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



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