So, two cases here, but this is a 26-year-old with intermediate UV IDs and episodes of vitreous hemorrhage in the right eye. Now, she comes in with this picture. What do you see here? It looks like there's some vitreous AIDS. And? Maybe there's some snowballs. Yeah. There's a picture on the optic nerve. It looks a little swollen. Well, there's some neobascularization on the optic nerve. Nothing here. And theography shows this. Looks like some NPD. Yeah. And a leakage out peripherally. And the nerve looks a little solid. All right. This picture has intermediate UV IDs. Is this vasculitis? Not necessarily. Not necessarily. So you can have vascular reactivity in the absence of true regimen vasculitis. You can have retinal vascular incompetence with leakage of dye into the picture, into the retinal substance, without really having true retinal vasculitis. Here's a 35-year-old lady on cell set who programmed tachyrolimus for kidney transplant. She has a history of memory number left for them. Kilomerular. Kilomerular. Now, she comes in with this. Actually, what do you see here? You're entraining vascular charge. Right. So, looks like she had surgeries, maybe. But not really. But then what do you do here? You do with underlying drugs. This is the absolutely normal leakage anyway. So, is this vasculitis? No. This is chronic vascular whitening without vascular Congratulations. But there truly have retinal vasculitis. You have to have very vasculated infarction. What's coughing and cheating? Cheating is actually infiltration of the space around the vasculature in the adventitian. Infarction with leukocytes. So that was just chronic history of either one of two things. Either retinal vasculitis or vasculate insufficiency global vasculated insufficiency with somebody with really a systemic hypo-profusion and therefore, it's the erosive of the vasculature. So not all cheating is very vasculate infiltration. Retinal vasculitis is retinal vasculate or very vasculate infiltration. It is a common occurrence in posterior intermediate UVAs. But in order for it to be the primary lesion, in order for it to be demarcated to retinal vasculitis, it needs to be the primary lesion. It needs to be either an endothelialitis or an inflammation of infiltration around blood vessels as the initiating lesion. Retinal vasculitis can be primary, and therefore focal. It can be localized into retinal hemorrhage. You can have local infarction, adjacent retinal exudation, or it can be diffused or secondary, which is what you see in UVAs. In this case, you see diffused capillary leakage, segmental staining of retinal vessels, optic nerve head, and macrodema. I like to call it inflammatory vasculopathy. You distinguish it from retinal vasculate. It's important to remember that even though we like to differentiate systemic vasculate, we like to look for a variety of systemic vasculates. It's crystal-dermal. All right, so even though we evaluate for systemic disease and systemic vasculitis, systemic vasculate is actually truly rare. And in this cohort of 1,430 patients from Oregon with octet inflammatory disease of which 14.1% had retinal vasculitis, only 11 or 1.4% of these patients had systemic vasculitis. So it's very rare. So we look for it. Because we look for inflammatory macrodermas, but we rarely find them. Is it 1.4% of the 14%? It's 1.4% of the 3%, so it's 2.41% in any patient. So retinal vasculitis can have very phlebitis, in which case it's primarily off the veins. And it can be arthritis, whereas it's primarily off the arteries. And everything in between. You can have mixed retinal vasculitis as well. Arteritis definitely leads to microinfarctions or large infarctions, sheathing and urinal dilation of the arteries, whereas peripherbitis can be a sheathing and cuffing where it's not influenced by branching or AV crossings. Patients generally come in with blurred or painless loss of vision, flutus cotodota, no symptoms with peripheral disease. Often is the case. Systemic manifestations do include oral, skin, and genital ulcers, as you can see with the chest disease. Arthritis, as you can see with Balearca and Nodosa, and with Wegner's, no called GP, Wegner was a Nazi for a few. He injected people with as much oxygen as he thought they could dull their ages into old age. But, so therefore, we no longer call it Wegner's, we call it Gretinomidus polyasidis. Neurologic disease, embolic disease, also features of many systemic disabilities. Clinical characteristics, you'll have vascular alterations or an examination, or an angiography. Very vascular, it is very, by this very larger arteriolytis, occlusive vascular apathy. And you should have, in most retinal vascularitis, signs of intraocular inflammation. Sometimes you won't really see it on examination. You have to make the patient look up and down and find those little spots that little bit yourself, or just a little amount of trace a lot of bit yourself. But you can't see papillitis as a reactive phenomenon. I did not. Oh. I don't think that. Thanks. Sorry. So if you read, oh, wait. Ah. Go away. So primarily arteriolytis does include lupus, BANs, or it shows HSD, BZB, and syphilis. These can cause primarily arteriolytis. Lupus, I'll discuss this later, but really doesn't cause a vasculitis so much as it does a vasculopathy. So you have to draw the distinction as to the micro-angiopathy. Primarily filbitis includes sarcoid and aloe vera, not truly a vasculitis, but has a very strong vasculidic component, paraviral toxo, and HIV. Combinations of arteriolytis and filbitis do include MS, the chest disease, and Wagner's. The last two are occlusive vasculitis, vasculities. There's many theories on mechanisms. Most vasculities are immune complex diseases or immune hypocessitivity reactions. Direct antibody-mediated vessel wall damage can occur, as it does in lupus, cellular immune responses, direct damage by infectious agents. After all, ARN, corn, CNP, red nitrous, these are all retinal vasculities with massive, very vasculin infiltration. So the direction that damage by infectious agents is often seen. Humor-mediated vessel damage disorder in unirregulation. There are often diseases, amongst others, that occur without systemic disease. Eel disease is one such disease. Irvan, or idiopathic retinobasculitis and neuroerectomitis, frosted bradjetitis, and scleritis are all diseases. These are all vasculitic inflammatory diseases. Without systemic disease, for the large part. A little atheroscleritis has a higher rate of association with systemic vasculitis than other diseases do. This is a 38-year-old male with a positive BPD. All of the labs are negative. Vasculitis in history is unremarkable. And he presents with a vitreous hemorrhage. It's probably that 0.4 or 0.5. We don't care about them. All right. We're looking at the total gestalt of the image. You can see that there's probably some possible sub-remover hemorrhage along the inferior arcade of the vasculature. And also, there's a small area of hemorrhage. Again, it's like it's deeper, the retina, along the branch that's coming up.  And neovascularization is the most common cause for this. And why did neovascularization occur? Increased bedge effluent. Why does that happen with peripheral or central non-profusion? And you see areas of non-profusion around here. But what's going on between blood vessels here and over here? So they're leaking, right? So you have leaky blood vessels. You have peripheral non-profusion and neovascularization. And a gentleman with positive PPD. Before we think about the diagnosis, we have a 47-year-old portion male with incidental findings on routine examination. He's PPD positive. What do you see here?  A little microadherosal, dilatation, and a little leakage from the disk here and here. So, eel's disease. Now, this is your quintessential isolated retinal basculitis in the absence of systemic disease. Now, this was, studies DB a lot, thought of DB-ENA in trajectory samples of 41.6%. ERM specimens when taken away from the positive for macrobacteria PPD genome by PCR almost haven't done. It's an adiabatic obliterative peri-basculitis. Neovascularization without recritis, without UVA, so the exception to the dogma that, you know, all of the retinal basculitis has some sort of stigma about the inflammatory disease. And a strong association with positive PPD. However, you can get all of these instructional retinal detachment. Vision is usually pretty good. Victor's hemorrhage is the most common cause of vision loss. Creeper-invaulce-verifilism, we're trying to make for Victor's hemorrhage. Immunodulatory therapy is of no help. Antidepressant therapy doesn't help either. So, it is thought to be a immune response to the TB antigen in patients who are previously exposed to the TB. Is it more characterizing to find them along with peripheral? It's usually peripheral. It's almost always peripheral. That's why it's usually, symptomatic usually patients have excellent vision until they come in with neurovascularization and Victor's hemorrhage. Victor's hemorrhage and neurovascularization is usually central, whereas the ischemia is normally peripheral. Now, you'll see a lot of this in India, in Iran. You'll see a lot of this in Asia, but very rare in the United States, we've got, you know, I don't see. I don't have one. You see the group cases. They usually bilateral? It's often bilateral. That's not a bad thing. It's okay to see bilateral. It's very often, you know that. It's actually usually, you know that. Okay. So, you're a 34-year-old lady with a acute loss of vision and a better high-adjusted interest cell was noted. In the interest of time, it was good for you. So this is, you can see some exudate around the retinal branches over there. And you see a little Victor's hemorrhage, maybe some old Victor's hemorrhage. And you see a little bit of sheeting, perhaps around here. Okay. Similarly, in the nasal retina, you see the same thing, micro-aneurysmally, even micro-aneurysmally, there's no validation of these blood vessels. Exudation and some vascular sheeting. Over here, you see these little bulbs, these little aneurysms, micro-aneurysms and micro-aneurysms. You see vascular leaky. You see a little bit of papillitis. So the leaky and obligerative peripheral vascular is right around here at the site of this micro-aneurysm. So do any ideas? Does this is an exudated retinal vasculitis? Anybody? And if you don't know this, find it. There's more papers on this that there are patients. Chris? No way. This is an entity known as herbaceous. For some reason, they like to test you on this. There's a rare condition with multiple secular aneurysms of the larger retinal arterioles. There's peripheral non-profusion. There's always some of these. Younger patients, indeed, doesn't work. They're sometimes useful. And it may regress rapidly. In some patients without intervention, some patients develop intractional retinal attachment. Once again, a really rare condition. But if you see this kind of thing in your boards, think about your retinitis. Neuroretinitis, which is often by lateral statute of validation, and occlusive benefits of literature, primarily arterial gastrinitis. First, looking at that, it kind of looks like a disease, but it's different in information. The first thing is that you have retinitis, which is important. The second thing is that you have neuroretinitis as well. So you can see the system of mycology. You can see that that delights. And you saw a little bit of vasculature healing, which you can see in quotes as well. It's not very good. So this is a rather large topic, and we'll just get a class over it for a little bit. This is a 76-year-old lady previously treated for a branch retinal vein inclusion by an outside retina specialist. She developed new symptoms in both eyes and also pulmonary symptoms. She's agco-positive. She's asin-lycin-positive, and she has interstitial tenses on her chest extra. She has some vitritus. Her vision is less than average. I don't remember what it was. What do you see here, Chris? So there's multiple kind of frosted vessels and kind of peri-vascular images all the way out of the far-forward frame. And it's largely peri-flavidus, right? Right, yeah. So you have peri-flavidus multiple, for example, it's a somewhat sanical fracture of the in-inclusions of the trinus. Little bit of peri-flavidus and anguorental damage. So she was seen by this retina specialist and laser was done because of the areas of non-privileged. Similarly here, once we saw her, she had a lot of retinoluschina, some resolution of the peri-flavidus, and maybe some macular atrophy which you can see better on the CT. And as we look at the angiogram, we find that there's areas of leakage and here there's occlusive vasculopathy. This is a patient with an occlusive vasculopathy. This patient had Wagner's numb. Positive... Sorry, she had sarcoidosis, so the candle wax dripping like vasculase, that's what you should see in your picture. Now, we're going to have a whole lecture on sarcoidosis, maybe a little bit. So I'm not going to go into the specifics of sarcoidosis, but this is what sarcoid vasculitis looks like. The tritus, peri-flavidus, which is a pretty gritty, candle-waxy appearance. This is the attach-de-bouge appearance. Sarcoidosis can cause primarily venous, occlusive vasculopathy. This is not my vision because I was three at the time. But as my four-year-old wife knows, I lack a lot of pan-UVAs and have a lot of vasculitis. Partially responsive to hydrolysis, corticosteroids, unremarkable... Well, every system was positive for recurrent ulcers, recurrent squirtle, skin lesions, painful elevated erythritis lesions, all the arthralgias and fevers, and a 35-quantum grade loss. This bilateral retinal vasculitis, arteriolar denuration, corolla infarct and retinal infarct. Now, this is the appearance. We had a pretty poor image of retina. I'm sure you're happy to know what you're doing. But you can see areas of retinal whitening, retinal vascular occlusion. You can see little hemorrhages within the retina. It's treated with prednisone three months later. Visual of beauty came back to pretty good. Beauty with cytokine and close seams. Once again, it's a whole new type of retina. A new type of retina was in my life. I was with them. So, lots of peripheral retinal whitening under my nearing courage. So what do you think this is? It's an occlusive vasculitis with multiple branch retinal arterial occlusion. Skin ulcers, genital ulcers, mouth ulcers. It's a chest. A chest. So it's just Turkish. So the sea with the little thing underneath. That's chest. I don't know. It's a chest disease. So it's an occlusive vasculitis. This is one of my patients. You can see peripheral and a loss of circulation. You see primarily an arterialitis. Vasculitis, sheathing around the artery. There's a lot of non-perfusion. And so many symptoms you can have. If you're in an illicit or a new system, you'll have buccal ulcers, abdominal ulcers. You can have genital lesions. You can have occlusive vasculopathies off the gut. So often patients present with intestinal obstruction. They often present with stroke. They often present with encephalopathy from diffused micro-angiopathy. As I said, it's named after a Turkish dermatologist. In fact, it's so common in Turkey. But in Turkey, they call it UVA. It's been used by Jets clinics. A French gentleman of pre-Korean also described the disease around the time. At the same time, so they called it the Jets disease in the lunch of Europe. The Japanese guy got no credit for the work. But the triad of symptoms that's been described is recurrent in drop-in inflammation, oral and emotional ulcers, and in lesions. Now, it's interesting when you look at the genetic component of this disease. It's common along the old silver, blood-created medias that you have, genetic dissemination. And interestingly, in northern Europe, in lunch of Germany, you have patients with the Jets disease from whom you cannot elicit any history of still-crued or Mediterranean ancestry. It turns out that in the 1300s, the dirt invaded all the way up into northern Europe with rape and pillage, emphasis of rape. And you ended up with a lot of genetic dissemination with the leprosy up in northern Europe. And so you'll have a lot of patients, even though you won't find evidence of still-crued ancestry, you can have some patients because this speaks to how true genetic history can never really be elicited. In the Asian phenotype, so I'm talking East Asian in Japan and in China, and in Vietnam, you'll find a high association with the HIV-51. Half of the type, however, that's not always the case. So in the European variant, you won't find that doing an HIV-55 or a V-51 is not really useful for the diagnosis of the Jets disease at all. But they'll ask you in your course, so I'm going to HIV-51 and V-51. I never test for that. 97% of patients will have oral health ulcers, genital ulcers, and those with 80 skin lesions.  You stick a needle just right under their skin and if they have a reaction, they'll freeze the blister. So you see the vesicular eruption in the track of the needle. So you'll have patients coming in with a kind of a demographic rash, but any time they get an abrasion, they'll get these vesicles. So that's something that you see very commonly in Vetset's disease. Occurant inflammation is almost a hallmark of this disease. It's more common than the penicillin. So the ACR has a criteria for diagnosis. The major criteria include the ulcers from the ghost of the skin lesions or at the end of the dose of acne. Eugenia is hypersensitivity with a vegetarian reaction. Genital ulcers, ocular inflammatory disease. Sorry about the slurring. Aripsychitis and courteritis, you can't see that. It's most commonly an occlusive vasculitis. Minor criteria include arthritis and intestinal ulcers, usually of an ischemic nature of literative vascular disease and neuropsychiatric symptoms, including encephalopathy or diffuse encephalopathy. So in order to have complete Vetset's disease, you need to have all four of the major symptoms. Incomplete, three major symptoms and four of the symptoms have been with one other major symptom. All of those symptoms. Occular disease most commonly manifests through three years after a systemic disease. If you ask a review, systems patients will usually say that they've already had genital ulcers that have resolved, oral ulcers that have resolved or are ongoing. Less than a third of patients actually initially present with ocular disease and most of those patients that you elicit in history will tell you about certain symptoms that they have thought enough and off. There's significant vision loss in three years in the vast majority of bilateral disease and the interesting thing about Vetset's disease is that it's this recurrent explosive information so patients will go years or months without any inclusive vasculitis and then suddenly have a flare. So a lot of people are kind of drawn into this well-subsidized sense of security because this patient has not had any flares in a year off immunosuppressive therapy but when you look at it, they have these huge sudden flares something brought on by pregnancy, by stress, by psychic or physical stress. We actually studied a bunch of these patients in San Francisco. We had them on remiccate and we took them off remiccate. They had an immediate time to relapse of 2.3 years as opposed to your journal Idiomatica's registration so it recurred almost immediately in 27 years. So it just is this waxing of any patient who won't go through this but just remember that it is a occlusive angiopathy either of the small arterioles or the larger arterioles this anomaly arterioles. There is some venous involvement but that is rare. Macular is the most common cause of blindness or non-reversible blindness. There is optic atrophy, vitreous hemorrhage and very rarely contractional or retinal detection. I have a question. When they get their retinal vasculitis is it also with vitritus and angiocyanin inflammation or can it be like azimuthamide if you don't know what they're having? Usually it's with, I mean, classification is described as a retinal vasculitis in the presence of an explosive UBI and it is thought to be one of the causes of hypopia on UBIIs. What are the others? Endophomitis. Always think of that first when you see a hypopia. You have HLA between seven disease and you have a chest disease. So those are the ones that you really want to think about. It's a lot of cases necrotizing, leukocytoplastic, monocytic, obstructive vasculitis and in fact, both the arteries and veins are primarily an arthritis. There's infiltration of neutrophils when it's an active inflammatory process and there is a process of admission. So, querogosteroids do work and they work really well. Glucicin was thought to be useful for systemic disease. I don't use it because it's useless. Psychosporin was useful in association with anti-metabolics. Anti-metabolics alone rarely work. Anti-cytocanthermia, and DNF is a rare drug exception for the use of HUMERA, or Adalimumabin, and inflixinab, in vicious disease and it works the best. In general, for red monobacteritis, anti-cytocanthermia, and DNF agents tend to work the best interferon has been used to make the patients feel awful and in very, very, very reticent disease, you can use cytotoxic agents, especially when there is evidence of inflammatory encephalopathy because these patients can die from stroke. So that's what this is, in a nutshell. Other occlusive vascularity, this is a patient that my colleague in Kenya at the time saw, he said, 11-year-old comes in with severe vision loss and no other symptoms was positive for Anka. This is his retinose condition. And look at this huge Shenifestive here. So this is an occlusive vasculitis. GPA or weakness can cause an occlusive vasculitis. And we'll discuss this more I think next month when we have our scleritis, our scleritis, that's true. That's the most common manifestation of red monobacteritis can happen. Yes. So, another patient says, these are some cases that I got from a colleague of mine, Patti Ababa. He's been practicing red enough for 35 years. 25-year-old, white male with onset and pleurigus in fluterus. Diagnosed with arthritis. Treated with for a four-day. Three plus cells in the AC. Two plus cells in vitreous. Has its multifocal red nitrous and hemorrhagic vasculitis. Who do you see? Once again, film photography, sorry, please. It looks like inferiorly there, there's some kind of some hemorrhage. And then I'm not sure if that's just camera artifact or if that's red and white. There's some white spots that looks like he's old to the desk. So, maybe ischemic, right? So, review systems, medias, myalgia, fever, chills, blood source, distinctively. Looks. What else? So, everything looks pretty good, except he is heart-free, right? He had an epididymal biopsy and it was seen to develop this lesion. Or is it? Oh, I'm not supposed to do that. Darryl. I know you're not a foot though. I must. I don't know. Is it like? Okay, that's a foot. Is it ear, thumb, and a dose? It's a nodule. Okay. On the skin. What do you do when you see a nodule? You find out too. Right. So, what do you see here? This is a blood vessel. Look at the tunica, intima, and the media. Even then, in the whole area. What's those little blue things? So this is lymphocytic infiltration of the entire vascular wall, no granulomas. And you have an occlusive vascular apathy with skin nodules, high ESR, high white gum, and lymphocytic infiltration within the blood vessel. So a nodule, boosted vasculitis, high ESR, or anybody? You could. All right. So this is Pee Weaver, Polyard, right in the nose. So this is actually a pretty ungone, but devastating disease.  You can treat this for psychophosphamide, and that's how serious it is. It is like an angiopositive vasculitis. Only angios are very positive. Psychophosphamide was the treatment of the day back in the 80s, but now we like to re-register it for this disease because it's a lot kinder and gentler. It was first described in 1866 by Kusmo. What else is he famous for? Kusmo respiration. Yeah, Kusmo breathing. You get metabolic acidosis. Uncommon disease, four to nine per million patients. It's the most common, it's most common in the fourth to fifth decade. It's more common in men. And then 80 to 90% five-year mortality. So this is probably a more severe disease than GPA. You get necrotizing vasculitis without granulomatosis. That's what the French differentiates it from Wagner's and the sources can affect any organ system. And it's a subacute disease presenting over weeks to months. You get abdominal pain, renal disease. And you get polyneuropathy, you get kind of this myositis. There are two different varieties. There's a macroscopic and the microscopic polyanthosis, the macroscopic polyanthosis is thought to be an immune complex mediated disease, although there are signs of primary endothelitis. You get amyretyl dilatation of vasculosecretic thrombosis. 30 to 70% have hepatitis B. So there is an association with hepatitis B. Other viruses that has been associated to include HIV, CMV, hepatitis A, hepatitis C, parvovirus and HDLV. There is an association with focal segmental glomerular nephritis, so do urinalysis, pulmonary disease. There is nasopharyngeal disease with collapse in his bridge, loss of the septum. It's diagnosed both clinically and physiologically. Unfortunately, Cianca and Bianca do not really do the trick. There is an elevated ESR, an elevated CRP, this vascular inflammation in 86% and that's testicular and it can't even be without symptoms. This patient did come in with testicular pain. Testicular biopsy is not favored. However, skin biopsies are often useful as are nasal and coastal biopsies. What do you mean by microscopic point? I think that it's higher. Generally, the smaller arterioles, it's the precapillary that's it. There's a skin lesion. You'll see if you do a biopsy of the nodule, it's usually the tiniest of arterioles that are affected. Which is why it's a necrotizing disease? Unlike you do it on his toe then that would have a higher risk. Yeah, so if you have a microscopic as opposed to a macroscopic, you're more likely to have a higher anchor at the anchor. Once again, this is a clinical diagnosis. This is a pathological and clinically oriented diagnosis. Testing is often negative. Three fourths of patients have renal disease and it is the primary cause of death while the heart condition is dosa. The second mostly in God's death is cardiovascular disease. One fifth to one half of patients have skin findings and about a third have some gastrointestinal disease who ask for colonoscopy and an upper GI series. You can have a non-deforming arthritis and an arthrologist so it's kind of like the arthrologist that you see which is also non-deforming arthritis. You can have peripheral nervous system disease, MSI features are as easy as and then do urinary disease. Occular manifestations occur in 10 to 20% in every tissue of the eye. You can have vascular inflammation of the epistereal and lumbul vessels. This is the most feature. However, you can also see iridus and neurophemological manifestations. Retinal vascularitis, vitreitis, coroidal vascular vascularitis with coroidal multilobular infarct and exudative retinal detachment as you see in any coroidal disease kind of posterior spiraeus-like picture when you do an FA, you'll see multilobular serious retinal detachment. Psychopostomioid verticosteroid retaximab is useful. ESR can be followed to indicate activity untreated as a 13% 5-year survival. With steroids alone, there's a 48% 5-year survival and if you use a combination regimen of this data it's from the pre-reduction days of the 5-year survival rate of it's less likely it's more likely you can kill with treatment so this is 60% 5-year survival with treatment. This is in the psychopostomioid days once again it's a standard retaximab we don't really have much data on it right now. Questions about BAN? This is a 30-year-old Asian lady with progressive bilateral visual loss this is the fundus examination and presentation there what do you see? So it looks like the media is there's maybe some haziness preferably it's a bad photo and then there is like all these hypopigmented dots you see that in the other adipose and some leakage of the blood vessels some of the conclusion out in the peripheral arterioles and venous sort of in the watershed zone and just as a close patient would have been diagnosed with SLE three months earlier and has been on IV as a prednisone for rheumatology and for rheumatology and has been on IV and SLE treated with anesthetes and the mylarios steroids very ages plasmapheresis dialysis transplantation and these days very much with immunomodulatory therapy we recommended plasmapheresis and IV so it's a wide range wide ranging disease as many presentations as increased B cell presentations repressed CD 17 sorry D 17 D helper 17 production so these are the suppressant modulated B cells immune complex deposition anti-phospholipid antibodies it's a chronic disease as multi-system involvement patients generally present with polyurethralgias polyurethritis skin lesions what are the common skin lesions in lupus malarage destroy lesions photosensitivity lesions renal disease is a killer pericarditis adenopathy other particular endothelial infestation such as anemia neurological disorders and ocular findings it has 20 years of hemorrhage it's pretty good age of onset is between 20 and 15 mean age is 30 women more than men black women white however you do see a certain subtype in Scandinavians there's a prevalence of one in 2100 so it's actually one of the more common inflammatory diseases so the ACR by the American College of rheumatology has a revised criteria for the infestation infestation malarage discoid rash photosensitivity rash skin manifestation oral ulcer arthritis sinusitis renal disorders most common cause of death neurological disorders such as micro angiopathy and encephalopathy hematological disorders so you can't have anemia immunologic disorders I don't know whether that's right but the new care antibody is one of the revised criteria for SLD to have a definitive diagnosis you need 4 of 11 ACR criteria ocular lesions are not one of the 11 criteria so ANA has a 95% sensitivity and it's really one of the only ocular inflammatory diseases where ANA is useful because you can follow it as the immunosuppressification and the SDNA has a pretty high sensitivity antiro antila lupus anticoagulant anticarburelipin antibody in the case of obstetric disease so multiple spontaneous abortions and in the case of obstetric disease so multiple spontaneous abortions and in the case of hypercoagulable disease such as venostasis disease retinal findings do parallel systemic disease angiography shows arterial and capillary non-profusion staining of blood vessels cotton bold spots CRAOs and CRVOs retinal amphibious hemorrhage similar findings as in hypertensive retinopathy with coroidal microinfarctions retinal microinfarction and nerve fiber microinfarctions which are cotton wool spots retinal neurovascularization can occur due to obstetric disease you can get serious retinal detachment so a more vocal variety not multi-lovely and you can get tractional retinal detachment remember that this is more for retinal angiography not so much retinal vasculitis it is probably brought on by diffuse endothelial damage somebody had a question I was going to say you see it so I guess you see more of an artery than it makes but it's a it's usually it's a micro-angio it's usually in the very very small vessels and capillary it's like the arterial and then the small tendules alright Lucas here's a 20 year old lady with a one month history of recurrent episodes of vertebral carrying loss and increased confusion sorry to go back to that one so there'd be no vitritis because it's like an angiopathy whether that's almost itis almost never I mean it's it's an itis but it's it's more of an endothelial itis why though the there's not much a new complex deposition in endothelial it's often the antibody that often targeted against endothelial cell surface protein endocardial lipid endopausal lipid you get small amounts of obliteration of the very small vessels it's an endothelial itis um there are cases where you can get there it is where you can get some vitritis but by and large this is more of a micro angiopathy remember the patients since this is not a very aggressive inflammatory disease you'll patients will often not present with popular inflammatory diseases they'll often present with other findings and you'll see you know God will splots on on screening visits or on routine eye exam sometimes they'll present with with micro angiopathy and sometimes they'll present with hyper-densiv retinopathy or choridopathy that's actually probably the most common cause of vision loss and lupus over the reclusive vasculopathy it's usually patients come in with uncontrolled hypertension from their renal disease and and that's why they have vision loss not so much the retinal angiopathy anyway alright this will speak to all of you so neurology consulted ophthalmology because this lady comes in with one-on history of recurrent episodes of vertigo loss increased confusion I think somebody will recognize this vision it was you who read it perfect too I think I know everybody knows what it is so when she was first seen she had some loss of vision and so left eye there's a couple of cotton wool spots for the retinal whitening I guess there's a very large cotton wool spot because well they're in the central right with the larger cotton wool spot which is what it is what's the right what's the CREO the huge cotton wool spot right it's true let me see here so there's a bluration of that superior arcade and it's hard to hear yeah six months later it comes in with this vision so a couple of large cotton wool spots in both eyes and xerography so there's some vascular sheathing there on the inferior arcade not sheathing just a little bit of leakage oh leakage okay then I think that's the same vessel from earlier with it's completely obliterated there superior yeah what is it here then there's some leakage there peripherally and then maybe some disc leakage as well completely uninvolved site over here right something that you didn't see on the television yeah what is it here some multiple enhancing lesions within looks like the ponds no not ponds no no sorry why are we doing it no of the one yeah corpus claus but there's also no I guess the enhanced lesions I was referring to are actually the so do you want the flare do you want right CSF is dark no T2 is CSF dark why don't we kill me so I can say you see colossal hyperwave density and on the flare you see these non-indeguos enhancements of the corpus colossus this is it's in the leesier this is the size of the flare those are enhanced lesions also enhancements not enhancements because there's no flare yeah there's no contrast there's no contrast but so hyper-density yeah hyper-density signal signal thank you together we can all be one hero diagnosis everybody knows this once again another disease where there are probably more papers and visions but so sex disease is an important one for you to know because they'd like to test it and because Nerozny consults you guys on this brief topic so initiated treatment with IVIG infusions and celsic so sex is a triad of encephalopathy hearing loss and multiple DRAOs women more than men three is to one age-uponset is a 9 to 58 but averages are on the end of the 30s multiple areas of CNS microinfarction with colossal and very colossal white matter changes a pro-coagulant state has not been demonstrated even though this is a micro-angiopathy there is elevation of factor 8 and anti-1 filibrand factor antigen for that start to represent endothelial damage brain biopsies with multiple areas of microinfarction endothelial injury typical of an anti-endothelial endothelial anti-endothelial cell injury syndrome however the antigen has not been identified treatment steroids work initially operating agents IVIG aspirin is a useful agent all therapies have a variable efficacy most patients tend to improve spontaneously with or without treatment although treatment is advocated and some patients do progress through dementia a reversible global encephalopathy so just a quick summary we have two minutes there are certain clinical entities that are associated with a rational vascular and systemic vascular disease some of which have been discussed some of which have not all they are trigonadosa Wagner's George Strauss Lymphertoid granulotosis which does include GBA but can include isolated granulotosis hypersensitivity vasculitis susax giant cell arthritis temporal endocrinosis other clinical entities do include all of these sargaridosis is probably one of the most common you can have some patients with ankylosing spondylitis age of 27 positive with retinobascular as Crohn's disease polymyositis tochiasis GCA lymphoma and leukemia can give you masquerade like syndrome certain infectious diseases certainly HSV VZB CMV are all viral retinitis this is whose primary lesion is a vasculitis HSV arthritis is a vasculitis of the iris HSV VZB sclerocariditis is a vasculitis of those structures and ARN is a vasculitis that's viral with massive very vasculinary filtration so that's why we use steroids there are isolated retinal vasculitis ills ARN toxoplasmosis can cause a retinal vasculitis and of course not to forget the most common cause of retinal vasculitis which is none at all or idiopathic retinal vasculitis it's important to ask about the epidemiological aspects race ethnicity place of birth and that can help you maybe narrow some things down but that's disease for instance comprehensive history do ask about every system in the body how would you know about this particular disease unless you ask about them clinical features and orthodontics amination do look at the cornea it's because you're in the redness of it doesn't mean you don't look at the cornea UVIS is their inflammation sometimes you really have to look for it make a patient look up and down so that you can perturb the pictures and actually see cells come up at you scleritis is their focal segmental or diffuse scleritis and then look at the pattern of retinal vasculitis is it arterial venous or both that can give you some clues for the border testing this is an area where we run into trouble this is what's recommended with the things in red are what I would think about to begin with definitely a CBC ESR and CRV CRV are important vasculomarkers because if you see a patient with retinal vasculitis and a high ESR then you're thinking systemic vasculitis ANA, ANCA, anti-DSDNA cryoglobulins in the setting of hepatitis B and C cryoglobulinemic vasculitis it does affect the retina therefore it's important to check for the viral hepatitis syndromes of course always check for syphilis always check for HIV in these particular patients all the rest are not really useful but all for some look at the evidence for oral thinning fluorescein angiography is of course super useful adjusted CT scan adjusted MRI can be useful but use it only sparingly when you have evidence of systemic symptoms tissue biopsies always the answer if you see lesions on the skin yes if you have idiopathic retinal vasculatus how far in review systems is negative I tend not to do so you don't do much more yes okay if you have you have to look at the clinical signs and then decide so if you have a lady who comes in with multiple branch retinal vein and put artery occlusions with encephalopathy and anti-OK fine but if you don't have any positive in the review system I tend to be a little bit cautious when ordering an MRI do you get idiopathic retinal vasculatus do you treat it how do you usually treat that? start with steroids think about methotrexate think about I use the same step letter but I have a much lower threshold to start a biologic because biologics and idiopathic retinal vasculatus anecdotally tend to work a lot better than that of course if you see anything to biopsy to biopsy that's important so retinal vasculatus is inflammatory disease and retinal vessels associated with drug and information it's rarely sorry it's usually idiopathic I don't know why that's given associated with it's usually idiopathic you're talking about idiopathic let's just say it's rarely associated with systemic disease it's often idiopathic but it's often associated with ocular specific or isolated ocular syndrome like vasculatus thyrosystemic workup is warranted because the diseases that it is associated with are very very dangerous lupus can kill you B.A.N. can certainly kill you lupus can kill you G.B.A. can kill you do rule out infectious etiologies very important systemic corticosteroids liverly very often hysteroids really are indicated because often these are bilateral diseases systemic immunosuppressive therapy is always useful except in certain cases such as ear disease where we know it does not work and doesn't really work that well either it's important to address the consequences of retinal vascular occlusion just like with any other retinal vascular occlusive disease with laser to decrease the VEGF load vitrectomy can be useful to rule out infectious disease but more importantly it's used to cure vitruse opacity and vitruse hemorrhage so it's an uncommon ophthalmologic condition with visual acuity it can indicate the worsening of existing systemic disease or be a herald for unidentified systemic disease and it often requires aggressive systemic therapy always look for it always think about it and then always think about potential systemic disease questions


So this morning, we're going to start off first with a demo. In True Chip Childers style, I'm going to start my morning off with a demo. So I wanted to bring up on stage someone that spent some time trying to bring the Cloud Foundry experience to Windows users, which is really exciting. And I'm excited to see and have someone come and showcase that on stage today. So this morning, first up, I want to bring up Sean Van Wong. She's a product designer from Pivotal to show us how to do remote debugging for Windows and Cloud Foundry. Come on up. Every time I hear that, I have this weird reflex. My Windows machine is rebooting. But thank you. I mean, this is something huge, bringing the Windows experience to Cloud Foundry. What made you go down this path? Yeah, I think in the past few years, we have observed that a lot of our customers who is in a dire need of Windows support and they have a lot of .NET workload that need to push to Cloud Foundry. Initially, we made a lot of workarounds for them to use whatever Cloud Foundry could have provided back then. But it became more and more clear to us that we actually need to have a dedicated team now to actually help bridge the gap between the Windows user world and the Cloud Foundry world. That is awesome. I know it's been desperately needed for a long time. And then today, you're going to show us some new tools that you've developed. Yeah. So yes, because Windows 2016 just provided the new Windows container technology. And that really is a game changer for Cloud Foundry users. Now, if you push your .NET app to Cloud Foundry with the Windows 2016 stack, you can leverage a lot more CF features such as CF SSH into the remote container. That is what I'm going to demo today. Well, that is super cool. So I'll let you go ahead and get started showing us how to do that. Cool. So this is a simplified and recorded demo of how to remote debug .NET app that you just pushed to your remote container. So we will start from publish your app and then remember to flag it as debug. And now you have published and let the build running. Now we're going to just move the file to a clean directory. Nora is our sample app that we always use for demo purpose. And then while you're moving your published application, you should also include the remote debugger provided by Visual Studio in the same folder with that application. And you should make sure that your remote debugger version works with the version of the Visual Studio of your choice. Now we're going to check some command line from the help documentation. The particular command that we're using right now is to being able to access a remote application without authentication requirements. So once we checked that, now we see a push with Windows 2016 stack. And with our HWC build pack, now we push it to a remote container. Now it's a staging application. So what's happening here? So now this application is successfully running. And let's do a web request to make sure that we could hit the end point right now. So now this application is running. As we just saw here, this is a fat finger. Ignore that one. OK, so now the application is running. It says, hello, I'm Nora, running on norah.humans.cf.app.com. And now this is the important part. Now we made CFSH possible. And now you can establish an SSH connection from your local host with your remote container. And you could do a port forwarding which attach the remote debugger port to your local host. Yeah. Thanks. This is a very, this is a really, it looks simple. It's just like a dash L and port forwarding. But what it allows us to do is now you have your remote debugger port attached to your local. Now you can, if something is crashing on the container, you can add breakpoints and debug it from your visual studio without leaving your local environment. So here we just did a check for the port, proved everything is running. And then now we just need to attach to a managed process here using the same port we just declared. Yeah, so now this start point is attached to our process. And you must see this loading that is running the process for this port forwarding attachment. And as it runs through, we're going to add a breakpoint to our demo app. So here we are. Now while this breakpoint added, let's try to hit the end point again. Now boom, here the script will stop at your breakpoint. And from here, you can check your logs and make sure your app is running. So this is a small feature we just provided to the .NET developers and the Cloud Foundry users. It's a very important step for us to bridge the, for the .NET developers on Cloud Foundry to leverage the most important, most advanced features in Cloud Foundry. Absolutely. Thank you so much. Thank you. That is a super awesome demo. And obviously .NET is an important workload for a lot of users. So thank you. Yeah, this is just a very simple demo. This afternoon at 2.45, Sanjay and Matt from my team is going to give a more in-depth presentation about the newest feature with Windows 2016 stack. Please go and check it out. Awesome. Thank you. Thank you so much, Sean Fun. Thank you. Thank you. Thank you.


Researchers and scientists agree that there is a great way to treat depression. In fact, this awesome treatment is 1.5 times more effective than any other treatment, including medication. If that's the case, why don't people like using this treatment? What is it about it that makes almost everyone dislike it? Depression is a pervasive and often debilitating mental illness that can have severe consequences for those who suffer from it. It is a serious and complex mental health condition that affects millions of people worldwide. It can cause feelings of sadness, hopelessness, and despair and interfere with everyday activities such as work, school, and socializing. In a work environment, depression can have detrimental effects as well. If depression isn't treated, it can hurt careers. It leads to presenteeism, which is when employees are at work but aren't doing their jobs, and absenteeism, which is when employees miss days of work. It may also hurt the performance of employees in many ways, such as their ability to concentrate and make decisions, manage their time, finish physical chores, interact with others, and communicate. Like most other health problems, the intensity and effects of this condition are lessened when it is caught early and treated well. But for those experiencing depression, finding effective treatments can be a challenge. Finding the best treatment for depression requires an individualized approach, as different treatments may work better for different individuals based on their unique needs and circumstances. Many people turn to medications, therapy, or a combination of the two in order to manage their symptoms. However, there is another, often overlooked, treatment for depression that has proven to be extremely effective for everybody. But nobody seems to like it. Despite growing scientific evidence of how effective this treatment is on depression, many people struggle to incorporate it into their daily routines, or worse, have the will to do it continuously. If it is so good, why is it that people are not adopting it? People may not like this way of treating depression for a number of reasons, including a lack of motivation, a lack of time, physical limitations, or a dislike for certain types of this method. One of the biggest problems with this treatment is that people don't want to do it. Many people find it hard to start a routine, or they lose interest in it over time. This can happen when they can't see a lot of progress, when the same routine gets boring, or when setbacks make you feel down. Lack of time is another reason. Sometimes people don't like it because it requires time. People who have a lot going on often don't have time for this method. Some people may feel like they don't have enough time in the day, especially if they have other jobs or commitments. The third reason is that they are unable to perform it physically. Some of these steps may be hard or hurtful for people with health problems or injuries. Some people might not want to do it because they don't think they have the skills or confidence in their bodies to do it. And finally, we just don't like it. It could be because most of us feel uncomfortable doing it, or we just don't like the pain and the hard work that come with it. No matter the reason, it's important to remember that there is no single solution to get past these obstacles. But there are ways to get around these problems and make this approach a more enjoyable and lasting part of a person's life. These include making goals that are realistic, finding things that are fun and interesting, doing them every day, and asking for help from friends, family, or a professional. And remember that it helps with depression and makes you feel better. Now, do you have any idea what this great treatment is? It's exercise. Exercise is one of, if not the, most effective mental health treatment there is. There is increasing scientific evidence showing the positive effects of exercise on mood states such as anxiety, stress, and depression. Exercise regularly can greatly enhance mental health and, interestingly, can enhance mental well-being just as much as psychotherapy. In fact, just 20 to 40 minutes of physical exercise can significantly improve anxiety and mood for several hours. For example, a 2006 meta-analysis of studies conducted by Klepp et al., and published on PubMed looked at the link between exercise and depression. The meta-analysis looked at articles that were published through November 2014 on Psychinfo, M-Base, Medline, Central, and Sports Discus. 900 participants were also included in a total of 23 randomized controlled trials. The research concluded that exercise is an effective way to treat depression. Also, a South Australian meta-analysis, which looked at data from more than 97 reviews, found that regular physical exercise is 1.5 times more effective than other treatments. One of the most important things that the study showed was that exercise is linked to a more positive and less negative mood. It means that the more a person exercises regularly, the happier and more positive his outlook on life is. On the other hand, lack of regular exercise can result in anxiety and negative thoughts. A 2013 study conducted by Rethorst and Tripp also showed that exercise is a great way to deal with depression. It said that regular exercise, such as aerobics, resistance training, or yoga, can lead to significant reductions in depressive symptoms. In fact, it has been shown that exercise interventions can help with depression just as well or better than standard treatments like antidepressants and psychotherapy. With regular exercise, your body will also create endorphins, which are chemicals that make you feel good. Endorphins help boost self-esteem and confidence, bring people together, and make you feel like you've done something good. All of these things are good for your happiness and overall health. People can greatly reduce their chances of getting depressed and improve their ability to deal with the signs they already have if they work out regularly. Exercise is truly a remarkable treatment for depression. In fact, not just on depression alone but in every aspect of your life. So, if you want to feel positive and happy, enhance mental health, increase emotional connections, or maybe find the love of your life in the gym or at a park somewhere. Exercise is the goat of all treatments. Can you see why exercise is the best treatment for depression? Like it or not, including exercise or physical training in your complete plan to treat depression is a must. And making exercise a priority and getting help from a doctor or personal trainer. People with depression can improve their overall mood and improve their ability to manage existing symptoms. Hi, I'm Emmy Golding, Director of Psychology for the Workplace Mental Health Institute. We hope you liked the video. If you did, make sure to give it a thumbs up. We have more and more videos being released each week, so when you subscribe, you'll get a notification letting you know when a new one's just been published. So make sure to hit that subscribe button and don't miss out on this vital information for yourself, your colleagues and your loved ones.


inspiring the confidence of the under-respect of our adversaries. Sailor, Marine and Airman, President Reagan's confident leadership and great personal courage have been an inspiration to our military men and women and reflect the utmost credit upon himself and our nation. But if this nation can stay on the course, it will not be so again. What this society will be safer as a result. And I can't think. But there's one other thought we'd like to make. Mr. President, eight years of your first inaugural address urged our citizens. And if I now may recall, on the behalf of my children and sisters just as a freedom movement, they're not represented. They gave their representatives their identity. They're going to take me and change this.