Pathophysiology of glaucoma in uveitis.
Glaucoma secondary to uveitis may occur by any one or by a combination of several different pathophysiological mechanisms. These include acute angle-closure due to iris bombé caused by posterior synechiae; chronic angle-closure due to peripheral anterior synechiae; and open angle glaucoma due to obstruction and/or inflammation of the trabecular meshwork. Secretory hypotony may mask impairment of outflow, while steroids used to treat the uveitis may further complicate the situation by causing a rise in intraocular pressure. Careful delineation of the pathophysiology involved is the cornerstone of successful management.
D000305:Adrenal Cortex Hormones / Q000009:adverse effects; D005901:Glaucoma / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D005902:Glaucoma, Open-Angle / Q000209:etiology; D006801:Humans; D007429:Intraocular Pressure / Q000187:drug effects; D009798:Ocular Hypertension / Q000209:etiology; D000267:Tissue Adhesions / Q000209:etiology; D014129:Trabecular Meshwork; D014605:Uveitis / Q000150:complications* / Q000473:pathology
D000305:Adrenal Cortex Hormones