Glaucoma is actually a group of eye disorders involving optic neuropathy. The disease is characterized by changes in the optic disc and loss of visual sensitivity and field. The signs and symptoms develop and progress in response to several pathologic factors, including increased intraocular pressure (IOP), retinal ischemia, reduced or dysregulated blood flow, and physiologic changes of the extracellular matrix of the optic disc.
There are two major types of glaucoma:
1) open angle
2) closed angle.
Either type may be a primary, inherited disorder, secondary to disease, trauma, or drugs; or congenital.
Primary open-angle glaucoma (POAG) is a bilateral, genetically determined disorder that accounts for 60% to 70% of all glaucoma cases and is usually found in individuals older than 50 years. Treatment is initiated in parents who are at risk for visual field loss with the goal of lowering the IOP to a level associated with decreased risk to the optic nerve (usually 25% to 30% reduction). Medications that are used to treat POAG include topical nonselective β-blocking agents, prostaglandin analogues (latanoprost, travoprost, and bimatoprost), brimonidine (an α2-agonist), and the fixed combination product of timolol and dorzolamide.
Angle-closure glaucoma, overall, accounts for 5% or less of all primary glaucoma cases, but it must be treated as an emergency when it occurs to avoid vision loss. The goal of initial therapy is a rapid reduction of the IOP to preserve vision and to avoid surgical or laser iridectomy which produces a hole in the iris. Acute attacks are treated with a combination of pilocarpine, hyperosmotic agents, and a secretory inhibitor (β-blocker, α2-agonist, and topical or systemic carbonic anhydrase inhibitors).
Several mediations may induce or potentiate intraocular pressure and thus increase the risk of increase the risk developing glaucoma.
The potential for this to ocular depends on the type of glaucoma and whether the patient is adequately treated for the condition. patients with treated, controlled POAG are at minimal risk of increased IOP induced by anticholinergics or vasodilators; however, they are very susceptible to glucocorticoid-induced increases in IOP. In patients with closed-angle glaucoma, any drug that produces mydriasis (a long-continued or excessive dilatation of the pupil) or swelling of the lens may produce angle closure.