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Hello, everyone. Uh Good morning for me. Anyway, it's great to have you with us on medical education. As always, uh, questions, always questions and answers in the chat. We really want you to ask as much as you want. No question is not a good question. We want all your questions, all your answers cos that's the only way we're gonna learn. So pop your answers in the, in the chat too. If, if there's any questions being asked, um, your feedback form will be in your inbox in an hour's time, please complete that I will be passing on all your feedback to Yarra and maybe depending on what you're saying in your feedback, maybe we can get Yarra on for another event next year, maybe. Um, so what we'll do is we'll fill out your feedback form and once you've done that you, your certificate will be on your medical account for you to download. Ok. So without any further ado I, we're all going to start to learn about introduction to inflammatory arthritis. You y Fabulous. Thank you, Sue. Good morning. Good afternoon. I don't know if it's good evening to anybody attending here. My name is Yara, um and rheumatologist and internist. I currently reside in there, but I received my um coli and clinical work assessments, right? I haven't got any disclosures today and I'm going to go straight onto the presentation. So when we say inflammatory, it is vital important for all of us to be able to tell whether this is actually inflammatory or it's not. And how can we tell before we go on to the details of what inflammatory disease is? We should be able to tell that this is actually an inflammation. So, on this slide, I'm I'm just um presenting um a small comparison between the two. So when we say inflammation, we know the cardinal signs of inflammation which are um having swelling, having hotness, redness, of course pain and tenderness to touch. While some of these may be present in inflamma in non inflammatory conditions, you wouldn't find hotness or redness. It might be, be painful. Yes, it might be tender. Yes. And it might be swollen but not hot and not bad. The next thing is the duration of stiffness and you might be surprised that also noninflammatory conditions can cause some stiffness usually in the morning, but also after a period of inactivity when it's prolonged. However, the duration of the stiffness is the one that tells us whether this is actually inflammatory. And if you have prolonged morning stiffness, some people say more than half an hour, some say more than an hour then this is inflammatory while, if it's brief, it lasts a few seconds or a few minutes, 10 minutes, 15 minutes, then this is not inflammatory. Um, the pain usually gets better with activity when it's inflammatory. And this applies to certain categories of inflammatory joint disease. But when it's not an inflammation, the pain gets better when patients rest. And in fact, the pain usually comes after activity. Um, when you do blood tests, you will find raise inflammatory markers, of course, with inflammatory er conditions, but those should normally be normal when it's not an inflammation. So now that you know, when er to say this is an inflammation and when to say this is not an inflammation, we're gonna move to give you some classification on how to classify inflammatory joint conditions. Now, in medicine, we like classification, especially when we have uh a huge number of diseases to study and putting them into categories, help us study them in a better way. Um and then uh in a better effective way. So the main entities are rheumatoid arthritis, whether this is seropositive or sero negative. Um And then we have uh another entity called seronegative spondyloarthropathies. And this is a group of four diseases that you know, which are ankylosing, spondylitis, uh psoriatic, arthritis, enteropathic arthritis and reactive arthritis. Then another group called crystal arthropathy. And we're gonna focus on two diseases here, the gout and the pseudogout or the CPPD arthropathy. And then finally, comes the infectious or the septic joint disease. Now, another way of um categorize um joint disease is simply to count, count the number of involved joints. So, if it's one joint, we call it mono mono for one arthritis. If it's um more than one, that's two, up to four, then this is oligo and anything um, of more than four, which is basically five is called poly. When it's a single joint involved, you should first and foremost think of a, a septic or an infected joint. Not because it's the commonest, but because it's the most severe and it could be the deadliest. The second one could be trauma again, not because it's the commonest, but because it is the one that requires more immediate treatment and then comes the famous crystal arthritis such as gout and pseudo gout. Next comes the oligo and in this category, we have um the seronegative inflammatory arthritides generally including the psoriatic, very active and opic and the peripheral um disease in the ANK spon. Also the juvenile inflammatory arthritis can present as oligo arthropathy, especially uh in uh the younger patients around the age of 2 to 4. And then comes the famous rheumatoid arthritis, which is typically a polyarthropathy and that involves more than five joints. Um Sometimes the psoriatic and the gi A might present with more than five joints involved at any one time. Now, we're gonna delve into more details and we're gonna start with the famous rheumatoid arthritis disease. Um I forgot to mention that um as, as uh what sue mentioned, if you, if you guys have got any questions, please write that down on a piece of paper. Um and, er, or put that in the chart and we're gonna answer that at the end uh to avoid interruptions. Now, back to our presentation, rheumatoid arthritis is by far the commonest inflammatory arthritis when it comes to autoimmune inflammatory arthritis. Um and uh it is estimated that it can affect up to one and in some studies, 2% of the population. So if you're walking um in the park and there are probably 200 people, at least two of those have rheumatoid arthritis. It is that common and the things that you need to know about rheumatoid arthritis are a lot of things. But for me, what has clinical relevance and what helps you say that this is actually the rheumatoid versus this is not rheumatoid is basically, it is a symmetrical disease. It is not a mirror image disease, but it's a symmetrical disease which means that it involves both sides of the body, meaning that if it affects the MCP joints of the right hand, it should affect the MCP joints of the left hand. And not necessarily, for example, if I say 2nd, 3rd on the right, it should be 2nd 3rd on the left. It can be anything, it could be 34 or 12 and five anything of these, it affects the small joints. So it has a predilection to small joints and you rarely will find rheumatoid arthritis affecting only large joints. It usually, most of the times affects smaller joints, the hands before the feet before any other joints and it usually spares the di s. So if you see someone's hands with DS only involved, then this is not rheumatoid arthritis. And if you, if you know someone who has rheumatoid arthritis with changes in the dips, then this is not because of their rheumatoid, it is more likely to be osteoarthritis or another condition when it comes to deformities. I've got a nice picture for you on the next slide. But if the patient was left without treatment and you will see that mainly in elderly patients who, uh had the active disease before the era of um, the current medications that we have, then, um, they could have ulnar deviation and this is simply the deviation of uh the fingers to the ulnar side. And this is because of sub laxation of the um, heads of the bones, um, at the MCP joints. Um, there's also the Boutonniere and the swan neck deformities. I'm gonna move to the next slide to show you these deformities. So, um, in the thumb there, you could see uh what you can call the Z deformity or the Boutonniere deformity of the thumb, which is basically, um uh and hyperextension of the distal er joint of the digit. You will also see the ulnar deviation of, of all the other fingers from a second, all the way to the fifth. They are all deviating to the er ulnar side. And you will see swan neck deformity, uh affecting the um P I PS and D I PS where the P I PS are hyperextended and the P IP um the, sorry, the P I PS are hyperextended, the D I PS are flexed. This is what we call swanic deformity. Basically because it looks like a swan back to the previous slide. The spine can be involved but mainly rheumatoid arthritis could affect the cervical spine. What is important about this is that if the patient is known to have deformities in the hands, they could also have problems with their cervical spine and specifically um um at the joint between C one and C two, which, which we call that plantar axial joint. This is important to remember if you have uh an older patient who has deformities related to their rheumatoid arthritis because it was uncontrolled severe disease, et cetera. And if those patients were about to undergo a surgical intervention under uh general anesthesia, they need to have the Atlanta axial joint assessed by lateral X ray prior to the operation because you know, when they go uh for a um for an um anesthetic, they will have to have their neck hyper extended and that might cause what we call sublaxus of that um C one over C two and that might cause an injury to the cervical spine. And you know how vital the cervical spine is. So, remember this now, um when it comes to calling it sero positive or sero negative sero positive, simply means that the patient should at least have one of one or both. Um rheumatoid factor. CCP positive. You know that CCP is more specific, which means it is on the only disease that causes CCP positivity is rheumatoid. However, rheumatoid factor can be positive in a multitude of conditions, including normal patients, normal people. So you're negative as having these two negative. If the patient has negative rheumatoid factor and negative CCP, but have all the other signs and symptoms, then they still have rheumatoid arthritis. Yeah. So having a negative rheumatoid factor and ne negative CCP on blood test does not exclude the disease. Ok. Right. And then you probably heard of what we call the das 28 score. And in rheumatology, we like scoring the disease activity simply because this gives us an idea on how well or ill controlled the disease is. And this has an implication on what medications the patients have access to and what medications they have indication to go on to on the next um level of treatment. So simply the das 28 score is um uh a way to tell us if the disease is active based on the number. And this is a simple calculation where we use the number of swollen joints, number of tender joints, we use either E SR or C RP. And we use the patient's assessment of how active uh their disease is. Um anywhere between zero and 100 where zero is no active disease and 100 is the most active disease they have ever had. Um And um on this slide, I'm showing you what joints are taken into account when we calculate the das 28. So it is both shoulders. Each one of those will count as one, both elbows. Again, each counts as one, both wrists and the and then the proximal uh uh interphalangeal joint and the MCP joints and the joints of the thumb. Also, you will notice the knees are involved, the hips are not nothing in the axial spine and nothing in the feet. Ok. So, keep that in mind as well. Whilst um patients might have active disease involving their toes. This is not taken into account when we do the S 28 and this is um uh probably AFA flow in this scoring system. Now, uh we've presented this already. Now, this is an important slide which shows us simply what an inflammation within the joint looks like. And um on the left side uh of on my left side uh of the screen, you will see a healthy normal joint in pink, you will see the joint capsule and then underneath that in orange color, you will see a healthy looking synovial membrane lined by cells that we call synoviocytes. It is thin, it is uniform, it is soft and um it produces enough fluid to er facilitate the movement um in within the synovial cavity, we call it the synovial fluid. Now, you will see the bone is healthy uh looking, uh it is uniform and it's covered um by a nice smooth um uniform uh thick layer of cartilage. When compared to the uh picture um on the right hand side, which is actually busy with lots of new cells that shouldn't be there. So you will see that the the joint with the joint capsule is actually looking bigger and boggier. That's because the synovial membrane is much, much thicker. It, it has become hypertrophic and hyperplastic more cells have grown. You see you will um have uh many layers of uh synoviocytes. Um You will see plenty of inflammatory cells, you will see b cells, you will see mature plasma cells, you will see new blood vessels formed there. Um So that causes the swelling, the hotness, the redness, of course, and the pain. And you will also see that some osteoclasts have arrived in the area and they have started eating on the bone and that's when the erosions happened. Keep that in mind, the bottom of the slide is also important and and it shows us what are the cytokines that are produced within the inflamed tissue um, that cause the damage to the joint. And why is this important? Because we are targeting these when we give treatment. So, the famous, uh TNF Alpha, we give anti TNF medications. The uh il 17, we again have developed Il 17, um, anti Il 17 medications. Um, there is the IL 18, um, um, and being developed at the moment. Um, and then when it comes to, um, the osteoclast, this is uh the ankle, which is the molecule responsible for activating the osteoclasts resulting in bone erosion. And there are medications that act as anti rankle medications, right? And we've discussed this already and we're gonna move on to the next category which is the sero negative spondylar arthropathy. And this includes uh a group of four conditions um listed here, the psoriatic arthritis, the ankylosing spondylitis, the reactive arthritis and the anti arthritis. Um talking um about the psoriatic arthritis in a bit more details. It is classically a rheumatoid factor, negative disease. So if you find um a patient with skin uh psoriasis and rheumatoid factor, positive, think twice before labeling them as psoriatic arthritis. Ok. And that's one thing, the other thing if the patient in front of you doesn't have active psoriasis, now you should ask about previous history of psoriasis in themselves in the first or second degree family members because this is a um a risk factor for developing psoriatic arthritis. Um in some patients, they might have joint disease that precedes the skin disease. Therefore, if the disease behaves like psoriatic arthritis, but they do not have psoriatic um uh skin lesions, then warn them that they might develop that in the future. However, some lucky patients will never develop skin disease. And that's about 5%. Uh 5 to 15%. The presentation of patients with psoriatic arthritis is mainly periarticular. So more than synovitis, they will have enteritis, they will have dactylitis, which is what we call sort of digit and they will have various tendonitis or tendinopathy, including that of achilles tendon and the pa the famous plantar fasciitis. Those are mm the main um pathology in in psoriatic arthritis as opposed to sinusitis and rheumatoid arthritis. Those patients will have oligo arthropathy, polyarthropathy or might as well have axial involvement. What you need to know when we come to treat these patients is that they can have an edema apart from hydroxychloroquine because studies have found that uh those patients will develop um a skin flare or will worsen a previously controlled skin disease. And if the patient um develops uh an acute flare of their joint disease, and there is no means but to give steroids, you can't help but to give steroids, then you have to give that for uh of course, the shortest duration possible. And the smallest dose possible. And you have to warn the patients prior to prescribing that, that once they stop the steroids, their disease, the skin disease might get worse. They need to be aware of this before making an this is Jack until the ede ARDS kick in or the flare up um phases away. Um The next condition we're gonna discuss here in the seronegative arthropathy is ankylosing spondylitis. And this is basically an axial, which means that involves the axial spine, including the shoulder and the hip girdle. But also it can present with peripheral joint disease. And each of these has different way of presenting itself and different treatment if you would and different response to treatment. And if you want to discuss the axial disease, then they usually start off with um uh an S IJ inflammation which is the sacroiliac joint. Um it can affect one or both joints, um causing pain, stiffness limitation in uh the ability to bend the patient's back. Um And um if uh the disease was not treated, then patients will develop um sclerosis which is basically um fusion between the two bones at either side of the joint. Um they might also have a facet joint inflammation along the axial spine anywhere in the thoracic spine, the lumbar spine or the neck. Therefore, um uh you should not exclude the disease if the lumbar area, for example, or the sacral joint is spread if the pain is higher up. Now, um imaging is very uh crucial when it comes to ankylosing spondylitis and X ray will be beneficial later in the disease. Once sclerosis has occurred. So you will not be able to see the uh joint space between the sacroiliac joint, it will be fused and the area will be replaced with new bone. However, uh our aim is to pick the disease before um we arrive late. And therefore, MRI comes and the patient uh should go an MRI scan. Um If you suspect the disease and you cannot um diagnose it with confidence on an X ray. So the MRI will show you active lesions at the time. The patient took the scan, the lesions will change quickly. So probably a couple of days later, the lesion that you saw on that scan might disappear. Um An important piece of information that she should supply the patient with with prior to going under the Mr machine is to try and avoid taking any steroids or any nonsteroidal medications which might mask the inflammation. How does the inflammation appear on an Mr scan? It will show areas of white, bright color indicating active inflammation uh on the uh stair sequence or the T two sequence. Um extra articular manifestation of ankylosing spondylitis. They uh sadly might have uh apical lung. Um I LD, this is rare but uh significant. They might have um aortic valve or aortic root, uh involvement, aortic root or aortic root dilation. So, look for these um if you need by physical examination, of course and um by um a simple chest x-ray, which might show you the aortic root dilation. Uh you might also want to, to arrange for an echocardiogram. If the patient has a significantly active uh ankylosing spondylitis, as I said before, they might have also peripheral joint involvement, which um is mainly the uh large joints of the lower limbs. Could be the hips, could be the knees, the ankles, usually large joints. Yeah. And um when we measure inflammatory markers, you will probably find them normal when the patient has only axial disease or slightly raised. But those can be significantly raised when um the patients have active peripheral disease. Um and again, when it comes to treatment, the axial spine will not respond to edema. The treatment that is methotrexate, sulfaSALAzine, et cetera, but the peripheral joints will respond. So this is important on uh on how and when to choose what medications. Ok. Um And you've all heard of these tests which will help you clinically um to be able to tell uh what joint is involved. So, the fiber test is a test that you do when you uh bend the knee. And um uh you do um flexion uh uh abduction and lateral rotation of the hip. And you, you um try and press hard on the uh leg to see where the pain will be reproduced. If the pain is reproduced in the S IJ, then this probably is um uh more of a confirmatory sign. If you would that there is S IJ involvement. However, the pain is actually in the hip joint itself, then um it's probably involvement of the hip rather than the back. Ok. The shoulder test is the test that you do when you put marks on the patient's back and then ask them to bend their back and measure the distance. And if the distance is shortened, this indicates that they probably have more stiffness or involvement of the lower back. Ok. Uh And then uh scoring system, we have the BA I score which was developed in both um in the United Kingdom. And this um uh has been uh used worldwide. It's a calculator, you can use it anywhere. Um uh You will find it on your computer or on, on your um phone. There are apps, et cetera, uh which measures uh the disease activity gives you a number and tells you whether the disease is active, um no activity, moderate or high activity. And again, this uh like the B dash 28 has a clinical implications on what stage of treatment we should uh escalate onto. Right. Next comes the reactive arthritis and you probably when you hear reactive arthritis, you will all think of the right triad where the pa where a patient develops, conjunctivitis, red eye, sticky eye, and then urethritis which is discharge and then develop arthritis. Thereafter, this is not common. The commoner reactive arthritis is one that is called HLA B 27 associated, which comes after bacterial infections such as the gonococcal, the chlamydia which are sexually transmitted. And then there, there are the stomach bugs, the Campylobacter, the salmonella and the shigella among others, uh those are usually associated with um HLA B 27 which is a test that some doctors uh choose to do. Uh the non HLA B 27 associated are those which happen after um any infection other than these uh microorganisms such as, for example, after a virus. Um It's important to say that sero negative inflammatory arthritides are associated with HLA B 27 and this is the, this is dependent on the race. So some races have higher level, higher positivity of HLA B 27 some have lower. And um when it comes to ankylosing spondylitis, 90% of patients are HLA B 27 positive. When it comes to reactive, it's somewhere between 20 to 50% et cetera, it's 70% and PSA um and, and this will lead you to the question to say, do I check B um HLA B 27 to confirm the diagnosis. The answer is no, the diagnosis is clinical. Um And the HLA B 27 is used for um research purposes, not diagnostic purposes. OK. The um reactive arthritis is self-limiting and don't forget to treat the inciting disease. So um take all the swabs, you need, give all the antibiotics, uh you need, give all the supportive treatment you need um give painkillers if you need and wait for the condition to uh subside. If it doesn't subside as quick as you want, you can give some steroids. Um risk of recurrence is there when it, when the patient has HLA B 27 positive. Um And if they don't, then the recurrence is unlikely. Ok. Uh Last of these is anterior paic, anterior paic means um bowel and which means these are related to inflammatory bowel disease. Um So it's basically the extraarticular manifestation of inflammatory bowel. It's the commonest one. and it can affect um either the axial spine or the peripheral spine or both the axial spine. Usually. Um uh is um the activity within the axial spine usually narrows the activity of the bowel. Um the peripheral joint, not necessarily. Um So basically this tells us that treat the bowel, the joints will sore themselves. Ok. Now, we're done with the sero negative entity. Um and we're gonna move down to the crystal arthropathy which is commoner, er, and the, the commonest two are gout and pseudo gout. And I'm gonna go on to slightly more details. Um uh talking about the gout here and gout is a common disease and um it's uh I would say uh over diagnosed, a lot of people are on treatment that they shouldn't be on. So, uh I I'm gonna give you a few hints on how and when to treat gout. So usually you have to um know the uh epidemiology of the disease, er, or who are um, the, um, a group of people who are at risk to develop gout, um, you should make the diagnosis right then decide to er, when and how to treat. You do not make the diagnosis based on the urate level in the blood. Never ever do that. Um, usually the patient is a male, um, older than 40 they will be overweight. They will have, um, consumed a lot of red meat, uh proteins uh probably they will consume alcohol. Um They might be hypertensive on diuretics and they might have renal impairment. Females are not spared. They are luckier but they will be affected. Um after menopause, um younger patients are also not spared, but it's very rare. And if you want to make a diagnosis of gout, you have to think twice or three times before making a diagnosis in a younger patient. It is rare. Um always ask about um familial um disease and al always look at the patient. If the patient looks like the one we we just explained, but they're not older than the age of 40 they might well have gout. So they're probably overweight. They consume a lot of red meat alcohol. Some of them, the young people might be hypertensive on diuretics and they might have renal disease. So age alone does not exclude but als but always think of risk factors and think of age and family history. Now, if um the patient has these risk factors and um uh the patient comes to you with a blood test that shows urate, uh, raised urate levels. Do I go and say, oh, you fit the criteria or the picture? You look like someone who will develop gout. You have raised levels in your blood. There you go. Take this treatment and start it. Congratulations. You have gout. This doesn't work like this. You should always have good history from the patient to um, say that, yeah, they have gout. So how do they present? Gout? Usually presents as monoarthritis and usually affects the big toe. And this is what we call podagra, usually it's unilateral. However, if it's chronic, if it's um been there for years and years, no treatment, then it might affect more than one joint. Uh And this is what we call polyarticular gout. And usually those will have what we call gouty toy. We'll go on to this. Uh shortly other joints could be the ankle, the knee, the elbow. And if you think the further you go away from the core, then the joints are more likely to develop gout. Why? Because it has to do with the solubility of the gout crystals in the fluid. If the joint is closer to the body, it is warmer and it's more soluble. If it's further down, it's cooler and it is more likely to develop the attack. The usual scenario, the patient is um at risk, they go to bed, they're fine. They are awakened with severe pain in their big toe, the knee, ankle, et cetera. This happened, suddenly the build up happened overnight. Over a few hours, they will wake up with swelling, hotness, redness pain. They feel as though they've broken a bone. They couldn't bear putting in footwear on or even the bedsheets. Um, this is usually self limiting, but until it limits itself, it is very painful. So most patients will seek either, uh, medical advice or will go on to take medications. They normally respond well to nonsteroidals if they can't take them. Um, and after excluding all the risk factors go on and treat with the highest um dose, uh, the patient could tolerate from um, a nonsteroid, uh, nonsteroidals with stomach protection. If they can't take that, then think colchicine or think steroids. Um, now, uh, this is one attack. Do I give, um, urate lowering medications? And before that, do I check their urates? The answer is no to both questions. Um, you do not check your rate during the acute attack simply because it can be normal, right? So you wait until the attack subsides and then you go on and check the urate level as baseline, it usually would be raised next. Do I go on straight and, and start um, urate lowering treatment? Cancer is well, it depends. So, normally we wait for the patient to have two or more attacks in any 12 p, uh, 12 months period or if the patient has gouty to five with raised your rates. Then you go on and treat. If the patient has chronic kidney disease, uh stage two or more, then you go on and treat. And if the patient had uh retrieved um u uh kidney stone, uh either spontaneously through passing it out uh from the urethra or um helped by um a urologist. Then this is an indication to treat. Other than that, you have to wait until the patient had, had two episodes of gout. But anything else to do? Yes, diet. So you have to advise patients to decrease their alcohol, the alcohol consumption, the red meat intake, um any extra protein supplements that they're on. Um they should um be well hydrated. Hydration is important and treat any underlying or provoking cause, for example, an acute infection, et cetera. Um So people who fast during Ramadan or for any other indication, they are at a high risk to develop gout. Um if they are not well hydrated after they break their fast, people around the festive period who um indulge in, you know, the cured meat boards and cheese and red wine and alcohol. Those are at higher risk to develop gout because people simply do not drink enough water in the cold months. So be ca be careful around this time of the year. Um If this applies to you, right? Um And normally during the attack, the inflammatory markers will be raised. Um And um if the patient comes to you with a swollen knee or a swollen ankle and you are good at aspirating the joint, you could stick a needle. There, take some fluid and take the fluid sample to the lab and ask them to look for crystals, which we are going to talk about in a second. So um uh the the fluid um taken from the Synovia will show very high level of white cell count, most of which are neutrophils. When it comes to gout, you will also be able to see gout crystals and how do they look like under the microscope. So, first of all, you have to make sure that the lab or the hospital has a fluorescent microscope. Um And under that microscope, the crystals will look like needle shaped and they will be negative bent. This is typical for gout crystals, right. This in the typical clinical scenario will confirm the diagnosis of gout if the picture looks like gout. But the crystals are thromboid and are positive by infringe. Then this is CPPD disease or or otherwise called pseudo gout. Another way to tell whether this is gout or pseudo gout is the joint involved. So pseudogout might affect the hand joint, the wrist more than gout would um um and on x-rays, the CPPD will show um a classical uh white stripe of calcification within the cartilage if you look at the X ray carefully. So this indicates pseudogout rather than gout Right. Um, the group of patients involved is probably the same, but CPPD is much, much commoner in the elderly. And of course, it does not have anything to do with um, the risk factors for gout, which are um in ingesting, um red meat and alcohol. But the pseudo gout can happen in an acute clinical illness, dehydration, um uh chronic kidney disease, et cetera. Ok. Right. So, now we've, we're talking about the inflammatory arthritis conditions in general. Now we're gonna talk about the lab tests and this is important. Um in rheumatology, we do lots of blood tests and it's important for you as a clinician to know what does each er result mean. Um in uh in the setting of an inflammatory arthritis, you will find that inflammatory markers are usually raised. This can be uh raised e sr raised C RP or raised ferritin. So ferritin is, is an acute phase reactant. Keep that in mind, some of those patients will develop anemia of chronic illness, especially if the disease was not well controlled. This means that they will have low hate B with normal M CV. Again, keep that in mind. Um rheumatoid factor and P usually uh within the correct clinical context, mean patient might have rheumatoid arthritis. And we talked about the HLA B 27 and we talked about the, the urate levels. The synovial fluid analysis is an important thing and we need to talk a little bit about um this in more detail. So when you aspirate the joint, you should look at the fluid when you've done that, uh enough times you will be able to appreciate what the con normal consistency of the synovial fluid should look like. If it's normal, it is more viscous, which means it's thicker and it's more um probably stringier and um uh stickier. While if it's more liquidy, more like watery, then this is more likely to be inflammatory, inflammatory might be clear, but it might be turbid and some blood. If the inflammation has uh been there for some time, when you analyze it, you will see plenty of vit B CS as opposed to um a few like up to 10, it should be sterile if you find any bacteria to think either contamination or indeed septic. Um If you see crystals under the fluorescent microscope, we've, we've um explained that already. So these are the things that you should be looking for when you do uh SYO through an analysis. So send that to chemistry, send that to cytology to count the cells chemistry to tell you um um the sometimes a ph um and um uh send that to the lab that will do the fluorescent microscopy and also culture the fluid to look for infection. Next comes uh imaging. We like imaging, but we only do that if clinically indicated. Um um x-rays, if the patient had had an inflammatory arthritis for a while, they will have periarticular erosions. They will have osteopenia and they will have loss of joint space. And if you remember them, the picture I showed you early on. Um you will remember well, why an erosion happened and why osteopenia happened within the joint vicinity, but we shouldn't wait until this happens. These are irreversible um damage changes. We should try and aim to detect inflammation as soon as possible. So, ultrasound help us. It is cheap. It is available, it's clean, it's noninvasive it if done. Um um in good hands, it will be able to detect earlier changes such as effusions that are small enough not to be detected clinically. It might detect smaller erosions before they become bigger and more noticeable on an X ray. It will be able to tell us if there is tendonitis or enthesitis in areas that you can't palpate. An Mr scan is preserved um for um the spine or deeper joints such as the hip. But also if uh you are looking for um injuries within tendons and cartilage um more famously within the joint itself. So the Mr scan uh has its own indications. All of these are good uh scan modalities, but you should know when and what to order now that you've um arrived at the diagnosis you need to treat and this is what the patients want, patients want to have a diagnosis and to be treated for all patients advise um them to uh do activity to remain active, do exercise. And if they can't help, um, doing that themselves, you can arrange for them to have physiotherapy. Very important physiotherapy is, um, their most important treatment modality in ankylosing spondylitis. Every single patient should learn how to exercise and to do that religiously daily. Some patients in fact treat themselves with exercise. Right. NSAID s come next. But you shouldn't, by any means, go through all of these, uh, one by one, you can give one or more uh at the same time. Um uh And this depends on your clinical judgment, you can give nonsteroidals or steroids, but not both. Um And then er dmard, some patients will need to start ASAP if you are confident enough about your diagnosis or if you feel um as though their condition is not going to improve spontaneously, such as um for example, gout which is not treated with edema by the way. And uh of course, the reactive arthritis dos and we've got a few of these, they are good. Um They are safe, they are uh effective, you can use one or a combination of those. Um But if they were not enough, if the patient had any contraindications or developed any allergic reactions or, or side effects, then you should go next to the biologics. And this is where the scoring system comes. You cannot jump immediately to a biologic if the disease was not active. OK. Right. And uh again, remember the er cytokines the um, the proteins responsible for inflammation. We are addressing these um with DMR S and biologics treatment goals. So, if you treat the patient, what is your goal? And what's the patient's goal? And, and you have to, er, state this early in the er, in the disease management process. Our aim is to control the disease, progress to control the pain symptoms. And then you need to prevent or decrease the frequency or the severity of the attacks. If they were to happen, you need to prevent joint damage and deformities. Very important. And of course, patients want to live their life, they want to go to work, they want to have kids, they want to have normal life as much as possible. Our aim to have uh patients in remission and if we can't then to keep the disease at low activity, um it is not acceptable that any patient in this day and a day and age still has an active disease um er without knocking all the available doors that you have, you should not spare any patient, any medication if you can uh offer that to them. Ok? And by this we come to the end of our presentation. Thank you all for listening. Thank you for coming and um happy to receive any questions. Thank you. Thank you. Wonderful. Thank you very much, sir. We'll give you a few minutes to up some questions in the chat if that's ok. Mhm. Perfect. So we wanna just cl that, that's lovely. You know exactly what you're doing. Yeah. So any questions anyone? Wow. Thank you very much. That was super informative. See, I think it's not until you actually listen to talks like yours that you actually realize my mum had arthritis. So we grew up with my mum having arthritis, but it's not until you hear talks in depth about certain things that you're like. Wow, there's so much more than there is. There is a, the, yeah, II think we don't know enough about arthritis yet. Uh, I think it is a science that's still developing and every day would learning about something new about how the disease happens, how it develops, what, um, genetics come behind the disease. Uh, what induces it, what makes it worse? Why does someone, um, have it and, and probably the brother or sister doesn't or the, or the twin doesn't. Um, there's a lot that we don't know. We know a lot but it's not enough and we shouldn't stop learning. Um, we've got some medications, we've got tons of medications for most patients. This is enough. But for a few unfortunate patients, this isn't enough. And some patients have had every single medicine under the sun and they still have active disease. Um, and that's where research comes and that's where medical students come. Um, they should know enough about medications and they should know when and what to use and how they can help us develop more? Yeah. Yeah. Totally. Yeah. I mean, so some, so are there some arthritis, uh, that is hereditary then or not? So, um, if it, it is caused by genes or if it's immune related, then you, as a daughter are at slightly higher risk than someone who doesn't have anyone in their family. Um, but is it directly hereditary? Now, this doesn't mean that if your mom has it then you will definitely have it. And there isn't a percentage to say, well, if mom has it, then 25% risk, I'll have it. No, it's not like that. It, there are lots of factors that um some genes, some um environment factors. Um some diet as, as you've seen um lifestyle, et cetera. Yeah. Yeah. Delegates I have you got any questions? No, I don't see any. They're very quiet. Please do pop your questions in the chat. Honestly. They can't be any worse than my questions. Please don't say that I have to let our delegates know I am not medical. I just organize and host you organize things. Yeah, and I am not the medical person. So my questions are normally quite basic but then it allows them to ask this hopefully. So please get typing, ask your questions. Um We just want your questions. Have you had any experiences? Is there anything you want some information on that you have within your workplace that you want to ask questions about? Now? Do you know how many people are attending today? We have got there. It's 24 people attending today and I don't know where they're from. Right. Oh, hang on. There you go. There we go. So. Oh, wow. Some of these words. So I'm not very good at pronouncing words. Ok. Can you let me read that for you? So, uh, that's question from Soha sheikh. Er, hello, doctor. It was a great presentation. Thank you. Soha. I have ra with ankylosing spondylitis. I'm on steroid medication. Still it's difficult for me in winters, there is a lot of stiffness in my neck and lower spine area, anything in daily diet, which can help me. Hm. Right. So, er so Leha having both conditions together is a bit tricky and at first and foremost, you should make sure you actually have both of these conditions together. Um uh most patients will not have two diseases at the same time. So you should make sure um to get the actual diagnosis right. Next comes um steroids will not help your back as you would uh want. Um and to answer your direct question, which is diet, um there is a lot of work er, on diet nowadays. Nothing proven so far. Um You cannot say that avoiding certain group of um food or drink will definitely help your er condition improve. And people talk about um gluten free. Some people talk about lactose free. Um some people talk about sugar free. None of these are proven to be effective. Really. Um Some people have tried uh and there is actually a study that was published recently um about er a spice turmeric. Um and some people take turmeric er capsules because it could stain et cetera. So they, they prefer to take it as a capsule. Um They compared people taking that and people who um took water, both were um equally effective. So basically turmeric doesn't help with inflammation. Ok. Sidra Hussein, although fibromyalgia is a separate condition. Is there much link between this and patients developing inflammatory joint conditions later on, right sidra. So, inflammatory joint disease increases the chance for people to develop fibromyalgia, not the other way round. So, if the patient has fibromyalgia, now they're not at a higher risk for inflammatory joint disease. In the future, you should make sure um your your diagnosis is correct. Do you actually have fibro fibromyalgia or is it an early inflammatory arthritis? Cooking? Uh Maruf Hasan besides rheumatoid factor, anti CCP antibody, what test is important in diagnosing rheumatoid arthritis? How long patient need to take steroids? How to taper safely? You are the best test, your knowledge. Your clinical expertise is the best test to say um with confidence the patient has or doesn't have rheumatoid arthritis. The blood tests, the x rays come to help you ascertain that. Yes, I've made the right diagnosis or I can with enough certainty, exclude the diagnosis. Um There isn't at the moment any more specific or sensitive tests to, um, when it comes to blood tests to say that this is rheumatoid arthritis. Um How, how long do they need to take steroids as short a period as possible? Uh And how to taper safely tapering? Depends on the initial dose. If you start high, you should give the patient longer time if you start low. Um, you can taper it quickly. Um, Afan Jaber, thank you. Um, does gout need prophylactic medications again? Afan the indication to treat is to prevent future attacks. If the patient ticks the uh boxes that we've mentioned in uh the presentation that is more than two attacks or one attack plus raised urate level plus all the other risk factors then yes, they need to have urate lowering medications to prevent future attacks. And thank you is from other delegates. Welcome. Perfect. Any other questions? Brilliant. Any other questions, any other follow ups to those questions? Is there anything that any answers that uh you've been given that you're like, oh, hang on a minute. But um please do pop them in the chat. Sorry. We, we like to challenge Yvonne. Great presentation watching from Zambia. Hello from Jordan. My question is, did you say we could prescribe both dmards and nsaids at the same time? Yes, you could. However, Dmard is your destiny. It is the medication that the patient needs to be on. Not the nonsteroidals. Nonsteroidals should be given for the shortest period possible because of all the side effects that they cause and because they do not control the disease I A they will not stop or prevent the disease from getting worse. But yes, they can be used if the patient is in pain or is having a mild flare. Wonderful. Thank you. Mhm. Got lots of. All right. Any other questions any more? For any more going on? As I said, you will get your feedback form. And if you can fill that out, there is a little bit in there that says about any other topics you would like? Oh, can we get the powerpoint? Great presentation? Clear, concisely, explain many things. Um There is a section in there that says, are there any other topics you would like covered within this category? Um I will be giving ya all your feedback. So if she's keen to do another teaching session in the new year, you know, we might be able to get her back on another teaching topic that you brought in there around arthritis, maybe you want to go into more depth into something then we can t and we'll see what happens. So um Power points should be live, right? They should be able to access these powerpoints later on. So I can, I can pop it on. It'll go on with catch up. So this talk will go on as catch up and so so will the slides. So yes. Definitely you can. I know it was so informative, wasn't it? You probably want to go back and watch it all over again. Yeah, so if that's it, we will say goodbye. Um I will say goodbye to your delegates. Um Thank you very much for joining us. It was lovely to have you and please look out for more medical education events and please fill out that feedback form. It really is important for us to give back that feedback to us because um because this is what helps them as well, it helps them to teach further going forward. You know, they really do value the feedback that you give. The honest feedback that you give feedback is an as well. So please do fill it out. So without any further ado, we will say goodbye. Um So we'll see you again soon.