 Today's material stuff that I have to go over, this is not really interesting stuff necessarily from an exciting clinical standpoint, but we're trying to highlight some of the material from a clinical standpoint to make it relevant for the residents, resident Chris. So for the residents, what I would try and do is read through this once and have some sort of note system where you can summarize what you think is important out of it, so you don't have to go back and read it again, and then as you go through your notes to review for OCAPs, if you read something and you're like, but I'm not sure what that means, go back and read that specific section, maybe just boost up or shore up your notes to make it a little easier. Essentially, this would be what this PowerPoint lecture would be for me if I were preparing for OCAPs is just sort of a note summarization of all of this information. It is chuck full of information. This section covers about 60 or 70 pages in this BCSE book, so it's going to be impossible to go through all of it here today in one hour, so again I'm going to try and highlight some of the findings there, some of the information I think is a little more useful, at least from a clinical standpoint, so that would be a lens I think we all know, you know blood supply depends on aqueous for nutrient delivering waste removal. Some interesting facts in terms of aging that we see with the lens, of course we know that it reflects light due to the difference in the index of refraction between aqueous and vitreous and the lens material itself. With aging we see an increase in lens curvature which should in theory increase the lens power, but there are very changes in the index of refraction of material that can cause either myopic or hypropic shift. Of course, classically we know if increasing nucleus chloride and cataract we tend to see a myopic shift and it increases that index of refraction. Size, this is something useful from a surgical standpoint, knowing what your typical size is of the human adult lens, which is about 9 millimeters in circumference and 5 millimeters anterior posterially, so the thickness is about 5 millimeters. That depth can be useful in terms of instruments, knowing what size your instrument is, as you're inserting it into the lens material, knowing what depth you can safely go to there. So, let's see. The capsule, from a clinical standpoint or surgical standpoint, we're mostly interested, of course, the posterior aspect of the capsule being very, very thin, two to four microns, you want to be gentle with that posterior capsule, just known as made out of type 4 collagen and it's an elastic membrane. The zonules, which support the lens, maintain a position. A few basic things you need to know about this, they originate from the basal laminate of the non-pigmented epithelium of the parsed plane and parsable cloud of the ciliary body. They insert in a continuous fashion in the equatorial region, both anteriorly and posteriorly, and with age, these directly equatorial fibers tend to regress, leaving more of the anterior and posterior fibers behind to support the lens. Lens epithelium is a single layer anteriorly. This is where the active replication is occurring in the anterior equatorial region, it's called the germitative zone. The newly formed cells will migrate equatorially and posteriorly to form new lens fibers in their dramatic cellular structure changes as that process occurs. You'll see them increase membrane protein, of course, lose their organ cells. As they do that, they depend almost completely on glycolysis for energy production, taking back to your biochemistry days undergrad. Let's see, anatomy of the nucleus cortex. No cells are ever lost from the lens. The oldest cells are going to be found in the nucleus, the center part of the lens, and the newest cells are the most outermost aspect of the cortex. If we look at the histology or morphology of the lens, there's really no distinction between cortex and nucleus. You can slice up the lens prep and put it under a microscope. You're not going to be able to tell a difference in terms of where that lens cell came from. So surgical texts that describe the endonucleus, the epinucleus, the cortex, that's a description of how that material behaves, the older lens cells versus the newer lens cells, and not necessarily a histological morphologic difference between those lens cells. This is all pretty boring. I won't bore you with that. Remember, in structural proteins, it's got a skeletal proteins. Yeah, I don't really see a lot of them. If they test you on this material, they're just mean, on the O-caps. So in terms of aging of the lens, there is an increase of the water insoluble proteins with age. As these proteins aggregate, we'll start to see opacification or reduced clarity. So scatters, lights, glare symptoms the patient might complain about, even though they don't have much of a cataract. It's probably from those types of changes. So let's see. A certain amount of that process, of course, is normal. Excess of this will begin to result in cataract formation. There's a good correlation with the amount of insoluble protein in a brunessant cataracts. There's a relative lens density. And some of the changes that appear to result in this, there's a loss of reduced form of glutathione, which is designed to help prevent oxidative change or stress. So we'll start to see disulfide bonds between protein material in the lens cells and other forms of cross-linking increase. And we get yellow and brown pigment deposition changes. Of course, that's what a cataract looks like. All of us, most of us have seen that in clinic. Let's talk about carbohydrate metabolism. This can be interesting in a few clinical scenarios. So we know that glucose can enter via both passive or simple diffusion and active facilitated diffusion mechanisms. Most of the glucose is phosphorylated by G6P2. Excuse me, G6P by the enzyme hexokinase. This is the rate-limiting step in glycolysis, about 70 to 100 times slower than any other enzymes in that system. Glucosexfosate will then pass either two pathways, anaerobic glycolysis, the rate-limiting step being phosphorylbucinase, which is regulated by feedback control. You only get two ATP produced through this system for one glucose molecule relative to 38 in the Krebs cycle, the oxidative metabolism cycle. So it's not real efficient use of glucose. This is due to low oxygen tension. See, 3% of glucose passes through oxidative processing. It's interesting that only 3% of glucose passes through oxidative processing but still creates about 25% of your lens ATP because of that difference in efficiency. When we look at experimental models, the lens can remain transparent without oxygen. It doesn't require oxygen, thus demonstrating the dependence on glycolysis, its ability to depend on glycolysis. We put it in a medium without glucose. It will not remain transparent. Glucose is absolutely required for that transparency. The other pathway that G6P will go through is the hexose monophosphate shunt. About 5% of it goes through that purses N80PH for fatty acid nucleotide biosynthesis and some of the oxidative stress pathways to help support those. All right, so let's talk about the diabetic cataract. Anybody without looking at this, anybody tell me how a diabetic cataract develops? Does anybody know? OK, we're going to learn today then. So we've talked about nonphosphorylated glucose. We'll enter the sorbitol pathway. In most cases, that's a very small amount that goes through that. Aldous reductase is the key enzyme. This Michaelis constant, 700 times that of hexokinase, affinity is inversely related to that. So you can see it's a very high constant. So obviously, the affinity is fairly low for glucose. It doesn't grab onto glucose very well. And thus, with normal levels of glucose surrounding the cell, very little of that glucose goes through this pathway. With higher levels of glucose, however, there's feedback inhibition of the glycolysis pathway. And thus, a greater amount of this glucose can be fed through the sorbitol pathway. Sorbitol is then converted to fructose by this enzyme here, which also has a low affinity for fructose. So again, the sorbitol pathway has multiple sort of checks, if you will, in the normal system where very little glucose is sent through that pathway. But if we have this feedback inhibition, a lot more glucose sitting around, eventually it starts to be processed through this. So thus, it takes a fairly high amount of sorbitol. It will build up in the setting of high glucose. This is how that happens. Sorbitol is poorly permeable. And of course, that is important to understand. And this mechanism of diabetic cataract is that if you have a lens bathed in a high glucose setting, we get lots of sorbitol retention or production with high glucose levels. We see a significant NADPH to NADH ratio, which also drives additional sorbitol activity. And this accumulated utilized NADP will also do the sorbitol pathway. It will drive the HMP shunt activity as well. But sorbitol and fructose will accumulate in the lens in the setting of high glucose. And this will generate osmotic pressures, which draw water into the lens, which will overwhelm energy-dependent pumps. It's trying to pump that fluid back out. Eventually, the lens fibers will swell and disrupt the cytoskeletal structure. And the lens becomes opacified. So that's how a diabetic cataract develops in the setting of high glucose. A sorbitol pathway, retention of sorbitol with osmotic stress, not causing the lens to swell. Do you have a question? Well, ultimately, is it the same endpoint as age-related cataracts? Or on, like, Mr. Pathology, would they look different? So this would look a lot like a cortical cataract in terms of cortical cataract is due to swelling of the lens structure. To be honest, I don't know if you looked at it histopathologically, whether it would look any different, a swollen opacified lens versus a oxidatively stressed lens. I guess if you looked at it with certain stains and not a pathologist, so this is conjecture on my part, it might look a little bit different. But most of the time I've read where I've read through this material when it talks about looking at things morphologically or histopathologically, it's really hard to distinguish between these things, between clear lens and a cataract lens as well. All right, so let's talk a little bit about oxidative damage protective mechanisms. So of course, we're all familiar with what free radicals are. It can be, of course, generated at low levels by normal metabolism, radiant energy. We have relatively low oxygen tension around and in the lens. And so the oxidative stress is likely not necessarily interacting with oxygen first, but acting directly on lens proteins and lipids. We have protective mechanisms to try and prevent this. Glutathione peroxidase, catalase, superoxide, dysbutyrate, vitamin E, and vitamin C, ascorbic acid. We know that increased levels of oxygen can result in cataract formation, and this is clinically relevant. This is seen in the setting of hyperbaric therapy and in the setting of atrectomy. We know we've atrectomized the eye. We remove the vitreous. The vitreous has a fair amount of vitamin C, among other oxygen utilizing or protective mechanisms for oxidative damage from oxygen. It also consumes oxygen. So as we remove that, oxygen tension increases in the posterior segments, and that will facilitate oxidative stress, damage, and lens classification of cataract formation. So that's why we often see that after atrectomy surgery, especially in patients who already have started some of this process over the age of 50. All right, so let's see. A couple of brief things off of this. Relative to aqueous and vitreous, know that the lens has a higher concentration of potassium and amino acids. I do remember seeing that on OCAPs. It has a lower concentration internally of sodium chloride in water. So there are these both passive gradients and active transport mechanisms that take advantage of this. It's referred to as the pump leak theory with this sodium potassium ATPase helping to maintain that. We won't belabor any of those. Accommodation and presbyopia. So this is somewhat clinically relevant. So the Hemmholz theory, which is sort of the theory that most of us sort of ascribe to in terms of how accommodation occurs, its syllabiotic contracts, increases diameter of the syllabiotic ring, which results in changes in zonular tension. So it's reduced zonular tension that allows the lens to increase in spherical curve in shape, particularly in the center anterior aspect of the lens. And this will allow us to increase the power of the lens allowing you to focus on something up close. The change in the central anterior capsule is, where it's more focal in that area is thought due to the relatively thinner anterior capsule centrally versus the equatorial. Remember we went through the thickness, I didn't highlight it too much, but it's a little thinner in the center and anteriorly relative to the anterior equatorial regions. Of course, accommodative response is going to be stimulated by the distance of the object you're looking at or blur, chromatic aberration is thought to maybe help stimulate that. Of course, parasympathetic intervation mediates it. Loss of accommodation with age, something just to be aware of is something you might see on the OCAPs. And adolescent has quite a bit of accommodated amplitude of 12 to 16 diopters. The age of 40 drops down to 48 diopters after age 50 decreases to less than two diopters, obviously. Most patients become symptomatic from a presbyopia standpoint assuming they're hematropic around the age of 45. The cause of this process is thought to be due to hardening of the lens, which increases over a thousand fold over a lifetime. Other possible contributing factors to presbyopia, lens dimension changes. Of course, we talked about the lens continuing to grow throughout life. So it might result in reduced, sort of reduced leverage, if you will. This is a ciliary body zonular system, as it enlarges. Loss of capsule elasticity with age, geometry of the zonular attachments, and sort of the loss that we talked about equatorially, maybe that plays a little role as well with age. Ambriology, this is just rope memorization. Try to know a few things about it, but don't worry about too many of the details. So I'm gonna skip over it, because it's really boring to me. Let's talk about, let's see, congenital anomalies. Congenital leafache is fairly rare. I've never seen it. Lenticonus and lenticlovus. So lenticonus, nice to know some of the associations with systemic diseases. So anterior lenticonus. Lenticonus is just a focal cone-shaped deformation of the anterior-posterior capsule. Posterior is more common. It's usually unilateral and sort of a sporadic finding. Anterior is often bilateral associated with Alport syndrome. So you see anterior lenticonus. Certainly ask the question if they've been diagnosed, and oftentimes they have. But if they haven't, suggest the primary doctor considering an evaluation for Alport syndrome. Let's see, retinoscopy in these cases will show this sort of central myopic, distorted reflex. Or it might, red reflex, excuse me, will show sort of an oil droplet look centrally. And the bulging may progress. You get sort of this myopic shift. Sometimes you get a focal opacity or a cataract in that area where the capsule is deformed. So the lens coloboma. We have two types, primary coloboma, which is just a wedge-shaped defect of the lens itself. It's isolated in a second area, which has sort of the same shape as this primary, but it's associated with a ciliary body, zonular defect, developmental anomaly, and uveal coloboma, essentially, as caused there. Sometimes you can get a focal cortical opacity. You get some thickening of the capsule in that area. Very common for the zonules either to be weak or absent in the area of the coloboma. So you need to be aware of from a surgical planning standpoint. Let's see, metendorb.it becomes a star. Exciting there. Peter's Anomaly. You'll learn about that in Quarantine. Microspherofakia. Most commonly seen in wheel marshesani syndrome, which is sort of the antithesis of Marfan syndrome. These are short patients with short, stubby fingers. It's inherited autosomal recessively. So just know that association, microspherofakia, wheel marshesani syndrome. Concerned with microspherofakia, we've got a small lens, it's spherical. It can block the pupil, increasing the risk for acute angle closure and glaucoma. Myotics will aggravate this as it will cause forward lens movement. So cycloplegic is preferred in this scenario to increase the tensile force of the zonules, bring that lens posteriorly, and reduce the anterior posterior lens diameter. Of course, an LPI is the treatments to try and help prevent that particular issue. Aniridia, I know about the association with the PAC-6 gene, which comes up with Peter's Anomaly as well. So this transcription factor is very important to the development of the cornea, the lens and the retina. So aniridia is essentially a panocular syndrome, though the aniridia is the most striking clinical feature when a general physician might be evaluating the patient because there's partial or near complete absence of the iris. But other findings that you'll notice on the limb exam or complete exam, you see some corneal panis due to limbal stem cell deficiency or failure. They can get a corneal epitheliopathy from that same problem. So corneal specialists are very familiar with aniridia because of the effect. You can also see a form of glaucoma thought to be due to some developmental anomalies of the trabecular mesh work. You can have foveal and optic nerve hypoplasia. So diminished visual function in general, which can result in nystagmus. It's nearly always bilateral and about two-third of cases are familial. So it's an inherited defect though. You can see sporadic cases associated with the wagger complex. You can get cataract as well, anterior, posterior, polar opacities can be present at birth. And within the first two decades of life, about 50 to 85% of patients will go on and on. So cataract is a likely problem early on. They have porzonules or porzonular integrity. So it's important to be aware of that in the surgical planning standpoint as well. So a few basic things about congenital cataract, about a third of them are syndromic. A third of them are isolated but inherited. And a third of them are just will be of unknown cause. You'll do a workup and you won't really find any specific cause. They occur in about one in 2,000 live births. And they're usually present at birth or within the first year of life. There are a number of different types that I won't necessarily spend a lot of time on in terms of what they look like. You can kind of review through that. I do want to talk a little bit about the polar cataract. If you've got an anterior polar cataract, they're typically small because they're a little bit further away from the nodal point of the eye. They don't require surgery necessarily because they don't impact vision as much, but they can result in an isometropias. It's important to monitor them closely for differences in refractive error and make sure that that's corrected. Posterior polar effects or posterior subcaps or cataracts are going to be often more visually significant because they are typically larger and closer to the nodal point of the eye. Of course, with a posterior polar cataract, I think most of us, at least residents, are probably familiar with the concept that they're associated with capsule fragility or in some cases thought to be a capsule defect. So it's always wise as you're going through surgical planning to be aware of that and adjusting your surgical plan to compensate for that. Essentially, we don't hydro-desect the lens. We only hydro-delineate. We try and remove the lens layer by layer to get to that final area where the capsule may be very fragile at the very end of cortical removal. Let's see, let me skip that. All right, so ectopia lentis can be congenital, developmental, or acquired. A subluxated lens is partially displaced. A luxated or dislocated is completely displaced from the pupil. This implies that the loss of essentially all of the zonules. Symptoms with ectopia lentis obviously decrease vision if that lens is de-centered. We can see marked astigmatism due to tilting of the lens, monocular diplopia, and iridodonesis if the lens is moving a lot. We've got a lot of zonular weakness or loss. Conflictations include, of course, cataract. We can see displacement of the lens into the interior chamber or into the vitreous cavity. If it's acquired, it's typically due to trauma. Systemic associations include Marfan syndrome, homocystinuria, aniridia, which we talked about congenital glaucoma. Less commonly, Ehlers-Danlos. Though you wanna be aware of it in patients with Ehlers-Danlos, there are a variety of different Ehlers-Danlos syndromes. Some of them are gonna be more likely to associate with ocular findings and others won't be. So trying to find that specific subtype will help. Hyperlysinemia sulfide oxidase deficiency. It can be an inherited isolated anomaly. There's an autosomal dominant inheritance pattern with that. So Marfan syndrome is a mutation of the fibrillin gene on chromosome 15, autosomal dominant inheritance. Although 15% don't have a family history, so maybe a sporadic genetic defect. These patients are tall. They have chest wall deformities. They have a dilated aortic root mitral valve prolapse. Commonly, there's a lot of concern about cardiac risk in these patients. 50 to 80% will show ectopia lentis. Usually, it's symmetric and it's superior temporal displacement. That's an OCAP question they like to ask. Zonials will remain intact. You'll see them, but you'll notice they're stretched and elongated, so you get a chance to see one of these cases with Dr. Crandall, who's probably the one that does the most cases. Myself and some of the other surgeons do them occasionally. You'll see that stretched elongated component to the zonials, they're weak, but still have some structural integrity. Let's see. They often will have significant axial myopia and they have increased risk of retinal detachment. They often require a bifocal at a younger age due to weak raps and accommodation maybe related to the zonular weakness. If you do a lensectomy, there's an increased risk of vitreous loss and retinal detachment in those cases. Obviously, more complex surgery. We'll skip homeocystinuria, hyperlysinemia. Let's talk a little bit about genetic contributions to age-related cataract. So identical and fraternal twin studies suggest that at least a portion of age-related cataract formation is heritable. So about 50% based on studies of cortical cataract development is thought to be genetic or heritable. This mutation, which I don't anticipate would ever come upon OCAP, so don't worry too much about it. And then they estimate based on different studies about 35% of nuclear cataract risk is genetic or heritable. Let's see. So this, of course, suggests there's some genetic links, underlying biologic pathways that would be important to assisting us in understanding potential targets for therapy that could put us out of business as cataract surgeons. So just ignore that aspect. Nobody do any research on that. It's bad for business. I know that there are actually some people looking at drops. I think they are designed to reduce the oxidative stress to the lens and theory might help to sustain greater accommodative amplitude into older age and may help to reduce at least nuclear cataract formation. I think it's been through a phase two trial with some success and so they may be moving to a phase three. Now it's interesting to see if that comes out. For those of you who are a little older, maybe sooner, hopefully sooner before you start getting reading glasses, right? So let's see, ectopia lentis at pupilae. This is autosomal recessive. So this has the, of course, the ectopia lentis lens subluxation, but also a pupil displacement, usually in the opposite directions. Pupils typically irregular and slit-shaped. And this is usually bilateral, but you'll see asymmetric clinical appearance between the two. Pupil dilates poorly and you'll see associated ocular anomalies, myopia, retinal attachment, cataract. Among others. Let's see. Let's talk a little bit about age-related lens changes, how they develop. Let's see, we've talked about aging effects, lens increasing in mass, thickness, and a loss of accommodated power over time. We know that with new layers of cortex, the central lens, to some degree, is compressed and hardens. We call nuclear sclerosis chemical changes and proteolytic cleavage of crystalline result formation of these very large protein aggregates. We have chemical modification with pigmentation. We see a decrease in potassium and glutathione, so there's greater oxidative stress risk, and that will result in opacification. Specifically, nuclear cataracts. Everybody over the age of 50 has some level of sclerosis, although it's usually very mild. This is, of course, a central opacity of the center portion of the lens, the oldest lens fibers, if you will. It's easier to visualize. The slow length that you can look at it with a well-dilated patient, the red reflex. Typically, it's very slow in terms of its progression, usually bilateral, but of course, as we all know, it can be asymmetric. It has a greater impact on distance vision compared to near, so patients typically are gonna have distance vision complaints with a nuclear cataract. Myopic shift is a very classic association with the nuclear cataract as it progresses due to increased index of refraction. We call second sight as a historical term for this myopic shift where they start to be able to see up close again without glasses. That's what that means. Let's see. The abrupt change in the index of refraction between the nucleus and cortex will sometimes result in monocular dyplopia as well, so those big changes in index of refraction can result in ghosting symptoms. They tend to have a little bit of a reduced color discrimination. You'll often hear patients at for cataract surgery describe changes in their color perception, particularly at the blue end of the spectrum. Histologically, it's difficult to identify differences compared to a clear lens, so as we talked about, I think you had the question about pathology. A lot of these things are just very hard to visualize histologically. On electron microscopy, maybe there's some increased lamellar whirls in some nuclear cataracts, but that's about the extent of the change you might see. So cortical cataracts are a local disruption of cell structure and mature lens fibers. We get membrane integrity compromise. We lose essential metabolites. We get extensive oxidation and precipitation of protein. This is usually bilateral, though it's often asymmetric. The effect on vision is dependent on where it's located, whether it's in the visual axis or not. Classic symptom is glare from focal light sources due to the focal nature of the cortical opacification. Progression is somewhat unpredictable. Sometimes it'll be very stable for a long period of time in other cases it will progress rapidly. Your first signs, you'll see vacuoles. When you see vacuoles in the lens, those are in the cortex, if you will, from an anatomic lens standpoint. They're not in the nucleus of the lens. You sometimes see, of course, water clefs in wedge-shaped opacity spokes, as we're familiar with them from the clinical standpoints. With complete opacification, capsule to nucleus, cataract is considered mature, so white cataract. Cortex takes up water and can cause swelling. This can result in what we call an intumescent cataract. It can be under significant pressure, which can create a greater risk for capsule problems as you try to do it. Capsulotomy, tear-outs, Argentinian flag sign, et cetera. So something to be aware of to try and manage that. When degenerated cortex leaks through the capsule, we call it hyper-mature. With further liquefaction of the cortex, you get this freely floating nucleus in the lens. We call it morgagnium. Histologically, you can see swelling and local disruption of the lens fibers, if you look at it, under the microscope. All right, posters of caps or cataracts. Usually these patients relate younger at onset. They'll often have glare and poor vision with bright lights or bright lit backgrounds. Lights will induce pupil constriction, so potentially greater impacts. If it's centrally located, especially on near vision, of course with the combination of pupil does constrict. Can't be age-related, but trauma, steroid use, inflammation, ionizing, radiation are associated with PSE formation. Histology, we have posterior migration of the lens epithelial cells from the lens equator with aberrant enlargement. Solemn cells called wevel or bladder cells. We, of course, know corticosteroids are strongly associated with PSE formation. It is related to dose and duration of treatment, so the higher the dose, the greater the duration, the greater the risk. It's been reported with varied forms of administration. Systemic, oral, or IV, but it's also been reported in cases of joint injections. Obviously, intraocular or topical administration, even with nasal sprays or other things in hailed forms, I have been associated with that. In children, you may see some regression if it's an early PSE with cessation of the drug. So sometimes reversal can be induced in a young patient, in older patients, that's not likely to occur. Other drugs I see of interest, the thysines, we'll worry about those. So we'll bring this up. So intra-lenticular foreign bodies, if it's not cupric or ferric in nature, so not copper or iron-based, the capsule compromises small and self-sealing, sort of fibrosis, it may be okay to leave that foreign body in place. You may get a focal opacity where that foreign body is located, so it depends on where it ends up. But it's certainly possible that in some cases, leaving the foreign body alone until the cataract becomes visually significant is reasonable. Well, that's ultraviolet radiation, so let's talk a little bit about that. Experimental evidence suggests that cataract risk is at least to some degree related to UV exposure, or at least that will increase cataract risk. So we've got epidemiologic evidence that shows there's an increased risk of cortical cataract with increased sun exposure. It counts for about 10% of total risk in temperate climates where you're exposed to greater amounts of UV radiation. ANSI standards, these are lens standards, will result in about an 80% reduction of UV transmission with prescription lenses or appropriately labeled non-prescriptioned sunglasses. Wearing a hat will reduce UV exposure by about 50%. So when patients are outdoors, wear a hat, wear sunglasses, and that's one of the reasons why is to prevent increased cataract risk. Oh, let's see, chemical injuries, so ciderosis, bulbide due to iron deposition, and the lens, TM, et cetera. You'll see a yellowish hue early on followed by a brown rusty discoloration of the lens if there's an iron-based foreign body that's left in the eye. Late manifestations include complete cataract and retinal dysfunction due to damage from the body, copper-based foreign body. You'll see deposits in decimates, membrane, anterior lens capsule, and other intraocular basement membranes and form a sunflower cataract, so there's petal-shaped deposits, yellow or brown pigment. It really is a visual consequence. If a foreign body has a high amount of copper, usually you get a severe inflammatory reaction with necrosis if it's not dealt with. Electrical injury, we talked about metabolic cataracts and diabetes, we talked about that. Galactosemia. So Wilson's disease, of course the classic Kaiser Fleischer ring, copper deposit in the decimates membrane, you can see a sunflower cataract with Wilson's disease as well if it becomes more advanced. Myotonic dystrophy can be associated often with a cataract that's usually a PSE cataract and usually at a younger age. So effects in terms of cataract development and nutrition, alcohol, smoking, risks for cataract formation, lower socioeconomic status, lower education level of poor overall nutrition. Conflicting results when we look at vitamin supplements, studies A-Reds showed no reduction. Did show some moderate protection against development of nuclear opacities. So lutein and zeaxanthine, which of course are really important to macular health, of great interest to Dr. Bernstein. Diet rich in high lutein foods has been shown to reduce the risk of cataract and then smoking and excessive alcohol consumption are associated with increased risk of nuclear. Opacities of course, macular degeneration as well. So cataract associated with uveitis, obviously thought due to the inflammation and the subsequent steroid therapy. They're often subcapsular either PSE and sometimes anterior subcapsular changes. You can see posterior synechia, the iris that lends capsule. Oftentimes the anterior capsule can be thickens and even fibrous. Fibrous people are remembering on that anterior capsule. Fuchs heterochromic erosiclitis is a specific uveatic syndrome that will present. It's usually unilateral, will present with cortical cataract in many cases. And 25% of cases will have spontaneous intraoperative and tear chamber hemorrhages. You get some bleeding during surgery. Typically they have a very good prognosis with surgery. They don't usually have posterior synechia and the inflammation is usually fairly mild. Let's see, cataract associated with ocular treatments we've talked about. Intractomy association and of course corticosteroid association. Hyperbaric oxygen therapy. So somebody who is undergoing hyperbaric treatments will often see a myopic shift. Although there's no change detected in the corneal curvature or axial length. So that's, it's presumed that it's in the lens in terms of changes in the index of refraction of lens material. In most cases the shift will resolve once the treatment is completed. Patients do have an increased risk of development of nuclear cataracts with significant exposure to hyperbaric oxygen. We talked a little bit about oxygen exposure to the lens with the tractomy and how that causes that. So a similar mechanism that increased oxidative stress. Pseudo exfoliation. So this is something that can be associated with a number of different ocular problems including glaucoma cataract and xonular issues. It's a fibrolegranular material is deposited in the eye and other organs. Systemically it's a basement membrane like material in the eye will be deposited on the lens. The cornea, the TM, iris, ciliary processes, anterior hyaluridic phase of the xonular fibers. You'll see little deposits on the lens capsule with an intervening clear zone corresponding to iris excursions. Pretty classic clinical appearance. You'll see atrophy in the iris, the pupil to margin, pigment deposition on the interior iris as well. They usually don't dilate well. You'll see increased pigmentation of the TM on the gonioscopy. Our concerns surgically when we're doing cataract surgery in these cases is the capsule's a little more fragile, zonular weakness is a greater potential problem. And then of course at higher risk for open-angle glaucoma can be a very aggressive form of open-angle glaucoma. It can be unilateral in clinical presentation but we always assume or presume that it is bilateral even if it's asymmetric clinically on exam. And it tends to be more apparent with increasing age. No question of age component to it. About these in glaucoma, I told you there's a lot of slides on this. It's really, demiology, oh that's it. Okay, so I think we've highlighted some, maybe too much of the information there but at any rate for the residents, just focus on trying to, with BCSE series, ideally trying to get through, particularly some of these less interesting components, trying to get through it, making some notes, things that you think are important, highlighting those and being able to go back and review those notes as opposed to having to go back and reread those areas. And then if the note doesn't make sense, go back and read that, just that small section. That's what I would recommend in terms of OCAP preparation that way. As you continue through your three years, you'll be able to just go back and review your notes for OCAP prep, particularly for this section which applies to the first 60 or 70 pages of this BCSE series. Does anybody have any questions about any of the material that we've presented today? Do we have any other questions? Sort of random question. We, I've occasionally had consults questions about people who had electrical injuries, like electric shock or like maybe injuries. Does the cataract development occur in those cases? I didn't know if you- There's a slide on that, let's go back to that. So electric shock, it can cause protein coagulation. Obviously cataract lens made out of protein can cause focal opacification. Cataract, it's more common with transmission of the current involving the head, so closer to the eye. Typically you're gonna see subcapsular and cortical changes. Sometimes they can be progressive, sometimes you'll see some regression or loss of the change, so it'll improve, especially in younger patients. And in many cases it remains very stationary. Have you ever seen those? You always tell us to come look and I'm like it's been a week, I'm sure they don't have a cataract yet, but. I would tell them in most cases they can be seen as an outpatient once they're discharged, set up an appointment, we'll do a dilated exam and look at things, document what's there. But unless they're complaining of significant vision changes, I tell them it's not appropriate for you to see them inpatient, it's not necessary. Other questions? In call you to ask for a consult, let's say you know what, that's not gonna cause an acute problem. Let's schedule an outpatient visit when they get discharged, focus on taking care of the electrical burn injury or other organ dysfunction associated with electrical transmission, cataracts at least of their concerns. All right. Other questions? We're gonna finish a little early, mostly because this is just hard to get through and it's very dry and I can see half of you nodding and bobbing your heads and that's okay because I fully expect that I'd be doing the same thing. All right. Thanks for coming. You're welcome.