Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content +++ INTRODUCTION ++ Glaucomas are ocular disorders that lead to an optic neuropathy characterized by changes in the optic nerve head (optic disc) that is associated with loss of visual sensitivity and field. +++ PATHOPHYSIOLOGY ++ There are two major types of glaucoma: primary open-angle glaucoma (POAG) or ocular hypertension, which accounts for most cases and is therefore the focus of this chapter, and primary angle closure glaucoma (PACG). Either type can be a primary inherited disorder, congenital, or secondary to disease, trauma, or drugs. In POAG, the specific cause of optic nerve damage is unknown. Increased intraocular pressure (IOP) was historically considered to be the sole cause. Additional contributing factors include increased susceptibility of the optic nerve to ischemia, excitotoxicity, autoimmune reactions, and other abnormal physiologic processes. Although IOP is a poor predictor of which patients will have visual field loss, the risk of visual field loss increases with increasing IOP. IOP is not constant; it changes with pulse, blood pressure, forced expiration or coughing, neck compression, and posture. IOP demonstrates diurnal variation with a minimum pressure around 6 pm and a maximum pressure upon awakening. The balance between the inflow and outflow of aqueous humor determines IOP. Inflow is increased by β-adrenergic agents and decreased by α2- and β-adrenergic blockers, dopamine blockers, carbonic anhydrase inhibitors (CAIs), meltatonin-1 agonists, and adenylate cyclase stimulators. Outflow is increased by cholinergic agents (eg, pilocarpine), which contract the ciliary muscle and open the trabecular meshwork, and by prostaglandin analogues and β- and α2-adrenergic agonists, which affect uveoscleral outflow. Secondary OAG has many causes, including exfoliation syndrome, pigmentary glaucoma, systemic diseases, trauma, surgery, ocular inflammatory diseases, and drugs. Secondary glaucoma can be classified as pretrabecular (normal meshwork is covered and prevents outflow of aqueous humor), trabecular (meshwork is altered or material accumulates in the intertrabecular spaces), or posttrabecular (episcleral venous blood pressure is increased). Many drugs can increase IOP (Table 65–1). The potential to induce or worsen glaucoma depends on the type of glaucoma and on whether it is adequately controlled. PACG occurs when there is a physical blockage of the trabecular meshwork, resulting in increased IOP. ++Table Graphic Jump LocationTABLE 65–1Drugs That May Induce or Potentiate Increased Intraocular PressureView Table||Download (.pdf) TABLE 65–1 Drugs That May Induce or Potentiate Increased Intraocular Pressure Open-angle glaucoma Ophthalmic corticosteroids (high risk) Systemic corticosteroids Nasal/inhaled corticosteroids Fenoldopam Ophthalmic anticholinergics Succinylcholine Vasodilators (low risk) Cimetidine (low risk) Closed-angle glaucoma Topical anticholinergics Topical sympathomimetics Systemic anticholinergics Heterocyclic antidepressants Low-potency phenothiazines Antihistamines Ipratropium Benzodiazepines (low risk) Theophylline (low risk) Vasodilators (low risk) Systemic sympathomimetics (low risk) CNS stimulants (low risk) Serotonin-selective reuptake inhibitors Imipramine Venlafaxine Topiramate Tetracyclines (low risk) Carbonic anhydrase inhibitors (low risk) Monoamine oxidase inhibitors (low risk) Topical cholinergics (low risk) +++ CLINICAL PRESENTATION ++ POAG is slowly progressive and is usually asymptomatic until onset of ... Your Access profile is currently affiliated with '[InstitutionA]' and is in the process of switching affiliations to '[InstitutionB]'. Please click ‘Continue’ to continue the affiliation switch, otherwise click ‘Cancel’ to cancel signing in. Get Free Access Through Your Institution Learn how to see if your library subscribes to McGraw Hill Medical products. Subscribe: Institutional or Individual Sign In Username Error: Please enter User Name Password Error: Please enter Password Forgot Username? Forgot Password? Sign in via OpenAthens Sign in via Shibboleth