الفهرس 
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Abstract
AMD is the leading cause of blindness in elderly Caucasians impacting significantly on patients their careers and National Health Service. Treatment is limited mainly to reducing the disease progression. The multifactorial aspect of AMD is well established with age, smoking and genetics being the most consistent associations.
Presently the debate continues as to whether non exudative AMD is a separate disease and perhaps a different aetiology to exudative AMD or whether they both represent a continuous spectrum of AMD i. e. clinical heterogeneity. However drusen size of more than 125μm appears to be the most discriminating feature in AMD phenotyping for progression to AMD.
AMD impinges on the practice of medical practitioners from various specialities, particularly ophthalmology, geriatrics, psychiatry and general practice. The recognition of the familial and sporadic forms of AMD by medical practitioners is paramount with the relevant preventive and screening interventions.
AMD was first recognized 130 years ago however much remains unknown. It will continue to present a major challenge to clinicians and researchers in the future.
New hope for old eyes is sustained by ongoing research on promising new AMD treatments. This combined with exciting new discoveries identifying genetic and environmental susceptibility factors paves the way for a brighter future for older generations.
As we enter a new era for AMD treatment we need to continue to increase public awareness of AMD. We should encourage healthy eating and cessation of smoking, and educate patients about the symptoms of AMD thus prompting earlier presentation to the ophthalmology service.
Better knowledge of AMD cell biology will lead to better treatments for AMD at all stages of the disease
The AREDS research study group has described a simplifed clinical scale to define risk categories for a five-year risk of developing advanced AMD in eyes without advanced AMD at baseline, or the risk in the unaffected fellow eye when advanced AMD is present in one eye at baseline.
It is a five-step scale (0–4) that predicts an approximate five-year risk of developing advanced AMD in at least one eye as follows:
0 factor, 0.5%; 1 factor, 3%; 2 factors, 12%; 3 factors, 25%; and 4 factors, 50%. The scale sums retinal risk factors in both eyes. The risk factors are the presence of one or more large drusen (>125 µm width of a retinal vein at the disk margin) and pigment stippling.
Each characteristic gets one point for each eye. Advanced AMD in one eye at baseline is given two scores. The presence of intermediate drusen (≥63–128 µm) in both eyes is given one score.
The AREDS trial also noted that the drusen area was stronger and a more consistent predictor of progression to advanced AMD than the drusen size.
However, for practical clinical purposes, the drusen number and type was used for calculating the severity score.
Patients should follow up for early detection of disease progression:
Patients with dry AMD should have a comprehensive dilated eye exam at least once a year. the eye care professional can monitor the condition and check for other eye diseases. Also if patient have intermediate AMD in one or both eyes, or advanced AMD in one eye only doctor may suggest taking the AREDS formulation containing the high levels of antioxidants and zinc.
Because dry AMD can turn into wet AMD at any time patient should get an Amsler grid from the eye care professional. Use the grid every day to evaluate the vision for signs of wet AMD. This quick test works best for people who still have good central vision. Check each eye separately. Cover one eye and look at the grid. Then cover your other eye and look at the grid. If patient detect any changes in the appearance of this grid or in the everyday vision during daily activities should get a comprehensive dilated eye exam.
SUMMARY POINTS:
1- Early lesions of AMD are located either between the RPE and its basement membrane (e. g., BlamD) or between the basement membrane of the RPE and the remainder of Bruch’s membrane (e. g., BlinD).
2- Focal and diffuse deposits between the RPE and Bruch’s membrane are called drusen.
3- Pathologic changes with AMD first appear in the inner collagenous zone and generally extend into the central elastic zone and outer collagenous zone, and the intercapillary connective tissue during later stages of the disease.
4- RPE cells with AMD have cytoplasmic “lipofuscin” granules due to incompletely digested photoreceptor outer segments.
5- Although rods gradually disappear with age, cones begin to degenerate only with advanced stages of non-exudative AMD.
6- Immunohistochemical studies have shown that drusen are composed of acute phase proteins, complement components, complement inhibitors, apolipoproteins, tissue metalloproteinase inhibitor 3, crystalline, serum albumin,. bronectin, mucopolysaccarides, lipids, mannose, sialic acid, N-acetylglucosamine, b -galactose and immunoreactive factors like IgG, immunoglobulin light chains, Factor X, and other components, termed DRAMS.
7- Soft drusen precede macular degeneration.
8- Soft drusen can lead to RPE atrophy, with resultant overlying photoreceptor atrophy and vision loss. When the vision falls below or equal to 20/30 the disease process is termed non exudative or dry macular degeneration.
9- Subretinal fluid, subretinal hemorrhage, RPE detachment, hard exudates, and subretinal fibrosis, all signs of exudative maculopathy.
10- GA is an advanced form of dry macular degeneration. This involves RPE atrophy with subjacent choriocapillaris and small choroidal vessel atrophy. This condition progresses slowly over years and often spares the center of the foveal avascular zone until late in the course of the disease