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Anatomy of the Eye By visual examination we can see Eyelids, cilia (eyelashes) and the openings of the tarsal (sebaceous) glands along the edges Palpebral fissure Lateral and medial canthi Lacrimal lake containing the lacrimal caruncle Plica semilunaris (loose fold of bulbar conjunctiva) Superior and inferior lacrimal puncta within their lacrimal papillae Bulbar and palpebral conjunctiva Sclera Corneoscleral junction (limbus) Cornea Pupil and iris Layers of the Eye Fibrous layer o Cornea o Sclera Vascular layer o Choroid o Ciliary body o Iris Neural layer o Retina o Optic disc (blind spot) Compartments and Chambers of the Eye Anterior Compartment o Anterior chamber Between the cornea and iris o Posterior chamber Between the iris, zonular fibres and lens Posterior Compartment o Vitreous chamber Between the lens and the retina Optic Nerve & The Visual Pathway Embryologically the optic nerve and retina develop as a diverticulum (outpouching) of the forebrain. The retina is made up of 3 layers: Receptor cells: rods & cones Intermediate layer: bipolar cells Ganglion cells whose axons converge at the optic disc, pierce the schlera and forms the optic nerve Optic Nerve The optic nerve passes through the optic foramen until it reaches the optic groove on the sphenoid. Here the fibres of the: Medial half of the retina (concerned with the temporal visual field) cross over in the optic chiasma Lateral half of the retina (concerned with the nasal visual field) pass back in the optic tract of the same side Optic Tract Most of the fibres of the optic tract end in the geniculate body. Some fibres are used for pupillary and visual body (head and neck reflexes) and bypass the geniculate body but go to the superior colliculus or pretectal regions. The reflexes are: Direct and Consensual Light Reflex Optic nerve -> optic tract -> pretectal nucleus -> accessory oculomotor nucleus (Edinger-Westphal) -> CNIII -> pupils constrict Accommodation Reflex When the eye follows a distant object brought close, three things happen Lens thickens by contraction of the ciliary muscles Pupil constricts Medial rectus muscles cause convergence This calls for a more complex pathway: Visual Body Reflex The visual body reflex is involved in: o Automatic scanning movements of the eyes & head that are made when reading o Automatic movements of the eyes, head & neck towards the visual stimulus o Protective closing of the eyes & raising arm for protection (followed by the reflex vocalisation: “Oh shit”) UV Light and the Eyes The Cornea and Lens The cornea and lens are the principal targets of UV radiation (UVR) damage, therefore, a brief mention of their histology. In both cases, light is transmitted through both structures because they are predominantly acellular internally and made up of parallel fibres allowing visible light to pass through them. The cornea is made up of 5 layers but 90% of it is made up of a stromal layer made up of parallel collagen fibres together with some sparsely separated keratinocytes. The lens is covered by a collagen capsule and has a simple cuboidal epithelium on the anterior surface. At the equatorial zone, they lose their organelles and elongate into fibres, which are pushed in towards the posterior pole of the lens. New fibres compress one on top of another in parallel forming the bulk of the interior of the lens. This differentiation is controlled by changing growth factor concentrations (Eg FGF, IGF, PDGF) along the surface of the lens. UV Radiation UVR is broken down into three main spectrums UVA (320-390 nm) UVB (290-320 nm) is most implicated in cancer formation. UVC (230-290 nm) UVB and UVA penetrate the cornea and exposure can come from o Direct sunlight o Reflections from Snow Sand Glass, chrome, concrete, shiny surfaces UVC is the shortest wavelength UV that is completely absorbed by the cornea. UVC exposure can come from High altitude snow reflection Welding arcs UVR causes tissue damage in two ways: o Molecular Fragmentation: molecules containing alternating double bonds (proteins, nucleic acids) resonate at UVR (especially UVB/C) frequencies and break. These then form new bonds causing DNA mutations and loss of protein function. o Free Radical Formation: pigmented molecules making up the vascular layer of the eye form long chains of alternating double bonds that are susceptible to UVR. The bonds can eject electrons that are captured by adjacent molecules (eg H2O + electron + H+ becomes H2O2), turning them into reactive oxides and peroxides that can break or create bonds within proteins and nucleotides causing DNA mutations and function loss. UV Vulnerability(5) The Elderly Basically, UV radiation catalyses reactions forming reactive molecules that are able to create or destroy bonds in other molecules (proteins, nucleotides) leading to tissue damage and loss of function. The body’s defence mechanisms protecting it from UV radiation include scavenger molecules: Carotene Superoxide dismutase Glutathione Vitamins C and E Caplains (mop up protein breakdown products in the lens(6) These become depleted in the elderly and macular degeneration and cataract formation is accelerated. Eye protection becomes even more crucial in this age group. Lightly Pigmented Individuals The lighter the eye pigmentation, the greater the prevalence of age related macular degeneration (it is almost unknown in genetically pure Negroes) Use of Photosensitizing Drugs A number of drugs absorb UV light and produce free radicals, damaging the retina and lens. These include: Phenothiazines (“Phenergan” and “Mersyndol” antihistamines, older antipsychotics) Allopurinol (common gout treatment) Tetracycline antibiotics Pathologies Likely To Be Caused By Exposure to the Different UV Spectra UVB exposure causes o Conjunctival damage Squamous cell carcinoma caused by prolonged and repeated damage to DNA by creating bonds between CC which DNA polymerase interprets as AA. TT forms in the growing strand, creating the C-T mutation signature of SCC caused by UVB Actinic conjunctivitis (acute inflammation caused by excessive exposure) Pinguecula (yellow deposit adjacent to the limbus) Hyperkeratosis Pterygium (release of stress induced cytokines producing a wedge shaped area of fibrosis, chronic inflammation, cell growth and angiogenesis(1) o Lens damage Cataracts Def: clouding or opacification of the lens 10% of cataracts are directly caused by UVB. Altogether 160,000 are treated annually in Australia(2) Pathophysiology of cataracts o UVB (and possibly UVA) causes changes in lens proteins either directly through molecular transformation or by production of free radicals, mainly, H2O2 , causing them to precipitate and become opaque. This process is exacerbated in certain chronically ill or elderly patients by the addition of small molecules to the proteins (post translational modifications): photooxidation products which accumulate in the elderly and bind to proteins Glycation in diabetics Cyanate from high urea levels in renal failure Excessive retention of copper (Wilson’s disease) and iron (haemochromatosis) produce reactive hydroxyl radicals o Changes to balance of growth factor concentrations at the surface of the lens (affected by corticosteroids, chemotherapy, cancers, metabolic disorders such as diabetes) prevents differentiation into fibres, causing nucleated cells to cover the posterior surface of the lens, causing a type of cataract (posterior subcapsular cataract). o Alteration of intracellular calcium metabolism causing the formation of calcium salts and binding to proteins causing light scattering. Corticosteroids mobilise Ca++ salts and are a major culprit. Nuclear Sclerosis o Because the proteins at the centre of the lens are the oldest (as old as the individual), cataracts often form here in the elderly and this type of cataract is called nuclear sclerosis. o Vascular Layer damage Choroidal melanoma is the most common cancer of the eyeball(3). UVA penetrates further and can cause damage to deeper structures within the eye o Lens Together with UVB contributes to cataract formation o Vascular layer Was originally considered the likely cause melanoma but this has since been found to be unlikely, with UVB remaining the main culprit(4). o Neural layer Macular degeneration UVC is completely absorbed by the cornea and causes o Photokeratitis: acute damage to corneal epithelium, stroma and in severe cases, endothelial cells of the cornea resulting in “snow blindness” or “welders arc eye”. Epithelial cells are shed into the tear film which can be seen as dots of debris. The exposed nerve fibre ending resulting in intense pain and an ongoing corneal reflex where the sufferer becomes “blinded” by blepharospasm (inability to open his eyelids). The main clinical signs and symptoms (which can appear several hours after exposure) of photokeratitis are: o Foreign body sensation o Gritty feeling o Tearing (containing conjunctival discharge and cellular debris) o Pain o Symptoms abate within two days with no permanent damage to the cornea. 1. Di Girolamo N, Wakefield D, Coroneo MT. UVB-mediated induction of cytokines and growth factors in pterygium epithelial cells involves cell surface receptors and intracellular signaling. Invest Ophthalmol Vis Sci. 2006;47(6):2430-7. 2. Council TC. Eye Protection From Ultraviolet Radiation. 2006. 3. American Society of Clinical Oncology. Eye Cancer | Cancer.Net. 2010; Available from: http://www.cancer.net/patient/Cancer+Types/Eye+Cancer. 4. De Fabo A, Noonan F, Fears T, Merlino G. Ultraviolet B But Not Ultraviolet A Initiates Melanoma. Cancer Res. September 15, 2004;64(6372). 5. Ultraviolet Vulnerability. In: Yanoff, Duker, editors. Ophthalmology. 3rd ed2008. 6. PATHOPHYSIOLOGY OF CATARACTS. In: Yanoff, Duker, editors. Ophthalmology2008.
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