Cataract

What is cataract???

What is the need to know

about it ?????????

62.6%

“BURDEN OF

CATARACT “

Global urban blindness

- 50 million in 2000

Will grow to

- 75 million by 2020 unless special efforts to arrest / reverse this

THIS BURDEN IS HEAVIER FOR A DEVELOPING COUNTRY LIKE OURS

WHYYY???????

poor uptake ofservices due to llack

Projected in population of pt information

the burden becomes heavier

in our countryOccurs a decade earlier

life expectancy

TREATABLE

CAUSE

OF BLINDNESS

•

VISION 2020 - RIGHT TO SIGHT

ANATOMY – LENS &ETIOPATHOGENESIS OF CATARACT

Who said …….. “ UNION IS AN ONION “

We can say…….

“ LENS IS AN ONION “

A REGULAR RECORD OF OUR AGE !!!

zonules

Do you know…!!!!!!!!!…

organ that grows through out life..???

Thickest basement membrane in our body..??

Least hydrated organ in our body…??

Structure with Highest protein content…….??

Blood supply of lens………. ??

CAPSULE : BY THE – Lens Epithelium FOR THE – Accommodation OF THE - Type 4 collagen

Capsule arround the lens is not uniform in thickness !! Thickest - para equatorial region Thinnest - at poles esp posterior pole

THICKNESS OF CAPSULE AT VARIOUS PARTS :-

EPETHELIUM : single layer of epithelium just beneath the ant. capsule , it forms

CapsuleLens fibers (ant. Preequatorial region)

That’s why,Oldest lens fibers are - DeepestOldest capsule is - Most superficial







EPITHELIUM : single layer of epithelium just beneath the ant. capsule , it forms

Capsule - anteriorlyLens fibers - posteriorly

(ant. Preequatorial region)


Post.capsule

Epithelium Cortex

Ant.capsule Nucleus

epithelium maturing to lens fiber

ANTERIOR POSTERIOR

ANTERIOR POSTERIOR

CORTEX & NUCLEUS: No cells (lens fibers) are lost As new fibers laid down – it crowds &

compacts the previously formed fibers

thus……., Center to periphery embryonic nuclei fetal nuclei infantile nuclei adult nuclei cortex BUT SURGICAL NUCLEUS & CORTEX????

As you travel from capsule towards nucleus through LENS

Age of fiber Density Protein conc. Enzyme conc. Glutathione O2 Conc.

Na+ K+ Amino acid

Inositol Ca2+ Glucose

LACTIC ACID

Active

Passive

NOTE :

O2 not allowed into the lens

Lactic acid from anaerobic metabolism –high conc. With in lens , so passively diffuses out

Aqueous is the only source of glucose,so it passively diffuses in

GLUCOSE

G – 6 – P

Triose – P

Pyruvate

Sorbital

FructosePOLYOL PATHWAY

CO2 + Acetyl CoA

KREB’S CYCLE CO2 CO2

NADP GSH

HMP Path (15%) NADPH GSSG Pentoses

Lactate

GLYCOLYSIS (50%) (Anerobic)

Aldose reductase

Reactive O2 species :- superoxide O 2

- H2O2 Hydroxyl ion.OH -

Inflamation Mitochondrial e- transport chain 2O2

- + 2H+

SOD

H2O2

GPX GSHAt cytoplasm 2 H2O

(HMP) NADPH GSSG PSH GR TT NADP GSH PSSG

Fenton’s reaction

At cell membrane Catalase H2O + ½ O2

LENS OPACITY Capable of causing some visual loss, measured as acuity loss

FUNCTIONAL CATARACT:

Len opacity causing visual loss sufficient to produce functional disability

CONGENITAL

METABOLIC

ACQUIRED TRAUMATIC

COMPLICATED

TOXIC

SENILE

INFECTIOUS

DIABETICMETABOLIC

Most common type of cataract,

Out of people aged bt,

52 – 64 yrs 4.6 % 65 – 74 yrs 18 % are with 75 – 85 yrs 46 % cataract

CATARACT IS ALWAYS,

But 3 mechanisms of great importance :-

OXIDATIVE STRESS PHOTOOXIDATION GLYCATION

2O-2 + 2H+

SOD

H2O2

GPX GSH

H2O GSSG

HMP NADPH PSH FREE RADICAL GR TT

NADP GSH PSSG

2

1 2

1

2

3

GSHwith aging Deterioration of mech. that protect against oxidative damage

CHROMOPHORE ???? Proteins & DNA are the chromophores in

lensLIGHTS ABSORBED, UVA UVB VISIBLE LIGHT All cells of our body are equally exposed to Light but why damage specifically occur in Lens…??????????

CHROMOPHORE

Direct photochemical Photosensitised

chemically changed chemically unchanged bt chromophore can cause it in another molecule eg. tryptophan

free radicals

LYCATION a condensation reaction bt amino grp of protiens &reducing sugars

GLYCATING AGENTS :- GLUCOSE G – 6 – P Ribose DHA (Oxidised ASA)

DIABETIC

Protien – NH2 + Glucose

EG Pdt (MORE IN CORTEX)

AGE Pdt (MORE IN NUCLEUS)

Crosslinking with protiens

conformational change aggregation

BrownPigmentation

To summaries as we grow older…….

Mitochondrial func.

Superoxide production

Loss of UV filters in nucleus

UV absorption

Photosensitisers

Total no: of photons absorbed

Every 5 th person visiting a physician is diabetic

Amount of AGEs

CORTEX – NUCLEUS interface develops

INDIA - DIABETIC CAPITAL OF THE WORLD

11.6% of urban indians are diabetic

3 to 4 fold increase in incidence of cataract in diabetic pts under 65 yrs,

High Diabetic age Poor control

Invites cataract earlier

Do You Think A Person Above 50 Is Going To come With Problem of cataract

Alone…….??????

CATARACT is always MULTIFACTORIAL

GSH PROTEIN MODIFICATION CATARACT

↓ GSH

↓Free a.a

↓Protein syn. loss of enzymes↓Glycolysis

↓ ATP

DIABETES

↑Glucose Sorbital

↓NADPH ↑G-6-P fructose

PROTEIN MODIFICATION

Croslinkng bt proteins

Aggregation of proteins

Na+-K+ ATPase

Ionic imbalance

↑Ca2+ osm shock

proteolysis

Malnutrition DIARRHOEA FAILURE

↑ Urea

↑ Cyanate

STEROID

↑Glucose Sorbital

↓NADPH ↑G-6-P fructose

↓ GSH PROTEIN MODIFICATION

Croslinkng bt proteins

Aggregation of proteins

Ionic imbalance

OTHER FACTOR INFLUENCING CATARACT :-

CONGENITAL

ACQUIRED

METABOLIC

TRAUMATIC

COMPLICATED

TOXIC

SENILE

INFECTIOUS

14% Of all cases of childhood blindness

20% - RUBELLA20% - HEREDITARY . DOMINANT 6% - WITH OCCULAR ANOMALIES35-50% - SPORADIC

5 % EACH

TAKE HOME……

Senile Cataract Is always multifactorial….

Poor control & high diabetic age…..

Congenital cataract – rubella,again is preventable

Public education- can result better utility of services

And…

Health & Medicine

Cataract