Glaucoma Overview

Glaucoma be categorized as

Glaucoma is a group of eye diseases that are characterized by progressive damage to the optic nerve and in which an important part is a relative elevation of intraocular pressure (IOP). Glaucoma is the second leading cause of blindness worldwide and the second leading cause of blindness in the US, where it is the leading cause of blindness in people of African ethnicity and Latin Americans. About 3 million Americans and 14 million people worldwide have glaucoma, but only half of it is known. However, glaucoma occur at any age, more than 60-year-old six times more frequently. Glaucoma be categorized as open-angle glaucoma Closed-angle glaucoma open angle glaucoma: classification based on mechanisms of outflow obstruction *, and refer to the table: cause developmental abnormalities of the angle, the Glaucoma: Classification based on mechanisms of outflow obstruction *, see table: narrow-angle glaucoma classification based on mechanisms of outflow obstruction *. As “chamber angle” means the angle is referred to, which is formed by the meeting of the iris and cornea in the periphery of the anterior chamber of the eye (aqueous humor production and flow.). > 98% of the aqueous humor exits the eye via the trabecular meshwork in the chamber angle and from there into Schlemm’s canal (Hauptabflussweg, especially in the elderly), or over the surface of the ciliary body in the choroidal vessels (uveoskleraler outflow). This drainage system not only acts as a mechanical filter and drainage path, but includes active physiological processes with one. Glaucoma are also still (in which the cause of the outflow obstruction or closure chamber angle is not known) in primary and secondary glaucoma divided (the outflow is prevented by a known disease), which account for> 20% of the adult forms. Open-angle glaucoma: classification based on mechanisms of outflow obstruction * Type causes Examples trabecular Idiopathic – Chronic open angle glaucoma juvenile glaucoma obstruction by erythrocyte ghost cells glaucoma Hemorrhagic glaucoma Macrophage Hemolytic glaucoma Melanomalytisches glaucoma Phakolytisches glaucoma pigmentary glaucoma uveitis (capsulare glaucoma) by neoplastic cells juvenile xanthogranuloma Malignant tumors neurofibromatosis nevus Ota by pigment particles Pseudoexfoliation by protein lens-induced uveitis glaucoma by drugs Corticosteroidinduziertes glaucoma Due to other causes ?-Chymotrypsininduziertes glaucoma Viscoelastic agents vitreous hemorrhage changes due to edema alkali burns iritis or uveitis, scleritis or episcleritis cause the eineTrabekulitis due to trauma chamber angle recessus due to intraocular foreign body Chalkose Hemosiderosis Posttrabekulär Obstruction Of Schlemm’s canal blockage of the channel (eg. As by sickle cells) collapse of the channel Other Increased episcleral venous pressure carotid cavernous fistula cavernous sinus thrombosis Idiopathic episcleral venous pressure increase Mediastinal tumors Infiltrative ophthalmopathy (thyreotroper exophthalmos) Retrobulbar tumors Sturge-Weber syndrome are obstruction of superior vena cava * It clinical Examples cited; no comprehensive list of glaucoma. . Adapted from Ritch R, Shields MB Krupin T: The Glaucomas, ed 2. St. Louis, Mosby, 1996, p 720; by permission. Angle-closure glaucoma: classification based on mechanisms of outflow obstruction * Type disturbances examples Anterior (pull mechanism) contraction of membranes Iridokorneales endothelial syndrome neovascular glaucoma Posterior polymorphous dystrophy surgery (. Eg corneal transplant) trauma (penetrating and nichtpenetrierend) – contraction inflammatory deposits – – Inflammatory membrane Fuchs Heterochromieiridozyklitis Interstitial keratitis by syphilis – Posterior (printing mechanism) with lens-induced pupillary mechanisms Intumescent lens subluxation of the lens Mobiles lenses syndrome Posterior synechiae pupillary in aphakia pseudophakia uveitis pupillary block glaucoma – Without pupillary block glaucoma Malignant (Ziliarblock) – cysts of the iris and ciliary body – Anterior displacement of the glass body by lens extraction – intraocular tumors Malignant Melanoma Retinoblastoma lens-induced mechanisms Intumescent lens subluxation of the lens Mobiles Lenses syndrome plateau iris syndrome – uveal edema after scleral buckling, panretinal photocoagulation or central retinal vein occlusion of the retinal tissue contraction Retrolentikuläre Persistent hyperplastic primary vitreous retinopathy of prematurity (retrolental fibroplasia) * There are clinical examples cited; no comprehensive list of glaucoma. . Adapted from Ritch R, Shields MB Krupin T: The Glaucomas, ed 2. St. Louis, Mosby, 1996, p 720; by permission. Developmental abnormalities of the angle that cause glaucoma: classification based on mechanisms of outflow obstruction * mechanism disorders High inserting the peripheral iris Axenfeld-Rieger syndrome Peters anomaly Incomplete development of the trabecular meshwork or Schlemm’s canal Congenital (infantile) glaucoma glaucoma that associated with other developmental disorders are angle block by contraction of fine strands aniridia * There are clinical examples cited; no comprehensive list of glaucoma. . Adapted from Ritch R, Shields MB Krupin T: The Glaucomas, ed 2. St. Louis, Mosby, 1996, p 720; by permission. Aqueous humor production and flow. Most of which is produced by the ciliary body of the aqueous humor, leaving the eye in the chamber angle, which is formed by the meeting of the iris and cornea. It occurs primarily via the trabecular meshwork and Schlemm’s canal. Pathophysiology The optic nerve extending axons of retinal ganglion cells carry the visual information from the eye to the brain. Damage to those axons lead to the destruction of nerve cells, resulting in optic nerve damage and visual field defects result. In the axonal damage, increased IOP plays (in unaffected eyes the average range is 11 to 21 mmHg) a role, either by direct nerve compression or decreased blood flow. However, the relationship between externally measured pressure and nerve damage is complicated. Of the people with an IOP> 21 mmHg (d. E. With ocular hypertension) develop only 1-2% / year (about 10% in 5 years) glaucoma. In addition, one-third of patients with glaucoma has no IOP> 21 mmHg (known as low-tension glaucoma or normal tension glaucoma). One factor could be that the externally measured IOP does not always reflect the true IOP; corneal thickness may be thinner than the average, which leads to a higher intraocular pressure measurement or thicker than average, wad leads to lower intraocular pressure measurement. Another factor could be that a vascular disorder affecting the blood supply to the optic nerve. It is also likely that there are factors within the optic nerve that influence susceptibility to damage. The IOP is determined by the balance between aqueous humor and Drainage. An elevated IOP caused by inhibited or impeded runoff and not oversecretion, which seems to be a combination of factors involved in the trabecular meshwork. In an open-angle glaucoma, the IOP is elevated because the outflow is insufficient, although the chamber angle not appear locked. When angle-closure glaucoma IOP is increased because the peripheral iris to the outflow mechanically blocked. Glaucoma var model = {videoId: ‘4604452640001’ playerId: ‘H1xmEWTatg_default’ imageUrl: ‘http://f1.media.brightcove.com/8/3850378299001/3850378299001_4817481336001_017-Glaucoma.jpg?pubId=3850378299001&videoId=4604452640001’, title : ‘glaucoma’, description: ‘ u003Ca id = “v37894257 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eIm inside the eye There are two fluid-filled chambers. (Also known as aqueous humor) Intraokularflüssigkeit is responsible for maintaining adequate pressure conditions inside the eye

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