Glaucoma, Primary Open-Angle
Primary open-angle glaucoma (POAG) is a chronic, progressive optic neuropathy which causes loss of the optic nerve rim and retinal nerve fiber layer (RNFL) with associated visual field defects. POAG is associated with increased intraocular pressure (IOP). Normal IOP is 10 to 21 mm Hg.
Prostaglandins should be avoided during pregnancy in the treatment of POAG.
Predominant age: usually >40 years
Prevalence in persons >40 years of age is ~1.8%.
Etiology and Pathophysiology
- Aqueous is produced by the ciliary epithelium of the ciliary body and is secreted into the posterior chamber of the eye. Aqueous then flows through the pupil and enters the anterior chamber to be drained by the trabecular meshwork (TM) in the iridocorneal angle of the eye. It then drains into the Schlemm canal and passes into the episcleral venous system. 5–10% of the total aqueous outflow leaves via the uveoscleral pathway.
- Impaired aqueous outflow through the TM leads to greater resistance in the aqueous drainage system and causes an increase in IOP.
- A family history of glaucoma increases the risk for developing glaucoma.
- TMCO1 genotype has been found to increase the risk of developing glaucoma among non-Hispanic whites.
- The myocilin (MYOC) gene was the first gene associated with POAG.
- Increased IOP
- Diabetes mellitus (DM)
- Positive family history
- Prolonged use of topical, periocular, inhaled, or systemic corticosteroids
- Systemic calcium-channel blockers
- Prior history pars plana vitrectomy
- Obstructive sleep apnea
- Corneal hysteresis (CH): a measure of the viscoelastic damping of the cornea; lower CH associated with faster rates of visual field loss
Higher dietary nitrate and green leafy vegetable intake has been associated with a lower POAG risk. Evidence suggests that nitrate, a precursor of nitric oxide, is beneficial for blood circulation.
- The vascular endothelium regulates the microcirculation via vasoactive factors with nitric oxide being one of them. Nitric oxide reduces IOP by causing relaxation of the TM and the Schlemm canal, resulting in increased aqueous outflow.
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