Glaucoma comprises a group of ocular disorders characterized by increased intraocular pressure, optic nerve atrophy, and visual field loss it is estimated that more than 80.000 people in the united state are blind as a result of glaucoma. The incidence of glaucoma is about 1,5% and is black between ages 45 and 65 years, the prevalence is at least five times that of whites in the same age group. In most cases blindness can be prevented if treatment is begin earlyClassificationMany terms are used to describe the various types of glaucoma : Primary and secondary glaucoma refer to whether the cause is the disease alone or another condition. Acute and chronic refer to the onset and duration of the disorder Open (wide) and closed (narrow) describe the width of the angle between the cornea and the iris. Anatomically narrow anteriorchamber angles predispose people to an acute onset of angle-closure glaucomaPrimary open-angle glaucomaPrimary open-angle glaucoma, the most common form, is a multifactorial disorderthat is often genetically being lost. Aqueous humor flow is slowed or stopped because of obstruction by the trabecular meshworkAngle-closure GlaucomaAn acute artack of angle-closure glaucoma can develop only in on eye in which the anterior chamber angle is anatomically narrow.the artack occus because of suddent blockage of the anterior angle by the base of the iris.Ather form of glaucomaNormal-tension glaucoma resemble primary open-angle glaucoma.in this type of glaucoma ,the optic nerve is damage even though intraocular pressure (IOP)is not high.secondary glaucoma may occur as a result of trauma that can disrupt the flow patern of aqeous humor.Etiology and risk factorsAbout 90% of primary glaucoma accurs in people with apen angles. Because there are no early warning clnical manifestations , it is imperative that regular ophthalmic examinations include tonometry and assessment of the optic nerve head (dick). The most common cause of chronic open-angle glaucoma is degenerative change in the trabecular meshwork, resulting, in decreased outflow of aqueous humor. Hypertension, cardioveskuler disease, diabetes, and obesity are associated with the development of glaucoma. Increased IOP alao results from weitis (inflammation of filtering structures). Encroachment by a rapidly growing tumor and chronic use of topical corticosteroids may also produce manifestations of open-angle glaucoma. Neither the cause of low-tension glaucoma nor the reasons prtis nerves are damaged even though the IOP is normal (i.e, between 12 and 22 mmhg) are known . people at higher risk for this from low-tension glaucoma are those with a family history of normal-tension glaucoma, people of japanase ancestry, and people with a history of systemic hert disease,such as irregular heart rhythm.Secondary glaucoma develops from edema, eye injury(hyphema), inflammation, tumor, or advanced cases of cataract of diabetes. Edematous tissue may inhibit the outflow of aqueous humor through the trabecular meshwork. Diayed healing of corneal wound edges may result in epithelial cell growth int the anterior chamber.PathophysiologyIntraocular pressure is determined by the rate of aqueous humor production in the ciliary body and the resistance to outflow of aqueous humor from the eye. IOP varies with diurnal cycles (the highest pressure is usually on awakening) and body position (increased when lying down). Normal variation do not usually exceed 2 to 3 mmHg. IOP and blood pressures are independent of each other, but variations in systemic blood pressure may be associated with corresponding variations in IOP. Increased IOP may result from hyperproduction of aqueous humor or obstruction of outflow. As aqueous fluid accumulates in the eye, the increased pressure inhibits blood supply to the optic nerve and the retina. These delicate tissues become ischemic and gladually lose function.Clinical manifestationsAcute angle-closure glaucoma causes severe pain and blurred vision or vision loss. Some clients see rainbow halos around lights, and some experience nausea and vomiting. Secondary glaucoma has the same clinical manifestations as acute angleclosure glaucoma. Visual field dfects are the result of the loss of blood supply to areas in the retina. The individual response to IOP varies, some clients sustain damage from high pressure, whereas others sustain damage from relatively low pressures, whereas others sustain no damage from high pressure.An ophtinalmoscopic examination shows atrhopy (pale color) and cuppling (indentation) of the optic nerve head. The visual fiel examination is used to determine the extend of perhiperal vision loss (see visual fields in chapter 64). In chronic open-angle glaucoma, a small crescent-shaped scotoma (blind spot) appears early in the disease. In acute angle-closure glaucoma, the fields demonstrate larger areas of significant loss of vision.In clients with angle-closure glaucoma, a slit-lamp examination may demonstrate an erythematous conjunctiva and corneal cloudiness. The aqueous humor in the anterior chamber may also appear turbid (hazy), and the pupil may be nonreactive. Increased IOP (