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Um they'll be transferrable to other exams as well for sure. Um So we'll jump into the first question. Um So a 45 year old woman presents to GP with joint pain. Her pain initially started in the, the right knee, but she has now developed pain and stiffness in her 1st and 3rd pharyngeal joints of the right hand. Her symptoms are worse in the morning and improve throughout the day. Uh Her past medical history includes achilles tendonitis, which she is undergoing physiotherapy for on examination. Her right 1st and 3rd digits are swollen with maximal tenderness over the distal pharyngeal joints. You've noticed that her nails also have an abnormal appearance and these are pictured below. Um Her GP completes a basic rheumatological screen which shows a raised C RP, but normal rheumatoid factor and anti CCP. What is the most likely diagnosis? So, I'll just give you a minute or so. Uh I think Matt's gonna put the pole up. Ok. Lovely. Like most people answered, I always give it sort of 10 or ses so seconds more. Ok, I think we're gonna, and it there. So, um yeah, most people answered uh correctly. The answer was uh d psoriatic arthritis. Um And there are a few reasons why that's the most likely diagnosis. Um So we'll go through them now. So the first thing we want to think about when diagnosing uh psoriatic arthritis is the joint pain. Um So that's sort of the, the core thing to think about in rheumatology anyway. Uh, but this patient has symptoms of inflammatory arthritis. So, pain that's uh worsen in, in the morning after a period of long rest, um with prolonged morning stiffness of more than 30 minutes. And then this, this pain improves with, with activity. So, moving, moving around. Um so that's just classically any inflammatory arthritis. So anything like a ra lupus and psoriatic arthritis, but you can actually look more at the pattern of uh the joint pain um in inflammatory arthritis. And that can give you some more clues about the diagnosis. So, psoriatic arthritis can take a number of different patterns and this compares to rheumatoid. Um as rheumatoid only typically takes one pattern and that's a symmetrical pattern that typically affects the hands. Um The patient in this case had an oligoarticular arthritis, which is the most common um type of pattern seen in psoriatic arthritis. And that's essentially just a joint um a pattern that affects less than uh four joints asymmetrically, but you can get other patterns as well. Um that can affect the spine and then if some patterns can be symmetrical as well. But that is the most common pattern in in uh psoriatic arthritis. Uh The next thing to look out for is skin changes. Um The most obvious skin change. Um If it was a really nice exam question, they just describe a psoriasis rash. So a um sort of plaque on the extensor surfaces that is red and crusty. However, in this question, it was slightly more challenging as um only nail changes were mentioned. Um So the one pictured was something called onycholysis. So that's just detachment of the nail um from its nail bed. But um as you can see on the picture, um down in the sort of er right hand corner of the screen, you can get a lot of different nail changes, so you can get pitting, you can get um just changing in colors, ridging. Um But the most common is this sort of onycholysis or, or pitting of the nails. Um The important thing to say with nail changes in psoriatic arthritis is that um and skin changes as well is that they're, they're actually not necessary for diagnosis. So you could get a really difficult exam question. Um They gave you no skin changes and no no rashes um or nail changes and they'd expect you to, to diagnose it. And there are actually a few more clues that you can um you can take from the history and the two things to look out for mainly that would point you towards psoriatic arthritis over another form of inflammatory arthritis would be dactylitis. So, sausage uh fingers, which is essentially just swollen digits. And that's pictured in, in the top right hand corner of the screen and enteritis. So that was mentioned in the in the stem as the patient had um some achilles tendinopathy. Um and that's also pictured in the top right hand of, of the screen as well. So those are two things to look out for that make you you think of psoriatic arthritis when the history isn't so, so clear, it's quite important to say that P psoriasis and psoriatic arthritis is really difficult to, to diagnose and it's, it's always done by a specialist in secondary care. Um And that's probably because there's no blood test that really points you towards psoriatic arthritis. It's in this group of um arthritis called sero negative arthritis or spondylar arthropathies. And I found a, a helpful way to remember those is uh the pneumonic pair. So, psoriatic enteropathic. So those associated with inflammatory bowel disease, um ankylosing spondylitis and reactive arthritis. They're all Seron, which means that um you can't do an antibody blood test to get you a diagnosis. So they, they can be quite difficult to diagnose. It's also important to say that sort of C RPS raised in, in active disease. And then if you x-ray the hand you get this penciling cup deformity, which I've got a picture of in the bottom right hand screen. Um but everyone got, most people got that right. Um I think we'll move on to the next question. Um So question two, a 56 year old man presents to the emergency department with an acutely painful right knee on further questioning. He tells you the pain started yesterday morning, reaching maximum severity at night and meant that he struggled to sleep at all. He describes the pain as stabbing and has also noticed that his knee is red and hot to touch and there's a picture of it below. Um His past medical history includes non hodgkin's lymphoma, which he's on chemotherapy for. And he's also got a duodenal ulcer on examination. His right knee is grossly swollen and erythematous. Um His observations are all normal. Um A joint aspirate is done um which shows negatively birefringent needle shaped crystals. So which is the most appropriate treatment most people have answered, just give it 10 more seconds. Ok. So a bit of a mixed bag of that one. So about 50% said colchicine and then the other answers were split at all about around 25% each at A and B allopurinol naproxen. So the correct answer is uh culture thing. Um And we're gonna talk about why that is um it was quite a difficult question. Um And I was a bit harsh on this one, but I, we, we can break this one into to two parts. Um First is need to figure out what the diagnosis is and what we actually have to, to treat. And there are a number of different clues in the questions then which point you towards a certain diagnosis. So the first one is, um, the patient's presenting with an acutely painful right knee, which is reaching severity in about 24 hours. So quite a fast onset. So immediately you're, you're not thinking about things like osteoarthritis or it could even be quite a, quite a fast onset for something like ra or psoriatic arthritis. So I think your your top differentials for this one straight away should be septic arthritis, a crystal arthropathy. So a gout or a pseudo gout and then he arthrosis and there's a few things that that point you away from some and towards gout is your most probable diagnosis. So, septic arthritis, the the patient is afebrile and systemically quite well. Um And so in exam questions, typically, patients will present with a fever. If they've got septic arthritis in real life, it's it's not so common. And I think uh sort of 40% of patients um won't have a fever presenting with septic arthritis. But it's definitely something to consider when someone's got an acutely painful knee. Um pseudogout. So stems normally mention a risk factor. So something like a hemochromatosis or a hyperparathyroidism, um that would normally be mentioned in the stem, but we don't have any mention of that in this one and then he arthrosis. So blood in the, the knee joint um that would normally precede some trauma, um which hasn't been mentioned. So at this point already thinking about those options, but specifically gout. Um and the, the next clue you have is this uh chemotherapy and, and he's, he's undergoing chemo for non hodgkin's lymphoma and quite an aggressive chemotherapy regime with three different drugs. And so chemotherapy is quite a big risk factor for gout. Um So the chemotherapy attacks the tumor. And uh essentially what happens is the contents of the tumor is released into the circulation. And these chemicals called purines um are released from tumors. Um when they're killed by chemotherapy and these purines are then um converted to uric acid by metabolism and this uric acid builds up and causes gout. Um So that's definitely something to, to bear in mind when you, you see a, a question stem of someone with a painful joint. Um but also under chemotherapy and then the final nail in the coffin almost is um this joint aspirate so negatively birefringent needle, needle shaped crystals. Um So, uh I'm not an expert on this by by any means, but essentially what the joint aspirate is looking at is just the fluid aspirate but under polarized red light. And then it gets this appearance which is described normally in exam questions. Um And I found a useful way of remembering which ones which is that um you can pair the ps together and you can pair the NS together. So pseudogout goes with positive birefringence, um and um negative birefringence goes with needles and that's also associated with gout. Um The other thing that they'll mention in exam questions from time to time is that um the appearance of the, the needles in er, pseudo gout, they're rhomboid shaped um whereas needle shaped in, in gout, um and it is also important to say that you don't get any crystals in septic arthritis. So now we've got our diagnosis of, of um gout, we can think about how we, we manage that. Um But first a bit more about gout. So it's the most common inflammatory arthritis. It's caused by um high uric acid levels in the blood due to purine breakdown and it typically affects 50 to 60 year old males. Um I think a doctor once said to me that it used to be described as the Henry the eighth disease as he used to suffer from it. Um Quite a lot cos he's in that sort of age demographic, but he's also got a lot of risk factors for it. So the risk factors being um sort of lots of red meat in the diet, lots of fish, lots of alcohol. Um So if you have a struggle to think about it in exam question, think of Henry eighth. Um So it typically affects the first um mesotarsal pharyngeal joint. So the the big toe and that's 70% of um people with gout or an acute gout flare. Um, the other 30% it will affect a, uh, another distal joint, something like the knee or the elbow. But these can be more difficult to diagnose and you probably have to do a joint aspirate. Um, if it's just affecting the big toe and it's clinically very obviously gout, you don't have to do a, a joint aspirate, um, comes on very quickly in 24 hours and resolves in, in 5 to 15 days. Um but in patients with chronic gout, um they tend to develop these, these to five or uric acid deposits and they can happen in any joint and, and typically in the ear as well. So the answer to the question was colchicine um in managing this acute flare of gout. Um So as per the nice guidelines, there are two options in managing an acute attack of gout, those being nsaids. So Naproxen was the option for an NSAID in this situation or colchicine. However, this patient had a duodenal ulcer. Um So nsaids are contraindicated. Um As if you sort of reduce prostaglandin synthesis with an NSAID, you have a greater chance of that ulcer uh bleeding because the stomach, um although the duodenum isn't protected as much by the prostaglandins. So NSAID S were contra indicated in this case. So colchicine is the only option. Um prednisoLONE is another option. You can use it second line. So if nsaids and colchicine are either ineffective or contraindicated. Um And then your allopurinol and Oxistat um are used in um, the long term management of gout. So they're both uric acid lowering therapies which work by inhibiting an enzyme called xanthine oxidase. Um And it was typically thought that these drugs make um acute effect of gout, bit of echo. Um, a few players of gout w um worse, um which means that you have to wait until, uh, the information is settled before starting someone on allopurinol or for boxer sta. Um So that was a, a tricky tricky question. And Julie, the author was there to, to catch, catch you out, but I've seen it done in quite a few exam questions. So it's good to, to bear that in mind. Um So moving on to the next question. Um So a 37 year old female attends Rheumatology outpatients following a referral from her GP after she presented with a number of different symptoms. These included a pruritic facial rash that spared the nasolabial folds, bilateral polyarthralgia of the hands and feet and generally feeling more fatigued than normal. She has no relevant past medical history and is not on any medication. So given the most likely diagnosis, which of the following investigations is most sensitive for diagnosing the condition. So most people have answered, let's give it a few more seconds fine. So just gonna end it there. So a bit of a split again, um most people are going for D, so A and A um but a few people going for A B and C as well. Um So the correct answer is D antinuclear antibody and we'll have a chat about why that is. So the first thing to do with this question, uh same as the last question is, identify sort of the condition we're talking about and, and what's going on and there are a few clues pointing to you towards one specific er condition and that's so lupus. And so the main um indication for lupus in this question is the malar rash. Um So this is a classic description of the malar rash or of the butterfly rash that is um characteristic of s and that's normally described in exam questions as a pri facial rash and it spares the nasolabial folds and there's two pictures of, of the rash down there, sort of resembling a butterfly on, on the cheeks. Um So that's the main thing that points you towards lupus, but we've also got polyarthralgia um that's in the hands and feet. Um and it normally affects quite a lot of joints and lupus, we also have constitutional symptoms. Um so fatigue, um other patients might have weight loss and malaise as well. And then the final thing is age demographics. So uh the, the classic lupus age demographic would be um a woman in her thirties. So it tends to affect um the sort of female to male ratio is 10 to 1. So 10 times many women get it compared to men and it normally the normal sort of incidences in th, uh, between the ages of 3040. Um, and I think most people got that based on sort of the answers, the more difficult part was thinking about lupus and then the sensitivity and specificity of, of blood tests and it can be quite a challenging thing to get your head around. I don't think it was um taught that well in lectures when, when we were in sort of 1st and 2nd year. So I try and do my best of explaining. It's quite a text, heavy slide um just for the benefit of, of notes after so sensitivity. Um first is essentially how good a test is at detecting people who really have a condition um or a disease. And if the test has a high sensitivity, um it's really good to detecting people who actually have the disease. Um And if a test has a low sensitivity, it means that it misses a lot of people who have the condition and therefore gets a lot of false negative results. Um So that's a lot of words, but I find the best way to explain it um to patients uh sort of in an osk scenario. Um or thinking about it in my head is that if you test 100 people with the disease, a test that's 90% sensitive. So relatively high sensitivity will pick up 90 of those 100 people. And this means that it's quite good as a rule out test. So if you've got a very sensitive test or a test, that's very good at picking up people with the disease and it comes back as negative. And that, for example, that's not rheumatological is amylase and pancreatitis. It means that if it comes back negative, you can quite confidently say, or you can say in, in this scenario, you can um with 90% sensitivity that you're 90% sure that this patient won't have the disease. Um and a helpful way of remembering that is um sensitivity snout. So it's got the n in the middle and out. Um So it's just a little way of remembering it. Uh On the other hand, specificity um is I correctly identifying people uh who don't have the condition. So if a test has a high specificity, it's really good at saying that someone doesn't have the condition when they actually don't. Um But if a test has a low specificity, it um can wrongly identify people who don't have the condition and mislabel them as having something which will give a false positive result. And a helpful way of thinking about this is if you test 100 people without the disease, a test that's 90% specific will label 10% of that population um as having the disease when they actually don't. And another example, of this would be uh your nitrites on a urine dipstick. And it means that um a test that's highly specific means that you can rule it in. So the opposite to, to sensitivity. A summary of that is essentially um sensitivity is not missing sick people and specificity is not mislabeling healthy people. Um And both are really important to use in conjunction when uh doing these rheumatological tests um as some have high sensitivity but low specificity and vice versa. So, when we think about Lupus and the actual question itself, um the correct answer was anti nuclear antibody. Um because that is by far the most sensitive test um for diagnosing lupus. Um and it's a very good rule out test, but it's not very specific. So it means that if 99% of um the patient population have lupus, then 99 per um 99% have a, a raised A N A who have Lupus. It means that you can be 99% sure if there's a negative A N A that they don't have lupus. Um but it's not very specific, which is the problem with it, which means that people with um rheumatoid arthritis, systemic sclerosis, all of these different rheumatological conditions will also have a raised A N A as well as some patients with the viruses as well. But in terms of sensitivity, um A N A is by far, er, the, the best one or, or the highest number in lupus in terms of the other options. Uh 20% of lupus patients are rheumatoid factor positive. And then we, we're looking at our DS DNA and our Smith antibodies. So these are antibodies, autoantibodies that are highly specific um to lupus. So they're basically only raised in lupus, but they're less sensitive, meaning that not all lupus patients will um have a positive DS DNA or a positive Smith. Um The other option in the question I think was antihistone. So this is just one to remember for drug induced lupus. And then um one final thing about lupus blood tests um is that CRP and complement are used um in the monitoring of active disease. So all these anti auto antibodies are useful in diagnosing the condition. But if you've got someone with Lupus and you want to see how their disease is responding to treatment. Um or if it's flaring, you want to measure CRP and complement and the reason you measure complement it is because C three and C four bind with autoantibodies. So your anti DS DNA and your anti Smith and your A N A and it means that your complement goes down in active disease. Um So yeah, very text heavy slide. But um hopefully when Matt sends out all the slides um later that will be be some use. It's quite a difficult topic to get your head around and II spent ages trying to get my head around it for finals. Um So yeah, moving on. Um next question. So a 56 year old woman presents to her GP with increasing pain, stiffness in her hands. She is currently under secondary care for rheumatoid arthritis for which she takes methotrexate. She admits that she's been under more stress recently. On examination, there is symmetrical swelling, um stiffness and tenderness of the 2nd, 3rd and 4th metacarpal, pharyngeal joints and the proximal pharyngeal joints bilaterally. Uh what is the most appropriate management at this stage? So I just give it 10 or so more seconds. Oh, So, yeah. Well, I think most people have answered. Um And so the majority of people have said oral prednisoLONE. The answer is actually I am methylprednisolone and we'll have a bit of a chat about why that is. So this question is just testing um understanding of nice guidelines. Um And uh this patient is having a flare of their rheumatoid arthritis, but in a general practice setting. So now say that the first line treatment for a flare of rheumatoid arthritis um in general practice is either a intramuscular steroid or an intra articular steroid. Now, because this patient has swelling of multiple small joints in the hand. Uh an intra articular steroid isn't the best option because you'd have to go into each one of those joints. Um And it im steroid is would give the the best coverage as it's more of a systemic therapy. Um I imagine im is, is preferred over oral steroids because it has a faster action. Um And that's really important in ra in, in preserving joint function as deformity can, can kick in pretty quickly. Um So that's why oral steroids are, are second line. And I imagine that's for people who are needle phobic and, and have other contraindications for, for having needles as well. You can add in nsaids um alongside, but they shouldn't be given as monotherapy. Um And probably the most important thing to say with this question is that if you're in the context of general practice, um it's really important to get some rheumatology advice, whether that's a sort of referral to rheumatology Hot Clinic um for a same day assessment or using the advice and guidance service in in general practice. Um because it sort of r rheumatoid arthritis can be quite difficult thing to get under control, especially when someone's having a flare. Um And this means that sort of a rheumatologist should, should have an opinion on that as well. And then on the, the right hand side of the screen is just a screenshot of, of the nice guidelines. Um So yeah, just summary of this one flare of rheumatoid arthritis, I think I am steroid cool. Um So next question, um a bit of a longer one. A 44 year old man presents to his GP with a persistent dry cough which started 12 weeks ago. He denies any hemoptysis but reports feeling more out of breath than normal. He also reports losing a significant amount of weight and has noticed a new rash appear on his legs which he was he would like looked at as well. He has no history of foreign travel and no relevant past medical history. His observations are all in normal range. Apart from he's got a raised temperature of 38 degrees. Cardiovascular and respiratory examinations are both normal. His calves are soft, nontender but he has several tender raised erythematous nodules on his shins. Bilaterally. The GP takes some bloods and orders an urgent chest X ray. The results are as follows. So his hemoglobin is in normal range. Um So are the platelets and so are the white cells but there is a raised calcium and a serum ace is done as well, which is normal. So out of these five, which is the most likely diagnosis. The chest x-ray is also pictured um on the right hand side. Great. You go. You've got a question in the chat which is um what would be the best site for im injection of the steroid relating to the previous question. So, II imagine it would be any large um muscle site. So the deltoid is probably the most common in general practice. Um but the glutes would be a good option as well. So any large muscle site, any other questions, just put them in the chat and and Matt will, will read that them out. I imagine. So, most people have answered. I was give it 10 or so more seconds. Oh, so yeah, most people are right with that 1. Uh 74% of people said Sarcoid um very well done. Sarcoid is the right answer. Um And we'll have a little chat about why that is. So, firstly, thinking about the history. Um So well, firstly, what is sarcoid? So sarcoid is this inflammatory disease? Um No one really knows what causes it. And essentially what happens is you get loads of these noncaseating granulomas being deposited in loads of different parts of the body, um which can cause a number of different symptoms. And granulomas are essentially just these group of a activated macrophages and they can bur into anywhere in the body. So the brain, the lungs, um the heart, the joints, the skin and cause a lot of different symptoms, which is is difficult as a, a medical student because you try and find ways for to, to remember things. And um I find that this, this is a, a good one for a Pneumonic because there's no real links, you can find between the symptoms as these granulomas can deposit anywhere. Um And the one that I used for finals was um a bugs life, um which I'm not sure if you've heard of before, but I found it was quite a good way to, to remember the different features of sarcoid. Um, so we'll go through that. Now. Um the first being arthropathy and arrhythmias. So, sarcoid um or granulomas can deposit in the joints and the heart, the heart can cause arrhythmias and heart block. And um the joints can cause arthropathy. I think it tends to be an asymmetrical polyarthritis. So lots of different um, joints affected. The next is er B Bell's palsy and bilateral hilar lymphadenopathy. So, Bell's palsy, um if there's a granuloma being positives in, in the facial nerve that could cause cause Bell's palsy, um which is one of the most common neuro manifestations. Um and then bilateral hilar lymphadenopathy, which was pictured on the, the X ray and we'll have a, we'll have a talk about that in a minute. Um If the granulomas go in the eyes, you can get uu uveitis. Um G stands for granulomas uh which are non caseating. That's quite an important feature of sarcoid. Um So if you were to have caseating granulomas on a biopsy, that would be um indicative of TB. So, non caseating is sarcoid, whereas caseating is TB and caseating is essentially what's um in the granuloma. So in TB, it's caseating cos it's filled with pus um or caseating is, is cheese like that's what, what II remember um s in the pneumonic is serum calcium um and ace elevated. Um So we had serum calcium that was elevated in this case. Um but serum ace was normal and we'll have a chat about why that is on the next slide. L is for lupus pernio and the liver being affected. So I've got a nice picture of lupus pernio pictured there. So it's this bright purple rash that's on the cheeks and on the nose as well. Um And you can differentiate that from the lupus malar rash. Um because this rash, lupus pernio um doesn't spare the nasolabial fault. As you can see I is interstitial fibrosis, um affecting the upper lobes. Um F is for a fever that's swinging. So, patients fever can go up and go down and then e is for erythema nodosum. So that's pictured in this picture up here. Um And it's normally described if you don't have a picture in um the exam as um painful, uh tender, raised nodules on the shins and it tends to be bilateral. Um And there's lots of things that can cause erythema nodosum. Sar sarcoid is only one of them um off the top of my head. I think pregnancy can cause it. Um the contraceptive pill, um lots of different drugs and, and certain malignancies as well. Um But sarcoid is definitely one of the most common causes. Well, in, in an exam setting of, of erythema nodosum. So in terms of investigations, um so just starting on the bloods. So lots of vague things can be shown on the blood. So the full blood count might show anemia, leukopenia, low platelets as well. Um which don't, doesn't really give you um that much help in diagnosing sarcoid in an exam setting. Um One of the main things to look out for is hypercalcemia. Um and this happens because the macrophages um in the granulomas in Sarcoid, they all release Vitamin D as part of their um or they activate Vitamin D sorry as part of their metabolism. And this means that you get more calcium absorption in the intestine. Um which means you get hypercalcemia. If your liver is affected, you get a raised A LP. Um and then serum ace is the other thing we're going to talk about. So, um I left it normal in this exam, stan just to really emphasize the point that it's not a very good test for diagnosing sarcoid. So the sensitivity is only 60% and it's only 70% specific and it's therefore, it's not really that reliable on the diagnosis of sarcoid. Um And you can have questions like this where your serum ace is normal, but they've got all of these clinical features of, of sarcoid. Um So that's definitely something to bear in mind. I mean sensitivity only, only 60% means that 40% of people um with sarcoid have a completely normal raise serum ace. Um So I just want to really emphasize that one um in terms of imaging. So a and, and other um the most common imaging finding that you'll get in exams there. B bilateral hilar lymphadenopathy. So I think only two things can cause that really. Um The other being TB um when I've circled it on the X ray, it's just um this sort of pacification or more whiteness by um bilaterally um as circled there. Um If you're going to do a CT scan, you'd, you'd probably see some upper zone fibrosis. Um And then the gold standard for diagnosis is a tissue biopsy of the granulomas to, to show these non caseating granulomas um under microscopy in terms of management. Um as with a lot of rheumatological things, steroids, um um are used but only when the disease is severe. So by that, I mean, organ threatening. So if there's um evidence of it being in the brain or the lungs, um or the heart, you'd use some steroids, but a lot of the time it's just a watch and wait strategy and these patients will have relatively regular follow ups in rheumatology clinic. Um So good to that sarcoid. Most one, most people got that one right. So, move on to the the next one. So a 59 year old woman is brought to the emergency department by her husband with symptoms of fever, shortness of breath, fatigue and sore mouth. She also notices a la a large number of bruises have appeared on her arms and legs in the last few days without any obvious cause. Her past medical history includes ra for which she takes methotrexate and she was recently treated for a diabetic foot infection. Although she can't remember the name of the, the drug she was prescribed for it. She had bloods taken, which showed the following results. So, her hemoglobin's low, her platelets are low. Her white cells are also low as are the neutrophils, lymphocytes and monocytes. So all of her um blood cells are low, which drug has caused her presentation, just give it 10 more seconds. Um Most people have answered the, the question. Cool. Um So most people um have got the right answer and that's uh b er co Trimox. A few people said a and then there's a scattering of people who said CD and E as well. So, yeah, well done. Um correct answer Co Trox and we'll have a talk about why that is. So, firstly, what's going on with all these blood tests and symptoms. So this patient has symptoms of bone marrow aplasia, which is essentially when the bone marrow isn't functioning how it should do and it's not working. And the main um clue that's happening is this, well, all of these abnormal blood results. So every single blood cell is low, there's not one specific one that's sticking out and that would indicate that there's something wrong with the production of the of the blood cells in the bone marrow. Um She also had quite a lot of symptoms that are associated with it. So a fever um that can be due to um increased susceptibility to infections because of low white blood cells. She also has some anemic features. So, shortness of breath and fatigue, um some bruising because of low platelets and a sore mouth, um which is quite characteristic of aplastic anemia. Um and this might suggest a thrush blood blisters or mouth ulcers. Um So quite vague with, with sore mouth. Um So yeah, a patient has bone marrow aplasia. Um And now we have to think what, what could be causing that. So she was on methotrexate and we have to think of what other drug could be um interacting with methotrexate to cause this clinical picture. And the answer is co Trimox. So, co Trimox is um made out of um trimethoprim component and a sulfa methoxo component um as well. And both these drugs inhibit folate synthesis um through the inhibition of dihydrofolate reductase, which is um one of the enzymes involved in folate metabolism. And um essentially these two drugs act synergistically together. So, methotrexate and trimethoprim and you get way more folate um inhibition than you should do. And this affects the bone marrow more than any other part of the body as the bone marrow is this rapidly um has lots of rapidly dividing cells. There's always cells being produced and there's lots of cell division happening there for which um folate is needed for. So, disrupting the folate metabolism um in 22 ways and by two drugs um will sort of compile on each other and you'll get this clinical picture of bone marrow aplasia in terms of other things. Um methotrexate can do. So it's quite good to have a good understanding of um side effects. Methotrexate can cause as it's probably the most common D mod mentioned in exam questions. Um So it can also cause a mucositis. Um So, um that's just sort of inflammation of, of the mouth and the mucous membranes, myelosuppression, which is a less severe clinical picture than this one. But essentially the same thing where the bone marrow is being suppressed. Um It can affect the lungs as well. So causing a pneumonitis sort of picture and that's the most common pulmonary manifestation. Um and it's sim sim similar to a hypersensitivity pneumonitis typically develops a year after starting the treatment. Um and patients will present with um a nonproductive cough and, and general breathlessness on the more severe end of, of lung complications. It can cause fibrosis which is irreversible um and can cause um really difficult breathing and breathing complications. Um And that the liver can also be a candidate for, for, for, for fibrosis as well. Um So, yeah, more difficult question that one, but most people got it right. Um But yeah, really good. Um Out of all the sort of rheumatological drugs, methotrexate is probably um one of the most important. So I have a really good understanding about how it works and, and the side effects it can cause we've got a couple of questions, Hugo, I'll try my best related to that one. We've got, are you worried about neutropenic sepsis? And then we've also got, um, as she's febrile, shouldn't we be starting, um, antibiotics? IV. Uh Yeah. Well, so you could definitely think about starting antibiotics. IV. Yeah, I mean, the clinical picture if we go back to the uh the last slide. Yeah, I mean, um I haven't mentioned that she's febrile. Oh no, she does. She is febrile and does have low white cells. So, yeah, we would think about neutropenic sepsis and we probably would start her on some IV antibiotics straight away. Um The important thing would be to not start her on a trimethoprim or a folate inhibitor, um type of antibiotic. Um And that's the only antibiotic that I know of that that works in this, this way. Um So yeah, absolutely. Should start an eye about antibiotics but not your trimethoprim or your cotrim. Um Are there any other questions? That was it? That was cool. I think we're gonna do another uh a a hematology revision session um at some point. So we'll definitely talk more about um neutropenic sepsis and um and related blood conditions then. Um So question seven. So only two more questions to go. You'll be, you'll be pleased to, to know um a 25 year old male sent to general practice with a two week history of lower limb joint pain. The specific joints are um that are painful are his right knee, left ankle and numeral numerous metatarsal pharyngeal joints. He also reveals that he is going to the toilet much more and that it hurts when he passes urine. He has also been using over the counter eye drops for the past few days as his eyes have been red and irritated. Um He also had a rash on his feet, which is pictured below. Um His only past medical history is that he was treated for an S ti four weeks ago. So given the most likely diagnosis, what would you expect to find if you aspirated the right knee joint? So most people have answered, I'll give it 22nd, I'll say seconds more. Ok. Um I'm gonna end the po so most people have said c so sierra gonorrhea, um and then, um about half of the rest have said b so chlamydia and then half um of the rest of the what have said e so no organism growth. So the right answer is actually e uh no organism growth. And we're gonna have a chat about why that is. Um So as I think everyone's sort of correctly identified, this patient has something called reactive arthritis. Um And that's characterized by the triad of um conjunctivitis, urethritis and arthritis. Um And a way you can remember that is um can't see, can't pee can't climb a tree. So urethritis, dysuria increased, urinary frequency conjunctivitis. Um less common of the triad seen in te 1010 to 30%. Um And that was hinted at in the the stem as he was using eye drops frequently. And then you get um all your, your cli tree is your asymmetrical polyarthralgia that typically affects the lower limbs. It is a lot less common in, in the upper limbs and the hands. Um So I think most people correctly identified that it was sort of reactive arthritis sort of picture. Um Oh and also to mention about this rash. So this rash is um I think it's less common in rats, arthritis um than the tria together, but it's worth knowing about. Um it's called Cra Crader blenorrhagicum. And it's essentially just these hyperkeratotic lesions that are on the soles of the feet um giving this appearance. Um You can also scale on the palms but it's less common. Um So that can be mentioned and that can throw people off in exam questions when they see that someone's got a rash on their feet but reacts to arthritis sort of picture. Um And it's most commonly caused by a chlamydia infection four weeks prior. Uh It can also be caused by gastroenteritis, um four weeks prior or a few weeks prior as well. It's like a a salmonella or, or an organism like that. Um It's one of these sero negative spondylar arthropathies um that we mentioned earlier. Um that's triggered by an illness and the difficult thing in this question was, um, so it's, it's, it's triggered by an infection. So, um, most people identified the, um, sexually transmitted infections are the options. But if you were to aspirate um, the joints, you actually wouldn't find any organism. And that's because reactive arthritis is caused by um, an inflammatory response. So, the immune system, um going against this chlamydia infection or, or gastroenteritis. Um, and that means that it's not the organism itself. That's, that's cau um causing the joint pain and, and the clinical picture, it's more the inflammatory process um due to immune system activation as a result of the illness a few weeks prior. Um and essentially the inflammatory process occurs in the synovium of the joint and causes um causes joint pain. Um It can last quite a long time. Um So 4 to 6 months and if you're seeing someone in general practice, you'd, you'd prescribe them nsaids in this acute phase of illness. Um However, if it goes on longer, longer than 4 to 6 months or it's really debilitating, um you can think about a referral to rheumatology and they can, they can prescribe stuff like sulfaSALAzine or methotrexate. Um The only other thing to mention really in regards to this question um is that it's HLA B 27 associated, which can sometimes sneak into exam questions. So, um it might be a patient who's got known inflammatory bowel disease um or another HLA B 27 associated condition. Um So yeah, quite a, quite a tricky question. Um But really emphasizing the point that it's not the organism that's causing the, the joint pain and it's not an infection that's causing the joint pain. Um or the clinical picture, it more this defective inflammatory response which is causing arthritis, urethritis, and, and conjunctivitis. Um Two. So move on to the last question. So you are an F two working rheumatology, outpatients. A 35 year old man attends clinic for a review of his ankylosing spondylitis, his back pain um is well controlled on oral nsaids. Um But it's read online that ankylosing spondylitis can affect other parts um of his body and he'd like to know more. Um And the question is, er which of the following is not associated with ankylosing spondylitis? Just give it 15 more seconds or so more. Cool. Um I think most people have answered. So a lot of people said b um and then uh a fair few people said d um and the next most popular was e so um this question is about sort of complications by closing and spondylitis and the correct answer was ea bi basal fibrosis. Um So, yeah, it's a classic presentation of ankylosing spondylitis, morning back pain stiffness that improves throughout the day. He's asked to know more about um other things that can happen. So, extra articular manifestations of, of ankylosing spondylitis and as it's a rheumatological condition, there's loads of different things that can, can happen. Um And a good way of remembering this is, it's the seven A si was a bit harsh in the question. Um And I used heart block block instead of atrioventricular block. So your seven A S are anterior uveitis, aortic regurgitation, um V block or AV no block, um apical fibrosis. So that's fibrosis of the upper lungs. It's one of the only conditions that causes um apical lung fibrosis, which is why bibasal fibrosis was, was the incorrect. Um was the correct answer as it was the only thing that that isn't um part of this, this list. Um And then other things are anemia of chronic disease, achilles, tendonitis and amyloidosis. Um So yeah, quite difficult to, to remember all of those. But if you're um if you're in doubt, think of the, the seven days and try to remember that one node block as it can be referred to as heart block in, in some questions. And the really important thing to emphasize is that ankylosing spondylitis is one of these weird conditions that can cause fibrosis of the upper lobes of the lungs instead of the lower lobes. Um And I think that's us done. So I think Matt's put a feedback link in the chat. Um And then everyone who completes the feedback link will get email slides. Is that right? Matt? Yes, that is right. Um It's a bit of briber bit of bribery. Yeah. Uh Thank you very much for joining us and obviously thank you, Hugo for that presentation. Um We got another one next Monday. Um And all the following Monday is basically up until finals at Bristol, which I think is end of June. Um I don't know when other universities do their finals, but thanks again for joining us, make sure to fill in that feedback link and we will see you next week. Thank you very much. Let me stop the recording.