Vitamin a presentation, Vitamin A Deficiency, Vitamin A toxicity

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Information about Vitamin a presentation, Vitamin A Deficiency, Vitamin A toxicity
Health & Medicine

Published on January 15, 2014

Author: dhruvendrapandey98



This presentation contains Importance of vitamin A, Sources of Vitamin A, Absorption,Transport and Excretion of Vitamin A, Vitamin A Deficiency, Vitamin A Toxicity, Required dose of Vitamin A, Nutrition, Nutrition deficiency

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.

VITAMIN A • Exits in 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


Absorption • 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

• 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 .

Transport • 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

STORAGE • The liver has 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.

Excretion of Vitamin A • Not readily excreted • Some lost in urine • Kidney disease and aging increase risk of toxicity because excretion is impaired

Functions of vitamin A • Vision (night, day, colour) • Epithelial cell integrity against infections • Immune response • Haematopoiesis • Skeletal growth • Fertility (male and female) • Embryogenesis

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

Functions of Vitamin A: Immunity • Deficiency leads to decreased resistance to infections • Supplementation may decrease severity of infections in deficient person

Functions of Vitamin A: 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.

Vision Cycle

The Visual Cycle

• Role in Prevention 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

Recommended daily allowances (RDAs) for Vitamin A

Units of measuring vitamin 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

Deficiency of Vitamin A

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

• Usually, Vitamin A 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

Health consequences • Xerophthalmia is 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

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

Night Blindness • Lack of 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.

Night blindness

Bitot’s Spot • These are 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.

Conjunctival Xerosis • Conjunctiva becomes dry and non wettable. • Instead of looking smooth shiny it appears muddy &wrinkled.

Keratomalacia • One of the major cause for blindness in India. • Cornea becomes soft and may burst • The process is rapid • If the eye collapses vision is lost.

Other Symptoms of VAD • Alteration of skin and mucous membrane • Hepatic dysfunction • Headache • Drowsiness • Peeling of skin about the mouth and elsewhere

Follicular hyperkeratosis

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) 1. biochemically determined concentrations of retinol in plasma or serum

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.

Criteria for assessing the 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%

Universal vitamin A distribution 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

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

Upper Level for Vitamin A • 3000 μg retinol • Hypervitaminosis A results from longterm supplement use (2 – 4 x RDA) • Toxicity • Fatal dose (12 g)

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)

Toxicity of Vitamin A Acute toxicity short-term megadose (100 x RDA); symptoms disappear when intake stops •GI effects •Headaches •Blurred vision •Poor muscle coordination

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

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

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

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