EYE AND AGING POWERPOINT PRESENTATION PPT

EYE AND AGING

1. EYE AND AGING DR. ASISHA ANILKUMAR JUNIOR RESIDENT DEPT. OF OPHTHALMOLOGY

2. ability to maintain physiologic homeostasis under conditions of biologic stress declines. In the phenomenon of aging, physiologic and anatomic changes should be universal to the species degenerative Progressive intrinsic

3. EYELIDS AND PERIOCULAR SKIN thinner and less elastic ↓ collagen and elastin with increased skin wrinkling ↓ eccrine and apocrine secretions ↓ basal epithelium proliferation &superficial desquamation Vessels more dilated and tortuous ↑ meibomian secretions ↓ pigmentation eyelashes and brow

4. PHOTOAGING OF EYELID SKIN Sun exposure creates additional changes in the aging eyelid influenced by numerous genetic and environmental factors. Genetic factors degree of melanin deposition efficiency of radiation induced repair to DNA.

5. ACTINIC KERATOSES ultraviolet light-induced changes epidermal acanthocytes irregular thickening of the stratum spongiosum (acanthosis) with hyperkeratosis and parakeratosis most common premalignant skin lesions

6. AGING EFFECTS ON EYELID MALPOSITIONS INVOLUTIONAL BLEPHAROPTOSIS bilateral with retained levator function decreased upper lid elevation, especially on upgaze

7. BROW PTOSIS. caused by generalised descent of the brow. ptosis is relieved by manually lifting up the brow

8. Dermatochalasis Ectropion Entopion

9. AGING CHANGES IN PALPEBRAL CONJUNCTIVA no decrease in goblet cell numbers increased vascular lumen size decreased number capillaries/mm2 thinning of connective tissue in substantia propria increased fragmentation of collagen elastotic changes are much less common

10. LACRIMAL GLAND AND DRAINAGE SYSTEM ↓ quantity and quality of tears increased periductal fibrosis Males < Females enlargement & proliferation of lacrimal ducts within palpebral lobes caused by stenosis

11. ↑ lymphocyte infiltration without known glandular disease. Production of immunoglobulin A and secretory component (acinar cells), antibodies, chemotactic factors, and leukokines subclinical dacryoadenitis ↓tear drainage - weakened lacrimal pump mechanism (secondary to changes in lid muscle and connective tissue compartment) or to an increased drainage resistance. widening of middle nasolacrimal duct in men

12. CORNEA no change in corneal diameter & thickness curvature becomes steeper astigmatism - ‘against the rule’ sialylated residues in mucin component - adherence of several bacterial organisms and susceptibility to corneal infection ↓ corneal touch sensitivity & corneal luster

13. FUCHS’ DIMPLES local atherosclerotic/ neurotrophic factors / by desiccation shallow, elliptical excavations 1.5–2 mm in diameter, with clearly defined edges, sloping borders, faint opacity in the floor Transient - last up to 48 h HPE - focal thinning / loss of surface epithelium, Bowman’s membrane or anterior stroma

14. HUDSON-STAHLI LINE Deposition of iron - cytoplasm of corneal epithelial cells Clinically - slightly brown best seen under cobalt blue illumination deeper cellular layers of the epithelium

15. EPITHELIAL BASEMENT MEMBRANE DYSTROPHY(COGAN’S DYSTROPHY) Bilateral Females Sporadic / AD alterations in attachment of epithelium to basement membrane

16. Collagen changes  polygonal opacities bordered by clear translucent lines which intersect around the opacities in a mosaic pattern. Appearance of ‘crocodile skin’ Term ‘anterior crocodile shagreen’ (mosaic shagreen of Vogt) bilateral

17. VOGT LIMBAL GIRDLE a linear yellow-white opacification of the corneal limbus Women more common nasally Type I - If separated from limbus by a clear interval Type II - confluent with the limbus, and the central edge is more ragged. HPE - degeneration of Bowman’s layer, anterior stroma, with deposition of calcium, hyalinization & elastotic degeneration

18. ARCUS SENILIS cholesterol, cholesterol esters, neutral fats phospholipids in peripheral corneal stroma separated from the limbus by a clear zone - lucid interval of Vogt

19. Band keratopathy calcium salts in Bowman layer, epithelial basement membrane and anterior stroma

20. Hassall-Henle bodies Arise from descemets membrane are localised thickenings in periphery of endothelium If occur axially in the corneal endothelium - called cornea guttata

21. CONJUNCTIVA epithelial thickness ↑ - tranparency ↓ subepithelial layers - thinning & atrophy, with elastin degeneration and hyaline deposition vessels demonstrate fusiform dilatations and increased varicosity PINGUECULAE. yellow-white, triangular patches in bulbar conjunctiva nasal > temporal

22. Concretions common and associated with ageing, appear as yellowish–white tiny cysts deposits epithelial debris including keratin located subepithelially in inferior tarsal conjunctiva become calcified / erode through the overlying epithelium

23. Conjunctivochalasis a fold of redundant conjunctiva between globe & lower eyelid Protruding over the lid margin exacerbated by inflammation, mechanical stress related to dry eye and lid margin disease. Conjunctival resection can be performed in severe cases

24. Aging of Iris Pigment loss  iris transillumination defect (pupillary margin) increased sclerosis of blood vessels Pupil smaller & less reactive with age thinning and flattening of stroma loss of iris crypts

25. TRABECULAR MESHWORK Gonioscopy - increased pigmentation of trabecular meshwork. shape change from wedge-shaped to rhomboid hyalinazation of basement membrane of epithelium reduction in trabecular endothelium decrease in circumferential area of Schlemm’s canal ↑ resistance to aqueous humor outflow may precipitate glaucoma.

26. AGING CHANGES IN THE AQUEOUS HUMOR a ↓of 2.5% per decade after the age of 30 years. Aging changes in epithelial cell metabolism basement membrane integrity ciliary process vasculature pattern

27. CHANGES IN AGEING LENS Weight and thickness increases Light transmission by lower wavelength decrease; light absorbance increases Light scattering increases Fluorescein property increases Alpha crystallins disappear from nucleus Betacrystallins - more polydispersed Loss of gamma crystallins

28. Proliferative capacity of lens epithelial cells decrease Enzyme activities decrease Increase in urea soluble proteins Glutathione and ascorbic acid levels decrease Loss of lipids, membrane and cytoskeletal proteins Loss of membrane potential and increase in Na and Ca

29. CATARACTOGENESIS Mechanisms Precipitation denaturation coagulation agglutination of soluble lens proteins

30. Mechanism

31. CHANGES IN GANGLION CELL AND NERVE FIBER LAYER 25% of ganglion cells More in alzheimers Lipofuscin accumulates Astrocytes ↓ number & thicker

32. Corpora amylacea whirls of eosinophilic material associated with degenerating and aging neural tissue.

33. CHANGES IN THE RETINAL CIRCULATION Differential rates of disappearance endothelial cells & pericytes formation of microaneurysms, vascular loops, shunts. Hyalinization, ↑ thickness of basement membrane FAZ - ↓from 0.7 mm in children to 0.5 mm by 40 yrs

34. CHANGES IN THE CHOROID AND CHOROIDAL CIRCULATION decreased density of choriocapillaris thinning of choroids migration of melanin from inner to outer regions together with decreased melanin content in the overlying RPE, increased visability of choroidal vessels appearance - tigroid fundus

35. FINDINGS IN CLINICAL APPEARANCE OF THE RETINA decrease in fundus reflex Peripheral microcystoid degeneration (outer plexiform layer region) ↓ increase incidence of senile retinoschisis

36. PAVINGSTONE DEGENERATION OF PERIPHERAL FUNDUS a well-circumscribed obliteration of choriocapillaris degeneration of outer retina and RPE at peripheral fundus locations

37. CHANGES IN BRUCH’S MEMBRANE collections of lipid material between basement membrane of RPE cells & inner zone of Bruch’s membrane known as basolaminar deposits or ‘early drusen’

38. AGE-RELATED MACULAR DEGENERATION drusen and RPE changes in the absence of another disorder Dry (non-exudative, non-neovascular) most common form90% Intermediate- large drusen Hyper/ Hypo pigmentation of RPE RPE atrophy  geographic atrophy Drusenoid RPE detachment

39. Wet (exudative, neovascular) less common more rapid progression to sight loss. The main clinical entities are: CNV, pigment epithelial detachment (PED) retinal angiomatous proliferation (RAP) polypoidal choroidal vasculopathy (PCV).

40. OPTIC NERVE No changes in axon numbers Thinnig of neuroretinal rim in nonglaucomatous aging eyes ↓ blood flow to neuroretinal rims Corpora arenacea (psammoma bodies) - arachnoid concentrically laminated noncellular bodies appear hyalinized and calcified

41. Corpora amylacea smaller, noncalcified, stain poorly with H & E (pale blue) not present in the meninges located within the neural substance, Lipofuscin accumulates in the aged optic nerve and disk

42. VITREOUS liquefaction of central vitreous increase in sodium hyaluronate after age 70 increase in soluble protein concentration increase in vitreous condensation Floaters

43. POSTERIOR VITREOUS DETACHMENT Separation of posterior vitreous from retina

44. Sclera ↑ scleral rigidity yellow appearance due to lipids changes in proteoglycan concentrations & ↓ decreased collagen turnover Development of senile scleral plaques

45. blue, brown, or slightly clear anterior to horizontal rectus muscle insertions bilateral expulsed leaving a crater in the sclera scleromalacia perforans well-defined margins lack of necrosis

46. Idiopathic sclerochoroidal calcification both eyes Geographical yellow–white multiple fundus lesions with illdefined margins supero / inferotemporal mid-periphery associated with vascular arcades USG- highly reflective choroidal plaquelike lesions with orbital shadowing.

47. THANK YOU