eye signs. Term xerophthalmia encompasses the clinical spectrum of ocular manifestations of VAD, from milder stages of night blindness and Bitot’s spots, to potentially blinding stages of corneal xerosis, ulceration and necrosis (keratomalacia) 2 biochemically determined concentrations of retinol in plasma or serum
    22 : Classification of xerophthalmia XNN ight blindness X1A Conjunctival xerosis X1BB itot’s spot X2 Corneal xerosis X3A Corneal ulceration/keratomalacia (< 1/3 corneal surface) X3BCorneal ulceration/keratomalacia (= 1/3 corneal surface) XSCorneal scar XFXerophthalmic fundus
    23 : Serum retinol concentrations serum retinol concentrations in a population constitutes the second major approach to assessing vitamin A status in a population, with values below a cut-off of 0.70 µmol/l representing VAD , and below 0.35 µmol/l representing severe VAD. a serum retinol concentration below a cutoff of 1.05 µmol/l has been proposed to reflect low vitamin.
    24 : Criteria for assessing the publichealth significance of xerophthalmia Clinical (primary) Night blindness (XN)* 1.0% Bitot’s spot (X1B) 0.5% Corneal xerosis and/or ulceration/keratomalacia (X2 + X3A + X3B) 0.01% Xerophthalmia-related corneal scars (XS) 0.05% Biochemical (supportive) Serum retinol (vitaminA) < 0.35 µmol/L (10 µg/dL) 5.0%
    25 : Universal vitamin A distribution schedule for preschool and lactating mothers Children 1–6 years 200,000 IU of vitaminA orally every 3–6 months. Infants 6–11 months 100,000 IU of vitaminA orally every 3–6 months. Lactating mothers 200,000 IU of vitaminA orally once: at delivery or during the first 8 weeks postpartum if breastfeeding or during the first 6 weeks if not breast-feeding
    26 : Recommended xerophthalmia treatment schedule 6 -12 months > 1 yr Immediately 100,000 IU 200,000 IU Next day 100,000 IU 200,000 lU 2–4 weeks later 100,000 IU 200,000 IU Severe Protein-Energy Malnutrition (PEM) Monthly until PEM resolves 100,000 IU 200,000 IU
    27 : Upper Level for Vitamin A 3000 µg retinol Hypervitaminosis A results from long-term supplement use (2 – 4 x RDA) Toxicity Fatal dose (12 g)
    28 : Hypervitaminosis A Acute Intoxication: Results when excessively large single doses >300,000 IU ingested Infants: n/v, drowsiness or irritability w/signs of increased ICP Adults: drowsiness, irritability, headache & vomiting Serum vitamin A values = 200-1000 IU/dl (N: 50-100 IU/dl)
    29 : Toxicity of Vitamin A Acute – short-term megadose (100 x RDA); symptoms disappear when intake stops GI effects Headaches Blurred vision Poor muscle coordination
    30 : Chronic Intoxication Results when >50,000 IU/day ingested for several wks or more Signs & symptoms in infants: Early are anorexia, pruritus, irritability, tender swollen bones w/motion limitation Alopecia, seborrhea, cheilosis & peeling of palms & soles Hepatomegaly & hypercalcemia observed Craniotabes & hyperostosis of long bones Elevated serum vit A levels confirms diagnosis Reversible manifestations when vitamin A discontinued
    31 : Chronic Toxicity of Vitamin A long-term megadose; possible permanent damage Bone and muscle pain Loss of appetite Skin disorders Headache Dry skin Hair loss Increased liver size Vomiting
    32 : Toxicity of Vitamin A Teratogenic (may occur with as little as 3 x RDA of preformed vitamin A) Tends to produce physical defect on developing fetus as a result of excess vitamin A intake Spontaneous abortion Birth defects
    33 : thanks

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