2. VITAMINS
• Are a class of organic compounds categorized as essential
nutrients
• Required by the body in very small amounts (Micronutrients).
• Do not yield energy; but enable the body to use other nutrients.
• Broadly divided into two groups: Fat soluble Vitamins (A, D, E
& K)
Water soluble Vitamins (B & C)
3. Vitamin A is also called retinol
Plays essential roles in vision, growth, & development;
maintenance of healthy skin, hair, mucous membranes; immune
functions & reproduction
Vitamin A includes preformed vitamin → Retinol
and pro vitamin → Beta carotene
1 mcg of retinol=1 mcg of retinol equivalent (RE)
1 mcg of B-carotene=0.167 mcg of retinol equivalent
(RE)(RE)
4. History
• Hopkins conducted an experiment in young rats (1906-1912).
• These were fed on casien, starch, sugar, lard and inorganic
salts. These rats failed to grow and died.
• An addition of only 3 ml milk enabled them to thrive! An
‘Accessory food factor’ was thus demonstrated.
• Mc Callum isolated it in 1913 and was named as Vitamin A.
Wald was awarded Nobel Prize for description of ‘dark vision’
and its association with Vitamin A
8. Absorption and utilization
Absorption and utilization depends upon the
• amount of fat in the diet
• Method of food preparation
• Rate & completeness of digestion
• Absorption is optimal when the body stores are depleted & when
optimal amounts of other nutrients are present
• Presence of Vitamin –E & hormone thyroxin enhances the
absorption of Vitamin -A
9. MECHANISM OF ABSORPTION
• Vitamin A esters are hydrolyzed in lumen of intestine by the
enzyme lipase
• The vitamin –taken by intestinal mucosa, where the vitamin is
etherified with palmitic acid
• These esters are absorbed & enter lymphatic & eventually into
circulation
• In blood vitamin esters – attached to ß lipoproteins & are
taken up by the liver
• The vitamin is released as retinol binding protein
10. FUNCTIONS
• Essential for normal vision
• Integrity and normal functioning of glandular and epithelial
tissue
• Supports skeletal growth
• Anti infective
11. MECHANISM OF ACTION
ROLE IN VISION: Retina contains 2 types of receptor cells:
Rods- Dim light vision
& Cones - Bright light vision
Rhodopsin - Light sensitive pigment in photoreceptor cells of retina
- Made up of retinaldehyde, bound to protein Opsein
- Excitation by a single photon results in transmission of
nerve impulse
-When light falls on rhodopsin it splits into Opsein &
all trans retinal
All trans retinal →converted to 11-Cisretinol
12.
13. The challenge
• Vitamin A deficiency (VAD) is the leading cause of
preventable blindness in children and increases the risk of
disease and death from severe infections. In pregnant
women VAD causes night blindness and may increase the
risk of maternal mortality.
• Vitamin A deficiency is a public health problem in more
than half of all countries, especially in Africa and South-
East Asia, hitting hardest young children and pregnant
women in low-income countries.
• Crucial for maternal and child survival, supplying
adequate vitamin A in high-risk areas can significantly
reduce mortality. Conversely, its absence causes a
14. Contd …..
• For children, lack of vitamin A causes severe visual
impairment and blindness, and significantly increases the
risk of severe illness, and even death, from such common
childhood infections as diarrhoeal disease and measles.
• For pregnant women in high-risk areas, vitamin A
deficiency occurs especially during the last trimester when
demand by both the unborn child and the mother is
highest.
• The mother’s deficiency is demonstrated by the high
prevalence of night blindness during this period. The
impact of VAD on mother-to-child HIV transmission
needs further investigation.
15. Facts
• An estimated 250 million preschool children are vitamin A
deficient and it is likely that in vitamin A deficient areas a
substantial proportion of pregnant women is vitamin A
deficient.
• An estimated 250 000 to 500 000 vitamin A-deficient
children become blind every year, half of them dying
within 12 months of losing their sight.
16. Problem of VAD in India
• In india level of Bitot’s Spot which was 2% in 1979 has
declined to 0.7% in 2001,indicates that it is public health
problem
Volnerability :-
Young children <the age of 3 years
Pregnant and lactating women
Sex:-
Male childen > female children
17. DEFICIENCY
• Signs of vitamin A deficiency are → 2 types
• Ocular and Extra ocular
• Ocular manifestations: are the most common ones.
Night blindness,
Conjunctival xerosis,
Bitots spots,
Corneal xerosis,
keratomalasia.
18. • First clinical sign of vitamin A deficiency- Conjunctivital
xerosis
• First clinical symptom of vitamin A deficiency-Night
Blindness
19. Signs and symptoms of Vitamin A
Deficiency
• Dryness, itching, redness of conjunctiva
• Night blindness (inability to see in dim light)
• Other signs of xerophthalmia : Bitot spots; Corneal
xerosis;
• Keratomalacia
• Dry, rough, itchy skin; rash
• Dry, brittle hair and nails
• Loss of acuity of senses: smell and taste
• Loss of appetite
• Anaemia, fatigue
• Poor growth
• Low immunity: Increased vulnerability to infections
• Increased risk of certain cancers
20. NIGHT BLINDNESS
• Initial ocular manifestation of vitamin-A
• Inability to see in dim light
• Condition may worsen unless the child is supplemented with
vitamin –A
• Condition may worsen in children suffering from diarrhoea
and other infections
22. XEROPHTHALMIA
It is a consequence of vitamin A deficiency in which there is
drying and thickening of the conjunctiva and ultimately ulceration
and destruction of the conjunctiva.
23. Pathophysiology:
• Vitamin A is necessary for the growth and differentiation
of epithelial cells, conjunctival and corneal epithelial cells
are involved in this process.
• Night blindness is the earliest sign of vitamin A
deficiency. Next phase is the loss of normal mucous cells
from the cornea
• Dryness causes keratinazation of the epithelial cells lining
the cornea
• Dull, hazy and luster (shine) less appearance i.e.
xeropthalamia
• Final consequence keratomalacia, Bitot’s spot may be
seen, which are glistering white plaques of desquamated
thickened conjunctival epithelium, usually triangular in
shape.
24. Causes of blindness:
• Vitamin A deficiency.
• Trauma, retinoblastoma.
• Cataract, other congenital eye anomaly.
• Diabetic retinopathy and hypertensive retinopathy.
25. Source of vitamin A deficiency:
Vegetables: carrot, papaya, pumpkin etc.
Green vegetables, tomatoes.
26. Ocular manifestation of vitamin A
deficiency
• XN: Night blindness.
• XIA: Conjunctival xerosis.
• XIB: Conjunctival xerosis with Bitot’s spot.
• X2: Corneal scar.
• X3A: Corenal ulceration with xerosis involving less than
1/3 rd of the cornea.
• X3B: Corenal ulceration with xerosis involving more than
1/3 rd of the cornea.
• XF: xeropthalmic fundus.
• XS: corneal scar.
27. Preventive measures
• Ensure breast feeding and the mother should be given
adequate vitamin A completed food.
• In pregnant mother doses of vitamin capsule in three
maternal visits or 1 capsule at least at last trimester.
• Sufficient dose of green leafy vegetables should be given
to the child.
28. Curative measures
1. Corneal lesion or severe illness or malnutrition:
– 1, 00,000 IU vitamin A intramuscularly.
– 1, 00,000 IU vitamin A in the following day.
– 1, 00,000 IU vitamin A on two successive days.
2. Non-corneal xerophthalmia, healthy and well nourished.
– Less than 14 years-1, 00,000 IU vitamin A orally.
– More than 14 years old-2, 00,000 IU vitamin A orally.
Operative measures:
• For restoration of the vision keratoplasty can be done if
there is corneal opacity.
29. CONJUNCTIVAL XEROSIS
First clinical sign of vitamin deficiency.
Conjunctiva becomes dry & non-wet table
Looks muddy & wrinkled instead of smooth & shiny
Most common in children aged 1-3 yrs
Associated with PEM
Most widespread & serious nutritional disorder leading
to blindness
Andhra, TN, Karnataka, Bihar, and WB → badly
affected states
30. BITOTS SPOTS
• Triangular, pearly white or yellowish, foamy spots on
bulbar conjunctiva on either side of cornea
• In young children→ Vitamin A deficiency
• In older children → Sequel of earlier disease
31. KERATOMALACIA
• Keratomalacia or liquefaction of cornea is a grave medical
emergency
• The cornea may be soft & may burst open
• The process is a rapid one & the vision is lost permanently
• Mostly associated with PEM
32. EXTRA – OCULAR MANIFESTATIONS
Non specific and difficult to quantify
Comprise follicular hyperkeratosis, anorexia, and growth retardation
Cessation of bone growth→ overcrowding of brain &
CNS →Paralysis from
cranial pressure
Damage to mucous membrane (loss of integrity of epithelial cells)
Mild vitamin deficiency →↑Morbidity & mortality
due to respiratory &
Intestinal infection
33. HYPERVITAMINOSIS
Acute symptoms are developed on ingestion of very large
amounts of vit-A:
Headache, drowsiness, sluggishness & peeling of
skin & palms
In Infants→ Sudden rise of intracranial pressure
Continued intake of excessive amount → Roughening of skin
Irritability
Coarsening & falling of hair
Head ache
Leukopenia
All these symptoms vanish on withdrawal of vit -A
35. Prevention and Control
• Improve the diet to include more intake of foods rich in vitamin A
• Reducing frequency & severity of contributory factors like PEM ,
respiratory infections, diarrhoea and measles
• Every half yearly a massive dose 200,000 IU of Vitamin A in oil (retinol
palmitate) is administered orally to preschool children(1yr -6yr)
• A massive dose 100,000 IU of Vitamin A to children between 6 months
-1 year of age
• ASSESMENT OF VITAMIN –A DEFICIENCY→ Population
surveys (clinical&
bio chemical
criteria)
• Was part of Child Survival Safe Motherhood before;
Now part of RCH Program
36. REVISED STRATEGY OF WHO FOR VISION
2020
• It has been estimated that blindness cost the world 25 billion
annually in productivity
• A global initiative has been taken initiated to reduce the
preventable & curable blindness by 2020
• Strengthening of vitamin –A supplementation; School eye
screening programme
• Treatment of minor ailments at primary level; ICDS, & IEC for
awareness
37. References
1. Park .k text book of preventive and social medicine, 23rd
edition, bhanarsidas bhanot publishers. 2015: 615-616
2. B rajvir, textbook of public health and community
medicine, published by department of community
medicine pune,and WHO. 1st
edition 2009: 731-732
3. Gupta M., Mahajan., Text book of Preventive and
Social Medicene, 3(Edn):533
4. http://www.who.int/nutrition/topics/vad/en/
5. Lal. Sundar, text book of preventive and social
medicine, 4th
edition, CBS publishers.2014:222-223
6. Yadav Dr. Sudeep, a book on pathophysiology,1st
edition, 2011 A.D: 211-212