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Glau and macular

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Focus on the aging eye:

Volume 3, Number 1

coma degeneration
2.5 HOURS CONTACT
Aging eyes are at higher risk for a number of diseases that can damage vision and may even cause blindness. In this second article of a two-part series, youll learn about two sight-threatening diseases and their treatments.
HEATHER BOYD-MONK, SRN, CRNO, BSN Assistant Director Emeritus of Nursing Education Programs Wills Eye Hospital Philadelphia, Pa. The author has disclosed that she has no signicant relationship with or nancial interest in any commercial companies that pertain to this educational activity.

BILL CHANDLER, 69, has noticed that when hes reading lately, the lines of type appear distorted and the center of the printed page seems to be blank. When he closes his left eye, he sees this change in the central (reading) visual eld of his right eye. Bill makes an appointment to see his primary care provider. After examining him, his provider is fairly certain that Mr. Chandler has the classic signs of age-related macular degeneration (AMD), a common ailment in older adults. He refers him to an ophthalmologist for a comprehensive examination. As you read in the rst article of this two-part feature on the aging eye (LPN2006, November/December), the eyes undergo age-related changes just as the rest of the body does. Some of these changes, like presbyopia, are inevitable and correctable. Others, like cataract, require surgical correction. But some age-related eye diseases, like glaucoma and AMD, are more seriousand though theyre usually manageable, they can also cause severe vision loss or blindness if left untreated. In this article, Ill explain how glaucoma and AMD affect the eye, and Ill review preventive measures and treatment options. Ill also review how you can help educate your patient with vision problems so that hell be able to enjoy the best vision possible. In my previous article, you were brought up to speed on presbyopia and cataract; now lets take a look at another

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common eye condition that can exacerbate with age: glaucoma. Too much (aqueous) humor isnt funny Glaucoma is dened as intraocular pressure (IOP) that damages the optic neurons. It results from inadequate drainage of aqueous humor, the clear uid that lls the eyes anterior and posterior chambers. Aqueous humor is produced by the ciliary body, the circular structure adjacent to the iris. Aqueous passes through the pupil, drains through the trabecular meshworka collection of tiny channelsand then enters the venous bloodstream via the Schlemms canal. When the ow of aqueous humor is impaired, elevated IOP can result. This increases pressure on the optic disc (optic nerve head), damaging the optic nervea bundle of about 1 million nerve bers that relays information from the eyes retina to the brain. Increased pressure on the optic disc can cause physical damage and loss of peripheral (side) vision. It was once thought that high IOP was the main cause of optic nerve damage in glaucoma. Although higher-than-normal IOP is a major risk factor, its now known that other factors must also be involved. This is because even patients who have normal IOP can develop glaucoma. Glaucoma affects about 2.2 million Americans, according to the National Eye Institute (NEI). Risk factors include: family history of glaucoma elevated IOP being African-American or Hispanic myopia or hyperopia previous eye trauma previous eye surgery increased age in susceptible individuals
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prolonged use of topical or systemic corticosteroids. Glaucoma is diagnosed based on results of a thorough patient history and a comprehensive eye examination. The examination includes the following tests: visual acuity test. This is an eye chart test that measures how well the subject sees compared with what a person with normal vision sees at 20 feet (6 meters). tonometry. The eye care provider applies anaesthetic drops to the eye, then measures the IOP using a tonometer. gonioscope. After instilling topical anaesthetic drops and viscous hydroxypropyl methylcellulose (Goniosol) eye drops, the ophthalmologist places a goniolens on the eye and, using the light source from the slit lamp, views 360 degrees of the iridocorneal angle between the iris and the corneaat the periphery of the anterior chamberto document if the angle is open, narrow, or closed. dilated eye exam. Short-acting dilating drops are placed in the eye (only after the other tests), then the eye care provider uses an ophthalmoscope to check the retina, blood vessels, and optic disc for damage. visual eld test. Ordered at a later time, this test documents subtle peripheral vision loss and an enlarged blind spot. fundus photographs. Steriophotography is used to document the initial state of the optic disc. Once a patient is diagnosed with glaucoma, his ophthalmologist will monitor disease progression with tonometry, visual eld tests, and optic disc photographs. As mentioned, elevated IOP is a major risk factor for most types of glaucoma. The Goldmann applanation tonometer (attached to a slit lamp) is considered the standard for

accurately measuring IOP. While looking through the slit lamp with a cobalt blue light lter, the ophthalmologist uses the slit lamps joystick to guide a sterile prism to rest against the cornea. A calibrated drum is turned with the other hand to atten (applanate) the cornea. The prisms myers (half circles formed like an S) must be in alignment to measure IOP accurately. Before this procedure can be done, a topical anesthetic is instilled so that the patient doesnt feel the prism, and a yellow uorescein (uorescent) dye is instilled to facilitate adjusting the myers. (Remember, normal IOP for most people ranges from 12 to 21 mm Hg.) Another test for monitoring glaucoma is fundus photography. The fundus is the back of the eye where the optic disc, vitreous, macula, retina, and retinal blood vessels are located. A specially trained photographer takes images using a customized camera mounted to a microscope. The photos help the patients provider monitor any glaucomatous changes in the optic disc. Glaucoma is actually a group of related diseases that share the common traits of optic neuron damage, gradual loss of peripheral vision, and (in many cases) elevated IOP. Lets take a closer look at how types of glaucoma differ. A slow road to sight loss Ninety percent of patients with glaucoma have primary open-angle glaucoma (POAG). This is a gradual disease process thats often called the silent thief of sight. If not diagnosed and treated, it slowly and irreversibly damages the optic disc by enlarging, or cupping, the central physiologic cup, causing loss of peripheral vision. One of the problems with POAG is that its usually asymptomatic in

Volume 3, Number 1

AREDS: What you need to know about a landmark eye disease study
The Age-Related Eye Disease Study (AREDS) was a major clinical trial sponsored by the National Eye Institute of the National Institutes of Health. The study had two major objectives: to learn more about the natural history and risk factors of age-related macular degeneration (AMD) and cataract to evaluate the effect of high doses of antioxidants and zinc on the progression of AMD and cataract. The AREDS included 4,757 participants ages 55 to 80 in 11 clinical centers across the United States. All participants had varying stages of AMD. Each was given one of four treatments: zinc alone, antioxidants alone, a combination of antioxidants and zinc, or placebo. The formulation evaluated by the AREDS researchers contained: 500 mg of vitamin C 400 international units of vitamin E 15 mg of beta-carotene 80 mg of zinc as zinc oxide 2 mg of copper as cupric oxide. Copper was added to the AREDS formulations containing zinc to prevent copper-deciency anemia, which may be associated with high levels of zinc supplementation. The study results showed that, although its not a cure for AMD, taking high levels of antioxidant and zinc supplements can reduce the risk of progression to advanced AMD by 25% in people at high risk for the disease. The AREDS formulation may also play a key role in helping people who are at high risk for developing advanced AMD retain their remaining vision. (These same nutrients had no signicant effect on the development or progression of cataract, however.) Those in the zinc alone or antioxidant alone groups also reduced their risk of developing advanced AMD, but at more moderate rates compared with the antioxidants plus zinc group. Those in the placebo group had the highest risk of developing advanced AMD. Is the AREDS formulation right for your patients? Heres what you need to know. Who should take the AREDS formulation? People at high risk for developing advanced AMD should consider taking the AREDS formulation. Advise your patient to see his eye care provider, who can tell him if he has AMD and is at risk for developing the advanced form of the disease. Warn the patient not to start taking the AREDS formulation before speaking with his eye care and other health care providers. Can a person take a daily multivitamin if hes taking the AREDS formulation? Yes. A daily multivitamin contains important nutrients that arent in the AREDS formulation. For example, an older adult patient who has osteoporosis needs to be concerned about taking vitamin D, which is not in the AREDS formulation. If the patients already taking daily multivitamins and his health care provider suggests the AREDS formulation, tell the patient to rst review with his provider all the vitamins and medications hes taking. Can a daily multivitamin provide the same high levels of antioxidants and zinc as the AREDS formulation? No. The AREDS formulations levels of antioxidants and zinc are considerably higher than the amounts in any daily multivitamin. Are there adverse effects associated with taking the AREDS formulation? About 7.5% of the participants assigned to the zinc treatments, compared with 5% who didnt take zinc in their assigned treatments, had urinary tract problems that required hospitalization. Yellowing of the skin, a well-known adverse effect of large doses of beta-carotene, was reported slightly more often by participants taking antioxidants.
Source: National Eye Institute, National Institutes of Health.

early stages, although a patient may complain that his eyes are bothering him, that he feels intermittent pain over the brow area, or that he sees halos around light sources. POAG is often discovered through tonometry performed during a routine eye examwhich is one of the reasons why regular eye exams are so important, especially if the patient has a family history of glaucoma. The eye care provider may discover glaucoma by detecting the diseases characteristically elevat-

ed IOP. However, the diagnostic triad of elevated IOP, optic disc cupping, and visual eld changes conrms a glaucoma diagnosis. Higher-than-normal IOP and changes in the optic disc are indications that the eyes aqueous humor outow is impeded. If the ophthalmologist detects these signs, hell examine the iridocorneal angle of the eye with the goniolens, which allows him to see whether 360 degrees of the angle are open, narrow, or closed. With POAG, the angle

appears open, but it doesnt drain the aqueous humor effectively. Blockage generally occurs in the sievelike channels of the trabecular meshwork. The eye care provider will also perform ophthalmoscopy to see if the optic cup-disc ratio shows signs of change. Seen through an ophthalmoscope, the optic disc has a central indentation, called the cup, thats normally about one-third the size of the disc; enlargement of the cup-disc ratio signals a problem.
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Fundus photography documents cup-disc changes, and may be performed while IOP is uctuating. As mentioned earlier, unchecked elevated IOP damages the optic neurons responsible for the peripheral eld of vision. The extent of this damage is assessed on a machine called the Humphrey Field Analyzer, a computerized device that detects even minute areas of decreased vision. A better treatment angle on glaucoma Although miotics (drugs that constrict the pupil) are sometimes used to treat glaucoma, the constricted pupils interfere considerably with the patients night vision (pupils dilate in dim illumination). A patient with the disease is more often treated with alpha-adrenergic agonists, prostaglandin analogs, betaadrenergic blockers, or cabonic anhydrase inhibitors (none of these drugs affects pupil size). Lets take a look at what these drugs do and review a few other treatment regimens for glaucoma management. For instructions on how to instill eyedrop medications, see the Skill Building department in the November/December issue of LPN2006. The most important point to remember when giving glaucoma eye drops is to occlude the puncta by pressing in the inner canthus (corner of the eye) to prevent systemic absorbtion of the drug. Nonselective beta-adrenergic blocker eyedrops like timolol ophthalmic (Timoptic, Timoptic-XE) reduce the production of aqueous humor, which lowers IOP. Remember that nonselective beta-adrenergic blockers also affect the heart and lungs, so they should never be given to a patient with a history of asthma or severe bradycardia. Alpha-adrenergic agonist eye50 LPN2007

drops like brimonidine ophthalmic (Alphagan) decrease production and increase drainage of aqueous humor. Prostaglandin analog eyedrops like latanoprost (Xalatan) are the most recently developed POAG medications. Latanoprost increases the uveoscleral outow of aqueous humor, which helps lower IOP. Carbonic anhydrase inhibitor eyedrops like dorzolamide ophthalmic (Trusopt) may also be used to lower IOP by stopping aqueous production. When IOP cant be controlled with maximal medical therapy, an ophthalmic specialist may use one of the following procedures to help control disease progression: Noninvasive argon laser trabeculoplasty is performed on the angle of the iris to open the channels of the trabecular meshwork. The procedure isnt a long-term x, though. A patient may require more than one trabeculoplasty, or he may eventually require more conventional surgical intervention (trabeculectomy). Trabeculectomy is a procedure in which a new outlet called a bleb (small bubble) is created under the conjunctiva that allows aqueous humor to disperse. Some glaucoma patients also receive a small tube, called a Seton implant, in the anterior chamber; this tube acts as a shunt for the aqueous humor to drain. Most Seton implants function by allowing better drainage of the aqueous humor from the anterior chamber, which in turn lowers IOP. Some, such as the Molteno and Baerveldt implants, allow free ow of aqueous humor. Other types, such as the Ahmed and Krupin implants, have valves that close automatically if IOP becomes too low so that aqueous humor ow is kept at an even rate. Postoperatively, patients are prescribed cycloplegic and steroid/

antibiotic eye medications. Cycloplegics, like scopolamine 0.25% (Isopto-Hyoscine) and atropine 1% (Atropisol, Isopto Atropine), dilate the pupil and temporarily paralyze the ciliary muscles. (Remember, the muscles of the ciliary body alter the accommodation of the lens, changing its shape to adapt to near or far vision.) This helps alleviate postoperative inammation of the iris and ciliary body. Patients must use extreme caution when instilling a cycloplegic drug. If the medication is inadvertently instilled into the wrong eye, it could cause an attack of angle-closure glaucoma. Lets see how this type of glaucoma differs from POAG. When glaucoma is an emergency Angle-closure glaucoma, also called narrow-angle or closed-angle glaucoma, is an acute conditionand its an emergency situation. It occurs when the lens enlarges and displaces the iris, pushing it forward. This narrows or closes the iridocorneal angle. A patient with angle-closure glaucoma presents with symptoms of sudden onset of blurred vision and extreme eye pain. About 5% of white Americans age 50 years and older have angle-closure glaucoma. Narrow angle glaucoma is more prevalent in patients of Asian ancestry. Signs and symptoms of an acute angle-closure glaucoma attack include: hazy cornea mid-dilated and xed pupil decreased or blurred vision red eye (injected conjunctiva) severe eye pain headache multicolored halos surrounding lights nausea and vomiting from pain. The eye care provider must quick-

Volume 3, Number 1

Vision changes with glaucoma and macular degeneration


Normal vision Glaucoma

Macular degeneration

ly assess the eye and test visual acuity before conducting a slit lamp evaluation, which includes tonometry and gonioscopy to identify if the iridoconeal angle is narrow or closed. With this type of glaucoma, the patients IOP may be as high as 50 mm Hg. Immediate treatment in the affected eye includes sequential miotic eye drops, administered to counteract the mid-dilated pupil and increase the eyes aqueous outow, and steroid eye drops, instilled to decrease the inammatory response. Beta-blocker drops are administered to decrease the production of aqueous humor. Intravenous acetazolamide (a carbonic anhydrase inhibitor) is administered to halt aqueous production, followed by an infusion of mannitol, which shrinks the vitreous. Only when the patients IOP has signicantly decreased is the attack considered under control. A day or two after an acute episode

of angle-closure glaucoma, the patient will likely undergo a noninvasive laser peripheral iridotomy (PI). The ophthalmologist makes a small hole in the peripheral iris to allow aqueous uid to ow from behind it directly into the anterior chamber. As a precaution, hell perform PI on the unaffected eye as well. Other types of glaucoma arent necessarily related to aging. They include: congenital glaucoma, in which a membrane (called Barkans membrane) in the angle of the eye prevents aqueous humor drainage. secondary glaucomas, which develop as complications of other medical conditions. The most common of these is neovascular glaucoma associated with diabetes. New blood vessels grow into the angle, blocking aqueous outow. Glaucoma may develop after an eye injury or as a result of an advanced cataract or an intraocular tumor.

Transient elevated IOP may develop following eye surgery. Uveitis (inammation of the iris, ciliary body, or choroid) may also have an associated glaucoma. pigmentary glaucoma, caused by akes of pigment from the iris blocking the trabecular meshwork and slowing aqueous humor drainage. No going back Lets return to Mr. Chandler for a moment. You remember that he complained of seeing distorted lines of words and a blank spot in the middle of the page when reading. His eye specialist conrmed what the primary care provider suspected: Mr. Chandler has AMD. AMD is a leading cause of severe and irreversible central vision loss in older adults. The degenerative changes of this chronic condition occur in the macula, an avascular part of the retina thats responsible for the
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clear central vision we need to perform daily activities like reading and driving. AMD occurs most frequently in white patients with light-colored eyes and infrequently in Asian and African-Americans patients. But the biggest risk factor for AMD is age: According to the Vision Problems in the United States report, published by Prevent Blindness America and the NEI, approximately 1.65 million Americans age 60 and older have the disease. An estimated 10% of Americans age 75 and older have some central vision loss resulting from AMD, but they retain peripheral vision. According to the NEI, middleaged, white people have about a 2% risk of developing AMD; those who are age 75 or older have nearly a 30% risk. These numbers will grow, according to the medical journal Archives of Ophthalmology. Because the average age of the U.S. population is increasingits estimated that by 2010, the majority of Americans will be age 45 and oldercases of AMD are expected to grow to almost 3 million by 2020. Established risk factors for AMD include: family history of AMD history of systemic high blood pressure gender (women are more likely to be affected) race (whites are more likely to be affected) smoking light eye color. Possible (not proven) risk factors for AMD include: low levels of the antioxidants selenium and zinc continued exposure to sunlight variants or deciencies of two genes that play a role in immune response. (The variants have been discovered in 74% of AMD patients studied.)
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Wet and dry A patient can have exudative (wet) AMD or atrophic (dry) AMD. Dry AMD is far more common: Between 85% and 90% of AMD patients have this form. The wet form of the disease usually leads to more severe central vision loss. Dry AMD is characterized by atrophic pigment epithelial changes that are usually associated with slow, progressive mild visual loss. Another entity seen in the aging and thinning macular tissues is deposits of complex lipids and calcium called drusen. Dry AMD is typically diagnosed when an eye care provider detects the drusen, which appear as yellowish spots, accumulating on the macula. Drusen are usually the result of debris from eye tissue that has broken down. Central vision loss may occur gradually with dry AMD, but the loss is never as severe as with wet AMD. An ophthalmologist testing a patient for AMD rst performs uorescein or indocyan green angiography. Fluorescein dye is injected into the patients arm vein. This allows the specialist to visualize and photograph retinal blood vessels. Wet AMD has different signs and symptoms than dry AMD. Metamorphopsiaa distortion of straight lines like the wavy lines of print that Mr. Chandler sawand a central scotoma (a blank spot in the eld of vision) may appear gradually over days or weeks. These visual distortions are the result of a choroidal neovascular net of leaking blood vessels that has formed under the macula. If wet AMD is diagnosed, the patient is usually given a simple test called an Amsler grid to take home and use on his own to monitor vision changes. An Amsler grid is a blackand-white card printed with a pattern resembling graph paper and a

dot in the central intersection of lines. The patient looks directly at the grid while focusing on the center dot; if any of the lines appear blurred, wavy, broken, or missing, hes instructed to call his eye care provider immediately. This can be a sign that the disease is progressing. Therapy for AMD We dont yet have preventive treatments for AMD, but patients have a number of options to help prevent or slow disease progression. Heres a review of the most common treatments. High-dose nutritional supplements of zinc, beta-carotene, and vitamins C and E have been shown to reduce the risk of progression to advanced AMD by 25% (see AREDS: What you need to know about a landmark eye disease study). A diet rich in fruit and vegetables is also recommended. Ocular photodynamic therapy with verteporn (Visudyne) has been successful in treating certain stages of wet AMD. During the procedure, a nonthermal laser light activates the verteporn, which occludes (closes) the leaky blood vessels. Vascular endothelial growth factor antagonists slow vision loss by inhibiting the growth of abnormal, leaky blood vessels that cause structural damage and vision loss. An example is pegaptanib sodium injection (Macugen), which has been approved by the U.S. Food and Drug Administration for treating both dry and wet AMD. If your patients already been diagnosed with dry AMD, he needs to be counseled on the importance of monitoring his vision daily with an Amsler grid and getting regular vision checkups (every 6 months to 1 year). Many current clinical investigations aim to develop effective pre-

Volume 3, Number 1

ventive strategies and treatments for AMD. At present, though, AMD is irreversible. If your patients already lost some central vision because of AMD, let him know about the resources available for visual rehabilitation, which include low-vision optical aids and support services. For example, MD Support, an international nonprot organization, offers a variety of patient-friendly links to goods and services (see On the Web for more information). Keeping an eye on good vision According to Prevent Blindness America, 50% of cases of blindness in the United States are preventable. Although we cant stop aging, we can take steps to maintain good health. Encourage your older patients to get regular eye checkups so that if a problem does occur, it can be diagnosed early enough to avoid vision loss or blindness. Patients who are ages 40 to 64 should have a comprehensive eye exam every 2 to 4 years. Adults age 65 or older should be

examined every 1 to 2 years. Remember, some of the injuries older patients sustain occur because poor vision prevents them from seeing obstacles clearly. Because vision and hearing changes can have a major impact on patient health and safety, the U.S. Preventive Services Task Force recommends regular vision and hearing screening for all patients age 65 and older. With vigilance, regular checkups by an eye care provider, and your help and advice, your patient will be able to keep the twinkle in his eyes for a lifetime. LPN Selected references
Aref AA, Schmitt BP. Open-angle glaucoma: Tips for earlier detection and treatment selection. Journal

of Family Practice. 54(2):117-125, February 2005. Bellmann C, et al. Age-related macular disease: How to assess the retina using scanning laser techniques. Aging Clinical and Experimental Research. 17(6):435-444, December 2005. Boyd-Monk H.The eyes have it: Understanding problems of the aging eye. Nursing made Incredibly Easy! 3(5):34-39, 41-46, September/October 2005. Kaiser PK, et al. Treatment of Age-related Macular Degeneration with Photodynamic Therapy [TAP] Study Group. Verteporn therapy of subfoveal choroidal neovascularization in age-related macular degeneration: 5-year results of two randomized clinical trials with an open-label extension: TAP Report No. 8. Graefes Archive for Clinical and Experimental Ophthalmology. 244(9):11321142, September 2006. Kanadani FN, et al. Structural and functional assessment of the macular region in patients with glaucoma. British Journal of Ophthalmology. August 9, 2006 (Epub ahead of print). Rosenthal B. Age-related macular degeneration (AMD): An overview. http://www.healthandage. com/Home/gid2=2233. Accessed August 3, 2006. Zhou B, Wang B. Pegaptanib for the treatment of age-related macular degeneration. Experimental Eye Research. 83(3):615-619, September 2006.

On the Web
American Academy of Ophthalmology: http://www.aao.org Glaucoma Research Foundation: http://www.glaucoma.org Macular Degeneration Partnership: http://www.amd.org MD Support: http://www.mdsupport.org/support.html National Eye Institute: http://www.nei.nih.gov

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Focus on the aging eye: Glaucoma and macular degeneration


TEST INSTRUCTIONS To take the test online, go to our secure Web site at http:// www.nursingcenter.com/ce/lpn. On the print form, record your answers in the test answer section of the CE enrollment form on page 54. Each question has only one correct answer. You may make copies of these forms. Complete the registration information and course evaluation. Mail the completed form and registration fee of $22.95 to: Lippincott Williams & Wilkins, CE Group, 2710 Yorktowne Blvd., Brick, NJ 08723. We will mail your certicate in 4 to 6 weeks. For faster service, include a fax number and we will fax your certicate within 2 business days of receiving your enrollment form. You will receive your CE certicate of earned contact hours and an answer key to review your results. There is no minimum passing grade. Registration deadline is February 28, 2009. DISCOUNTS and CUSTOMER SERVICE Send two or more tests in any nursing journal published by Lippincott Williiams and Wilkins together and deduct $0.95 from the price of each test. We also offer CE accounts for hospitals and other health care facilities on nursingcenter.com. Call 1-800-787-8985 for details. PROVIDER ACCREDITATION: Lippincott Williams & Wilkins, publisher of LPN2007, will award 2.5 contact hours for this continuing nursing education activity. Lippincott Williams & Wilkins is accredited as a provider of continuing nursing education by the American Nurses Credentialing Centers Commission on Accreditation. Lippincott Williams & Wilkins is also an approved provider of continuing nursing education by the American Association of Critical-Care Nurses #00012278, (CERP Category A), California CEP 11749, District of Columbia, Florida #FBN2454, and Iowa #75. LWW home study activities are classied for Texas nursing continuing education requirements as Type 1. Your certicate is valid in all states.

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CE

2.5
CONTACT HOURS

Focus on the aging eye: Glaucoma and macular degeneration


GENERAL PURPOSE: To provide the nurse with current information about glaucoma and age-related macular degeneration (AMD) in the older patients. LEARNING OBJECTIVES: After reading the preceding article and taking the following test, you should be able to: 1. Discuss the risk factors and symptoms of glaucoma and AMD in older patients. 2. Describe the current diagnostic work up, management, and prevention of glaucoma and AMD. 1. Which statement about glaucoma is correct? a. Patients who have normal intraocular pressure (IOP) can develop glaucoma. b. Glaucoma results from inadequate drainage of the vitreous humor. c. High IOP is the cause of optic nerve damage in glaucoma. d. Increased pressure on the optic disc can cause loss of central vision. 2. Each of the following is a risk factor for glaucoma except a. female gender. b. African-American ancestry. c. myopia. d. previous eye surgery. 3. Which of these tests are used to diagnose glaucoma? a. uorescein angiography and ophthalmoscopic examination b. Amsler grid and fundus photography c. Humphrey Field Analyzer and laser trabeculoplasty d. tonometry and visual acuity test 4. Ninety percent of patients with glaucoma have a. closed-angle glaucoma. b. primary open-angle glaucoma (POAG). c. neovascular glaucoma. d. narrow-angle glaucoma. 5. Which of the following may be early symptoms of POAG? a. yellow spots on the macula and loss of central vision b. sudden onset of blurred vision and extreme eye pain c. intermittent pain around the brow area and halos around light sources d. distortion of straight lines and a blank spot in the central eld of vision 6. Which assessment nding is diagnostic of glaucoma? a. decreased IOP b. deposits of complex lipids and calcium in the macula c. change in the optic disc-cup ratio d. choroidal neovascular net of leaking blood vessels 7. Which categories of medication are used to treat glaucoma? a. selective beta-blockers and immunosuppressive agents b. alpha-adrenergic agonists and nonselective beta-adrenergic blockers c. antihistamines and biologic response modiers d. diuretics and anti-inammatory agents 8. Which of these medications are prescribed following glaucoma surgery? a. brimonidine ophthalmic (Alphagan) and timolol ophthalmic (Timoptic) b. latanoprost ophthalmic (Xalatan) and dorzolamide ophthalmic (Trusopt) c. verteporn (Visudyne) and pegaptanib (Macugen) d. scopolamine (Isopto-Hyoscine) and atropine (Atropisol) 9. Which of the following is a risk factor for angle-closure glaucoma? c. female gender a. smoking d. obesity b. Asian ancestry 10. Symptoms of an acute angle-closure glaucoma attack include each of the following except a. severe eye pain. b. decreased or blurred vision. c. distortion of straight lines. d. red eye. 11. Which type of eye drop is administered to decrease the production of aqueous humor? a. steroid drops b. nonselective beta-blocker drops c. miotic drops d. saline drops 12. The procedure performed on the angle of the iris to open the channels is called a. laser trabeculoplasty. b. ocular photodynamic therapy. c. trabeculectomy. d. laser peripheral iridotomy. 13. Which statement correctly differentiates wet AMD from dry AMD? a. The wet form leads to more severe central vision loss. b. The dry form is less common. c. The wet form is also known as nonexudative AMD. d. The dry form quickly advances to become the wet form. 14. Which of these risk factors are associated with AMD? a. dark-colored eyes and Asian heritage b. previous eye surgery and prolonged exposure to sun c. diabetes and poor circulation d. light-colored eyes and Caucasian heritage 15. Which statement about AMD is correct? a. Vision loss from AMD is generally reversible with prompt treatment. b. AMD is characterized by peripheral vision loss. c. Middle-aged persons have a 20% risk of developing AMD. d. Dry AMD is caused by aging and thinning of the macular tissues. 16. Which of these treatment options is used to slow the progress of AMD? a. low doses of zinc, beta-carotene, and vitamins C and E b. ocular photodynamic therapy c. prostaglandin analog d. pachymetry 17. Which statement about prevention of agerelated eye disorders is correct? a. Adults age 65 and older should have an eye exam every 2 to 4 years. b. Taking high doses of antioxidants and zinc can prevent AMD. c. Glaucoma can be prevented by taking high doses of copper and beta-carotene. d. Patients with dry AMD should have a vision examination every 6 to 12 months and use the Amsler grid daily.

ENROLLMENT FORM LPN2007, January/February, Focus on the aging eye: Glaucoma and macular degeneration
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