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Vitamin a presentation, Vitamin A Deficiency, Vitamin A toxicity
Vitamin A deficiency (VAD) is a significant nutritional issue in low-income countries, critically affecting vision, immunity, and overall health. Symptoms of VAD include night blindness and various forms of xerophthalmia, which can lead to blindness in children. Effective management involves supplementation and monitoring, particularly among high-risk groups such as infants and pregnant women.
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Vitamin a presentation, Vitamin A Deficiency, Vitamin A toxicity
- 2. Introduction • Vitamin Adeficiency (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. VITAMIN A • Exitsin 3 forms: • all trans-retinol • long chain fatty acyl ester of retinol (main storage form) • retinal (the active form in the retina) • Retinoic acid is also considered to be physiologically active • Pro vitamin A or carotene can be converted to retinol in vivo
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- 6. Absorption • Retinoids • Retinylesters 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
- 7. • Approximately 80%is absorbed. • It is passed along with fat through the lymphatic system into blood stream. • Absorption is poor in case of diarrhea, jaundice and abdominal disorder. • Absorption increases if taken with fat. • Vitamin A which is not absorbed is excreted within 1 or 2 days in feces .
- 8. Transport • Transported viachylomicrons from intestinal cells to the liver • Transported from the liver to target tissue as retinol via retinol-binding protein, which is bound to transthyretin
- 9. STORAGE • The liverhas enormous capacity to store in the form of retinolpalmitate. • under normal conditions a well-fed person has sufficient Vitamin A reserves to meet his need for 6 to 9months or more.
- 10. Excretion of VitaminA • Not readily excreted • Some lost in urine • Kidney disease and aging increase risk of toxicity because excretion is impaired
- 11. Functions of vitaminA • Vision (night, day, colour) • Epithelial cell integrity against infections • Immune response • Haematopoiesis • Skeletal growth • Fertility (male and female) • Embryogenesis
- 12. Functions of VitaminA: 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
- 15. Functions of VitaminA: Immunity • Deficiency leads to decreased resistance to infections • Supplementation may decrease severity of infections in deficient person
- 16. Functions of VitaminA: Vision • Retinal is a necessary structural component of rhodopsin or visual purple, the light sensitive pigment within rod and cone cells of the retina. • If inadequate quantities of vitamin A are present, vision is impaired.
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- 19. • Role inPrevention of cardiovascular disease • Antioxidant capabilities • ≥5 servings/day of fruits and vegetables • Role in Cancer prevention • Antioxidant capabilities • Lung, oral, and prostate cancers • Studies indicate that vitamin A-containing foods are more protective than supplements • Other Roles in • • • • Age-related macular degeneration Cataracts Acne AML
- 21. Recommended daily allowances (RDAs)for Vitamin A
- 22. Units of measuringvitamin A Each μg RAE corresponds to • 1 μg retinol, • 2 μg of β-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
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- 24. High risk group • • • • • • • • • • • Infancy Childhood Pregnancy Lactation Urbanpoor Older adults Alcoholism Liver disease (limits storage) Fat malabsorption Increased excretion as in cancer & UTI Low protein intake resulting in deficient carriers
- 25. • Usually, VitaminA Deficiency (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
- 26. Health consequences • Xerophthalmiais the most specific VAD, 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
- 27. Classification of xerophthalmia •XN Night blindness • X1A Conjunctival Xerosis • X1B Bitot’s spot • X2 Corneal Xerosis • X3A Corneal ulceration/keratomalacia (< 1/3 corneal surface) • X3B Corneal ulceration/keratomalacia (≥ 1/3 corneal surface) • XS Corneal scar • XF Xerophthalmic fundus
- 28. Night Blindness • Lackof vitamin A causes night blindness or inability to see in dim light. • night blindness occurs as a result of inadequate pigment in the retina. • It also called tunnel vision. • Night blindness is also found in pregnant women in some instances, especially during the last trimester of pregnancy when the vitamin A needs are increased.
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- 30. Bitot’s Spot • Theseare foamy and whitish cheese-like tissue spots that develop around the eye ball, causing severe dryness in the eyes. • These spots do not affect eye sight in the day light.
- 31. Conjunctival Xerosis • Conjunctivabecomes dry and non wettable. • Instead of looking smooth shiny it appears muddy &wrinkled.
- 32. Keratomalacia • One ofthe major cause for blindness in India. • Cornea becomes soft and may burst • The process is rapid • If the eye collapses vision is lost.
- 33. Other Symptoms ofVAD • Alteration of skin and mucous membrane • Hepatic dysfunction • Headache • Drowsiness • Peeling of skin about the mouth and elsewhere
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- 35. Assessing vitamin Astatus 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) 1. biochemically determined concentrations of retinol in plasma or serum
- 36. 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.
- 37. Criteria for assessingthe public health 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%
- 38. Universal vitamin Adistribution schedule for preschool and lactating mothers • Children 1–6 years 200,000 IU of vitamin A orally every 3–6 months. • Infants 6–11 months 100,000 IU of vitamin A orally every 3–6 months. • Lactating mothers 200,000 IU of vitamin A orally once at delivery or during the first 8 weeks postpartum if breastfeeding or during the first 6 weeks if not breast-feeding
- 39. Recommended Xerophthalmia treatment schedule 6-12 months • Immediately 100,000 IU • Next day 100,000 IU • 2–4 weeks later 100,000 IU > 1 yr 200,000 IU 200,000 lU 200,000 IU • Severe Protein-Energy Malnutrition (PEM) Monthly until PEM resolves 100,000 IU 200,000 IU [email protected]
- 40. Upper Level forVitamin A • 3000 μg retinol • Hypervitaminosis A results from longterm supplement use (2 – 4 x RDA) • Toxicity • Fatal dose (12 g) [email protected]
- 41. 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 [email protected] IU/dl (N: 50-100 IU/dl)
- 42. Toxicity of VitaminA Acute toxicity short-term megadose (100 x RDA); symptoms disappear when intake stops •GI effects •Headaches •Blurred vision •Poor muscle coordination [email protected]
- 43. 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 [email protected]
- 44. Chronic Toxicity ofVitamin 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 [email protected]
- 45. Toxicity of VitaminA • 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 [email protected]
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