DIP Episode 110 - ABIM/Medicine ITE/USMLE Step 3 Review Series 8 (Rheumatology 2)

Okay, welcome. My name is Devine. I am a PGY-1 transitional year resident. That's ultimately going into radiology and this is episode 110 of the Divine Intervention Podcasts and in this podcast I will be continuing my review for the American Board of Internal Medicine exam and the Medicine Intrins exam slash step three. And in this episode we'll be continuing our discussion of of rheumatology. So let's just jump right into it, right? So what if you get a question about like a 25 year old guy comes in with like low back pain, tells you the doc I feel stiff in the morning. I can like extend my back much but as I sort of workout, if I workout for like two hours, I sort of feel a lot better. What are you thinking about? Well, I hope you're potentially thinking about like ankylose and spondylitis, right? So I'm just basically using this vignette to begin at a discussion of the seronegative spondylathropathies, right? So what are some key things about the seronegative spondylathropathies? You want to keep out the back of your mind for these exams. The first thing is you want to keep in mind that this thing is mainly affect the spine, right? So the affect your axial skeleton for the most part. And one thing that is almost like a pathonomonic hallmark of these diseases, and again, I'll talk about them in a bit, is enthocitis, right? And thocitis is just a boss phrase to mean inflammation of a region where ligament or tendon mits bone. Okay? So for example, right?

If you look at the uakili, right? Like ligaments and tendons and medium bone at that point or at your elbow, right? So those are common areas of inflammation in these are seronegative spondylathropathies, and also in the spine as well, right? Me, if I will say milling the spine. And I mean for the most part, these things are all a rheumatoid of factor negative, right? And then you want to remember for sure that these are all associated with like HLEB27, right? Although having a positive HLEB27 does not mean you have a seronegative spondylathropathie, right? I mean, like HLEB27 is found in almost like 10% of the world's population, right? So you kind of want to be careful with that. In fact, this is a very nice way for them to integrate bio stats with this, right? So having a positive HLEB27 is kind of sensitive for seronegative spondylathropathies, right? But it's not specific. Okay? So that's something to keep in mind. And the thing is what are the four diseases that fall under this? There's actually more than four, but the four you need to know for your exams, right? So there's the psoriatic arthritis, right? The numonic, you probably remember from step one is the numonic pair, right? So the piece for psoriatic arthritis, the ACE for ankylose and spondylathus, the I is for like IBDS associated in therapy, right? And then the R is for like the reactive arthritis. It was previously known as writer syndrome, but people don't use that term anymore.

So what's the way this thing's classically present? I just gave you that, right? So it's going to be a young person, the completely low back pain, it's worse in the morning, better during the day, especially when they work out. And these people, right, they may classically have like eye problems as well, right? In fact, many patients with a seronegative spondylathropathies, they tend to get a U Vitis. Okay? So getting a slick lump exam, maybe the correct next best step, or as in a question, you see on one of these are tests. So, and I mean, they have like some classic findings on image and especially like ankylose and spondylitis, they tend to have like bilateral secret relitis, right? So they tend to affect both of the acycrophiliac joints, but I'll give you some exceptions to that. And then in addition, these people, especially like angst, bond again, they tend to have like the bamboo spine, like the fused spine, right? So what are the big things we want to know about these, right? Let me say some generalities. The thing I'll just tell you is, there are many similarities between the IBD associated and therapy and sorry, I mean, IBD associated arthritis and ankylose and spondylitis. So I'll kind of recommend learning both together. These two conditions, they tend to have like the symmetric like spine involvement or like symmetric like secret reliat joint involvement, right? And the thing is, many patients that actually have ankylose and spondylitis, kind of like IBD, right?

They tend to have inflammation of their gut as well. And the thing is, these people that have these two authorities, they usually do not have peripheral joint involvement. They can, but it's rare, okay? Contrast this with the pair of like the psoriatic arthritis and the reactive arthritis, these people tend to have lots of peripheral joints involved in addition to the axial joint involvement. And then another thing is, instead of having like the symmetric secret reliat joint involving that you see in anxpond and IBD associated arthritis, these people tend to have like asymmetric involvement of the secret reliat joint. So that's one thing you kind of want to think, keep at the back of your mind on these exams. So if we sort of talk about them one by one, right? So I mean, kind of start at a kylose and spondylitis. Again, I've sort of given you the classic presentation, young man, low back pain, worse in the morning, better with working out. They have the synthesitis, right? So those classic things that I've already mentioned. But there are some high-youth things you sort of kind of want to keep at the back of your mind that are testable on these exams with regards to ankylose and spondylitis, right? So the thing is, remember when I've always talked about at Lanto axial instability with rheumatoid arthritis and juvenile idiopathic arthritis and down syndrome, right?

These people that have ankylose and spondylitis, again, before you send them for surgery or anything that will involve extensive neck manipulation, you want to make sure that you get an extra of the cervical spine with views, inflection and extension, right? To rel out at Lanto axial instability. So you don't get burnt. And one other weird thing, they love to test on exams with regards to ankylose and spondylitis is that these people, for the most part, especially if they get treated, they tend to have a pretty normal life expectancy. I have no clue why they love this on these exams, but they love to test it for some reason. So just sort of keep that at the back of your mind, right? And again, I already talked about the eye problems they may have. They may have like the anterior uviitis. So notice, I said anterior uviitis, not posterior anterior uviitis, right? So again, the slit lump exam may be the next best step in diagnosis for these people, especially if they come in presenting with eye pain. Okay? Again, I'm repeating it. anterior uviitis, not posterior posterior uviitis. If you see posterior uviitis on an exam, thanks, sarcoids, sarcoids, sarcoid. Okay? There are many things that can cause posterior uviitis, but I'll tell you this on an exam. If you see posterior uviitis, the only thing I really want you to think about is sarcoidosis. Okay? And again, I already talked about again, how you see the bamboo spine on imaging.

These people can actually get an intestinal long disease, right? So like restrictive disease where they will have like the normal or slightly increased fiv 1 to every serious show, but they will have a reduced dlc, right? That's what tells you that they are dealing with long fibrosis. I mean, I don't know exactly how high you'll this is, but the thing is most rheumatologic diseases that cause intestinal long disease, they tend to cause fibrosis of the base of the lung. And kilosis, pondylitis is kind of like its own thin. It actually tends to cause fibrosis of the apex of the lung. So that's like a relatively unique finding on exams with regards to an kilosine spondylitis associated in testicial long disease. And again, remember, these people can have inflammation of their guts. And one other thing you may also want to keep in mind, right? So they can give you an exam question. It's like classic and kilosine spondylitis. And then they tell you that this patient has like a new murmur, right? They tell you that it's like it's it's a holosis, stoic murmur that is sorry, it's a dastolic murmur that is radiating all the way back to the left low external border. If you see that, you really want to, especially if the pulse pressure is wide. So let's see, they have like blood pressure of blood blood pressures of like 150 over 50. Think about aortic regurg. Aortic regurg is actually relatively common in patients with ankylosein spondylitis.

In fact, ankylosein spondylitis increases your risk for aortic dissection. Okay. So that's one of those weird bizarre associations you want to keep at the back of your mind for tests. And then I mean, the IBDS, IBDS associated arthritis, right? So that will classically present patient with like a history of like Australia, collides or Crohn's. And then they have like many of the same findings as ankylosein spondylitis. That pretty much seals the deal for you on this test. So there's really not much I'm going to see there. And the thing is, like I said, right, these people tend to have more axial involvement. Remember, I talked about these things as a pair. I said that ankylosein spondylitis has many commonalities with with IBDS associated arthritis. So most of the time, these people tend to have involvement of the axial skeleton. Okay. Not necessarily the peripheral joints, but here's the kicker. Involvement of the axial skeleton has no correlation with disease activity in the gut for patients that have IBDS associated arthritis. However, if a patient has like peripheral joint involvement and they have like IBDS associated arthritis, the amount of peripheral joint involvement actually correlates with the amount of inflammation they have in their bowels. Okay. It's just one of those weird things. I don't foresee being something that shows up on an exam, but it looks like something that a GI doc will feel very good or rheumatologist will feel very good about pimping you on.

So I guess I'm just going to go ahead and through this in as an added bonus for you. So again, the level of axial involvement does not correlate with disease activity in the gut for IBDS associated arthritis, but the level of peripheral joint involvement certainly plays a, like has a very strong correlation with the amount of inflammation in the gut. And then like I said, I'll talk about the last two together, right? So like the psoriasis arthritis and the reactive arthritis, previously again known as Ryder syndrome, right? So the psoriasis obviously they will have psoriasis, right? So they will have like these are silver scale lesions on extensor surfaces, right? Nothing special there, right? But these people tend to have a lot of nil findings on these exams, right? So those are things you sort of kind of want to keep at the back of your mind, right? So for example, they'll have like nil pitting, right? So literally like a pit, like a hole, they'll have like lots of little dots on their nil bed. They can actually give you a picture of that and sort of want you to identify that on an exam, right? And the thing is they can have like these are sausage digits, right? So literally their fingers look like sausages, right? They have a lot of like soft tissue swelling and all that crap. And then they can actually have a separation of the nils from the nil bed, right? That the fancy medical term for that is on equal license, right?

I mean, that's why we go to medical school instead of saying like your nil separating from your nil bed, we see the word on equal license, right? So that that's like the medical term for nil separating from the nil bed. But anyhow, so psoriasis and all these finger find like nil findings, finger findings, think about a psoriatic arthritis. And then for the reactive arthritis, I mean, you probably remember this from your USMLE exams, like your step one step to CK, it's like a triad, right? So like the can see can pee can climb a tree, right? So so again, the trend is can see. So because they have conjunctivitis can pee because they have a urethritis, it tends to be a sterile urethritis. So your cultural, you want your not going to grainy bugs and then can't climb a tree, right? For the arthritis, right? So this arthritis, like I said earlier, it tends to be an asymmetric arthritis, right? It tends to affect like very few joints, it doesn't usually affect many joints, like you have in the neck, other seronegative, or spondyloa, apathy. Right? So it tends to affect very few joints, like one or two joints. And again, they have the conjunctivitis, they have like the sterile urethritis. So again, you're not going to find any bugs. And the thing is this triad, right? I mean, again, I love the way they float these trads in internal medicine, even if most times, they're actually pretty rare in the real world, right?

So it's very rare to find a vision that literally has all three things going for them at the same time, right? And I mean, how does this classically presented an exam? It'll be a person that like usually like a young person like recent GI or Giu infection, right? So like the, they have like a recent like bloody diarrhea from like Campilo Bacter or Shigella or Samonella, or the metalluriperson that had like a recent like your senior infection, or it can be a person that recently had let's say like a sexually active young person with all these risky behaviors, right? So you're thinking like Clamedia on that those circumstances, those are like the classic, classic, classic presentations. And then they get into trouble. And then after like weeks afterwards, they say like, Oh, Doc, my knee hurts. Right? If you see that, you really want to think about a reactiva throi. And again, these people culture them up the wazoo. Usually, I'll say like almost always you do not find any bugs. Okay? Because basically it's not these bugs is not like a persistent infection that's causing your symptoms. It really is like your immune system reacting to the bugs that are causing these symptoms that you're going through. So I'll tell you this, you basically never want to give antibiotics for reactiva throi. It is on any of these exams. The only time you give antibiotics is if they clearly give you evidence of an ongoing infection where you identify the bug if you idea bug find given type of attacks.

But I'll tell you this, I have very rarely, if maybe only once or twice, ever seen antibiotics, be the correct answer in a question that dealt with reactiva throi. So again, sort of keep that at the back of your mind. And then another thing you want to keep in mind with these are question with these are reactive arthritis questions is they usually have one or two findings, right? On some part of their body, right? So they may describe like this person having like like some kind of like a ring shaped ulcers on the on the penis, right? So they can like show you like a penis picture. And then you see these things that sort of look like shallow ulcers, they're kind of like round, right? So like ring shaped ulcers on the penis, that finding is what is known as a sersonate balanitis, right? So sersonative, I'm not mistaken, it's spelled as a C I R C I N A T E, right? So like sersonate a balanitis, balanitis, right? Because it's on the penis, right? So again, something you want to keep at the back of your mind. And then the thing is sometimes they may show you their extremities and you may see like these like splotchy lesions, sometimes you can see them under the feet. That's the thing that's known as a caradoderma blanoragica, okay? Caradoderma blanoragica, just encourage you just sort of like look this up online, you'll see some pretty gross and nasty pictures. There's a reason why it did not go into the first place.

I love dermed, love the material, but I just can't stand that looking at those kinds of things. So, so how do you treat these as seronegative as ponly lot of thropothics in general? The thing is when you're thinking of treatment, right? Because this is one very nice thing that your friends that write these exams try to confuse people with. Whenever you see a seronegative spondylathropathy, ask yourself, what is the part of the skeleton that is involved for the most part? Do they have a lot of axial involvement or do they have a lot of peripheral involvement? Because the manner of treatment is similar, but there are some key differences, right? So, for example, if they have the axial skeletons involved, right? So like they're spying, the secretariat joints. The first thing you pretty much want to start with is an onset, right? And you also recommend physical therapy. So like, NSAI Ds, NSAI Ds, NSAI Ds, physical therapy. If your NSAI Ds are not cutting it, your next line on the test is to consider a TNF inhibitor, okay? Is to consider a TNF inhibitor, okay? So, the next line is to consider a TNF inhibitor. If they have axial involvement. If your TNF inhibitor does not work, then they probably won't go this far on an example. If your TNF inhibitor doesn't work, your next line are the more exotic immune-based therapies, right? So like you probably heard of Stellara on TV.

This drug known as a ostekinumab is like a month for people taking step three, it's a monoclonal antibody against the interlooking 17 and interlooking 23. Those work really well for the seronegative or spondylothropy thesis, especially again, if you have axial involvement. Another one you may see on an exam is something called a secukinumab. Secukinumab, I think it's called like a centax. It's a monoclonal antibody against IL17. Sorry, I'm in spoke. Ostekinumab is a monoclonal against IL12 and 23. Secukinumab is a monoclonal antibody against IL17. This is more for people that are taking step three. I'd be surprised if you saw that on the medicine training or the American, the ABIM abort exam. So here's one thing that is super, super, super important. So pay attention here. You absolutely positively do not want to use a demard for the treatment of axial lesions in the setting of a seronegative spondylothropy. If you pick a demard, that will be the wrong, I can pretty much guarantee you, that will be the wrong answer in a test. Okay. They have done lots and lots and lots of studies and they've shown that demards do not work for axial involvement of the seronegative spondylothropy thesis. No one really knows why or at least from my looking through the literature, there's no real reasoning, but that is the guideline. So you definitely want to keep that at the back of your mind.

So please do not pick methyl trexit as treatment for axial like primary like axial involvement in a patient that has like ankylose and spondylytis, for example. But if these people have a lot of peripheral joint involvement, again, they won't be ambiguous on a test. They'll make it very clear, very obvious. Then again, your first line, think of your insets. Okay. Another thing you could potentially use as first line, I'll say for the most part, insets are correct, but you can actually use demards here. Okay. So this is where demards come into play like your methyl trexit, your hydroxychloroquine, your sulfosalazine. These drugs work well for peripheral joint involvement in the seronegative spondylothropy thesis. Okay. If your insets or your demards fail, you can proceed to your TNF inhibitors. If your TNF inhibitors are not caught in it, then again, you can proceed to the exotic therapies already talked about, right? So like your secukino map, your or stekinumab and stuff like that. So I'm again, you really, I know you'll be like, oh, define this is loyal. I promise you, I have taken these exams and I've treated lots of people for these exams. These things are certainly not loyal. I'll tell you that right now. Okay. So what if you get a question about a patient that they tell you that it's a 25 year old guy, he tells you that doc, my, oh, let's say it's more like a 40 year old guy, right? So 40 year old guy says doc, my, I have like low back in the morning, I feel stiff.

If I workout, things get better. And then you're like, hmm, it sounds like you have on kilos and spawn the light is and then you get imaging. And then you notice that the sacrileac joints are speaking span. So like no problems with the sacrileac joints. If you see that, what are you thinking about? And then let's assume they show you imaging where you see like, like calcifications in front of the vertebral body, so like anteriorly, and you sort of see them across multiple vertebral body levels. What disease are you thinking about? Well, I hope you're thinking about this. This is a low yield concept. But it's one of those things that if you, it's, it's very easy to identify, they don't make the question hard because most people will get it wrong, right? But this person has something called diffuse idiopathic skeletal hyperostosis or dish, okay, or dish. They love to test this on exams. Really? But it's one of those things where like step three, you're like, you see, I'm like, I have no idea. Or even these body exams, you're like, I have no idea, okay? They love to test this every so often. So I keep, definitely keep this at the back of your mind. Basically, they will give you a presentation of a person you're like, Oh, this is an kilos and spawn the light is what you get imagine, like plain fill, plain film, I imagine. You're like, this person's secretariat joints look good.

Or they tell you that, Oh, there is no evidence of secret Ilyaca joint inflammation or sclerosis or whatever. If you see that, then it is not ankylose and spawn the light is, it is this diagnosis known as dish, okay? So the kicker is the absence of secret light is. So it's like ankylose and spawn the light is minus secret light is equals dish, okay? So and these patients, they tend to get most of their symptoms in the neck. So they'll say, like, Oh, they have like trouble moving their neck. And sometimes they may even tell you that, Oh, on imaging, they find extensive ossification of the anterior longitudinal ligament. If you see that buzz word, just I mean, pretty much stop reading the question and pick the answer that says dish, okay? Or they may tell you that, Oh, on imaging, they find like multiple bridging osteophytes. That's another boss phrase, multiple bridging osteophytes. So essentially, these people have osteophytes that are joining multiple multiple vertebral bodies. Again, if you see that, think about that's why it's called bridging, because you're joining multiple vertebral bodies together. So this will have like spinal fusion. If you see that, think about think about a dish. And these people tend to have like risk factors, right? Like most of their risk factors are like metabolic syndrome kind of risk factors. So like being obese, having diabetes and stuff like that. And really for the most by these people, again, NSAZ, NSAZ, NSAZ physical therapy, right?

And sort of like trivia on the line metabolic issues. And this is actually again, one of those weird disorders that have an association with Atlanta axial instability. You see divine, you've repeated Atlanta axial instability so many types. Why do you think I'm repeating it? You think I'm repeating because I love to like hear myself talk, not really. I'm repeating because they test this thing like it shows up on pretty much every USM in the exam. A lot of these medicine board exams and even the medicine in training exam. Okay, so before a person has surgery or you approve them to start sports, if they have a history of Down syndrome or rheumatoid arthritis, or juvenile idiopathic, idiopathic arthritis, one kilosum spondylitis or dish. So diffuse idiopathic skeletal hypostosis, you need to obtain cervical neck X-rays held in with the neck held, cervical X-rays with the neck held in flexion and extension to rule out Atlanta axial instability. Again, you do not want to disengage the head from this spinal cord. No one ever comes back from that. Right? So you don't want that. Okay. So I think that's all I'm going to say about those arthritis. Now, what if they give you a question about like 60 year old guy, let's assume, you know, he loves his cold beer. He just had like met a few friends last night. They had like a few cold beers. They ate a lot of crabs. And let's assume like he has a history of hypertension and he takes like, he takes like HCTZ for his hypertension.

And then he comes to the hospital, comes to the ED and says, Oh, doc, my leg, my my leg hurts a ton. Right? I mean, you probably know what I'm going after here. He says, my leg hurts a turn. It's my big toe. It hurts so bad. In fact, if air blows over my big toe, it just hurts like crazy, right? Like it's like almost like pregnancy, like pain, although to be honest, I mean, I've treated patients with gout. I also had a chance to be at like BB deliveries. I think I will say that golf pain feels nothing. At least just from being at a delivery and seeing a patient with gout, delivery in a child is probably if not one of the most painful experiences. A person will ever experience in their lives. Thank God for anesthesia and epidurms. So when you see your mom or you see a lady that's pregnant and delivering a kid, you better respect them, right? Because that is certainly something I wouldn't, that is something I would not want to go through myself. So be grateful, be grateful for moms, they put in a lot of work. So just shout out to my mom, I guess, okay, so back to this. So this person obviously has gout, right? And how does gout present again, acute onset, right? Super bad pain. And usually for some reason on these exams, they love to see that the pain started at night, okay? That's like the classic presentation, the patient will be like in extreme pain. And again, it'll be monoaticular.

So it will only be one joint that will be involved on your exams, especially like in the acute phase, right? So this person has gout, right? So this basically here, I'm going to be talking about the crystalline atropathids, although I probably will only spend time on one today, because there is a lot of high ill things that you love to test with gout. So I will go through all the high ill stuff. And then next, when I pick up these are rheumatology series again, we'll go through the rest of the crystalline atropathids, right? So what's the path of physiology behind gout, right? You already know it's from the monosodium are ureth crystals, right? So don't forget these boss phrases, right? I probably learned for step one step two, these people tend to have like the needle shaped negatively by refringent crystals, right? So if you see that boss word stopped in the question, it's gout pretty much, okay? And the thing is you may say, okay, divine, why does this hurt? The thing is, there is a gout hurts is right? So when you have the inflammation, what I think is these needles shaped crystals, basically like, perforate neutrophils that come to like the site of inflammation, when you prefer neutral fields, remember neutrophils contain a lot of badness on the inside. So when you prefer it them, they release all these badness into the joint. And then you have like massive, massive, massive inflammation.

That's why you then have a really bad day if you're having a, if you're having a gout flea. And you may say, okay, so divine, where do these monosodium ureth crystals come from? The thing is, these monosodium ureth crystals, they come from one of two processes, is either you're making too much of them, right? So you're an over producer or you are not excreting these ureth acid crystals as quickly as you showed. So you're an under excreter. And the thing is, for the most part, most people that have gout are under excretors of ureth acid, right? So pretty much like almost like 90, 92% of patients that have gout are under excretors. So you may ask, okay, so divine, how can people over produce a ureth acid crystals? I mean, there are many ways you can be an over producer, but I'll say that usually, if you're taking these exams, the usually go after one of two people, right? The go after a person that is getting chemotherapy treatment for a lymphoma, right? Remember, those lymphomas, the chemotherapy tends to work like super awesomely. So a lot of cells die at once, right? And guess what? When a lot of cells die at once, what do you think they release into the circulation DNA, right? And if you break down DNA, you can alter you ultimately basically get to ureth acid, right? So if you're breaking down like your purines, your purines ultimately get broken down to ureth acid. So that can be an example of over production as the theology of a person's a goutier attack.

Another one that you'll probably more more likely see on step three is if the subscriber person that has like a lesh my hand syndrome, right? So remember, that's like a HGPRT deficiency. If I remember correctly, I believe HGPRT is like the hypoxanthane, one in phosphorybosotransferase. So those people have like a HGPRT deficiency. So the appearance salvage pathway doesn't work. If your period salvage pathway doesn't work, well, you're going to have a lot of problems. Like you have problems like biting your basically like chopping your fingers off. But in addition, they will also have gout because they cannot salvage purines. So you have increased flocks through Zanthinoxides to the production of ureth acid. So those are the people that tend to be over producers on exams, okay? But pretty much everyone else is an on the excreter, right? And these people, I mean, they tend to have like risk factors on the exam, like they tend to have antecedents like having like the metabolic syndrome or drinking a ton of booze, right? So a lot of alcohol being on a diuretic, right? So remember like your your diuretics like your thiazides, your lube diuretics, they actually decrease the excretion of ureth acid. So that can sort of put you in trouble relatively quickly. If you're also like aspirin, right? So let's say it's a person that has like cardiovascular disease and you're on like low dose aspirin.

So like your a 1 milligrams every day, that actually increases your risk of gout as well, right? Because the thing is low dose aspirin. So like the a 1 milligram aspirin, that actually decreases the excretion of ureth acid. But paradoxically, when you get to much higher doses of aspirin, that actually increases the excretion of ureth acid. So pay attention to this, it is actually being on low dose aspirin that increases your risk of having hyper urethemia that that can then predispose you to having gout, right? And then other things like red meat, right? That's another like classic risk factor on exams. And again, usually gout on exams shows up at the big toe, right? So like the first MTP of the big toe. And I mean, gout, what are some bad things that can happen down the line with gout, right? So the thing is these monosolium ureth crystals, they can build up over like years, right? And then if they build up build up build up build up build up, they form something known as toe fi, right? And the thing is, I mean, think about it, right? Sort of think of it this way, let's assume you live in a one bedroom apartment, and it's just you, right? And let's say you're like a clean person, you love to keep your apartment clean. I'm kind of like that. So you want to keep your apartment clean, you don't want your apartment being dirty, everything is like speak and span the way you want it to be.

And then let's assume you then begin to harbor, like you're bringing like 10 other people to live in the up in that apartment with you. Chances are that apartment is not going to stay clean. It's going to stay like dirty, going to stay destroyed or something right? Things will not be where they should be, right? So that's kind of like the way that these toe fi behave, right? They begin to build up around joints and guess what they do? They destroy soft tissue, they destroy joints, okay? So that's something you want to keep at the back of your mind. So toe fi is something that you see in long standing gout, in long standing gout. So the way gout will you again present, you'll present as a monoacicola throitis, right? You'll be a cute onset, right? And I mean, obviously you don't have like some crystal ball to tell you that, oh, you know what? Maybe this is this, you don't have something that says, oh, this is definitely gout. I mean, it could be an infection, it could be a septic arthritis, right? So obviously you want to get an atrocentisi so you tap that joint, right? And usually if it's gout, you'll see like white blood cells in the tens of thousands, okay? It can almost look like a septic arthritis picture, but you do the polarized light, whatever, you see the needle shaped, like negatively by refringent and needle shaped crystals, and you see a ton of neutrophils, okay? So you see those things, you don't see any bugs, and you know you're dealing with gout.

And the thing is on imaging, right? In gout, right? Like usually, you'll see like, especially if they have like toe fi, you'll see like these like radio loosened sort of like punched out lesions in the involved joints. So you may see, but define these are crystals and all that, well, why, why are they radio loosened? Think about it, right? So go back to your study for step one. What is the only kidney stone that is radio loosened? Those are your uric acid stones, right? So that should kind of make sense that, oh, like this to fight, which again, basically like conglomerates of uric acid crystals, they look, they are radio loosened on imaging, you just see a lot of soft tissue swelling, but actually those things are a lot of like uric acid crystals that have been deposited. So how do we treat gout? The thing is, first things first, they will try to trick you on these exams and try to make you measure uric acid levels. Do not, especially like in the acute phase of gout, do not measure uric acid levels. Don't be tempted to pick that answer. If you pick that answer, you're going to get it wrong. Do not like resist that temptation. Just think of angry divine face telling you to not pick to not pick an answer that says to measure uric acid levels. That is almost always a bad idea on these exams. Now, so how do you treat an acute gout attack? Right? So pretty much you start with endsets, right? So in the methamphetamine, ibuprofen, they work pretty well. Okay?

Another thing you could potentially use is steroids, right? So you can like inject steroids into the joint, especially if it's like one joint that is involved, or you can take like oral or like IV steroids, those work pretty well. Again, if a person has a history of diabetes, chances are given a steroid may not be the best idea in the world. If a person has a history of like peptic ulcer disease, or they have renal failure, maybe given an inset is not the best idea in the world. Another thing you can also actually use a cutely for gout is coaches in macochesins like third line these days on these exams. So keep that at the back of your mic. And the thing is your friends that write these tests, they love to give you multiple correct answers. They will give you like an inset, they'll give you a steroid, they'll give you coaches in, and you're like, hmm, which one do I pick? If a person has like no risk factors, no contraindications, go ahead and pick insets. But it's in our, the thing I will tell you that again, is like the classic thing, they do do to people on exams. If they give you multiple correct answers, being a good test, they can tell you that you should just basically look for some kind of contraindication. Okay, look for some kind of contraindication.

So these people, right, the contraindication for example, to an inset maybe that, oh, they have renal failure, or they have like a CHF, or they have like a peptic ulcer disease, they're obviously for those people, you don't want to give an inset, you want to consider something else. So another, I guess principle of treatment in the acute phases, if the person is not on chronic like gout therapy, already, in the acute phase, do not start gout, so let's say they've never been on alopeurino, do not start alopeurino in the acute phase of gout, or if they already on alopeurino, do not stop the alopeurino, okay, do not stop the alopeurino, do not increase the dose, don't change anything, just keep things as this, okay, so do not increase or start like a chronic gout med in the acute phase of a gout attack, okay, so if they are not on alopeurino, don't start it, if they already keep the occurring dose, okay, don't change anything, because if you make any change, that will increase the risk of worsening their flare, or increase the risk of having more flares.

So that's pretty much how you treat acute gout, so how do you treat chronic gout, right, so do you treat chronic gout gout, like your post-or child drugs are your Zanctin Oxidis inhibitors, right, remember Zanctin Oxidis converts some, basically makes your recacet, so if you inhibit the enzyme, you no longer make your recacet, then these people don't get into trouble, right, so what are your classic drugs here, those are drugs like alopeurino, drugs like a febboxo stat, right, or febuxo stat, whichever floats your blood, remember, if you even look at the spelling febuxo stat, Febuxo, S-T-E-B-U-X-O, S-T-E-T, so X-O tells you it's a Zanctin Oxidis inhibitor, okay, so those are like almost like your first line agents for chronic gout. And remember, these Zanctin Oxidis inhibitors, one super, super high-yield thing you want to keep in mind is that they can have like some bad drug interactions with is a thioprin, remember is a thioprin, occasionally you may see it on the exams referred to as a six-megaphtal purine, those drugs are broken down, one like metabolic pathway for those drugs is through Zanctin Oxidis. So if you give us Zanctin Oxidis inhibitor, you will stop metabolizing is a thioprin to inactive by products. So your is a thioprin will build up and you can get like a profound bone marrow suppression.

So you want to be careful, you either want to like lower the is a thioprin dose or stop the is a thioprin dose or maybe use a different drug, okay, so that you don't get into, you don't get into trouble here. So those are again the big things you want to keep in mind with your Zanctin Oxidis inhibitors, right? And the thing is these drugs, I guess let me sort of take like a small detour here, right? So you're like, okay, divine, how do we want to like, what are we treating this gout to, right? So the thing is usually try to treat it to keep the uric acid levels like below like six milligrams per deciliter. So that's usually kind of like your target. If a person has like to five, your target is a little lower, like you're trying to treat to like a target of like five milligrams per per deciliter. So like a uric acid level that is less than five milligrams per deciliter. Now, what are some other drugs you can use to treat gout chronically, right? So you can use like this drug of probenesid, right? So probenesid is something that's known as a uricosuric agent, right? So probenesid increases your excretion of uric acid. But let me go ahead and tell you this right now. Probenesid is almost always the wrong answer on tests, because you literally need to meet many like super specific conditions to be able to give probenesid as treatment for gout. So what are some of those conditions, at least what are the ones that show most commonly on an exam?

First thing first is the person has to be an under excreter of uric acid. That's the first thing. And then they also have to have like no reno failure. If they have reno failure, they cannot be on probenesid. Another thing is they must never have had like some kind of kidney stone from gout, right? So they must never have had like nephrolythiasis. And then another weird one, right? So this one, they love to like slot it into questions is if they've had, if they have like two five or they've had like two five in the past, then these people cannot be on probenesid. So basically, right, very few people leave any if any prescribes probenesid in the real world, because again, there are like way too many conditions you have to meet. You cannot have reno failure. You cannot have had a tofos. You cannot have kidney stones. So I'll just tell you this. This is pretty much never the right answer on exams. But if you check all boxes, then you can go ahead with probenesid on a test. So pretty much, I'll say for the most part, you want to go ahead and avoid the sensor like the plague on exams. I've seen it being correct like once or twice, but again, those are under like very specific situations where basically you check all these boxes, I just mentioned. And then some other drugs you can use for a chronic treatment of gout. So these drugs are like super, super expensive, right? So like your Uricase analogs.

So drugs like a pig lotty case or as buri case, basically, so they accord Uricase analogs, right? So the thing is birds, they actually have the sense I'm known as Uricase because birds can go that water for a long, long, long period of time, right? So birds, because the arenas like super constant treated, birds don't want to get like stone problem. So they can convert this uric acid to something known as Alantoin. So A, double L, A, N, T, O, I, N. So Alantoin, it's water soluble. It's easily excreted. So the thing is drug companies have devised Uricase analogs, right? Like big lotty case or as buri case, they basically convert Uric acid again to Alantoin, something that is very soluble. So it's much easier to excrete. So these people, uh, these drugs are like super effective, but with super effectiveness comes super cost. They are very, very expensive. Okay. So those are things you want to keep at the back of your mind. And again, if you notice, this thing is an analog of like almost like an animal product. So you can already begin to envisage the kinds of side effects that may pop up with these drugs, right? So these drugs, they cause a lot of, um, they can cause like some immune problems, right? So like they can have people can have like, um, like an affelactic reaction to these drugs, right? In fact, I'll tell you this. Usually if a person is placed on this, these are Uricase analogs. Usually it's like IV therapy.

You get like, I don't know how often it is like once a week or once every two weeks or something like that. You want to track these people's are Uric acid levels because if the Uric acid levels are going down, then that's good. That means the drug is working. It's actively converting the Uric acid to a lantoin. But if a person is on piglotticase, raspberry case, and the Uric acid levels are rising, that's an ominous sign because it means that the Uric, the means that the piglotticase, raspberry case you're giving them is not having effect. And the reason is not having effect is that the person has potentially made antibodies against it, right? And if a person is making antibodies against these Uricase analogs, they potentially have an affilaxis in their future. So when you see that, you want to go ahead and stop the infusion, stop the drug so that you don't get into trouble. And another thing is these, these, these drugs, so right, I said that, oh, the Uric acid analogs, so they help you convert Uric acid to a lantoin. The thing is, as you're going from Uric acid to a lantoin, it's kind of like a reduction reaction. So in the process, you actually make hydrogen peroxide as a byproduct. Well, is there a particular enzyme deficiency that makes it hard for you to handle hydrogen peroxide? Think back to your step one exam. So this is G6 PD deficiency, right? So like glucose, six-force feed dehydrogenase deficiency.

So on exams, if a patient, especially like the telltale side of this on exam is like African American person with gout that you want to start on these Uricase analogs, you probably want to avoid them, okay? Or you want to test them for G6 PD deficiency first before starting, okay? Because these drugs are, again, they are for the most part contraindicated in patients that have a G6 PD deficiency. So, so the thing is, I mean, another common question is like, oh, how do I know when to start this chronic gout therapy? Pretty much if you have more than one gout attack a year, right? That's, that's, excuse me, that's pretty much a criteria. So if you have like two attacks in a year, you get started on these are chronic gout therapies. Or if you have like complications of gout, so like you're really having like chronic kidney disease, or you're already having like nephrolithiasis, so like kidney stones, or you're already having like two fine, okay? And then, on those circumstances, go ahead and study these people on a, on a chronic gout therapy. And the thing is when you start gout therapy, you actually in addition to like giving the alopeia in, for example, you actually want to add like, like, kochisin, or like an n-set alongside for like a couple of months, actually, after you start, so that you don't get flares in the internal, okay? So you can start them on like kochisin at the same time or n-set at the same time, or like low dose, like oral steroids, okay?

You basically continue these agents for usually it's about like six months. After you've kind of like hit your like target uric level, right? So like you're less than six milligrams per deciliter or less than five milligrams per deciliter if you, if you have a two fine. So you continue for like a pretty long time, usually a couple of months before you stop and then just keep them on the alopeia. So I think that's where I'm going to stop, but I think before I round up, since we've been talking about like HLAB, something HLAB, whatever, let me just mention some high-yield ones that tend to pop up quite commonly on exams, right? So HLAB 27, right? You already know if you see that, you're thinking about your seronegative, uh, spondylothropathesis, right? Um, is there a particular HIV drug that you need to test for certain HLA before you start? I hope you're thinking about a back-a-veer, okay? Before you start a person on a back-a-veer, you better check for HLAB 57, okay? Because people that have HLAB 57, they are pretty supposed to have in like a life-threatening hypersensitivity reaction to a back-a-veer. Now, what's the HLAB that's a social-bechette disease? That's HLAB 51, okay? And then there's this one that's like super, super low-yield, but it tends to affect mostly like Asians, but, and I mean it's super rare, but it's something that may just pop up out of the blue on a test.

If a person has like HLAB 58, if you want to be a little more specific like HLAB 58, 0, 1, these people actually predispose to having like a life-threatening hypersensitivity reaction to alopurino, okay? So for these people, um, and again, it will be an Asian on your test. So like an Asian sort of kind of keep all like some like Korean person, like Korean or like Chinese. Keep that at the back of your mind before you start in alopurino. But again, it's super rare. It may, you may never see it in the real world like ever, but it's something that may shop on a test, okay? So definitely keep this at the back of your mind. And again, as I do whenever I round up, um, just want to throw it out there that I do offer one on one tutoring for many exams, right? So like the USML is step one exam, step two CK, step two CS, step three, the medicine training exam, the EBI and board exam. And you may say like, oh, divine, but you're going to be all, how do you tutor for the EBI exam? If you're interested in the story behind that, just send me a message and I can give you some more details. Um, and then also if you have like an acquaintance that it's in, uh, undergrad and need student for like organic chemistry, general chemistry, physics, biochemistry, physiology, histology, I have a tutor in for all those things.

And then if you're a met student applying to residency, so like an era's application or a college student applying to Met School, so an AMCA's application, I do offer like one on one consulting for those things again, like application prep, interview prep, personal statements, mock interview, stuff like that. Um, pretty much everyone I've worked with has matched most of them at their first choice. So, uh, take that for what you will. So, um, I hope you find this podcast to be helpful. I know it was kind of long when I promise you this stuff I discussed today, super, super high yield for the three exams that I just mentioned. So I wish you a wonderful day. Um, but to go on a quick soap box, I am glad that, um, the raptors are doing a great job. My, my main guy, a co-I Leonard is a silence in, uh, Gordon state. Um, I just feel like Gordon state, uh, a little humility will probably go a long way, uh, with some of your players. So, uh, hopefully we seal the deal on Monday and, uh, the raptors, uh, get their first, uh, MBA finals, uh, championship. So I'll see you in the next podcast. Have a wonderful night rest, sleep well and God bless you. Thank you.

PsA (Psoriatic), AS (Ankylosing), IBD-associated arthritis, RA (Reactive).

Can see (conjunctivitis), can pee (sterile urethritis), and can't climb a tree (arthritis).

HLA-B27.

AS/IBD tends to have symmetric axial/sacroiliac involvement; PsA/RA tend to have asymmetric peripheral joint involvement.

Needle-shaped, negatively birefringent monosodium urate crystals.

None (NSAI Ds/MTX are generally safe; the key warning is not to use DMAR Ds for axial involvement, as they are ineffective).

Multiple bridging osteophytes joining multiple vertebral bodies, in the absence of sacroiliitis.

The axial skeleton.

Anterior uveitis (not posterior).

HLA-B*57.

Perforated neutrophils releasing inflammatory contents upon crystal recognition, leading to massive inflammation around monosodium urate crystals.

Metabolic syndrome/obesity; chronic diuretic use (especially thiazides); low-dose aspirin use.

Below 6 mg/dL, or ideally below 5 mg/dL if the patient has tophaceous disease.

Uricase analogs (e.g., Pegloticase).

The axial skeleton.

Anterior uveitis (not posterior).

HLA-B*57.

Perforated neutrophils releasing inflammatory contents upon crystal recognition, leading to massive inflammation around monosodium urate crystals.

Metabolic syndrome/obesity; chronic diuretic use (especially thiazides); low-dose aspirin use.

Below 6 mg/dL, or ideally below 5 mg/dL if the patient has tophaceous disease.

Uricase analogs (e.g., Pegloticase).