Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Um Hi, everyone. We're just gonna start the rheumatology. So we have uh Doctor Ta with us. He's kindly agreed to do rheumatology. He's a medicine registrar. Um So I'm just gonna hand it over. So again, he can't see the questions in the chat at the moment. So please ask questions at the end. Thank you. OK. Hello everyone. My name is I'm on acute medicine uh register at Kings Mill Hospital today. I will be talking about rheumatology. Uh you know, uh 40 45 minutes. Absolutely not enough to cover all rheumatology topics. But I have tried to mention the most important topics which is important for you guys in the sorry exam. Uh Let's start. So today we will be talking about uh multiple topics, osteoarthritis, rheumatoid arthritis, polys, dermatitis. I've tried to uh make every two diseases, uh two similar diseases together. So you can memorize better osteomalacia, Vitamin E deficiency, sle ankylosing spondylitis, scleroderma. And, and, and at the end of the slides, I've tried to mention uh some high, some important points and the questions which is not maybe mentioned in the slides, but it's very important for you guys in the MS exam. Ok. Let's start with the osteoarthritis and rheumatoid arthritis, which is, I think the most common, uh, two diseases in rheumatology and have, uh, plenty of questions in, in all exams. So, let's start with osteoarthritis, rheumatoid arthritis with the pathogenesis, which is very important, you know, osteoarthritis is a mechanical cause, wear and tear. You will, uh, see this, uh, term wear and tear, it's mechanical. So most likely risk factors will be trauma, obesity and age. On the other hand, uh we have rheumatoid arthritis, which is an autoimmune disease. Ok. Uh So risk factors will be most likely people with HLA dr four HLA is a human leukocyte antigen which is like um receptor antigen on some cells uh which is like associated with autoimmune rheumatoid arthritis. Uh rheumatoid arthritis um is an autoimmune. So there should be some anti autoantibodies which is very important. You should know rheumatoid factor is one of them, rheumatoid factors is positive in around just 80% of people with rheumatoid arthritis. Some questions in the ma uh they sometimes ask about rheumatoid factor. What is rheumatoid factor? You should know about uh that rheumatoid factor is an IgM antibody against uh IgG specifically FC region. Some question. Yeah, they mentioned about this. The more specific uh autoantibody for rheumatoid arthritis. It is what we call anticyclic central related peptide antibody uh which like anti CCP, which is more specific for rheumatoid arthritis. They I think in, I'm sorry, they ask, uh, uh, very commonly about, uh, this, uh, uh, antibody for rheumatoid arthritis. So, keep it in your mind for the presentation. Both of them, they come with joint pain. Ok. But presentation is very, very important to know the differences between osteoarthritis and rheumatoid arthritis, osteoarthritis. As we said, it's mechanical mostly, uh, trauma, mostly with use. So in the question, they will mention for you pain after use and more specifically, it will say like pain worse at the end of the day, this is like more pathognomonic for osteoarthritis. And because it's mechanical, most likely it's just asymmetric joint involvement. So you'll hear the patient is like I have right knee pain, maybe just left knee pain. Uh like asymmetry could be bilateral joint pain, but one of them will be more than the other. OK. On the other hand, for the rheumatoid arthritis, mainly people or the question will mention for you mainly pain or morning stiffness, which is better with use. OK. So at the end of the day, uh the pain will be better in comparison with the osteoarthritis. OK. And as long as autoimmune, it's autoimmune disease, rheumatoid arthritis, we will see also in the question sometimes um systemic uh symptoms like fever, fatigue, weight loss, which we don't see in osteoarthritis. Ok. So these are most important differences be between osteopal and rheumatoid arthritis. There's another important thing you should know uh between these two diseases, which is the joint findings OK. Next slide, I will show you a picture which shows the these uh differences. But what I want you to know in these two diseases, which is very important specifically in the questions. Um We all know about D IP, distal interphalan osteoarthritis D IP is almost always affected but in rheumatoid arthritis, D IP is never been affected. OK. So this is a good, uh, a good thing to, uh find in the question to differentiate between two these two diseases uh and rheumatoid arthritis. D IP, as I said, it's not affected but MCP, metacarpophalangeal joint is almost always affected, which is not affected in the osteoarthritis. So you should keep it in your mind. D IP, osteoarthritis, MCP and rheumatoid arthritis. So the question, if it mentioned to you D IP is affected, most likely you're going to think about osteoarthritis. Ok. Uh Treatment wise, I'm not go in details in treatment but mainly uh osteoarthritis, you know, first line, maybe paracetamol, just acetaminophen, uh an acid and the steroids. Ok. And then just more severe cases, maybe we'll go for surgery for rheumatoid arthritis. Uh an and steroids still used. Ok. And we have also another uh disease modifying agent like methotrexate sulfaSALAzine, uh et cetera. And we have biologic agent. It depends on the severity of the rheumatoid arthritis, which is uh like TNF alpha inhibitors like infliximab or dili. Some questions about people who has rheumatoid arthritis and who are started on TNF alpha inhibitors. Usually some question they ask about what's the side effects on TNF alpha inhibitors? The most common side effects that you should keep in your mind for the, for the exam purposes, it's TB reactivation. T NFF inhibitors will cause uh TB reactivation. So keep it in your mind. Well, in this slide, it shows two pictures. This picture showing osteoarthritis changes. This is the normal part and this is osteoarthritis. If we can look, firstly, there's narrowing in the space which is very important in osteoarthritis, uh secondary to mechanical wear and tear use to or OK. In joint, finding most important things that you will see, as we said, narrow space, osteophytes formation here. And uh if you can see here, subchondral cyst and we will see subchondral sclerosis. OK. These are the most uh uh features for osteoarthritis. On the other side, if you look to the rheumatoid arthritis, what's obvious it's not narrowing in the space, it's most likely increase in sinovial fluids. Ok. And the most common things that starts with rheumatoid arthritis, it's the erosions. Ok. So you will see mainly erosions here, increase in sinovial fluids and this will lead to penis formation. Panus is a granulation tissue uh as a result of like uh synovial fluid accumulation here. OK. So, these are the differences in uh in joint affected in osteoarthritis and rheumatoid arthritis if we can look to this picture, which is very important. Ok. Uh In this picture. Uh, if we can see these are, which others are there? These are the distal internal joints. D IP, as we mentioned, D IP is only affected in osteoarthritis, not, not rheumatoid arthritis. OK. And if you look here, um, and the joint findings for osteoarthritis. D IP is always involved and we call it Heberden nodes. OK. Sometimes they ask about the name. OK. Just keep it in your mind. OK. And this one, it's proximal pharyngeal joint. P IP IP is can be affected in both rheumatoid and uh osteoarthritis. OK. Uh But in osteoarthritis, it's affected, we call it uh bouchar joint here if you look bouchar nodes, heb nodes. So make sure to know uh these two names and which one related to which joint? OK. This picture obviously show swan neck, swan neck can be seen in rheumatoid arthritis. OK. Sometimes the, you will see this picture. It's related to rheumatoid arthritis in this picture as well. Uh We call it boutin. So if you look here in joint findings, OK. There's a swan neck, sorry, there's one neck here and but uh in this joint, but like because of P IP is severely affected in rheumatoid arthritis and some ligaments might be affected. This will cause hyperextension of the uh D IP. It's not affected D IP, but it looks like hyperextended. So, rheumatoid arthritis. D IP is not affected. OK. Yeah, I made a slide after each uh topic. OK. So at least, uh, uh, I mentioned the buzz words and, uh, which is important in the, in, in the exam. Ok. So what you should know, like mainly, uh, from osteoarthritis and rheumatoid arthritis for osteoarthritis. You should keep in mind it's mechanical wear and tear. That's very important. Worse at the end of the day. That's very important as well. Um, and as we said, D IP is involved and it's asymmetric joints for rheumatoid arthritis. The best word for rheumatoid arthritis, autoimmune and TCP is very important, erosions morning stiffness as we said, and it's getting better with use. OK. And metac joint is affected and it's symmetric as it is autoimmune. OK. I've mentioned here some very important points. OK. Which uh they ask about it very commonly in M sra. OK. Which is the poor prognosis uh features for uh rheumatoid arthritis. Some question they will ask you. Uh One of the following is the most uh uh one of the following is a poor prognostic features. They will bring one of these or it will ask about which one of the following is uh a good prognostic features and it will uh they will bring all of these uh uh options with changing one of them. So, rheumatoid factor, if it is there, as we said, rheumatoid factor is only present in 80% of people. So 20% with rheumatoid arthritis, they don't have uh rheumatoid factor. So, rheumatoid factor is positive. This is a poor prognosis. OK. Anti CP also poor prognosis, poor function sets and presentation x-ray if you see early e organs, OK. Uh Within like less than two years of the onset of the disease. This is a poor prognosis as well. OK. Extra extraarticular features like nodules, uveitis, whatever uh else this is poor HD four and in onset. So keep in mind all of these uh poor prognostic features. OK. So next two diseases we have polymyositis and dermatomyositis. OK? When you say myositis, from the terminology myositis, inflammation and myopathy, OK. So patients will come with uh uh mainly muscle weakness, mus muscular pain. OK. What you need to know about polym myocytes and Dermatomyces. It's both like chronic autoimmune diseases. So there will be uh autoantibodies and rheumatology. Antibodies is very, very important and every exam they will ask about antibodies. OK. So in polymyositis, we have nonspecific uh antibodies ana a positive CK might be high. But these are nonspecific antibodies. OK. The most uh the more specific antibodies which is uh anti G one, which has a uh uh another name which called TRN synthetase. OK. Sometimes in the questions, uh you will not find anti G one but you'll find antihist RNA synthetase. So keep in mind both names for you. OK? Antis RP as well. Anti me two. OK. This is three antibodies you can see in both polym myocytes and dermatomyositis. But the most uh specific uh one like anti one is more specific to polymyositis, an two and uh Dermatomyces more. OK. But still you also can be seen in both of them. The difference between poly and dermatomyositis from the name. OK. The only difference is the skin involvement. OK. In polymyositis, it's mainly just muscles. Ok. So you'll see patients with proximal muscle weakness. Ok? But in Dermatomyces, you will find skin involvement. If you can see um the skin can be involved. Here. We call it guru papules. OK? Where hand is affected or it can affect eyes, we call it hill. OK? Or it can affect the whole face and the chest. Here we call swollen face. OK. Uh What I want you to know in dermatitis if you look to the facial rash here, nasolabial folds is affected. OK? Because uh in the next upcoming slides, I will mention in sle e which nasolabial folds are always spared. OK. So this is a, a good uh difference. You should know about dermatomyositis, uh facial rash and sl E OK. One more thing you need to know about dermatomyositis. It is very important in question specifically for increased risk of occult malignancy. And more specifically, it's a gi malignancy. OK. So any patient who comes with dermatomyositis, uh uh after confirmation, we should think or at least rule out malignancy. So maybe some question they will ask you, what is the next step? Sometimes it will be uh a colonoscopy to rule out any uh gi malignancy. So this is very important to keep it uh in your mind. OK. As I said, this slide, just the buzzword uh polymyositis, you should know about anti one and no skin involvement in dermatomyositis. Know about an to skin involvement and malignancy association. These are very important uh what you should know uh uh when you read the question. OK. Next we have osteomalacia and rickets. OK? Osteomalacia and rickets both are defect in mineralization of the bone. OK. But rickets will be in uh Children which they do. They have growth plates still and osteomalacia in others. Ok. So the most common cause of osteomalacia and rickets is Vitamin D deficiency. Ok. So when we say Vitamin D deficiency, Vitamin D deficiency can happen due to uh uh feeding, not eating well, whatever, but osteomalacia and can be caused by many things. The most common thing that you should know is the Vitamin D deficiency. Ok. In this slide, there's an X ray uh findings for uh osteomalacia and rickets. Ok. Uh I'm not sure how common they ask about it. OK. But the most important two things you should know bow leg here, bowing of the legs. OK. As you can see this is in rickets. And the other thing is rhetic rosy. This one or uh sometimes you can see uh pseudo fractures as well. So these are quite common features, seeing an X ray. The more important thing that you should know here is, as you said, it's the most common cause is Vitamin D deficiency. So when Vitamin D is low, this will lead to low calcium absorption from the kidney. Ok. And as a result of low calcium, as a compensatory mechanism, parathyroid hormone will go up. Ok. But I want you to know about the uh function of the parathyroid hormone. This is very important. Sorry, because um they will ask you about many questions about th parathyroid hormone, calcium, Vitamin D phosphate. DLP. So you should know about the mechanism of action of parathyroid hormone specifically on the kidney. Because parathyroid hormone has effect on the kidney and has effect on the intestine which is a bit different. Ok. The mainly what we need to know here is about effect on the kidney. Ok, parathyroid hormone on the kidney, it increase the absorption of calcium and increase excretion of phosphate. Ok. So here in osteomalacia, Vitamin D low calcium, low. Ok. Then as a compensation, parathyroid hormone will go up because of low calcium. Ok. Uh we call this secondary hyperparathyroidism. Ok. And the parathyroid hormone effect on the kidney will be increased excitation of phosphate. So serum phosphate will be low. Ok. And of course, alp will be high because of hyperactivity of osteoblasts. Ok. These effects is very important in the next slide I will mention to you uh different diseases with different uh effect on parathyroid, calcium, Vitamin D and phosphate. Ok. This table shows uh osteomalacia, Vitamin E deficiency. I think we covered most of uh the differences. Uh We can go next. Ok. Osteomalacia rickets. Uh you should know defect mineralization. Most common cause is Vitamin E deficiency. And as we said, uh low calcium, high parathyroid which will lead to low phosphate and high uh alkaline phosphatase. Ok. Next disease which is uh a very common systemic lupus erythematous, which we call it sle. Ok. Sle is a chronic autoimmune disease. OK. You should know that this chronic autoimmune disease because of immune complexes. It will cause uh many or organ damages and the patient will uh present with um multiple findings. OK. The organ damage in sle will will be caused mostly due to type three hypersensitivity reaction. Sometimes it can be type two, but the most common cause is type three hypersensitivity reaction. And sometimes they ask about this and the question uh in exams. OK. So chronic autoimmune disease, uh organ damage happened due to uh type three hypersensitivity. Uh Also also there is an association uh for sle with the complement system complements will be low. OK. So this will lead to decrease in the clearance of immune complexes. OK. So when immune complex has increased, OK, it will start to accumulate in uh different organs and cause a damage to that here in this slide. OK. Uh There's a Pneumonic rash or pain. OK. In this pneumonic, it will at least uh cover most of the findings of sle like rash, mostly as we said, malar or discoid. And what we mentioned here, if you can remember here, nasolabial fs are spared. OK. But in, as we said, in Dermatomyces, it was involved. OK. Arthritis involved sys like pleuritis, pericarditis also can be affected hematologic disorders like cytopenia, oral nasopharyngeal ulcers can happen as well. Renal disease is very common. OK. Photosensitivity you can see in sle antinuclear antibodies. OK. So you will see A N A positive and another more specific antibody which is anti stranded DNA and anti uh uh Smith uh antibodies. OK. And antiphospholipids, OK. These are more specific, this is not very specific. OK. Uh I remember uh yesterday, I've got a patient uh referred to me by a GP. OK. Referred to me as AK three. She was a young lady in thirties. OK. When she came to uh E AU, I've seen her, OK. She has AKI three in the time I saw her, OK. You can see puffy face, lower limb edema rash on the face, typical rash. OK. So uh we were investigating about uh likely sle and in the history, you can find like strong family history of sle. So sle is a bit like you, you still can see sle in uh in, in, in your clinical uh work. We have two things can happen uh in sle patients, Libman sac endocarditis, lupus nephritis, Libman endocarditis, you know, endocarditis can be caused mostly by bacteria, vegetation and treatment by antibiotics, whatever. But in sle patients because of these immune complexes which can uh cause vegetation and go to uh uh valvular heart valves, uh specifically more to the aortic and mitral valve can be affected. So, it is uh nonbacterial um uh endocarditis. Ok. And treatment should be like treating uh the cause not antibiotics. Lupus nephritis is also very common. As I said, the patient, uh main presentation was AKI three. OK. So lupus nephritis can be nephritic or nephrotic. Ok. The lady I saw she has proteinuria, she has uh puffy face edema. So, uh it's very common to have uh lupus nephritis. OK. And the most common causes of death, initially, mainly renal disease. Ok. So these are mostly the features of, uh, I said, oh, keep it in mind before we go to the exam. It's autoimmune type three hypersensitivity, ana anti Smith, anti double standard DNA. Ok. Low complements also very important rash and spare nasolabial foods. OK. This is uh, like buzzword. If you find it in the question, most likely go to a OK. Another important thing that you should know there is a drug induced lupus. There's some medication that can mimic uh, uh, sle but it's not like autoimmune. Ok. Uh, they, uh, they asked about it, uh, very commonly. Ok. There are four common medications. Ok. You should keep it in mind. Procainamide, hydrALAZINE, isona quiNIDine. Ok. These are the most common, uh, four medications but also other medication like minocycline, methyldopa chlorproMAZINE, TNF alpha inhibitors all uh can cause uh drug induced lupus. OK. Mostly. Uh in the question, they said patient with TB started on isona it. OK. And he developed blah, blah, blah, blah. So it will be dark induced lupus. So it will ask which medication can cause dark induced lupus. So keep it in your mind. This is very important. Uh We have an closing spondylitis, ankylosing spondylitis. OK. Let's start with the terminology. Ankylosing. Do you know what it means? It means fusion? OK. Uh uh This ankylosing means fusion and spondylitis. Spondyl means axial skeleton, litis mean inflammation. So we are talking about inflammation of axial skeleton that lead to uh fusion of vertebrae. OK. So it, it is considered as uh HLA B 27. Uh 1 of the HLA B 27 we have ankylosing spondylitis. We have reactive arthritis, we have IBD, we have psoriatic arthritis. All of these, we call it HLA B 27 C one negative spondylar arthropathy. OK. But ankylosing and spondylitis is very common and very important and especially in the exams. OK. It's more common in males. OK. The uh the most common features or, and the question you will see typically, typically young man, OK, with lower back pain and morning stiffness, which is better with uh use with exercise. OK. That a bit like similar to rheumatoid arthritis. But you differentiate that with a young man with lower back pain. OK. It will come the same as morning stiffness. So when you see morning stiffness in the question, you will think about rheumatoid arthritis and closing spondylitis. OK. So, read the question very carefully. Uh for patient with ankylosing spondylitis. Uh on the clinical examination, you will see a reduced flexion, lateral flexion and for more flexion and we call it sometimes ser test. So, uh if a patient with ankylosing spondylitis, maybe uh next step would be do er test to see if there is any reduced uh for deflection. Ok. There are other findings associated with ankylosing spondylitis, which is also important. OK. Pneumonic phase, apical fibrosis, uveitis, aortic leakage, a tenonitis block amyloidosis. OK. Uh which is uh a bit common with ensing spondylitis. But what you need to know, HLA B 27 males young, lower back pain and uh reduce for flection. Ok. So young male, lower back pain. Yeah. As we said, actually B 27 and x-ray sacra like joint, bump spine on X ray. OK. So if some question, they say uh they will uh present the patient as the atypical ankylosing spondylitis. And they will ask you what is the uh best diagnostic uh test for that? And then the question you would see like B 27 or x-ray sacroiliac joint. OK. But HLA B 27 is very important, but it's not the definite diagnostic test. OK. So if you see in the, in the answer, HLA B 27 and x-ray sacro joint, no x-ray sacro joint. It is uh the diagnostic uh uh next step for ankylosing spondylitis. But the definite uh diagnostic test will be an MRI. MRI will be the best uh scan for ankylosing spondylitis. But if uh MRI is not in the options and you can find x-ray, you can pick x-ray, not actually B 27. This is a very common mistake happen sometimes. Ok. Next we have sle derma, systemic sclerosis. It's all also uh chronic autoimmune disease. OK? That can affect uh multiple organs, mainly renal respiratory G and cardiovascular. OK. Renal you know uh patient can come with renal crisis. We call it renal crisis. And the very important thing that you should know in uh Marineo, a patient with who came with like a three renal crisis. Next step will be ace inhibitor. We all know that ace inhibitor is nephrotoxic, but it's the drug of choice for renal crisis. Ok. So any patient with seroma came with renal crisis. Next step, start him on ace inhibitors. That's very important. OK. Pulmonary uh respiratory uh findings. You will see interstitial fibrosis and it might lead to pulmonary hypertension. Ok. Uh There's another uh uh organs affected like uh gi is feature dismotility, cardiovascular as well. OK. What you need to know in scleroderma, systemic sclerosis, there are two types. OK? We have diffuse scleroderma. We have limited derma. OK. Um From the name diffuse unlimited diffuse, there will be widespread skin involvement. OK. Limited Cloderm will be uh limited skin involvement in the diffuse scleroderma. The most common antibody that you should know it's anti S cl 70 antibody. OK. It has another name that you should also know. Sometimes they ask and the answer you will find anti DNA to poisoner one. You will not find anti ac 70. OK. So you should know uh both names. OK. This is for the diffuse sle derma. On the other hand, the limited scleroderma, the antibody, uh the common antibody for limited scleroderma is anti centromere. OK. So, scleroderma, systemic sclerosis. If it mentioned to you anticentromere, this is limited anti C 70 or anti DNA to poiser. This is diffuse scleroderma in the limited scleroderma. It causes the Crest syndrome. What is the Crest syndrome? From the name you can use? See, it's calcinosis. Ok. Calcinosis like in this picture. This is calcinosis of the fingers of the tip of the fingers. Ok. Uh calcium deposits will be on the skin. This will uh cause thinning of the nails, thickening of the skin and looks like this picture is calcinosis. The other c is anti syndrome. So you can reme remember this or is Raynaud phenomena. Raynaud phenomena is also associated with limited scleroderma is a fetal dysmotility, sclerodactyly and telangiectasia. Ok. So in the question, I think it's uh not difficult to differentiate uh limited scleroderma. They will mentioned to you Crest Syndrome mainly OK. And it will ask what antibodies associated you. So you will go for anti syndrome. Uh Next we have Ehler. Uh we'll talk about and the next will be Marfan. OK. Ehler, maybe we all uh you know, it's a collagen synthesis defect. OK. That will lead to three things, hyperextensible skin, hypermobile joints and tendency to bleed what you need to know. Aler Dandel has uh four types. OK? It's not just Aler Danel Syndrome. We have inheritance and inheritance. It's not the most common uh type. OK. Inheritance can be autosomal dominant and the inheritance one w which was associated with barry, aneurysm and organ rupture, which is uh a bit more serious. The other types, hypermobility, classical type, vascular type, uh hypermobility. It's the most common type. OK. But what you need to know also the type of collagen affected. OK. And the classical type, the most common type of collagen affected is type five collagen and in the vascular type, it's type a three pro collagen. OK. So we have four types. We have the features of hilar D and it's collagen uh synthesis defect. Which type of collagen classical type is type five vascular type is type three. Here in the picture, you can see uh A B OK. Marfan syndrome. We all know Marfan syndrome. Marfan syndrome. It's an autosomal dominant connective tissue disorder. OK. It's a defect in the fibrillin, uh uh A fibrillin protein. OK. That is uh present on a gene on a chromosome 15. OK. So autosomal dominant connective tissue disorder defect and uh fibrillin gene on a chromosome 15. OK. Features we all know the features of Marfan most likely. Uh in the question, it will mentioned to you tall stature. Ok. High palate Arno Pictus excavator pis scoliosis. Uh But the most important thing that you keep it in your mind absolutely toll. Uh heart involvement is very common. OK? And it's the most common cause of death, which is aortic dissection. So, heart involvement and uh morphine will be dilation of the aortic sinuses. This is seen in 90% of morphine people. OK? And this will lead to aneurysm, aortic dissection, regurg and uh mitral valve prolapse. OK. So, keep in mind you uh these features, the other um very important feature in Marfan. And you can find it in the most of the questions. It's the eye involvement. It will, it will cause a marine upward lens dislocation. That's very important upward lens dislocation because some other diseases like homocysteinuria, it can cause downward lens dislocation. So in Marfan, uh it's upward, that's uh like buzzword and the questions that uh will lead you to the answer. OK. And as we said, aortic dissection is the most common uh cause of death in Marfan people. OK. So before I put this slide, because it's very, very important this slide and many questions uh they ask about it and it will help you a lot uh to find the correct answer. Ok. It's I put here all the diseases. Most of the disease is very important. Ok. Calcium phosphate alkaline phosphatase and parathyroid hormone. Ok. When you read the question, it, they will mention the question, calcium, liver phosphate alp and parathyroid hormone. Before interpreting this um this slide, we should remember the parathyroid hormone function. As we said it uh over the kidney, it increase the absorption of calcium and increase the excretion of phosphate. Ok. So parathyroid hormone itself can cause high calcium and low phosphate. Ok. So before we talk about all of the diseases, I want you to know um uh like the pathognomonic for each one. OK. Look on the osteoporosis and osteoporosis. Osteoporosis is not very common to ask about. But osteoporosis, if you look all calcium phosphate, alpina and parathyroid hormone, all are normal as well as the uh osteoporosis. Ok. So in the question, if they ask you, uh all are normal and what's the diagnosis you will go for osteoporosis directly? OK. The other pathognomonic that you need to know? Ok. For the Paget disease, I know we didn't mention in the slides and many rheumatologist topics not mentioned, but at least you should know about Paget disease. Uh pathognomonic for that it's isolated, raised alkaline phosphatase. OK. So in the question, it will uh come, the only AP is raised calcium phosphate and PTH will be normal. OK. So that's very important in osteopor. Is all normal in Paget only AP is raised. Ok. And let's go for osteomalacia, primary hyperparathyroid and kidney osteomalacia. We talked about it. We said Vitamin D deficiency, this will lead to low calcium, low calcium as a compensation, parathyroid hormone will increase and this will make phosphate low. Ok. And the LP will be increased because of uh hyperactivity of the bone. Ok. Hyperparathyroid and CKD is very important to differentiate between uh both of them because the only difference between them is the phosphate. When we say hyperparathyroidism, that means what that means, parathyroid hormone excess. Ok. Kidney is fine, no defect in the kidneys. So we will go for hyperparathyroidism. Ok. What we said the effect of this, it will increase the absorption of calcium and reduce phosphate, increase excretion of the phosphate. So when we say high calcium, low phosphate, high uh PT this is primary hyperparathyroidism. On the other hand, look on the kidney when we say chronic kidney disease. So that means the kidney is not functioning well. Ok. What's the function uh uh of the kidney? It will reabsorb calcium and excrete phosphate. So, if this function failed. Ok. So calcium will be low, it will not be absorbed. Ok. And phosphate will not be excreted. Ok. So phosphate will be high. Ok. And as a result of low calcium parathyroid will go up will be high. Ok. So this will call be called as secondary hyperparathyroidism. This is the primary. Ok. So this table is very important. I know you need to revise it quickly later. OK? But many questions will ask about this uh lab values. So keep it in your mind. Now, at the end, I know we have maybe around 10 minutes. OK? Not sure if we'll uh finish. But I've tried to mention some points or questions that is not included in the slide, but it's still very important for a mass exam. OK. Let condo calcinosis. If you see chondrocytes in the question, most likely diagnosis is osteomalacia and closing pseudogout. OK. We didn't mention about pseudogout and gout, which is very important topics as well, but I don't think we have time. OK? But chondrocalcinosis is pathognomonic or was work for pseudogout. Keep it in your mind. OK. Next dry eyes, dry mouth, arthralgia. OK. If you see these words in the question, this means Sjogren syndrome. OK. We didn't mention Sjogren but uh I love to uh bring this slide so I can highlight it as well because and exams they, they like to ask about Sjogren Syndrome, but most of the question will contain uh dry eye, dry mouth and arthri. And sometimes they ask about uh the autoantibodies for Sjogren, which is an anti, OK. Keep it in your mind these features. OK. This question, elderly man is investigated for bone pain, known to be deaf. OK. Raise the LP and skull X ray show thickening of the body. OK. So elderly man raised the LP, isolated, raised the LP and he's deaf. What we think about mainly Paget disease. OK. Paget disease. As we said, it's isolated, raised alkaline phosphatase. It will make the bone thicken. Ok. Why patient came with deafness or at least um uh because of the cranial nerves affected, this nerve will be affected uh by the thickening of the bone. Uh in Paget disease. OK. But the mainly you should know it's isolated, raised LP, it's associated with Paget disease, which one of the following uh are most characteristic of temporal arthritis. I know temporal arthritis is not mentioned as well, but um let's talk about it. Temporal arthritis, uh OD arthritis, most likely there's association with anti uveitis, intermittent claudication associated with heavy smoking, eosinophilia, hypertension. All are at least nonspecific. The most specific one is association with polymyalgia, rheumatica. Ok. So polymyalgia, rheumatica. Uh no, that there is association with temporal arthritis and treatment will be absolutely steroids. OK. Which one of the following most associated with rheumatoid arthritis? Ok. Let's go one by one X ray finding include subluxation. That's correct. That's true for rheumatoid arthritis. Ok. Commonly affect the large weight bearing joints. Do you think this is rheumatoid? No, this is osteoarthritis that affects the large weight bearing joints. Ok. D IP. As you said, this is osteoarthritis, carpal, carpal joint can can happen in both rheumatoid and osteoarthritis. Patient typically have unilateral symptoms. This is most likely we said asymmetry, unilateral more with osteoarthritis, not rheumatoid. X-ray findings include uh subchondral subchondral sclerosis. If you go back to the slide, you see the picture more likely with osteoarthritis. OK. Next question. Yeah. OK. If you look at this question, uh lab results, yeah, a question. It definitely you will have one of these questions. OK. So low calcium. OK. Raised phosphate, raised the LP and raised, uh P th what we think about? Ok. Do you remember what we said about osteomalacia, about primary hyperparathyroidism and D, right? OK. So and let's go one by one for parathyroid hormone if it's go up. OK. What's the function reabsorb calcium and excrete uh uh phosphate. So low calcium will lead to high parathyroidism. Uh But why phosphate is high phosphate is high? That's because kidney uh is not able to excrete phosphate properly. Ok. So in this case, most likely let's start budget disease. We said isolated ap sorry osteomalacia. We said Vitamin D deficiency, low calcium parathyroid will go up. OK. And phosphate will be low. OK. That's in osteomalacia in CKD. As we said, calcium will be low and phosphate will be high, which is in this question. So the answer most likely will be CKD. OK. And that's the difference with primary hyperparathyroidism. OK. So because in primary hyperparathyroidism, the phosphate will be low. So if, if you go back to the this uh table, that's very important and many questions will come on this table. OK. So very very. OK. So we talked about this. OK. Which one of the following antibodies is most associated with diffuse cutaneous systemic sclerosis. OK. Last question. Uh when we, when we say diffuse systemic sclerosis, we have diffused and limited. We said the diffuse one associated with anti uh S CL 70. OK. And anti poisoner one. OK. But it's not in the question. So let's go one by one. Anti centromere. You said it's associated with the limited uh systemic sclerosis. Anti Smith associated with anti TTG and anti endomet associated with celiac uh C anca associated with Wigner. Uh So we remained with a NAAN A can uh can be positive in systemic SARS. So, but it's not very specific. So if you can find anti cycle 70 you can choose A N A which one of the following uh antibodies is associated with Sjogren syndrome. Sjogren, we didn't talk about it but we mentioned it's associated with an anti anti me two. We said it is with dermatomyositis anti one with polymyositis anticentromere with limited systemic sclerosis anti anilla with Sjogren. Auntie Smith with a OK. So this question, 68 year old man present with three week history of low grade fever, myalgia uh in the shoulder girdle. He also reports a transient loss of vision in his left eye, given the most likely diagnosis which of the following lab investigation is the most useful diagnostic test before going to the diagnostic test. So 68 elderly came with proximal muscle weakness and eye involvement, loss of vision. So the main thing we think about is giant cell arteritis and polymyalgia mea. Ok. So the uh the most useful diagnostic test will be ESR OK. ESR would be high in most of the patients which of the following is associated with good prognosis in rheumatoid arthritis. Yeah, we talked about it early in the slides. OK. We said rheumatoid factor present is a poor prognosis. OK. So a negative will be a good prognosis. OK. Hladr four P, rheumatoid, no suggest all of these are poor features for rheumatoid arthritis, which of the following side effects uh is associated with the use of Etanercept. Uh I mentioned this slide just like to highlight your brain about uh some medication side effects. Etanercept is TNF alpha inhibitor. OK. And what I told you earlier in the slide TNF alpha inhibitor is most likely associated with reactivation of TB. That's very, very important thing they commonly ask about this. OK. I think uh it's six o'clock, I think a couple of minutes more. Ok. Uh 64 male patient came with CKD stage three and type two diabetes. OK. Came with pain and swelling at the right first meal joint on examination, joint is hard and tender to touch although he can still flex the big toe. What is the most appropriate initial management? Ok. So from uh the presentation looks like patient has gout. OK. So what will be the treatment of gout for this patient? Ok. Called chic prednisoLONE or all of the quickly, quickly. Uh the answer here will be called chin. Ok. Why not nsaids? Why not prednisoLONE? Not anai? Because patient has D3, we can't use NSAIDS prednisoLONE. Why not? Because patient has type two diabetes and steroids will uh worsen his diabetes. So we left with colchicine. Why not allopurinol allopurinol not, not used for the acute uh flare, mostly colchicine. Uh last slide, methotrexate side effects. It's very important that you should memorize. Usually they ask about uh methotrexate side effects most commonly mucositis, my suppression pneumonitis, pulmonary fibrosis and liver fibrosis. Sorry, I was very quick maybe, but we don't have too much uh time to cover most of the thing. Uh Hopefully I cover the most important uh points in rheumatology. Ok. Do you have guys any questions? Ok. Thank you so much, Doctor Tarek. That was a really good presentation. Um I think we have a few questions. Um What age groups is most common? Take? Where, what can I see the questions if you just go up, you'll be able to, they're uh a little more up, I think. Yeah, that's, that's where it started. Ok. Yeah. Uh sle more commonly, more commonly in the presentation you will see young lady, young female lady came with uh either kidney involvement rash, uh or the uh different other uh other findings of the sle but age group will be most likely young female around thirties, forties, maybe. Ok, I syndrome or does it describe the histopathology better? Yeah. Diffuse qualifer, as I said, sle lupus nephritis, we call it mainly lupus nephritis. Uh can be uh nephrotic and nephritic or nephritic. Ok. Diffuse proliferative is one type of uh uh of the nephritic um uh findings. Ok. Um They will not ask you about what type of nephrotic or nephritic, but most likely they will call it just lupus nephritis. But you should know it can come as nephrotic or as nephritic. So uh proteinura or uh no proteinura doesn't like uh uh specifically lead you but it's uh uh nephritis may be kidney affected. OK. Budget. What do they mean by budget? Yeah, budget. We didn't talk about it. But budget, as I said, II think they were answering your question when you Oh yeah. Yeah, maybe. Yeah, that's correct. Isolated. Uh OK. D Yeah, that's correct. That's a question. What are the answer for the rheumatoid? The question? Which question let me go back to the slides which rheumatoid question if they can tell me, is it this one the poor prognosis? Is it not sure if that's one? But uh we mentioned about rheumatoid arthritis. Um a good and poor prognosis. Uh at least keep in mind uh the poor prognosis for uh rheumatoid arthritis. If you want me to go back to the slides for, for, I think it was that I think it was that one. The x, which one, the x-ray question, I think it's when the question came up. Uh, this one, this one. Yeah. Uh, yes. Um, as I said, if you, uh, if you want to all the findings between, uh, rheumatoid and osteoarthritis, you can, but if you go on that, it will be easier for you. Ok? If you don't know about subluxation and, uh, rheumatoid arthritis, you can go, uh, the next one, a large weight bearing joint, as we said, osteoarthritis mechanical. So it affects more likely the large, uh, uh, weight bearing joints. Ok. So this is for osteoarthritis D IP we said it os osteoarthritis, carpal, metacarpal, it's not speak for rheumatoid. It can affect uh, osteoid. Ok. Unilateral, definitely with osteo not rheumatoid subchondral cleis. This is also definitely with, uh, osteoarthritis, not rheumatoid. Ok. There are subchondral cyst can come with both of them. OK. But cleis is more likely with, uh, rheumatoid arthritis. If you want to go back, uh, in the beginning here, uh, you have these two pictures which can show you, uh, Subchondral Cyst subs here. You can see, uh, Bruns, I know you, but if you go to the slides here, the finding you will find, uh, subluxation, it's there. Ok. Uh, as I said, it's sometimes difficult to memorize all of the, uh, uh, differences, but at least try to, uh, uh, rule out, uh, most of the options. Ok. What else? Thank you very much for focusing any other questions guys? How often do anti antibodies predict silly just or different? Yeah. Ok. Uh There's sle there's antiphospholipid syndrome. Ok. In SL E the most specific uh antibodies is anti Smith. OK. Yeah. So they sometimes ask about this question. OK. It's not anti, not A N or not uh anti uh double, it's anti Smith. That's the most specific uh antibodies for antiphospholipid syndrome. Ok. Uh There's other an antibodies, OK, which is anticardiolipin antiphospholipid antibody syndrome. OK. So it's a bit uh different from se antibodies. OK. And um antiphospholipid syndrome most likely in the question, you will find uh thrombosis. Maybe the question we me mention to you, uh pregnant lady has three previous miscarriages, uh DV TPE. OK. So this is more go with antiphospholipid syndrome and or it will mention anticoagulin uh uh antibodies or antiphospholipid antibodies. OK. But in sle less likely to come with miscarriages, less likely to come with thrombosis. The typical presentation for sle will be a young female lady, came with AK, came with a rash uh and with a strong family history. So this is how you can differentiate between both of them. Uh Any other question? Hope I answered all your queries. Thank you so much, Doctor Ta. That was a brilliant presentation. You managed to cover a lot in very little time. Thank you so much. Uh You will come any time. Thank you very much. Uh Hopefully, I didn't take a long time. Just seven minutes. No, no, it's really good, really helpful. Ok. Yeah, if you need anything, you can uh email me, send me, ask me any question. I'm happy to help you. Sure. Thank you so much. If anyone comes up with any more questions, I'll send you a message. Thank you very much. Thank you. Bye bye. See you later.