NUTRITION DISORDRS-VITAMIN DEFICIENCY &

EYE

DR. CHRISTINA SAMUELM.S OPHTHALMOLOGY,

FELLOW AT SANKARA EYE HOSPITALCHENNAI

NUTRITIENTS

Chemical substances that constitute food and are responsible for the functions of food and also protect the body from various disorders

Types of nutrients

Macronutrients Proteins carbohydrates Fats

Micronutrients Vitamins Minerals

INTRODUCTION- Vitamins

Vitamins may be regarded as organic compounds required in the diet in small amounts to perform specific biological functions for normal maintenance of optimum growth and health of the organism.

WHAT IS VITAMIN A?• The term “vitamin A” makes it sound like there is one particular nutrient called

“vitamin A”, but this is not true. It is a broad group of related nutrients.• Vitamin A is a broad term for group of unsaturated nutritional organic

compounds, that includes retinol, retinal, retinoic acid, and several provitamin A carotenoids, among which beta-carotene is the most important.

VITAMIN A is an Essential Fat soluble vitamin occuring in the following forms:

Pre formedRetinoids (retinal, retinol, retinoic acid)Found in animal products

Pro vitamin ACarotenoids Must be converted to retinoid formFound in plant products

HISTORY

It is recorded in history that HIPPOCRATES cured night blindness(about 500 B.C)

He prescribed to the patients Ox liver(in honey)which is now known to contain high quantity of vitamin A.

By 1917, Elmer McCollum et al at the University of Wisconsin–Madison, studied the role of fats in the diet and discovered few accessory factors. These "accessory factors" were termed "fat soluble" in 1918 and later "vitamin A" in 1920.

In 1919, Harry Steenbock (University of Wisconsin) proposed a relationship between yellow plant pigments (beta-carotene) and vitamin A.

In 1931, Swiss chemist Paul Karrer described the chemical structure of vitamin A.

Vitamin A was first synthesized in 1947 by two Dutch chemists, David Adriaan van Dorp and Jozef Ferdinand Arens.

Structure of vitamin A

NOMENCLATUREPROVITAMIN A : β-CaroteneVITAMIN A1 : Retinol ( Vitamin A alcohol)VITAMIN A2 : 3 –Dehydro-retinolVITAMIN A ALDEHYDE : RetinalVITAMIN A ACID : Retinoic acidVITAMIN A ESTER : Retinyl esterNEO VITAMIN A : Stereo isomer of Vitamin A1, has 70 –80%

of biological activity of Vitamin A1.

CHEMISTRY• Vitamin A is composed of ‘β-IONONE RING’ (CYCLOHEXENYL) to

which ‘POLY ISOPRENOID SIDE CHAIN’ is attachedPolyisoprenoid chain –all trans configuration, contains 4

double bonds, has 2 methyl groups with terminal carbon having ‘R’ group

‘R’ Group –alcohol/aldehyde/acidβ-Ionone ring –contains 1 double bond with 3 methyl groups

Sources of vitamin A• Animal : Fish Liver oil, Butter, Milk, Cheese,

Egg Yolk

• Plant : All Yellow –Orange –Red –Dark Green fruits & vegetables like Tomatoes, Carrots, Spinach, Papayas, Mangoes, corn, sweet potatoes.

RECOMMENDED DIETARY ALLOWANCE Unit of activity is expressed as ‘RETINAL EQUIVALENT’ (R.E.) / ‘INTERNATIONAL UNIT’ (I.U.)

1 Retinal Equivalent = 1μg of Retinol OR 6 μg of β-carotene1 I.U. = 0.3 μg of Retinol OR 0.34 μg of Retinyl acetate OR 0.6 μg

of β-caroteneInfants & Children : 400 t0 600 μg/dayAdults (Men & Women) : 600 to 800 μg/dayPregnancy & Lactation : 1000 to 1200 μg/day

FUNCTIONS OF VITAMIN AVISIONGENE TRANSCRIPTIONIMMUNE FUNCTIONEMBRYONIC DEVELOPMENT AND REPRODUCTIONBONE METABOLISMHAEMATOPOESISSKIN AND CELLULAR HEALTHANTIOXIDANT ACTIVITY Recent work suggests that, outside the retina, vitamin A is

chiefly concerned with mucopolysaccharide synthesis and stability of lysozome membranes. Children aged three months to four years are most commonly affected.

METABOLISM LIVER STORES 90% OF VITAMIN A

ACTIVE METABOLITES • TRANS RETINOIC ACID • CIS RETINOIC ACID

REGULATES EXPRESSION OF KERATIN AND MUCINS

RHODOPSIN IN VISUAL CYCLE

VITAMIN A DEFICIENCYMost susceptible populations:

Preschool childrenOlder adultsAlcoholismLiver disease (limits storage)Fat malabsorption

Vitamin A deficiency may result from :-Dietary insufficiency of Vitamin A / Precursors-Interference with absorption from intestineseg: diarrhoea, malabsorption syndrome, bile salt deficiency-Defect in the transport due to protein malnutrition

–‘Kwashiorkar’-Defect in the storage due to diseases of liver

Tissues chiefly affected –‘Epithelial’ principally which are not normally keratinised

Includes epithelium of respiratory tract, gastrointestinal tract, genitourinary tract, eye & paraocular glands, salivary glands, accessory glands of tongue & buccal cavity and pancreas

Fundamental change: Metaplasia of normal non-keratinised living cells into keratinising type of epithelium

OCULAR MANIFESTATIONS OF VITAMIN A DEFICIENCYXEROPHTHALMIA The term Xerophthalmia was given by a joint WHO and

USAID committee in 1976 to cover all the ocular manifestations of vitamin A deficiency including the structural changes affecting the conjunctiva, cornea and retina and also the biophysical disorders of retinal rods and cones functions.

XEROPHTHALMIA CLASSIFICATION(modified) (1982)

WHO CLASSIFICATION • XN-NIGHT BLINDNESS

• X1A-CONJUNCTIVAL XEROSIS

• X1B-BITOT’S SPOT

• X2-CORNEAL XEROSIS

• X3A-CORNEAL ULCER<1/3RD OF CORNEAL SURFACE

• X3B-CORNEAL ULCER>1/3RD OF CORNEAL SURFACE

• XS-CORNEAL SCAR

• XF-XEROPHTHALMIC FUNDUS

XN :NIGHT BLINDNESS(Nyctalopia)

Earliest symptom of xerophthalmia in children Diminished visual acuity in ‘dim light’(Insufficient adaptation

to darkness)Defective rhodopsin function.

Night blindness, per se, is not pathognomonic of vitamin A deficiency, being also a feature of various eye diseases e.g. retinitis pigmentosa, Oguchi's disease, choroideremia, gyrate atrophy of the choroid and retina, onchocerciasis and occasionally congenital.

If nutritional in origin the symptom will disappear after consumption of about 30,000 I.U. of vitamin A daily administered as cod or halibut liver oil

X1A CONJUNCTIVAL XEROSISCharacterised by:One or more patches of dry, lustreless,nonwettable conjunctiva.Interpalpebral conjunctiva(commonly temporal quadrants)Severe cases involves the entire bulbar conjunctiva.Desribed as ‘emerging like sand banks at receding tide’when child ceases to cryCan lead to conjunctival thickening,wrinkling and pigmentation.

X1B BITOT’S SPOTSBilateralBulbar conjunctiva in the interpalpebral areaCommonly in temporal quadrant.Raised triangular greyish/silvery white spots/plaques.Firmly adherent to conjunctivaFoamy keratinised epithelium(corynebacterium xerosis)

X2 CORNEAL XEROSISDry lustreless appearance of corneaEarliest change is punctate keratopathyBegins in the lower nasal quadrantBilateral punctate corneal epithelial erosions Can progress to epithelial defects Reversible on treatment

X3A & X3B CORNEAL ULCERATION /KERATOMALACIAStromal defects occur in late stages due

to colliquative necrosis leading to corneal ulceration ,softening (melting) and destruction of cornea(keratomalacia)

Corneal ulcers may be small or largeStromal defects involving less than 1/3rd

cornea usually heal leaving some useful vision

Large stromal defects commonly result in blindness.

Small ulcers 1-3mmOccur peripherallyCircularSteep margins and sharply

demarcated

Large ulcersMore than 3mmOccur centrallyInvolve entire cornea

KERATOMALACIA N MALNUTRIRION, DIARRHOEA, MEASLES & PARASITIC INFECTIONS COMMON IN MALNUTRIRION, DIARRHOEA, MEASLES & PARASITIC INFECTIONS GENERALIZED SOFTENING OF STROMA

SLOUGHS

DESCEMETOCELE

PERFORATION

XS CORNEAL SCARHealing of stromal defects results in corneal scarringSize of the corneal scar depends on the size and density of

corneal defect.

XF XEROPHTHALMIC FUNDUSUncommon in occurenceTypical seed like lesionsWhitish/yellow in colourRaised lesisionsScattered uniformly over fundusAt the level of optic disc.FFA reveals these dots to be focal retinal pigment epithelial

defects Rarely these patients can present with scotomas corresponding

to the area of retinal involvementRespond to vitamin A therapy with scotoma disappearing in 1-2

weeks and retinal lesions fading in 1-4 months

2. Parenteral therapy: IN CASES OF -severe disease -unable to take oral feeds -Repeated vomiting and diarrhoea -malabsorption Intramuscular injections of water miscible vit A

preparation Dose – 1,00,000 IU(Half the oral dose)

Local ocular therapy-Intense lubrication-instilled every 3-4 hours Topical retinoic acidTreatment of keratomalacia and corneal ulcerTreatment of corneal perforation

PROPHYLAXIS AGAINST XEROPHTHALMIA1.Short term approach

-Periodic administration of vitamin A supplements-WHO recommended ,universal distribution schedule of vit A for prevention

is as follows:i) Infants <6months (not being breastfed)—50,000 IUii)Infants 6-12 months and any child <8kg – 1,00,000 IU every 3-6monthsiii)Children over 1 year and under 6 years --- 2,00,000 IU orally every 6 monthsiv)Lactating mothers – 2,00,000 IU orally once at delivery or during next 2

months to maintain level of vitamin A in breast milk

PROPHYLAXIS

Under vitamin A supplementation program through Reproductive and child health program(RCH) and now National Rural Health Mission(NRHM)

-- Children between 9 and 36 months of age are to be provided with vitamin A solution every 6 months starting with 1,00,000 IU at 9 months of age along with measles vaccination and subsequently 2,00,000 IU every 6 months till 36 months of age.

2.Medium term approach- fortification of food with Vit A

3. Long term approach- Promotion of adequate intake of Vit A rich foods in high

risk groups particularly preschool aged children on a periodic basis and to mothers within 6-8 weeks after childbirth

Other measures like nutritional education,social marketing, home or community garden programs and measures to improve food security.

HYPERVITAMINOSIS A

Ingestion of large amounts of preformed vitamin A from the diet, supplement intake or medications

Acute:Single doses of >3,00,000 IUHeadache ,Blurred vision,nausea ,vomiting,

drowsiness,irritability i.e signs of raised ICP(Benign intracranial hypertension)

Serum Vit A values-200-1000 IU/dl

Chronic – long-term megadose; possible permanent damage ( >50,000 IU/day for several wks)Bone and muscle painLoss of appetiteSkin disordersHeadacheDry skinHair loss Increased liver size-Manifestations reversible when vitamin A discontinued

DEFICIENCY OF VITAMIN B1{THIAMINE} Can result in Corneal anaesthesia Conjunctival dystrophy Corneal Dystrophy Acute Retrobulbar neuritis

DEFICIENCY OF VITAMIN B2{RIBOFLAVIN} FUNCTIONS- plays an important role in cellular growth It acts as a co – factor for a number of enzymes involved in

energy metabolism. SOURCES Eggs , liver, green leafy vegetables Milk

DEFICIENCY MAY CAUSE

KeratitisSusceptibility of cataractPhotophobiaBurning SensationConjunctival irritationVascularization of Cornea

DEFICIENCY OF VITAMIN C

It may be associated with haemorrhages in the conjunctiva, lids, anterior chamber, retina and orbit.

It delays wound healing it causes bleeding of gum Effective anti-oxidant Protects eyes against u.v rays Delays cataract formation < more than 300 mg>

SOURCES Citrus guava mango Amla Pineapple

DEFICIENCY OF VITAMIN D

It may be associated with Zonular CataractPapilledema Increased lacrimation

VITAMIN E

FUNCTIONS Potent anti-oxidant Prevents ARMD

SOURCES Broccoli Carrot Spinach Fish

OMEGA -3- FATTY ACID

Functions Essential fatty acid –used to produce new cells , muscle, nerves and

organs Protects against ARMD, dry eye syndrome

SOURCES Fish walnut flax seeds

ZINC

This trace mineral has a protective effect on early ARMD Acutely concentrated in the eye and hence very important

SOURCES Almonds Wheat germs Dairy

SELENIUMHelps in treating : Retro-bulbar pain Oedema Grave’s disease

SOURCES

Turkey Brazelnuts Tuna

LEUTIN AND ZEAXANTHIN

THEY ARE XANTHOPHILS- CAROTENOIDS THEY ABSORB EXCESSIVE LIGHT ENERGY TO PREVENT DAMAGE MESO ZEA XANTHINE IS PRESENT IN THE RETINA FROM INGESTED

LEUTINS.

FUNCTIONS Anti-oxidants Prevents ARMD