Vitamins -Water soluble -Fat soluble Vitamin A -fat-soluble vitamin ingested in the diet in two forms. -as retinol itself from animal sources or -as provitamin carotene from plant sources

1. VITAMIN A
Hamisi Mkindi,MD5,SFUCHAS,2014
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2. INTRODUCTION
• Vitamins
-Water soluble
-Fat soluble
• Vitamin A
-fat-soluble vitamin ingested in the diet in
two forms.
-as retinol itself from animal sources or
-as provitamin carotene from plant sources
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3. Vitamin A deficiency(XEROPTHALMIA)
• literally means (xeros= dry ; ophthalmos = eye)
dryness of the eye
• Most important cause of blindness in children in
the world.
• Important factor in the cause of stunting which is
more prevalent than malnutrition.
• Important cause of ocular morbidity among
patients with chronic liver disease and lipid
malabsorption, and is a major cause of blindness
in developing countries
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4. Prevalence
• Global
• Africa
• Tanzania
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5. Vitamin A: Retinol
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6. Vitamin A
• main molecular structure contains a cyclic part
and a non-cyclic chain with 5 double bonds in
the all-trans position.
• A functional group is found at the end of the
non-cyclic part which can be an alcohol
(retinol), an aldehyde (reninaldehyde), a
palmitate (retinolpalmitate)
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7. Physiology
• Vitamin A intestinal mucosal cells,
carotene is converted to retinol and, along with
the directly ingested retinol, is esterified to
palmitic acid.
• Retinyl palmitate Liver(stored).
• In requirement for vitamin A, retinyl palmitate is
hydrolyzed, and the reconstituted retinol travels
via the blood stream, attached to retinol-binding
protein (RBP), to the tissue where it is needed.
Lymphatic
system
Absorbed
from SI
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8. Physiology cont
• Adequate body stores of zinc and protein are
necessary for the formation of RBP.
• Eye:vitamin A has a pivotal role in the
functioning of the retina and the conjunctiva.
• Retina contains two distinct photoreceptor
systems,the rods and the cones.
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9. Physiology cont
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10. • Vitamin A is the backbone of the visual pigments
for the rods and the cones.
• Rod cells: the aldehyde form of vitamin A (retinal)
and the protein opsin combine to create
rhodopsin, which is the photosensitive pigment.
• When light hits the rod cells, the pigment
isomerizes, which leads to the nerve impulse and
results in the visual signal.
• The pigment is broken down to opsin and the
stereoisomer of retinal.
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11. • Conjunctiva:vitamin A is necessary for the
maintenance of the specialized epithelial
surface.
• A lack of vitamin A leads to atrophic changes
in the normal mucosal surface, with loss of
goblet cells, and replacement of the normal
epithelium by an inappropriate keratinized
stratified squamous epithelium.
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12. • Also,the substantia propria of the cornea
breaks down and liquefies (colliquative
necrosis), resulting in keratomalacia.
• Vitamin A deficiency affects the retina,
conjunctiva, and cornea, and the signs and
symptoms tend to occur in a reliable
sequence.
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13. Risk factors
• Both an insufficient input and an increased need can
result in the deficiency.
• Infections of the gut, malabsorption, worm infestations
and particularly giardiasis decrease vitamin A
absorption,PEM.
• Recommended daily intakes
• Adult: 750 µg
• Pregnancy: 750 µg
• Breastfeeding: 1200 µg
• Children:
• < 1 yr: 300 µg
• 1-4 yr: 250 µg
• 4-6 yr: 300 µg
• 7-9 yr: 400 µg
• 10-12 yr: 575 µg
• 13-15 yr: 725 µg
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14. The WHO classification of vitamin A
deficiency is as follows:
• XN Night blindness
• X1A Conjunctival xerosis
• XIB Bitot’s spot
• X2 Corneal xerosis
• X3A Corneal ulceration/keratomalacia
-involving one-third or less of the cornea
• X3B Corneal ulceration/keratomalacia
-involving one-half or more of the cornea
• XS Corneal scar
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15. XEROSIS
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16. BITOT SPOT
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17. KERATOMALACIA
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18. Diagnosis
• Clinical:Night blindness and xerosis are the
initial signs of vitamin A deficiency, followed
by formation of Bitot’s spot.
• Serum levels of vitamin A
• CIC.
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19. Treatment
• Considered and emergency.
• Large and repeated doses are therefore given.
• Associated illnesses should always be Rx.
• Oral therapy: The oral regimen of vitamin A is 200,000 IU
on day of presentation, next day, and 2–4 weeks later.
• Children less than 1 year of age or less than 8 kg should
receive half the dose of the above dose. Repeat 200,000 IU
every 6 months up to 6 years of age to prevent recurrence.
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20. Prevention
• Dietary diversification.
• Fortification.
• Supplementation
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