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VITAMIN A DEFICIENCY
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)
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)
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
SOURCES
SOURCES
• Widely distributed in animal foods as preformed vitamin A and
plant foods as provitamins (carotenes)
• Animal foods: Liver, eggs, butter, cheese, whole milk, fish and
meat.
• Plant foods: Green leafy vegetables, carrot, Yellow
fruits (mango, papaya & pumpkin)
Avocados
Fortified foods: Vanaspati, Margarine, milk
Plant foods rich in vitamin-A
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
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
FUNCTIONS
• Essential for normal vision
• Integrity and normal functioning of glandular and epithelial
tissue
• Supports skeletal growth
• Anti infective
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
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
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.
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.
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
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.
• First clinical sign of vitamin A deficiency- Conjunctivital
xerosis
• First clinical symptom of vitamin A deficiency-Night
Blindness
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
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
Bitot spots Keratomalacia
Conjunctival Xerosis Keratomalacia
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.
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.
Causes of blindness:
• Vitamin A deficiency.
• Trauma, retinoblastoma.
• Cataract, other congenital eye anomaly.
• Diabetic retinopathy and hypertensive retinopathy.
Source of vitamin A deficiency:
 Vegetables: carrot, papaya, pumpkin etc.
 Green vegetables, tomatoes.
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.
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.
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.
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
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
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
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
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
RECOMMENDED ALLOWANCES (ICMR)
GROUPGROUP RETINOL (mcg) orRETINOL (mcg) or B-CAROTENE (mcg)B-CAROTENE (mcg)
Man 600 2400
woman 600 2400
Pregnancy 600 2400
lactation 950 3800
INFANTS(0-12)
months
350 1200
CHILDREN
1-6 Yrs
7-12 yrs
400
600
1600
2400
ADOLSCENTS
13-19 Yrs 600 2400
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
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
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
THANK YOUTHANK YOU

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VITAMIN A DEFICIENCY

  • 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
  • 6. SOURCES • Widely distributed in animal foods as preformed vitamin A and plant foods as provitamins (carotenes) • Animal foods: Liver, eggs, butter, cheese, whole milk, fish and meat. • Plant foods: Green leafy vegetables, carrot, Yellow fruits (mango, papaya & pumpkin) Avocados Fortified foods: Vanaspati, Margarine, milk
  • 7. Plant foods rich in 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
  • 21. Bitot spots Keratomalacia Conjunctival Xerosis Keratomalacia
  • 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
  • 34. RECOMMENDED ALLOWANCES (ICMR) GROUPGROUP RETINOL (mcg) orRETINOL (mcg) or B-CAROTENE (mcg)B-CAROTENE (mcg) Man 600 2400 woman 600 2400 Pregnancy 600 2400 lactation 950 3800 INFANTS(0-12) months 350 1200 CHILDREN 1-6 Yrs 7-12 yrs 400 600 1600 2400 ADOLSCENTS 13-19 Yrs 600 2400
  • 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