vitamin a presentation, vitamin a deficiency, vitamin a toxicity
DESCRIPTION
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 deficiencyTRANSCRIPT
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
Sources
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)
2. 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 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%
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 > 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
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)
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 toxicityshort-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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