Chemical Forms of Vitamin A Vitamin A refers to a group of fat-soluble retinoids, including: 1.1 Preformed Vitamin A (Active forms) Retinol (alcohol form) Retinal (aldehyde form) Retinoic acid (acid form) Retinyl esters (storage form) These are found in animal-derived foods. 1.2 Provitamin A (Precursors) Carotenoids, especially beta-carotene, from plant sources. Must be converted to retinol in the body. --- 2. Absorption and Metabolism 2.1 Absorption Occurs in the small intestine. Requires bile salts and dietary fat for micelle formation. Retinyl esters are hydrolyzed to retinol by pancreatic lipase and intestinal enzymes. 2.2 Transport Retinol is re-esterified in enterocytes and packaged into chylomicrons. Transported via the lymphatic system to the liver. 2.3 Storage Liver stores ~90% of the body's Vitamin A as retinyl esters in hepatic stellate (Ito) cells. 2.4 Mobilization and Circulation When needed, retinol is released from the liver bound to retinol-binding protein (RBP) and transthyretin. 2.5 Cellular Uptake Target cells take up the retinol-RBP complex via specific receptors. Inside cells, retinol is converted to retinoic acid, the active form that regulates gene expression. --- 3. Physiological Roles 3.1 Vision 11-cis-retinal is a component of rhodopsin, essential for low-light (scotopic) vision. Light converts 11-cis-retinal to all-trans-retinal, triggering a neural signal. 3.2 Gene Expression Retinoic acid binds to nuclear receptors (RAR and RXR) and regulates gene transcription. Important in cell differentiation, especially epithelial cells and immune cells. 3.3 Immunity Supports T-cell differentiation, mucosal integrity, and antibody production. 3.4 Reproduction and Development Crucial for embryogenesis and spermatogenesis. Controls limb patterning and organogenesis. 3.5 Skin and Mucosa Promotes epithelial differentiation, inhibits keratinization. Used topically in acne and psoriasis (e.g., tretinoin, isotretinoin). --- 4. Deficiency of Vitamin A Causes Malnutrition Fat malabsorption syndromes (e.g., celiac disease, cystic fibrosis) Liver disorders Symptoms Night blindness (nyctalopia) – early sign Xerophthalmia – dryness, Bitot’s spots, keratomalacia Increased infections – especially respiratory and gastrointestinal .

1. MI Project, Gandhinagar
VAS Programme
Training Programme for Medical
Officers
By:
District Extender

2. Technical aspect Of Vitamin - A

3. What are Vitamins ?
Vitamins are elements
1)Which are needed in very small amount
2)Essential for body functions like growth,
maturity and reproduction.

4. Vitamins Can Classified into two types
Vitamins Can Classified into two types
A
D
E
K
B C
Fat Soluble
Water Soluble

5. What is Vitamin - A ?
Vitamin A was found by Mc Collum around 1907.
Vitamin A is a group of similar biological compound,
which is used by the body as retinol for biological
function
Vitamin A works together with enzymes and co-
factors ( substances that assist enzymes)

6. Contd…
•It is needed for normal vision.
• It is essential for healthy & glowing skin.
• It is necessary for overall growth
especially for skeletal development.
• It provides resistance against infections by
increasing the immune response of the body.

7. Vitamin A compounds
Animal Sources Plant Sources
Retinol Retinal
Retinoic Acid
Carotenoids
(Preform vitamin A) (Precursor of Vitamin A)
b Carotene
Precursor of vitamin A converts into the preformed vitamin
A. Precursor of Vitamin A conversion depends on the bio-
availability and bio-conversion.
Retinoids

8. Sources of Vitamin A
Sources of Vitamin A
Animal Sources Plant Sources
Fish And Meat
Milk And Cheese
Green leafy vegetables
spinach,carrots,peas,banana
pumpkin, sweet potatoes,
tomatoes
Fruits : papaya,orange,
mango, watermelon, plums

9. Daily Requirements of Vitamin A
Group
Retinol
(mcg)
b-Carotene
(mcg)
Man 600 2400
Woman 600 2400
Pregnancy 600 2400
Lactation 950 3800
Infants 0-12 months 350 1200
1-6 years 400 1600
7-12 years 600 2400
Adolescents 13-19 years 600 2400
Adult
Children

10. Etiological Factors of VAD
Etiological Factors of VAD
Insufficient Intake:
Inadequate breast feeding
Unaffordable Vit. A rich food
Others:
Widespread poverty
Low literacy among women
Excess Loss:
Various Disease conditions
Increased Requirement:
During Pregnancy & Lactation
Low birth weight
Rapid growth condition
Reduced Absorption:
Infections
Zinc Deficiency in the body
Protein Energy Malnutrition

11. Deficiency of Vitamin A
Deficiency of Vitamin A

12. Depleted VA stores
Declining VA Stores
Reduced Serum Retinol
Reduced Child Survival
Epithelial Metaplasia
Impaired Dark Adaptation
Xerophthalmia
Blindness
Sub Clinical
VAD
Clinical
VAD
N
o
r
m
a
l
Severely Deficient Time
Stages of Vitamin A Deficiency

13. Deficiency of Vitamin A
Deficiency of Vitamin A
Night Blindness
Keratomalacia
Bitot’s spot
Conjunctival Xerosis
Xerophthalmia

14. VITAMIN A DEFICIENCY (VAD)
Night Blindness :-
• It is the first symptom of xerophthalmia.
• A child cannot see to get around after dark or in a dark room.

15. Conjunctival Xerosis
Conjunctival Xerosis
The conjunctiva which covers inner aspects of
upper and lower eyelids and the white portion
(sclera) of the eye becomes dry and non- wettable
Instead of looking smooth and shiny, it appears
dry and wrinkled.

16. Corneal Xerosis / Ulceration
• The cornea becomes dry ( Xerosis ) , if the disease is not
treated , the Xerosis can progress within hours to an ulcer of
the cornea.

17. Bitot’s spot
•Bitot’s spots are accumulations of keratin & Saprophytic
bacilli which form foamy cheesy material on the conjunctiva,
often in association with other signs of xerophthalmia such as
night blindness.
•They may differ in size, shape and location , they have a
similar appearance.
•

18. Corneal scar
Corneal scar
• It can lead to perforation of the cornea.
•At this stage, a corneal scar remains in the eye.
•If the scar is treated early, blindness can be prevented.

19. Keratomalacia
Keratomalacia
•It is a liquefied and ulcerated stage of the
Xerophthalmia of cornea
•The cornea becomes soft and may even
burst with discharge of fluids.
• If the disease is not treated , a corneal ulcer can lead to
“melting” or “wasting” of the cornea ( Keratomalacia )

20. Prevention & Control of
Vitamin A Deficiency

21. Sr no. Criteria
Prevalence
in (%)
Clinical signs of VAD
Children 2-5 years of age
1 Night Blindness (XN) >1.0
2 Bitot's spot (XIB) > 0.5
3
Corneal Xerosis(X2) and Corneal
Ulcers(X3) >0.01
4 Corneal Scars (XS) >0.05
Women of Child Bearing Age
1
Night Blindness (XN) in recent
Pregnancy >5.0
Biological sighns of VAD
Preschool children
Serum retinol < 0.7 micromol/L or
20 ug/dL >15.0
WHO/IVACG cut-off criteria for public health significance
WHO/IVACG cut-off criteria for public health significance
of Vitamin A deficiency (VAD)
of Vitamin A deficiency (VAD)
IVACG: International Vitamin A Consultative Group

22. Strategies to control VAD
Strategies to control VAD
Promotion of consumption
Improvement of
Dietary Intake
Food Fortification
Programme
Implementation of
VAS
Direct Indirect
Promotion of
Breast Feeding
Control of Infection
Immunization,
hygiene, safe water