vitamin A deficiency disease - Xerophthalmia. anatomy of eye, wald visual cycle, cause,sign symptom,treatment and prevention of Xerophthalmia.

1. Xerophthalmia
Vitamin - deficiency
Md . SajibAl Reza
Lecturer
Nutrition and Dietetics
College of Nursing Science Dinajpur
Dinajpur, Bangladesh
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4.  Pre-formed vitamin A / Biologically active vitamers: Retinol/
Retinal/ Retinoic acid ► Found only in animals
(human milk, liver, especially fish liver oil such as cod, shark, mackerel, egg yolk,
milk and dairy product such as butter, ghee, cheese, curd, fortify processed
foods include sugar, fats, oils, condiments)
 Occurs as retinylesters of fatty acids in membrane bound cellular
lipid and fat-containing storage cells.
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 Pro-vitamin A: Carotenoids (α-carotene, β-carotene, xanthophyl,
lycopene, chlorophyll) ► Found only in plants
(dark green leafy vegetables like spinach, amaranth; yellow and red fruits and
vegetables like pumpkins, carrots, tomatoes, squash, drumstick, peaches,
papaya, mangoes, apricots, jackfruit, banana, oranges)
 Occurs in cellular lipids, embedded in chloroplasts or the pigment
containing portion of chromoplast.
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5. Provitamin a : β-Carotene
Vitamin a1 : Retinol (
Vitamin A alcohol)
Vitamin a2 : 3 –Dehydro-
retinol
Vitamin a aldehyde : Retinal
Vitamin a acid : Retinoic
acid
Vitamin a ester : Retinyl
ester
Neo vitamin a :
Stereoisomer of Vitamin A1,
has 70 –80% of biological
activity of Vitamin A1.
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6. ☻Pro-vitamin A, carotenoids are converted to retinol by a cleavage
enzyme in the intestinal mucosa.
☻Absorption of retinol and β-carotene by mucosal cells.
☻Retinol is re-esterified with fatty acids and unconverted
carotenoids incorporated into chylomicrons in the intestine.
☻ Chylomicrons enter into the blood.
☻ All retinylesters are present in the chylomicrone are taken by the
liver and stored as retinyl palmitate.
☻ Retinylesters are broken down and re-synthesized in the liver.
☻ Free retrinol bound to retinol binding protein (RBP).
☻ The retinol is bound to cellular retinol binding protein (CRBP) by
RBP.
☻More than 90% of body supply of vitamin A is stored in liver cells
and secretes vitamin A in the form of retinol, which is bound to
retinol-binding protein.
Hydrolysis in intestine
Pancreatic esterase
Retinylesters of diet
Retinol + Free fatty
acids
Presence of bile salt
Wow..oo
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9. • β-Carotene is cleaved in the intestinal mucosa by carotene
dioxygenase, yielding retinaldehyde, which is reduced to
retinol, esterified and secreted in chylomicrons together
with esters formed from dietary retinol. [Arranged serially]
• The intestinal activity of carotene dioxygenase is low, so
that a relatively large proportion of ingested β -carotene
may appear in the circulation unchanged.
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10.  Liver (in stellate cell) has an enormous capacity for storing
Vitamin A in the form of retinol palmitate.
 Under normal conditions, a well fed person has sufficient
Vitamin A reserves to meet his needs for 6-9 months or
more
 Free retinol is Highly active but toxic, so it is transported
in the blood stream by combining with retinol binding
protein (RBP) (produced in the liver)
 So, in severe protein deficiency, production of retinol
binding protein prevents mobilization of liver retinol
reserves.
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11.  For normal vision in dim light.
 Maintaining the integrity and normal
functioning of glandular and epithelial tissues
which lines intestinal, respiratory and tracts as
well as skin and eyes.
 Supports growth (skeletal growth)
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12.  Retinol and retinoic acid function as steroid hormones. They
regulate the protein synthesis thus involved in cell growth and
differentiation.
 Synthesis of certain glycoproteins.
 Essential for the maintenance of
proper immune system
 Carotenoids function as antioxidants and reduce the risk of
cancers. May protect against some epithelial cancers.
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14.  Retinal helps in dim and bright
light visions.
 Rods for: Normal vision (Black
& ) + vision in
(present in retina)
 Cones for: Colour vision +
visual acuity (present in retina)
 Rod contain rhodopsin (made up
of 11-cis retinal + opsin)
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15.  The term “visual cycle” was coined by George Wald in the mid
1900’s to describe the ability of the eye to “re-cycle” vitamin A for
the synthesis of visual pigments (wald,1968)
 The visual cycle is the biological conversion of a photon into an electrical signal in the
retina.
 The processing of visual information begins in the retina with the detection of light by
photoreceptor cells.
 The photoreceptor cells involvedin vision are :
1. rods.
2. cones.
 Both the rods and cones contain chemicals that decompose on exposure to light and in
the process,excitethenerve fibres leadingfromthe eye.
 light sensitive chemical in the rods is called rhodopsin and that in the cones is called
cone pigments/colour pigments.
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17. 1. Bleaching of rhodopsin:
 When exposed to light, the
colour of rhodopsin changes
from red to yellow by a
process known as bleaching.
 Bleaching occurs in a few
milliseconds and many
unstable intermediates are
formed during the process.
2. Reformation of rhodopsin:
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18. :Normal vision/dim light vision:
 When light strikes 11-cis retinal opsin
convert to All trans retinal.
 At the same time opsin is dissociates.
 The conversion of rhodopsin to opsin
and all trans retinal occurs through
many intermediates reaction.
 1st stage: a light signal is converted
into atomic motion.
 2nd stage: this atomic motion is
converted into nerve impulse.
 3rd stage: this impulse is transmitted by
the optic nurve to the brain.
 This is followed by Dissociation of all
trans retinal from opsin.
 Immediately isomerized by retinal
isomerase to 11-cis retinal.
 This 11 cis retinal combines with opsin
to regenerate rhodopsin to complete
visual cycle.
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20. :::::::::::::COLUOR vision: ::::::::::::
■ Cone cells contain 3 different reninal
which produce color vision
- Porphyropsin ▬►Red
- Iodopsin ▬► Blue
- Cyanopsin ▬► Green
■ When light strikes the retina, it
bleaches one or more pigments
depending on the color quality of the
light.
■ These pigments are converted/splits
to all trans retinal and opsin.
■ Red if porphyropsin is split, green if
iodopsin is split, blue if cyanopsin is
split.
■ If mixtures of the three are converted
the color read out on the proportion
of the three splits.
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21. PRIMARY CAUSES OF DEFICIENCY – Vitamin A deficiency
SECONDARY CAUSES OF DEFICIENCY:
 PEM
 Infections
 Measles virus commonly affects the eyes.
 Fat malabsorption.
 Liver disorders effects storage of Vitamin A.
 Failure to synthesize chylomicrons and RBP.
 Xerophthalmia arises when the diet contains practically no whole
milk and dairy product such as butter, cheese, curd etc.
 Diet contains very limited amounts of fresh fruits and vegetables.
 Xerophthalmia and keratomalacia both occur in the first year of
life amongst artificially fed infants.
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22. Code Ocular sign
XN Night blindness
XIA Conjunctival Xerosis Dryness of the mucous membranes of the eyes
XIB Bitot spots Xerosis conjunctivae with Bitot spots
X2 Corneal Xerosis Dryness of the eye cornea
X3A Corneal ulceration or
Keratomalacia
Ccorneal ulcer is < 1/3 the surface of the
cornea
X3B Corneal ulceration or
Keratomalacia
Corneal ulcer is >1/3 the surface of the cornea
XS Corneal scar Scar
XF Xerophthalmia
Fundus
With images such as "cendol“
► XN, XIA, XIB, X2 can usually heal back to normal with good treatment.
► In stage X2 is an emergency that must be treated immediately because in a few days
could turn into X3.
► X3B X3A and if untreated can heal but by leaving defects that can even lead to total
blindness if the lesion (abnormality) of the cornea is extensive enough to cover the entire
cornea (cornea optical zone).
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23.  First evidence and symptom of vitamin A deficiency.
 It is not a disease itself but a symptom of several eye
diseases.
 Lack of Vitamin A first causes Night blindness or
nyctalopia
 It is the inability to see in dim light especially in late
evening.
 It occurs due to impairment in dark adaptation.
 The condition may get worse if Vitamin A is not taken,
especially if they suffer from diarrhoea and other
infections.
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24. Rods contain a receptor-protein called rhodopsin. When light falls on rhodopsin, it undergoes
a series of conformational changes ultimately generating electrical signals which are carried
to the brain via the optic nerve. In the absence of light, rhodopsin is regenerated. The body
synthesizes rhodopsin from vitamin A, which is why a deficiency in vitamin A causes poor
night vision.
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25.  It is the first sign of Vitamin A deficiency.
 The conjuctiva becomes dry and non-wettable.
 It appears muddy, thickened, pigmented and
wrinkled (instead of clear, smooth and shiny)
 The pigmentation gives the conjunctiva a “smoky”
appearance.
 Caused by deficiency of tears or conjunctival
secretions.
 These reflects a past deficiency of vitamin A.
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27.  They are triangular shape, greyish white or
yellowish, foamy spots or plaque on the
bulbar conjuctiva on either side of the
cornea.
 Look like a fine foam with many tiny
bubbles.
 Due to its increased thickness.
 Usually bilateral
 In young children, it indicates Vitamin A
deficiency.
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29.  The cornea appears dull, dry and non-wettable and eventually
opaque.
 First appears hazy & then granular.
 This stage is very serious.
 In more severe deficiency, there maybe corneal ulceration
 The ulcer may heal leaving a corneal scar which may affect
vision.
Cause: This is because glands in the conjunctiva no longer function normally.
 This leads to loss of tears and also loss of mucous, which acts as a ‘wetting agent’.
 The lack of mucous together with lack of tears not only leads to the dry
appearance but also increases the risk of infection.
Concequences: The drying is followed by a softening/melting
of the cornea with ulceration and areas of necrosis.
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30. Corneal xerosis with corneal ulcer
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31.  It is the liquefaction of the cornea. This is an medical
emergency.
 The cornea (a part or the whole) may become hazy, soft
and may burst open.
 Corneal ulcer are usually circular and punched out in
appearance.
 Rapid necrosis, corneal melting/softening, perforation,
prolapsed of intracellular contents.
 Red or look surprisingly white, swollen,
 Epithelial defects in periphery of cornea.
 This process is rapid and if the eye collapses, vision is
lose.
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33.  The most severe form of xerophthalmia is keratomalacia in
which more than one-third of the cornea is affected.
 The whole of the cornea may become soft and melt.
 Melting and clouding of the cornea (the clear layer in front
of the iris and pupil)
 Ulceration may lead to – perforation of the cornea, prolapsed
of the iris, loss of ocular contents.
 Destruction, inflammation, lesion, abrasion, injury of the eye
content and iris, a condition called KERATOMALACIA.
 The cornea may become edematous and thickened, and then
melt away.
 Ulcers may extend to centrally.
 This occurs because the structure of the collagen in the
cornea is affected by a process known as necrosis.
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35. X3A – Corneal Ulceration X3B – Corneal
Ulceration/Keratomalacia
Small ulcers Large ulcers
1-3mm More than 3mm
Occur peripherally Occur centrally
Circular Involve entire cornea
Steep margins and sharply
demarcated
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38.  The retina has white dots around the periphery of the fundus.
 Characterized by typical
► seed like
► raised,
► whitish/yellow
► scattered uniformly over the part of the fundus
► at the level of optic disks.
 Pale yellow spots near the course of the retinal vessels and in
the retinal periphery.
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40.  Vitamin A deficiency should be treated urgently.
 Nearly all the early stages of Xeropthalmia can be reversed
by :--
Administration of MASSIVE DOSE of 200,000 IU (or
110mg) of retinol palmitate orally on 2 successive days.
 ALL children with corneal ulcers are given Vitamin A
whether or not a deficiency is suspected.
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41.  In developing countries, supplements of vitamin A
palmitate in oil 60,000 RAE (200,000 IU) per every 6
months are advised for all children between 1 and 5
years of age
 Infants < 6 months can be given a one-time dose of
15,000 RAE (50,000 IU), and
 Those aged 6 to 12 months can be given a one-time
dose of 30,000 RAE (100,000 IU).
 Those aged > months can be given a one-time dose of
30,000 RAE (200,000 IU).
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42. Timing Vitamin A dosage
Immediately on diagnosis
<6 months of age 50,000 IU
6-12 months of age 100,000 IU
>12 months of age 200,000 IU
Next day Same age specific dose
At least 2 weeks later Same age specific dose
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43. • Administration of large
doses of Vitamin A
Short term
• Fortification of foodMedium term
• Reduction or elimination of
factors contributing to
ocular disease
Long term
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44.  The strategy is to administer single MASSIVE DOSE of Vitamin
A in oil (retinol palmitate) orally.
Age group Dose Duration
Children <12months 1,00,000 IU Once every 4-
6months
Children >12months 2,00,000 IU Once every 4-
6months
Child bearing age 3,00,000IU Within 1month of
delivery
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45.  FORTIFICATION of certain food [such as dalda
(vanaspati), margarine & dried skimmed milk] with
Vitamin A.
 Fortification is successful only if the chosen food is
consumed in sufficient quantities by groups at risk.
▐▐▐ Golden rice is a variety of rice (Oryza sativa) produced
through genetic engineering to biosynthesize beta-carotene,
a precursor of vitamin A. It is intended to produce a fortified
food to be grown and consumed in areas with a shortage of
dietary vitamin A.
Golden rice (right) compared to white rice (left)
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46. ► REDUCING or ELIMINATING the frequency and
severity of contributory factors to ocular disease (PEM,
respiratory tract infections, diarrhoea, measles)
► To consume green leafy vegetables or other Vitamin A rich
food
Sources:
 human milk, liver, especially fish liver oil such as cod, shark,
mackerel, egg yolk, milk and dairy product such as butter,
ghee, cheese, curd,
 The diet should include dark green leafy vegetables, deep- or
bright-colored fruits (e.g., papayas, oranges), carrots, and
yellow vegetables (e.g., squash, pumpkin).
 Vitamin A fortify processed foods include sugar, fats, oils,
condiments)
 Carotenoids are absorbed better when consumed with some
dietary fat.
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Which food contain
more vit-A ?

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49. GROUP RETINOL(mcg) ẞ CAROTENE(mcg)*
ADULTS
Man 600 4800
Woman 600 4800
Pregnancy 800 6400
Lactation 950 7600
INFANTS
0-6months 350 -
6-12months 350 2800
CHILDREN
1-6yrs 400 3200
7-9yrs 600 4800
ADOLESCENTS
10-17yrs 600 4800
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50. i. To consume green leafy vegetables or other Vitamin
A rich food
ii. Promotion of breast feeding
iii. Improvements in environmental health (such as
ensuring safe and adequate WATER SUPPLY,
maintenance of SANITARY LATRINES to
safeguard against diarrhoea)
iv. Immunization against infectious diseases (measles),
prompt treatment of diarrhoea and other infections
v. Better feeding of infants and young children
vi. Improved health services for mothers and children
vii. Social and health education
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51. Vitamin A supplementation is an integral part of this
programme. It covers children up to 5 yrs of age.
Administration of MASSIVE dose of Vitamin A up to 5yrs
of age.
 First dose of 100000 IU with Measles vaccination at
9 months.
 Second dose of 200000 IU after 9 months (at 16-18
months, with DPT booster).
 Subsequent doses of 200000 IU, every 6 months up to
the age of 5yrs.
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52.  Serum retinol level-Normal range is 28 to 86 μg/dL (1 to 3
µmol/L). The level decreases in vitamin A deficiency.
 Serum RBP level
 Serum zinc level is useful because zinc deficiency
interferes with RBP production.
 An iron panel is useful because iron deficiency can affect
the metabolism of vitamin A.
 Albumin levels are indirect measures of vitamin A levels.
 Complete blood count (CBC) with differential if anemia,
infection, or sepsis is a possibility.
 An electrolyte evaluation and liver function studies
should be performed to evaluate for nutritional and volume
status.
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53.  An EXCESS intake/ Vitamin A toxicity can be acute
(usually due to accidental ingestion by children) or
chronic.
 Both types usually cause headache and increased
intracranial pressure.
 Acute toxicity also causes nausea, vomiting, and
anorexia.
 C h r o n i c toxicity also causes sleep disorders
changes in skin, hair, and nails; papillar oedema;
abnormal/enlarged liver test results; and, in a fetus,
birth defects.
 HIGH intakes of carotene may colour plasma and skin.
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54. • 1 molecule of β carotene = 2 molecule of retinol.
• 1μ g of preformed retinol = 6 μg of β carotene.
 1 Retinal Equivalent = 1μg of Retinol OR 6 μg of β-
carotene
 1 I.U. = 0.3 μg/mcg of Retinol OR 0.34 μg of Retinyl
acetate OR 0.55 mcg of retinol palmitate OR 0.6 μg
of β-carotene.
1 mcg of retinol = 1 RE
1 mcg of ẞ-carotene = 0.167 mcg of RE
1 mcg of other carotenoids = 0.084 mcg of RE
1 RE = 3.333 IU of Vit. A
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55.  Vitamin A is required to maintain specialized epithelia (such
as in the cornea and conjunctiva).
 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.
 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. In addition, the substantia
propria of the cornea breaks down and liquefies, resulting in
keratomalacia.

56. Thank
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