Primary Open-Angle Glaucoma: Pathogenesis and Clinical Findings • Risk factors -> Incr IOP, Incr age, African-American heritage, positive family history, diabetes mellitus, myopia, vascular disease • Genetic predisposition -> Incr susceptibility of individuals with mutations in MYOC gene encoding myocilin, OPTN gene encoding optineurin, or NTF4 or WDR36 genes. • Steroid responsiveness -> Incr IOP in response to intra- or peri-ocular steroid administration -> Altered myocilin production in trabecular meshwork => Primary Open-Angle Glaucoma -> Calcium ion influx and NO in retinal ganglion cells -> Retinal ganglion cell injury -> Astrocyte and glial cell proliferation and alteration in ECM or lamina cribosa -> Optic nerve head remodeling - Direct mechanical damage to optic nerve head - Ischemic damage due to compression of blood vessels supplying the optic nerve -> Decr axoplasmic flow, Decr delivery of nutrients, deprivation or neuronal growth factors, oxidative injury, and initiation of immune mediated damage -> Apoptosis of retinal ganglion cells - RNFL thinning and glaucomatous cupping observed on fundus examination - RNFL thinning and glaucomatous cupping observed on optic disc or peri-papillary RNFL imaging -> Progressive VF defects => End-stage visual field loss with retained small island of central vision #Secondary #OpenAngle #Glaucoma #pathophysiology #ophthalmology
