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EPIDEMIOLOGY AND ETIOLOGY

Over 66.8 million people worldwide have glaucoma making it the second leading cause of blindness worldwide.3 In the United States it is estimated that 2.22 million people are affected by POAG, and by 2020 this number will increase to 3.36 million. The prevalence varies with race and ethnicity and it is three to five times more prevalent in African Americans than Caucasian Americans. The prevalence of POAG increases with age and is rarely seen in patients less than 40 years of age.1'4'5 Of patients diagnosed with POAG, 15% to 40% actually meet the criteria for normal-tension glaucoma (NTG).1'2 Ocular hypertension is present in about 3 to 6 million of the U.S. population, however, less than 10% will have progression to POAG within 5 years.6

The prevalence of PACG is lower than POAG and varies significantly by race and ethnicity. It is low in patients of European descent (0.09-0.16%) but higher in patients of Chinese (1.3%), Eskimo (2.9-5%), and Asian Indian (4.33%) descent. PACG is

also more prevalent with increasing age and among females. '

RISK FACTORS

Primary Open-Angle Glaucoma

O Practitioners can play an important role in eye care by assessing patients for risk factors and referring to an eye care specialist for appropriate screening and evaluation. Risk factor evaluation is essential in determining the frequency of comprehensive eye exams for patients (Table 61-1). It is also useful in deciding when to start therapy and determining the sequence of pharmacotherapeutic or surgical treatment modalities.1

The five primary risk factors associated with POAG are family history, age, race, central corneal thickness (CCT), and elevated IOP (Table 61-2). Patients who have first-degree relatives with POAG are at a higher risk of developing glaucoma than patients with no family history of POAG. Even though IOP is no longer a diagnostic criterion, it is associated with an increased prevalence and progression of the dis-157

ease. ' ' CCT has recently been recognized as a risk factor for POAG. The Ocular Hypertension Study (OHTS) found patients with ocular hypertension and thinner CCT (less than 555 |im) had a greater risk of progressing to POAG.1,6,9

The five major risk factors identified for PACG are hyperopia, family history of PACG, age (greater than 30 years), gender, and Eskimo or Asian ethnicity (Table 61-2). Patients who are hyperopic, female, or of Eskimo or Asian ethnicity tend to have more shallow anterior angles which predispose the eye to angle closure. Advancing age is associated with a decrease in the depth of the anterior angles because the lens becomes thickened and is displaced toward the anterior portion of the eye. Patients who have first-degree relatives with glaucoma are atgreater risk for developing PACG with a prevalence of 1% to 12% for Caucasians.7,8,

PATHOPHYSIOLOGY

The pathophysiologic alterations seen with POAG optic neuropathy are not fully understood. Elevated IOP is clearly associated with damage and eventual death of optic nerves; however, optic neuropathy can still occur in patients with normal IOP. Optic nerve degeneration without elevated IOP indicates the presence of independent factors that contribute to the death of the optic nerve. The key to understanding the patho-

physiology and treatment of POAG relies on an understanding of aqueous humor dy-

namics, IOP, and optic nerve anatomy and physiology. ' ' Aqueous Humor

The eye is separated into two segments by the lens: the anterior segment and the posterior segment (Figs. 61-1 and 61-2). The anterior segment of the eye is separated by the iris into the posterior and anterior chambers. The ciliary body, a ring-like structure that surrounds and supports the lens, produces and secretes an optically neutral fluid called aqueous humor through the diffusion and ultrafiltration of plasma. The nonpig-mented epithelium of the ciliary body secretes the aqueous humor into the posterior chamber. Aqueous humor formation can be modified pharmacologically through the a- and ^-adrenoceptors, carbonic anhydrase, and sodium and potassium adenosine tri-phosphatase of the nonpigmented ciliary epithelium.

After the transport of aqueous humor into the posterior chamber, it flows through the pupil into the anterior chamber where it provides oxygen and nutrition to the avascular lens and cornea. Aqueous humor then exits the anterior chamber through the trabecular meshwork and drains into the Schlemm's Canal, which drains aqueous humor into the episcleral venous system.

Eighty percent of aqueous humor drains through the trabecular meshwork which is a lattice of connective tissue that surrounds the anterior chamber. The size of the trabecular meshwork can be altered by the contraction or the relaxation of the ciliary muscle. Stimulation of muscarinic receptors on the ciliary muscle causes contraction which in turn causes the pores of the trabecular meshwork to open, increasing aqueous humor outflow.

FIGURE 61-1. Anatomy of the eye. (From Lesar TS, Fiscella RG, Edward D. Glaucoma. In: DiPiro JT, Talbert RL, Yee GC, et al., eds. Pharmacotheraphy: A Pathophysiologic Approach, 7th ed. New York: McGraw-Hill, 2008:1552.)
FIGURE 61-2. Anterior chamber of the eye and aqueous humor flow. (From Lesar TS, Fiscella RG, Edward D. Glaucoma. In: DiPiro JT, Talbert RL, Yee GC, et al., eds. Pharmacotheraphy: A Pathophysiologic Approach, 7th ed. New York: McGraw-Hill, 2008:1552.)

A second pathway, uveoscleral outflow, comprises the other 20% of aqueous humor drainage. In the uveoscleral pathway, aqueous humor exits the anterior chamber through the iris root and through spaces in the ciliary muscles which then drains into suprachoroidal space. Uveoscleral outflow can be pharmacologically modulated by adrenoceptors, prostanoid receptors, and prostamide receptors. 5 1-15

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