logging in or signing up anterior uveitis hari_yadav_2009 Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 3243 Category: Education License: All Rights Reserved Like it (4) Dislike it (0) Added: October 06, 2010 This Presentation is Public Favorites: 1 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript UVEITIS : UVEITIS HARIKRISHNA CHANDRAKANI Mamata medical college Titans batch khammam INTRODUCTION : INTRODUCTION The uvea is the middle portion of the eye. The term derives from the Latin word for grape, since anatomists once thought that the peeling of the outside of the eye left a grape-like structure beneath. The anterior portion of the uvea includes the iris and ciliary body; the posterior portion of the uvea is known as the choroid . Inflammation of the anterior uveal tract is called anterior uveitis, and is synonymous with iritis. When the adjacent ciliary body is also inflamed, the process is known as iridocyclitis. Terms used to describe uveitis posterior to the lens include vitritis, intermediate uveitis, pars planitis, choroiditis, retinitis, chorioretinitis, or retinochoroiditis. CLASSIFICATIONETIOLOGY PATHOLOGY OF ANTERIOR UVEITIS : CLASSIFICATIONETIOLOGY PATHOLOGY OF ANTERIOR UVEITIS CLASSIFICATION : CLASSIFICATION Anterior uveitis: It is inflammation of the uveal tissue from iris up to pars plicata of ciliary body. subdivided into Iritis : in which inflammation predominantly affects the iris. Iridocyclitis : in which iris and pars plicata part of ciliary body are equally involved, and Cyclitis : in which pars plicata part of ciliary body is predominantly affected. continue. . . I. ANATOMICAL CLASSIFICATION continue. . . : 2. Intermediate uveitis : Intermediate uveitis refers to inflammation localized to the anterior vitreous, pars plana of ciliary body and peripheral retina. 3. Posterior uveitis : It refers to inflammation of the choroid (choroiditis). Always there is associated inflammation of retina and hence the term ‘chorioretinitis’ is used. 4. Panuveitis : It is inflammation of the whole uvea. continue. . . conti. . . II. CLINICAL CLASSIFICATION : II. CLINICAL CLASSIFICATION 1. Acute uveitis : It is a sudden symptomatic onset and the disease lasts for about six weeks to 3 months. 2. Chronic uveitis : It is an insiduous and asymptomatic onset. It persists longer than 3 months to even years and is usually diagnosed when it causes defective vision. III. PATHOLOGICAL CLASSIFICATION : III. PATHOLOGICAL CLASSIFICATION 1. Suppurative or purulent uveitis. 2. Non-suppurative uveitis. It is subdivided in two groups (Wood’s classification). (i) Non-granulomatous uveitis. (ii) Granulomatous uveitis. IV. ETIOLOGICAL (DUKE ELDER'S) CLASSIFICATION : IV. ETIOLOGICAL (DUKE ELDER'S) CLASSIFICATION 1. Infective uveitis 2. Allergic uveitis 3. Toxic uveitis 4. Traumatic uveitis 5. Uveitis associated with non-infective systemic diseases 6. Idiopathic uveitis ETIOLOGY : ETIOLOGY The etiological concepts of uveitis as proposed by Duke Elder. 1. Infective uveitis: Modes of infection a.Exogenous infection.. i. Perforation of corneal ulcer ii. Postoperatively b. Secondary infection i. Spread of infection from neighbouring structures e.g: acute purulent conjunctivitis. (pneumo-coccal and Gonococcal), keratitis, scleritis, retinitis, orbital Cellulitis. ii. Endogenous infections e.g: Entrance of organisms by the way of bloodstream conti. . . continue. . . : Types of infectious uveitis : i. Bacterial infections: Tubercular,leprotic,syphilitic,brucellosis(granulomatous) Streptococci,staphylococci, pneumococci and gonococcus.(pyogenic) ii. Viral infections: Herpes simplex, herpes zoster and cytomegalo inclusion virus (CMV). iii. Fungal uveitis : Aspergillosis, Candidiasis Blastomycosis. continue. . . conti. . . continue. . . : iV. Parasitic uveitis is known in Toxoplasmosis, Toxocariasis, Onchocerciasis Amoebiasis V. Rickettsial uveitis: Scrub typhus Epidemic typhus continue. . . conti. . . : 2. Allergic (hypersensitivity linked) uveitis i . Microbial allergy Escape of the organisms or their products from the primary source of infection into the bloodstream causes sensitisation of the uveal tissue with formation of antibodies. At a later date a renewal of infection in the original focus may again cause dissemination of the organisms or their products (antigens); which on meeting the sensitised uveal tissue excite an allergic inflammatory response. Eg : Tubercular lesion in the lymph nodes or lungs. conti. . . continue. . . : ii. Anaphylactic uveitis. e.g :serum sickness and angioneurotic oedema. iii. Atopic uveitis. It occurs due to airborne allergens and inhalants e.g : seasonal iritis due to pollens,danders of cats, chicken feather, house dust, egg albumin and beef proteins. continue. . . conti. . . continue. . . : iv. Autoimmune uveitis. It is found in association with autoimmune disorders such as Rheumatoid arthritis, Wegener’s granulomatosis, Systemic lupus erythematosus, Reiter’s disease. In phacoanaphytic endophthalmitis, lens proteins play role of autoantigens. Sympathetic Ophthalmitis an autoimmune reaction to uveal pigments. continue. . . conti. . . Slide 16: v. HLA-associated uveitis: HLA-B27. Acute anterior uveitis associated with ankylosing spondylitis and also in Reiter’s syndrome. HLA-B5: Uveitis in Behcet’s disease. HLA-DR4 and DW15: Vogt Koyanagi Harada’s disease. continue. . . Slide 17: 3. Toxic uveitis : i. Endotoxins Acute pneumococcal or gonococcal conjunctivitis is due to microbial toxins. ii. Endocular toxins E.g: Uveitis seen in patients with blind eyes, long standing retinal detachment and intraocular haemorrhages is due to endocular toxins. iii. Exogenous toxins causing uveitis are Irritant chemical substances of inorganic, animal or vegetative origin. Drugs producing uveitis (such as miotics and cytotoxic drugs). Slide 18: 4. Traumatic uveitis: Direct mechanical effects of trauma. Irritative effects of blood products after intraocular haemorrhage. Microbial invasion. Chemical effects of retained intraocular foreign bodies and Sympathetic ophthalmia in the other eye. Slide 19: 5. Uveitis associated with non-infective systemic diseases: Sarocoidosis, Collagen related diseases (polyarteritis nodosa (PAN), Disseminated lupus erythematosus(DLE), Rheumatic and rheumatoid arthritis), Metabolic diseases (diabetes mellitus and gout). Disease of the central nervous system (e.g., disseminated sclerosis) and Diseases of skin (psoriasis,erythema nodosum). Slide 20: 6. Idiopathic uveitis : i. Idiopathic specific uveitis :the conditions which have certain special characteristics of their own. e.g :pars planitis,sympathetic Ophthalmitis. ii. Nonspecific idiopathic uveitis the conditions which do not belong to any of the known etiological groups, more than 25% cases of uveitis fall in this group. PATHOLOGY : PATHOLOGY 1. Pathology of suppurative uveitis: Purulent inflammation of the uvea is usually a part of endophthalmitis or panophthalmitis. It is characterised by an outpouring of purulent exudate and infiltration by polymorphonuclear cells of uveal tissue, anterior chamber, posterior chamber and vitreous cavity. As a result, the whole uveal tissue is thickened and necrotic and the cavities of eye become filled with pus. Slide 22: 2. Pathology of non-granulomatous uveitis: It consists of marked dilatation and increased permeability of vessels. Breakdown of blood aqueous barrier with an outpouring of fibrinous exudate. Infiltration by lymphocytes, plasma cells and large macrophages of the uveal tissue,into anterior chamber, posterior chamber and vitreous cavity. The inflammation is usually diffuse. iris becomes waterlogged, oedematous, muddy with blurring of crypts and furrows. conti. . . Slide 23: As a consequence its mobility is reduced, pupil becomes small in size due to sphincter irritation and engorgement of radial vessels of iris. Exudates and lymphocytes poured into the anterior chamber result in aqueous flare and deposition of fine Keratic Precipitates(KPs) at the back of cornea. Due to exudates in the posterior chamber, the posterior surface of iris adheres to the anterior capsule of lens leading to posterior synechiae formation. continue. . . conti. . . Slide 24: In severe inflammation, due to pouring of exudate from ciliary processes, behind the lens, an exudative membrane called cyclitic membrane may be formed. After healing, pin-point areas of necrosis or atrophy are evident. Subsequent attacks lead to structural changes like atrophy and fibrosis which cause adhesions, scarring and eventually destruction of eye. continue. . . Slide 25: 3. Pathology of granulomatous uveitis : In this,there is infiltration with lymphocytes,plasma cells, with mobilization and proliferation of large mononuclear cells which eventually become epithelioid and giant cells and aggregate into nodules. Iris nodules are usually formed near pupillary border (Koeppe’s nodules). Similar nodular collection of the cells is deposited at the back of cornea in the form of mutton fat keratic precipitates. Necrosis in the adjacent structures leads to a repairative process resulting in fibrosis. Keratic precipitates (KPs)Clinical photograph of a patient withgranulomatous anterior uveitis showing mutten fat KPsand broad segmental synechiae. : Keratic precipitates (KPs)Clinical photograph of a patient withgranulomatous anterior uveitis showing mutten fat KPsand broad segmental synechiae. Thank You : Thank You You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.