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Ok. Hi, everyone. Um My name is I'm gonna be doing um the first um lecture for the um BR SMS K part of the crash course. Um So we're gonna be doing rheumatoid and other inflammatory arthritis. And then also we're gonna move on to back pain for the second part. Um So just a quick recap of um year one. So there's two main divisions of arthritis. So you've got the inflammatory arthritis and on examination, you'd probably see the joint is quite hot, swollen, might be red as well. Um And the three kind of main divisions within that would be either an infective cause. So, for example, something like septic arthritis, um another cause can be crystal arthritis. So it could be gout where you've got um urate crystals building up or it could be um pseudogout where you've got the calcium crystals building up. Um And then the third inflammatory cause would be immune mediated. So something like rheumatoid arthritis, which will speak about quite a lot. Um lupus or it could be a seronegative arthritis which we'll also touch upon later. And then the second division would be uh degenerative arthritis. So that would be something like osteoarthritis. Um, so just quickly touching upon septic arthritis cause I think it was in the slides. Um, it's usually unilateral. So you'll only really find it affecting kind of one side. It will never be bilateral. Um, it will come on quite acutely. Um, and there'll be a hot swollen joint. Um, I think more often than not to the knee. Um, but that's not to say it couldn't happen in another joint. Um And it's an emergency. So, um you need to, first of all, aspirate the joints um and to confirm it is septic. So to send it for microscopy culture and sensitivities to find out the organism that's causing it. And then straight after aspirating giving IV antibiotics. So fluoxil um just to kind of cover it to prevent any joint damage before you get the results from the microscopy and culture back. Um And then in order to treat it, you need to do a surgical lavage. So wash out the joints and get rid of all of the infected kind of fluid that's in there. Um in terms of autoimmune arthritis. Um So as you said before, there's the rheumatoid arthritis, lupus and then seronegative arthritis. Um And I think we'll speak about rheumatoid arthritis. Um So, first of all, what is it? So it's a chronic autoimmune disease that mainly affects the Synovium. And you've got the synovial membrane found at three key paces that they want you to know So it's the synovial joints. So for example, your proximal interphalangeal joints um in your fingers. Um or it could be the Tenosynovium. So this is just synovium that surrounds the tendons. Um or it could be bursa which are fluid filled sacs. So you've got one near the E quinone. So literally like kind of near your elbow. Um There's a fluid filled sac there. Um in terms of a quick summary, so usually females are affected, more than males tends to occur between the ages of 30 to 50. Um And in terms of what causes it, it's a mixture of genetic and environmental factors um which will speak about on the next slide. Um in terms of key features and how to like distinguish it. Um So it will, it will mostly be symmetrical and it will involve multiple joints. Um There'll usually be pain, swelling and um prolonged morning stiffness. So that's last um stiffness lasting more than 30 minutes in the mornings. Um And if it's not treated and caught quite early on, it can lead to joint destruction. So, in quite advanced disease on radiographs, you'll see um joint erosions. Um It's also a systemic disease which means it's got a lot of like manifestations that don't just affect um kind of the like synovium and the joints. Um It you can, it can affect like the lungs, um the eyes um and other things like that, tons of key autoantibodies for it um, you just need to know there's rheumatoid factor and also anti CCP antibodies. Um, and in terms of the pattern of the joints involved, um, it can affect small and large joints. Um, but it particularly affects the hands and the feet. Um, and the most common joints that you need to know that are affected are the MCP joints. So the knuckles, the pip joints. So in the finger, um, you've got the wrists which are often affected the knees, the ankles and the metatarsophalangeal joints, um which are basically like the equivalent of the knuckles in the hand, but in the feet. Um so we spoke a bit about extra articular features. So kind of the features of systemic inflammation that you may see would be fatigue, fever, weight loss. Um Those are quite good ones to remember in terms of specific to um organ systems. Um So as we said, um it can affect the lungs and you may get some lung nodules that could be interstitial lung disease. So you might get some fibrosis of the lung tissue, um or there could be pleuritis. So just inflammation of the pleura of the lungs in terms of um the eyes, you could get epis scleritis and there's a picture there which just shows redness. Um There's, you could also get vasculitis, the inflammation of the vessels. Um There's also neuropathies. Um There's something called Felty Syndrome, which is an important kind of triad of conditions. Um So you get leukopenia, so reduction in white cells, um you've got splenomegaly and rheumatoid arthritis. Um in terms of subcutaneous nodules, um what those are defined as as they are like central areas of necrosis and they're surrounded by histiocytes. Um and also a peripheral layer of connective tissue. And um if you see these, these basically just suggest that um the person's disease is quite severe and it also has been shown to have a link to rheumatoid factor, which is one of the antibodies. And so talking a bit more about like the split between the genetic and environmental causes. Um So what they did was twin studies. Um so they looked at Mozy twins who have, who share the exact same DNA and they looked at dizygotic twins who have, who share 50% of their DNA. Um And they looked at the concordance of rheumatoid arthritis. So they said if one of the twins has rheumatoid arthritis, what are the chances that the second twin will also have um rheumatoid arthritis? And they concluded that if the monozygotic twin concordance rate was higher than the dizygotic twins concordance rate um that there would be some sort of genetic component. Um and just to kind of illustrate this bit more, make it a bit more clear if the concordance rate was 100% for example, in monozygotic twins, then you could probably say that the disease is purely genetic. Um However, this wasn't the case for rheumatoid arthritis and the concordance rate for monozygotic twins was 15%. However, dizygotic was 4%. So it still shows that there was a genetic component, but there are obviously other factors which we'll speak about. Um And in terms of the strongest genetic risk factor is HLA D four. So that's a really key point to remember um in terms of other factors, um it's also being female is can increase your risk. Um And it's not too sure why this is. But um it's just thought that it could be potentially because the immune system can get modulated during pregnancy and altered that way. Um So it can kind of propagate these autoimmune conditions sometimes in terms of environmental factors. Um So, it's been shown smoking causes citrullination of proteins in the lung epithelium. Um And as we spoke about earlier, there's the anti um cyclic citrullinated protein peptide antibodies. Um And so, obviously, those may get activated because of the citrullination. Um It's also the microbiome can have an impact, poor oral health. So for example, something like dental caries could increase the risk of rheumatoid arthritis and also a particular bacteria called porphyromonas gingivalis, which will cause a citrullination of proteins. Um in terms of the like shared epitope if we're talking about genetics. Um I know it mentioned it on the slides and I always used to be a bit confused as to what it was, but it's basically just a five amino acid sequence um in the position 70 to 74 of the HLA DL chains. Um And when you look at this along with smoking, they synergistically increase the risk of rheumatoid arthritis. Um So it's a nonlinear increase in risk and it kind of will exponentially increase the risk of rheumatoid arthritis when they're found in conjunction. So, looking at um the HLA classes a bit more, um I know you probably haven't done this since pom. Um But it's kind of helpful in actually remembering um the differences between rheumatoid arthritis and closing spondylitis. Um So, in terms of HLA class one, so under those come HLA A B and C um and HLA class one is expressed on every single cell. And usually what happens is cells will present the peptide um or antigen with HLA class one to the um CD eight T cells. So the killer cells um in terms of HLA class two, the only kind of HLA that comes on this is HLA D um for now um