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The ageing eye

Changes in the posterior segment with age

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he focus of this article is the changes found in the vitreous and retina as a person ages. Most practitioners immediately think of age-related macular degeneration, which is covered in another chapter in this series. However, we forget that the vitreous changes as we age, and these ageing changes are crucial in the evolution of posterior vitreous detachment, and the subsequent relationship with retinal detachment.
once it has occurred, it may account for retinal detachments occurring in areas where there are retinal holes. Another less common ageing change in the vitreous gel is asteroid hyalosis, in which calcium salts are found in (usually) one eye. The aetiology of these calcium salts is unknown, and they have been estimated as occurring in one to two per thousand of the population. They are clearly more common with age, but no other systemic associations have been found, although in the past some studies have questioned whether diabetes could be a cause. A PVD may be symptomatic or asymptomatic. It has been reported that up to 10% of symptomatic PVDs cause retinal tears, and these are classically described as horse-shoe or u-tears as the tear may look like a horse-shoe or a u-shape. When the PVD occurs, it may detach completely or incompletely, and has been reported to cause vitreous haemorrhage in up to 50% of individuals. However, often the haemorrhages are very small, and may be difficult to see. It is important to understand that few symptoms may mean major pathology, and so the symptom of a change in floaters in any patient as they age should be considered to be a patient with a potential retinal detachment until that possibility has been carefully excluded. Certain PVDs carry a higher risk than others, and myopes are the group strongest at risk of PVD causing pathology. Although PVDs tend to occur in older people in their sixth and seventh decades, they may occur earlier in myopes. Patients with peripheral retinal degenerations are also at a higher risk of retinal tears, holes and detachment. Other high risk PVDs are in patients who previously had cataract surgery, those with a family history of retinal detachment and in those patients who present with a dense vitreous haemorrhage, reducing vision. Peripheral retinal degeneration causes much concern to optometrists and ophthalmologists. In fact, many of the retinal degenerations are not particularly age related. For example, lattice degeneration, which affects up to 8% of the population, does not seem to be very age related. It is more common in myopes, and is present in up to 40% of retinal

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All layers of the retina undergo age changes, and many may contribute to the end-stage of visual loss from age-related maculopathy, either geographic atrophy or subretinal neovascularisation. An understanding of these ageing changes allows us to understand some of the age-related signs which can be observed when examining an eye.

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Chris Hammond is Honorary Consultant at the Twin Research and Genetic Epidemiology Unit at St Thomas Hospital in London and Consultant Ophthalmologist in the West Kent Eye Centre, at the Princess Royal Hospital in Orpington, Kent.

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Vitreous gel
The vitreous gel has a volume of around 4ml in emmetropic eyes, although this may be much larger in myopic eyes. It is attached at the vitreous base, which is a 3-4mm wide zone straddling the ora serrata, and also attached to the disc and macula. These attachments form a crucial importance in the aetiology of retinal detachment. The vitreous gel is clear, and transmits 90% of visible light, with a refractive index of 1.335. The vitreous, which many people assume to be rather like an amorphous liquid gel, as in gels used to lubricate eyes, actually has quite a formed structure. It consists of a framework of a very specialised type of collagen, called vitrosin. This is type II collagen; type I collagen is found in skin and bone. The hyaluronic acid in the gel accounts for this viscosity, and both the hyaluronic acid and the vitrosin are concentrated in the cortex of the gel, allowing structure and attachment. Because the vitreous needs to be clear, the water content is high at 98%, and rather than being an inert structure, the turnover time of water is in fact around 10 to 15 minutes. There is an active exchange of electrolytes within the gel, which is similar to the aqueous, but the glucose levels are very low adjacent to the retina. In ageing eyes, the vitreous gel changes its structure. Synchisis senilis occurs, in which the gel becomes more liquefied, and also syneresis, which describes the process of the gel collapsing in on itself, and therefore pulling on the retina where the attachments are found. The collapse of this gel leads to a posterior vitreous detachment. A posterior vitreous detachment (PVD) is an ophthalmic emergency, as it may be the precipitating factor for retinal tears to develop, and also

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detachments. Snail-track degeneration is also associated with retinal holes and tears, as is white-without-pressure, which has been associated with giant retinal tears. Because of these associations, there has been some debate about appropriate management of patients in whom retinal degenerations are found. Clearly, it is not practical to refer 8% of the population to ophthalmologists for screening, or treatment for this problem, and the current advice seems to be that patients who are asymptomatic with lattice degeneration do not need a Hospital Eye Service referral. However, they should be warned that as they may be at a higher risk of retinal detachment in the future, any symptoms of posterior vitreous detachment require urgent assessment to exclude retinal pathology. Although retinal tears and holes may occur in the lattice degeneration, it has been found that in many patients with lattice, the actual tears or holes causing the retinal detachment are not actually in the areas of lattice that were seen before the PVD. Therefore, lattice degeneration should be treated as a sign of a high risk eye in the context of PVD, but does not necessarily need prophylactic treatment. The management of patients who have asymptomatic holes or tears within retinal degeneration is less clear: in asymptomatic patients, routine referral is advised for the ophthalmologists to make the decision about whether treatment should be performed or not. Acute symptomatic PVDs in the presence of retinal degeneration usually require urgent referral to exclude significant pathology. The symptoms of PVD are either floaters or flashing lights (photopsia). The photopsia in PVD are almost always in the temporal field of the affected eye, and often happen in a vertical line which patients will describe as a flicker of lightning. The photopsia are very transient, and are usually only seen in dim light or at night, or when patients move their eyes. Longer lasting photopsia tends not to be due to PVD and is often due to migraine or other problems. Few PVDs cause photopsia alone, and in one series was only found to occur in 6% of patients. More common complaints were floaters alone which occurred in 44%. Remember that few symptoms may mean serious pathology, and so any sudden change in floaters may indicate an acute PVD which may, in up to 10% of cases, be associated with a retinal break. In the series cited previously, 50% of patients with an acute PVD presented with both floaters and photopsia. A PVD in association with a rhegmatogenous retinal detachment will usually produce a field defect and, if the macula is involved, reduced visual acuity. Examination of a patient with an acute PVD ideally requires examination of the anterior retina, as it is here that the vitreous base and strongest attachment to the retina

Figure 1
A Weiss ring formed following a posterior vitreous detachment (by courtesy of Trevor Warburton)

occurs. This cannot be achieved without pupil dilation. Indirect ophthalmoscopy with a slit lamp biomicroscope lens or with an indirect ophthalmoscope has great advantages over direct ophthalmoscopy in this regard. Firstly, a large area of field is visualised (40 with a 20 dioptre lens on indirect, compared to 10 with a direct ophthalmoscope). The magnification is reduced from 15-fold with a direct ophthalmoscope to x3.5 with a 20 dioptre lens, so this enables more wide areas of the retina to be carefully examined. In addition, optical distortion is reduced with indirect ophthalmoscopy and a stereoscopic view of the retina is achieved as well as some depth of focus. There is also stronger illumination and resolution; the peripheral retina can also be seen. The working distance is longer so that when performing a careful examination of the whole retina, you and the patient are not as close to each other for such a sustained period. It is important to realise that even with a slit lamp biomicroscope lens such as a super field or 90 dioptre lens, the retina anterior to the equator is still not easily seen. Although it enables the vitreoretinal relationship to be identified and holes can be seen in lattice more easily than with an indirect ophthalmoscope, if one needs to carefully examine the anterior retina, then a contact lens (e.g. Goldmann triple-mirror) is required, or scleral indentation which can sometimes detect holes which were not previously visible. Clearly, in practice, an optometrist must make a judgement as to how high risk a PVD is, and decide on whether and when referral is required. A very important sign to look for in the context of PVD is that of pigment cells (tobacco-dust) in the vitreous. This is known as Schaeffers sign and, if positive, means that there is a retinal tear until proved otherwise. Examination of an eye looking for these tobacco-dust cells is vital. The slit lamp light is set on a narrow, bright beam and focussed behind the lens in the anterior vitreous. The patient is then asked to move their eye up and down and then

look straight ahead, and while examining the swirling vitreous opacities, the practitioner needs to look for tiny pigment cells, which are brown in colour. Rather like looking for cells in the anterior chamber, they glint in the light, as in a cinema in which dust is seen through the projector light. Practitioners who have never seen this sign should contact their local vitreoretinal unit and ask if they can attend a clinic to view one. Once seen, it will always be easy to spot the sign again, and most vitreoretinal surgeons will be happy for you to examine their patients and look for Schaeffers sign. In the context of a patient with an acute PVD, and positive Schaeffers sign, the patient requires same day urgent referral to exclude retinal pathology. Other signs to look for in a PVD are the Weiss ring (Figure 1), which is the condensed portion of the vitreous that was attached to the optic disc floating in front of the disc. It is not often seen in PVD, but when it is, it is a clear sign that a PVD has recently occurred. Sometimes the posterior vitreous face can be seen flapping in the vitreous when the patient moves their eye, but this can sometimes be difficult to tell in ageing vitreous gel from other vitreous floaters. In one study at St Thomas Hospital, all patients with Schaeffers sign positive were found to have a retinal break or detachment, whilst patients with a PVD who did not have tobacco-dust cells were very unlikely to have pathology. Unfortunately, the rule is not 100% valid, and this is when optometrists are required to use their judgement. We will all be familiar with patients who report a change in their floaters some weeks or even months previously, in whom there is no overt abnormality on dilated fundoscopy, and most of these patients in the absence of any pigmented cells in the vitreous, will not require hospital referral. In an acute very recent onset PVD, however, an optometrist will need to decide whether referral is still indicated even in the absence of tobacco-dust.

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Rhegmatogenous retinal detachment is an age-related disease, and while it is most often associated with boxers and with eye injuries, the majority of retinal detachments occur in elderly patients at the time of a PVD. Retinal detachment is reported as occurring in around 1:10,000 of the population per year. However, up to 5% of the population may have asymptomatic retinal breaks, and this is another reason not to treat every patient in whom a tiny retinal hole is found. An acute retinal detachment shows signs of a PVD, and in addition there may be a relative afferent pupil defect, reduced intraocular pressure, occasionally a mild anterior uveitis, as well as the expected retinal breaks, and a convex, slightly opaque corrugated retina where the retina has detached, which is usually mobile in early stages. It may be stiffer and less mobile in longstanding or recurrent detachments when some proliferative vitreoretinopathy is occurring.

lower turnover in the retina. The retinal photoreceptors and ganglion cells are part of the central nervous system, and therefore do not replicate in life. This means that they are vulnerable to accumulative changes with age. The biggest stress is oxidative stress, which is cellular damage caused by reactive oxygen intermediates (ROIs) produced during chemical reactions, and in particular relating to the energy associated with light. Some of these ROIs include free radicals, peroxides and single oxygen species, all of which cause oxidative damage. The retina is very susceptible to this damage, as it has a very high oxygen use and therefore there are numerous chemical reactions producing ROI. Also the retina is high in polyunsaturated fats which are associated with oxidation. The most obvious cause is the continuous exposure to light that the eye undergoes, causing oxidation.

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Choroid
The choroid is part of the uveal tract, and is divided into three layers the vessel layer, capillary layer and Bruchs membrane. It is an extremely important part of the eye as it is responsible for the nutrition of the outer third of the retina, as far as the outer plexiform layer. The blood supply of the choroid comes from the posterior ciliary arteries in the main, and choroidal vessels are lined by fenestrated endothelial cells, and are most dense at the macula. The circulation is formed into lobules, and while it has previously been thought that the choroidal lobules had spaces through which blood flowed freely, there is now some evidence that these lobules are in fact end arteries which are rarely clinically important in terms of vision loss from circulatory problems. The inner two thirds of the retina are supplied from the retinal arteries, and the retina requires a large

Retina
Before the specific age-related changes in the posterior segment are described, it is important to remember that the retina contains many layers, and these all have a very complex growth factor homeostasis (Figure 2). There is interaction between the numerous cells and layers, and indeed between the retina and the choroid posterior to it. The tight junctions which form the blood brain barrier are probably very important, and their breakdown may contribute to age-related pathology. In response to the question, Why does the retina show changes with age?, the answer is that the retina undergoes considerable stresses during a persons lifetime. Unlike so many parts of the body, such as the corneal epithelium where there is a very high turnover of cells, there is a much

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Figure 2
The layers of the retina are illustrated in this figure. The most important area of change in the ageing eye is Bruchs membrane, which lies between the choriocapillaris and the pigment epithelium (by courtesy of David Kinshuck)

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Photoreceptors

Retinal pigment epithelium Bruchs membrane Choroid

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amount of oxygen. Its respiratory rate is twice that of the brain, and half of the energy requirements come from the photoreceptors. The choroid changes with age; doppler ultrasound suggests reduced choroidal blood flow with advancing age. Indocyanine green (ICG) imaging, which is similar to fluorescein angiography but involves a scanning laser ophthalmoscope being used with ICG highlighting the vessels, shows fewer choroidal arterioles and reduced fluorescence intensity with age. The cause of this is not clear, but it has been speculated that it is due to an accumulation of waste, as well as retinal pigment epithelial layer ischaemia. Bruchs membrane is the innermost layer of the choroid, and is between 2mm and 4mm thick. It is divided into five layers the basement membrane of the capillary endothelium which is next to the choroidal circulation, then a collagen bilayer with an elastic fibre layer (rather like a sandwich filling) in between the two. The innermost layer is the inner basement membrane of the retinal pigment epithelial cells. There are no tight junctions in Bruchs membrane, and so it is not a barrier to the flow of oxygen and nutrients. However, the changes in Bruchs membrane with age are a hallmark of the ageing eye, and are probably very important in the aetiology of age-related macular degeneration (AMD). The most obvious sign of ageing in Bruchs membrane is the accumulation of basal linear deposits (Figure 3). These

deposits are waste material, probably from the retinal pigment epithelium, and consist of lipofuscin. This is formed from lipids and oxidised damaged outer segments of the photoreceptors. This lipid rich layer forms a diffusion barrier to the water soluble constituents of plasma and, in addition the lipidisation of the membrane creates a cleavage plane, potentially allowing the growth of choroidal new vessels to beneath the retina. Lipofuscin deposition is seen from the age of 45 onwards, and is strongly age related. Although it cannot be directly visualised on ophthalmoscopy, there are techniques using autofluorescence which allows the pattern of lipofuscin deposition to be seen, although this cannot be reliably quantified. The barrier to diffusion also occurs from the age of 45 onwards, but interestingly, the prevalence of visual loss from age related maculopathy really only occurs in the eighth and ninth decades to a significant degree. We do not yet know whether a critical amount of basal linear deposits are required before visual loss, or whether other phenomenon are occurring in addition to the lipofuscin deposition. Drusen are deposits beneath the retinal pigment epithelium (Figure 4). They are usually divided into two sorts hard and soft. Hard drusen are small, punctate yellow dots, which can be found in the macular region but also throughout the retina. They are seen in up to 80% of individuals as they age, and become more common with age. They can regress and

may precede atrophy of the retinal pigment epithelium, choroid and outer retina. Hard drusen on their own do not constitute a sight-threatening risk, and in some families they are inherited dominantly where you may see numerous drusen at the posterior pole in quite a young individual. However, some studies have suggested that more than 20 hard drusen within the macular region are in fact a risk for later visual loss from AMD. Soft drusen are larger, and the definition of larger is more than 63 microns, which is half the diameter of a retinal vein as it crosses the optic disc. They are paler than hard drusen, and may be yellow or grey or white. Soft drusen may precede retinal pigment epithelial detachment and choroidal neovascularisation, and the more soft drusen there are, the larger they are, and the more confluent they are. All these signs are significant risk factors for exudative macular degeneration. Therefore, patients with soft drusen and/or retinal pigment epithelial changes need to be warned about the possibility of future visual loss, and to report immediately if they notice any sudden change in their vision, in particular metamorphopsia (distortion). However, they do not necessarily need referral as there is currently no treatment for soft drusen.

Ageing retina
The retina consists of nine separate layers identified on light microscopy, and the important areas that change with age are the retinal pigment epithelium and the photoreceptors. There is some evidence that some of the support cells between and around these layers also change and that there is some degeneration with age. Certainly, a loss of ganglion cells has been shown, and it has been postulated that the loss of a foveal reflex that is often seen with age is due to loss of the inner limiting membrane. In addition, it has been demonstrated that the inner limiting membrane can actually be pulled off the retina in a posterior vitreous detachment, without any loss of function.

Figure 3
Basal linear deposits are seen in Bruchs membrane, causing it to be thickened above the choriocapillaris and below the RPE (by courtesy of David Kinshuck)

Lipofuscin in the RPE cells

Retinal pigment epithelium

Thickening of Bruchs membrane The RPE is a single layer of post-mitotic cells. It is an active selective barrier and therefore is the most important barrier between the choroidal circulation and the retinal pigment epithelial cells. In addition, it regulates nutrition of photoreceptors. It also acts as a solar barrier, protecting against excess light damage to the retinal photoreceptors, and also mopping up ROIs. The RPE phagocytoses the outer segments of the photoreceptors, and therefore is of vital importance in the health of these cells and therefore the vision. The RPE also forms the blood-brain barrier at the back of the eye. The changes in the RPE with age seen are a loss of cells, as well as a pleomorphic change in the cells. In particular there is

Figure 4 Drusen are seen below the retinal pigment epithelium as round deposits, elevating the RPE and the retina

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loss of the melanin granules, which are antioxidant and are responsible for detoxifying the antioxidants and the ROIs. They also bind zinc and other drugs. As discussed earlier, the RPE may be responsible for the increased lipofuscin accumulation in Bruchs membrane, in a sense, because it can no longer cope with the constant turnover of rod and cone outer segments, and therefore waste accumulates. The RPE has a complex interaction with the choriocapillaris, and epidemiological studies have shown that retinal pigment epithelial changes at the macula are a risk factor for visual loss from AMD.

Photoreceptors
There are around 120 million rods, and 6.3 to 6.8 million cones. The rods are absent at the fovea and have a ratio with the ganglion cells of around 100:1. The photoreceptors are in a continuous turnover, and the outer segment discs have a turnover of around 9 to 13 days. The rod disc shedding is maximal in the morning, and cone shedding maximal at dusk. These are probably mediated through melatonin. With age, the photoreceptors do change. In healthy ageing eyes, the cone numbers appear fairly stable, but the parafoveal rods do reduce by around 30%. Reduced dark adaptation is seen in elderly patients, with good vision, and this may reflect this reduction in rods. The rods, however, appear more vulnerable than cones. The rods degenerate over thick subretinal epithelial deposits such as drusen, while the cones can actually survive even over disciform scars. This means that potential treatments of trying to replace the RPEs or surgically move the retina to a more healthy area of RPE have some clinical justification.

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macula, particularly concentrated in the fovea which is where light is concentrated. They are found in the receptor axon layer and in outer segments, and the origin is felt to be dietary. They protect the central retina from blue-light damage and oxidative stress. Macular pigments are found in green leafy vegetables such as spinach, as well as in orange vegetables such as orange peppers. The evidence that they are involved in AMD is that reduced levels have been found in patients with AMD compared to controls, and it seems that patients with high levels of macular pigment are at lower risk of AMD. One study has shown that a high intake of macular pigment is protective for AMD, and supplement studies are now just starting, to see whether supplementation will prevent vision loss in AMD. Zinc is in a high concentration in photoreceptors and RPE cells. Deficiency of zinc leads to abnormal dark adaptation. It has been postulated that there are reduced levels in older eyes. Zinc is an antioxidant also, and modifies plasma membranes with vitamin A. It is, however, toxic in high doses.

Other diseases
There are many other conditions which rise in prevalence with age. Examples of these include epiretinal membranes, macular holes, naevi and, of course, subretinal neovascularisation associated with AMD.

Conclusion
The eye, as it ages, shows structural vitreous changes, which may result in a PVD and therefore carry a risk of retinal detachment. In addition, there is reduced choriocapillaris blood flow, and accumulation of waste products (lipofuscin) in Bruchs membrane, which is derived from the RPE. Subretinal epithelial deposits are seen, known as drusen, and there is some evidence that there is reduced RPE function (with loss of rods) with advancing age. Large, soft drusen and RPE changes predispose the eye to subretinal neovascularisation. It is felt that oxidative stress, particularly blue light and the high oxygen usage of the retina, is important in the aetiology of many of the changes seen in ageing eyes.

Antioxidants
Antioxidants are present in high concentration in the retina. They stabilise ROIs without themselves becoming unstable, and examples include vitamin A, C, E, macular pigment and zinc. The Age-related Eye Disease Study research group (AREDS) study, which was a large multicentre prospective supplement study, showed that high dose antioxidant vitamins and zinc may reduce vision lost in patients who already have significant age-related maculopathy although there was no obvious effect in people without obvious age-related changes. Interestingly, many of the patients in the study were already taking simple vitamin supplements, and it may be that there is a reduced absorption and bioavailability of vitamins in the elderly as well as in some cases reduced intake. Macular pigment has become a very interesting area of research in the aetiology of age-related macular degeneration. The macula lutea is so named because the lutea is the yellow seen from the macular pigments concentrated in that area. The main two macular pigments are lutein and zeaxanthin, and are only found in the

References
1. Age-Related Eye Disease Study Research Group (2001) A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Arch. Ophthalmol. 119: 1417-36. 2. Boulton M, Dayhaw-Barker P (2001) The role of the retinal pigment epithelium: topographical variation and ageing changes. Eye 15 (Pt 3): 384-9. 3. Beatty S, Koh H, Phil M, Henson D, Boulton M (2000) The role of oxidative stress in the pathogenesis of age-related macular degeneration. Surv. Ophthalmol. 45 (2): 115-34.

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MCQs Module 5 Part 8 of the ageing eye series

light exposure at the retina b. Reactive oxygen intermediates include single oxygen species c. Macular pigment deficiency results in impaired dark adaptation d. Antioxidant supplements may reduce vision loss in age-related macular degeneration 8. The retinal pigment epithelium: a. loses melanin granules with increasing age b. allows free diffusion of nutrition to the retina c. consists of five layers of cells d. increases the number of cells with advancing age 9. Which one of the following statements is correct? a. Hard drusen are seen in the majority of elderly people b. Soft drusen are less than 63 microns diameter c. Drusen are found above the RPE d. Drusen are the result of infarcts in the choroidal circulation 10. Which one of the following is NOT associated with age? a. Rhegmatogenous retinal detachment b. Lattice degeneration c. Epiretinal membranes d. Asteroid hyalosis 11. Drusen are seen in what proportion of the elderly population? a. 20% b. 40% c. 60% d. 80% 12. Which one of the following statements is incorrect regarding zinc? a. It is in a low concentration in photoreceptors and RPE cells b. Deficiency of zinc leads to abnormal dark adaptation c. It is an antioxidant d. It is toxic in high doses
An answer return form is included in this issue. It should be completed and returned to: CPD initiatives (c4397g), OT, Victoria House, 178-180 Fleet Road, Fleet, Hampshire, GU51 4DA by September 3, 2003. Under no circumstances will forms received after this date be marked the answers to the module will have appeared in our September 5 issue and scores sent electronically to the accrediting bodies.

The ageing eye Changes in posterior segment with age

Please note there is only ONE correct answer
1. Age-related lipofuscin deposits in Bruchs membrane are called: a. basal laminar deposits b. basal linear deposits c. basal lutein deposits d. basal laminar flow 2. The vitreous gel: a. is viscous because of collagen b. attaches more firmly to the ora serrata with age c. has a 90% water content d. has a volume of around 4ml in emmetropic eyes 3. Age causes: a. pigment cells tobacco dust in the vitreous b. increased melanin granules in the RPE c. a reduction in parafoveal rods of 30% d. a reduction in the number of cones by 30% 4. Bruchs membrane: a. forms an important part of the blood-retinal barrier b. is the innermost layer of the choroid c. is around 0.5mm thick d. phagocytoses the outer segments of photoreceptors 5. a. b. c. A posterior vitreous detachment: is always symptomatic always causes a Weiss ring causes retinal tears in up to 10% of cases d. causes photopsia alone in 50% of cases 6. Which one of the following statements is correct? a. The choroid supplies nutrition to the inner two thirds of the retina b. The choroid shows reduced fluorescence intensity on ICG angiography with age c. Ischaemia of the choroid results in loss of photoreceptors d. Blood supply to the choroid is derived from the anterior ciliary arteries 7. Which one of the following statements is incorrect? a. Oxidative stress results from blue

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