DIP Episode 108 - ABIM/Medicine ITE/USMLE Step 3 Review Series 7 (Rheumatology 1)

Okay, good evening. My name is divine. I am a PGY1 transitional year resident. Now it's ultimately going to be going into radiology. This is episode 108 of the Divine Intervention podcast. And into this podcast episode, I will be continuing our review for the ABIM exam, so the medicine board exam. Again, like I said, like I said on my website, these are also useful for like the medicine-entraining exam that you take every year as an internal medicine resident. And also the USML is step three exam, because the USML is step three exam tends to test a lot of internal medicine concepts. So this will be series seven with that, and today I'm going to be talking about rheumatology. So let's jump right into it. But the first thing I'll say, actually let me see a few quick things about rheumatology. So I'm going to talk to you on the exam. I would kind of highly encourage you to know the classic imaging findings of many of the diagnosis in rheumatology. The medicine board exam, they actually do love to test imaging quite a bit. They will make it like heart imaging. They will make it something that is very zero recognizable, but I'll encourage you to be able to sort of like recognize those things, right? And then another useful thing is just sort of paying attention to patterns, right? And that's one thing I'm going to try to do today. I'm going to establish like pretty classic patterns of many of the rheumatological diseases.

And again, this will be a series I will make more rheumatology podcast that you to this exam. Again, I want this to be something you can just listen to on your week home from work or something like that. And one thing I'll say is some people have actually many people have asked me to try to put this podcast on an Apple podcast. And I promise I have tried multiple times. I don't know, I just keep getting into an air like getting like an error message. It just never seems to go through. I don't know if it's something with the website or what, but I promise I will keep trying, I will keep trying my best to figure it out. It's probably especially after in 20 years, I'll probably try to devote a couple of hours and see how see how things go. Okay. So, right? So the one of the main diagnoses you want to be able to make on your test with regards to rheumatology is arthritis, right? You know that there's rheumathyl, there's osteoarthritis, there's the spondyloarthropathies and what not, right? But the thing is when you're trying to make the diagnosis of arthritis, right? Usually it makes sense to try and ask yourself, is it an inflammatory arthritis or non-inflammatory arthritis? If it's not inflammatory, you're probably thinking more about like, oh, right? So like osteoarthritis, if it's more inflammatory, you're thinking more about rheumathyl arthritis, right? There's many other things that can cause those patterns, but those are the mainstream ones.

And I'll talk about the non-mainstream ones as we proceed, right? And then if a person has like a symmetric arthritis, right? You're probably thinking more about like rheumathyl arthritis, it tends to cause like symmetric joint involvement, like, oh, they will say like, oh, both of my hands hurt and stuff like that versus osteoarthritis that is more asymmetric, right? Or the spondyloarthritis, that the spondyloarthropathies those also tend to be asymmetric, right? And then I mean, if you check like the joint fluid, if the whitesand count is less than 2000, right? You know, you're thinking more about the non-inflammatory authorities, right? And usually the neutrophil, like, percent of that whitesand is usually less than 25%. So contrast that with like a septic arthritis where the whitesand is almost always graded and 50,000 on these tests. And the neutrophil percent is usually graded than 75%. Right? So that's something you want to keep at the back of your mind. So what if they give you a question about like a 65-year-old guy comes in and says, Doc, my legs have been hurting for the past six months, six months, and it's like both of my knees hurt, but my right knee hurts more than my left, right? And let's see this guy, his BMI is 36, right? If you see all those things, the guy is obese, he's having an asymmetric joint pain, right? And let's assume you do a physical exam, you don't see any redness or like soft tissue swelling or anything of that sort, right?

You can pretty much make the clinical diagnosis of osteoarthritis on the other circumstances, right? So what are the big things you see with osteoarthritis on exams, right? So again, like I said, they'll have asymmetric joint involvement. So it's not the entire joint that will be involved. It will be like one side of a joint that is involved, although obviously for a person has like late stage of osteoarthritis and they'll have like multiple, most of the joint involved. But I'll tell you this, usually on exams, let's say for example, if they have like inflammation in the knee, right? It usually, I mean not because it's a non-inflammatory arthritis, but if they have like knee involvement, for example, it will be like the medial side of the knee. So the insides of the knee that hurts the most, okay? It's not going to be the entire joint. And then the extremity involvement is again, usually symmetric, right? So let's say they may say, oh, both of my knees hurt, but one hurts more than the other. They tend to have like more symptoms than one joint compared to the contralateral joint and the other extremity, right? And then you want to know the classic things you find on imaging, right? So you'll find like the osteophytes, it's an osteophyte, it's almost like extra bone that you find within the joints, like around the joint. And then don't forget like your sclerosis, right?

So basically if you look around the articula cartilage part of the joint, if you see things becoming like white, if you see more white, it's just something that happens that's kind of like reactive remodeling because the articula cartilage is being like essentially worn down, right? And then you also can observe a sub-contral assists. So sub-contral means cartilage, right? So below the articula cartilage layer of the joint, if you look below, and you see like almost like punched out like black, right? So like more of you loosen parts below the articula cartilage, that's what's known as a sub-contral assist. And I mean, I believe the pathophysiology involves like some of the joint fluid, sort of hernating through the defects in the articula cartilage. And again, don't forget, if you tap that joint, the white count will be less than 2,000, the percent of the neutrophils will be less than, it will be less than 25 percent. And don't forget that these people, right? Again, because it's a non-inflammatory arthritis, they will tend to have, they will tend to have like a negative ESR, an ESR that would not be significantly elevated. So just something to keep at the back of your mind, right? And again, remember, because it's a non-inflammatory arthritis, these people would not have, they would not necessarily have joint stiffness. So if you have joint stiffness, it will be for less than an hour in the morning.

And then they will have like their joint pain, sort of getting worse, because right, as you bear more weight on the joint, it hurts more, right? So those are the big things you want to keep in mind. And then also don't forget kind of like the distribution of the arthritis, right? So the thing is, osteoarthritis tends to affect the DI Ps, so you're most distal, knuckles, right? So the knuckles that are closest to your nails, right? So they'll have, it affects like the DI Ps, it also affects like the first couple meter couple joint, right? So like the, almost like the base of your thumb towards the wrist, osteoarthritis, loss to, loss to, loss to affect that joint. And then it also affects the PI Ps, right? So sort of contrast that with like rheumatoarthritis that loss to affects like the wrist, the MC Ps, the PI Ps, right? Versus again, osteoarthritis that tends to torch your DI Ps, your first couple meter couple joint and your PI Ps. In fact, the most commonly affected joints in rheumatoarthritis, and I mean, in osteoarthritis, in the hand at the DI Ps, okay? At the DI Ps, that's actually very high you to know for example. And remember that thing I said that on imaging, you may find like extra bone, that extra bone usually kind of grows off to the side in the joints, that's what's known as an osteophyte. The thing is, when you have those osteophytes, right?

They can cause like soft tissue like impingement and they can sort of cause pain or they can sort of cause like deformities, right? That you can see on a physical exam, right? So those osteophytes, if you find them in the PI Ps, those are the things that are known as the bushards, notes. But if you find like these osteophytes in the DI Ps, those are the things that are known as the Herberdeens notes. So people are like, oh, divine, how do I remember that crap? Let me just tell you how, right? So your PI Ps, if you're just sort of going towards your nail, you'll have your PI Ps come first before your DI Ps, right? In the self-same way, B comes before H in the alphabet. So that's kind of like the way to remember the progression with that. And again, I already said, if osteophyte is affecting the knees, you hurt more on the inside, right? So it basically affects like the medial TBIO femoral compartment, right? And I guess there's this kind of osteophyte that me look like, he has like some similar findings to rheumatoid arthritis. It's called a Rousiv osteophyte. It almost always shows up, in fact, I'll tell you for all intents and purposes on any exam you take, it should show up in the hand. That's it. Show up in the hands for the most part, and it tends to affect women that are kind of like around a menopause. And most of the joints damage, it's usually like in the DI Ps, usually in the DI Ps. Again, so how do we treat osteophytes arthritis, right?

So you can tell your patients to lose weight, right? I mean, Beno Bis is actually like a big risk factor for osteophyte. If you lose weight, you can actually improve many of your many of your symptoms, right? And remember, don't sort of mix this up, right? So remember, obesity increases your risk of osteophyte. What obesity actually decreases your risk of osteoporosis, right? Because remember, when you weight beer, right? If you're obese, you're constantly weight beer. So that will make your bones even stronger, right? So that decreases your risk of osteoporosis, but it increases your risk of osteoporosis. So weight loss works pretty well in osteoporosis, but also don't forget, right? If you want to treat your classicly treat with like a sedaminofin, I will say in general, on an example, you should probably consider going with a sedaminofin first, instead of an insect. So a sedaminofin first, the instead of an insect, but if you don't see a sedaminofin as an answer choice, go ahead and choose an insect. Remember, a sedaminofin is not an insect, okay? A sedaminofin is not an insect. It works centrally. It is not an insect.

And then, if a person has like pretty severe osteoarthritic symptoms, and let's assume we have like a contraindication to take in insects, and it's just like one joint when they're where they're having a pretty severe symptoms, another acceptable thing you can do on the exam is to actually go ahead and inject corticosteroids into that joint, although that's usually like a rare scenario that presents on tests. Okay, so I think that's all I'm going to say about osteoarthritis, okay? So I think it's probably useful to maybe try and compare and contrast osteoarthritis as I discuss the rheumatoid arthritis, right? So I say that osteoarthritis tends to be asymmetric joint involvement. That's different in rheumatoid, in R.A. you have like symmetric involvement of the joint, right? So usually, like if you look at let's say like knee rheumatoid arthritis, both the medial side and the lateral side of the knee joint will be affected, okay? And remember that unlike osteoarthritis that tends to affect the PI Ps, the DI Ps, and the first CMC, rheumatoid arthritis tends to affect more of like the wrists, affects your MC Ps and your PI Ps, it does not affect the DI Ps for the most part on exams, right? And remember these people's joints will be like warm, you'll be red, unlike osteoarthritis where you have like stiffness less than an hour, right?

The stiffness is usually greater than an hour in a rheumatoid arthritis and unlike osteoarthritis where your symptoms sort of get worse as the day goes on because you're more weight bearing, rheumatoid arthritis as you sort of work out those joints, it actually gets better as the day proceeds. Being stationary makes your rheumatoid arthritis symptoms worse because by moving that extremity, you're sort of like shaking off the inflammation if you may, right? And the thing is on physical exam, there's some pretty classic things you can find in rheumatoid arthritis, right? So like one thing you can find is an honor deviation, right? So basically it's like the entire like hand is deviating towards the owner's side, right? Remember your owner's side is the pinky side of that extremity. So as you all hands are deviating towards the pinky side, that's what's called an honor deviation, right? And then the thing is all that inflammation in the joint can actually cause something known as joint subloxation, right? So it's like the joint sort of move in like weird directions, right? And that can create something that you've probably heard of, you've probably heard of the buttoinear deformity and the swan neck deformity, right? So let me just give you a quick clue here and this will make your life a profoundly easy.

So the thing is, I mean if you listen to one of my super early podcasts on like the central dog most study, always encourage people to try to learn the least amount of information, they'll enable them to control the most amount of knowledge, right? So you can see people they try to memorize every no-concrete of crap that's not a smart way to learn, right? You want to learn, learn like some small information that you can then build other information on from scratch, right? So for example, to remember like, oh what is swan neck, what is buttoinear? Literally all I remember is I just remember that like the term like S-F, right? So like S-F, like S-E-F, S-E-F, in that order. So the swan neck deformity, that's the S, right? Again, if you're going from proximal to distal, you go with your PIP first and then your DIP, right? So in your swan neck deformity, you have extension of your PIP and then you have flexion of your DIP. So flexion of your DIP means that like your last knuckle for your fingers, it is kind of pointing downwards, okay? So that joint, your DIP is held in flexion. So remember S-E-F swan neck deformity, extended PI Ps flexed DI Ps, that's all you need to remember. Then just remember that the other one is the other one, right? So buttoinear's deformity has to be the exact opposite. So like flexed PIP and an extended DIP, but again, you don't have to remember that. Just remember the S-E-F and you should be good to go.

And again, because it's an inflammatory arthritis, right? These people have soft tissue swelling and stuff like that. And the thing is osteo-romatoid arthritis, they love to test many high-yield scenarios with it, right? Many very great high-yield scenarios. So basically, I'm going to try to tell you like all the different ways they can test rheumatoid arthritis on your exam, right? So one way they can test rheumatoid arthritis on your exam is to tell you about a person that has had like long-standing rheumatoid arthritis and the person is going for like an elective, some kind of elective procedure, some kind of elective surgery. And then they ask like, what's your next best step in management? You definitely want to make sure that you get like x-rays of the neck, right? So like you want to get like a C-spine x-ray with like flexion and extension views. Because remember, rheumatoid arthritis has a strong association with something known as atlanto axial instability. Remember your atlas and your axis like C1, C2. With all the destruction that happens in rheumatoid arthritis, you can destroy. You can destroy that joint. And if you destroy that joint and let's say you go to surgery and anesthesia sort of manipulates your neck to intubate, you can basically disengage the presence head from the rest of the body, right? And you can essentially like severe the spinal cord. And I mean, that patient is likely going to die, right? So you don't want to do that.

So before if you're doing pre-ops as like an internal medicine resident, and a patient has like long-standing rheumatoid arthritis, you absolutely positively need to send them for a C-spine x-ray with flexion and extension of views. Very important to do that. And other people that can have atlanto axial instability just for purposes of test taking, people with Down syndrome, right? Keep that in the back of your mind. The classically they present that this will probably be more for step three. They will describe a person, has a history of Down syndrome, and the person is about to start participating in sports. You want to go ahead and get that C-spine x-ray that's with flexion and extension views. And then also don't forget stuff like patients with ankylose-inspondylitis, that's on the classic group of patients that can get atlanto axial instability. And then the fourth group that are tested on exams will be the patients that have a GIA. So Juvenile, Idiopathica, arthritis. So just keep those four patient populations at the back of your mind. Ankylose-inspondylitis, GIA, rheumatoid arthritis, long-standing, and come on divine think. Okay, let me reel them off again. Ankylose-inspondylitis, rheumatoid arthritis, GIA, and Down syndrome. Okay, those are the four patient populations that you sort of want to make sure you reel out atlantoaxing instability. And they test this all the time on the ABA exam. They tested a ton on the USMLA exam.

So it's just one of those high yield things you want to keep at the back of your mind. And if I remember incorrectly, they love to test that crop as well on the surgery on the surgery shelf exam. Okay, so that's one key thing you want to keep at the back of your mind, right? And remember, rheumatoid arthritis, right? Those people have chronic inflammation so they can have like a normal acidic, a normal chromic, normal chromica, anemia, right? So they'll have like anemia of chronic disease. Remember anemia of chronic disease, it's usually normal acidic on exams, but it could also be a macrositic, right? It could also be macrositic. But remember that in anemia of chronic disease, those people's fervent will be high, right? On like patients that have like macrositic anemia from iron deficiency, remember iron deficiency anemia is the most common cause of macrositic anemia. But if you have macrositic anemia and anemia of chronic disease on like iron deficiency anemia, where the fervent is low, and in anemia of chronic disease, the fervent is high. Okay? So that's one thing you want to keep at the back of your mind. Okay, and again, right? Obviously, they'll have like the high SRCRP because it's an inflammatory arthritis. They'll have like a white count in the, if you do like tap their joint fluids. So if you do an athrocentesis, the white count in that joint fluid will be more than 2000, right?

And remember, these people can have, there are some key antibodies you want to know, right? So don't forget your RF antibodies, right? So your rheumatoid factor, remember your rheumatoid factor is like an IgM antibody against the constant region of IgG. So it's an IgM antibody against the IgG, right? It's one of the antibodies you'll find in RA. And remember that it's sensitive for RA, right? It's not specific for RA. So just sort of keep that at the back of your mind. But the other classic antibody, right, is like the anti-CCP antibody. So like the anti-cyclic, citrally-nithid peptide, or polypeptide antibody, that's more specific for rheumatoid arthritis. And usually if you sort of combine like positive, our rheumatoid factor, positive CCP, the person has rheumatoid arthritis, end of story. You don't have to argue that any further. And again, your classic image in findings in rheumatoid arthritis, right? Don't forget your periodicula osteopenia, right? So again, periodicula, parachyminis around the articula part of the cartilage, right? So you look at the cartilage, right? And you see like black above and below the joint. So let's say you're looking at the knee right, is like, oh, like below the joint, you're seeing like a lot of black above the joint, a lot of black, right? So like more radio loosensy, that sort of gets you thinking about, come on, divine think, that's what you'll get you, gets you thinking about the parachycula osteopenia, right?

Remember, if you osteopenic, right, there's less calcium in that bone. So because there's less calcium, you have less x-ray attenuation, right? So your things are a little more radio loosens. And then don't forget, actually, you want to not forget your boss, this boss phrase, your marginal erosions, it's kind of like an animal came on like bits the side of the joint. The classic way you'll see it on image is, if you look at the sides of the joint, you see like, it's like a part of the joint is missing and it's kind of like missing like a curved fashion, that's what's referred to as a marginal erosion, right? And remember, rheumatoid arthritis, again, it can involve many other parts of the body, right? It can cause like intestinal lung disease, you can see people that they will have like pneumoconiosis in the setting of rheumatoid arthritis. I remember that's what's known as coupline syndrome, right? And it doesn't have to be a coworker's pneumoconiosis only. It can be any kind of pneumoconiosis. If you see that rheumatoid arthritis, that's a coupline syndrome. So the coupline, that's what I see. So kind of like the test prep company, but instead of a put a C for that, right? And then if they can give you a question about a patient, has rheumatoid arthritis and then they tell you that they have like a large spleen and then they give you like a low white blood cell count. You really want to think about something known as felty syndrome, under those circumstances, right?

So the way I remember the findings in felty syndrome is the mnemonic runs. So like R-A-N-S, the R-A stands for rheumatoid arthritis, obviously, and then the N stands for neutropenia, and then the S stands for spleenomegaly, right? And again, they won't give no sane question right? Or we'll say, oh, a patient with rheumatoid arthritis presents with neutropenia and spleenomegaly, no, no one is going to do that crap because that's what you're expecting. You're probably going to be in for a root-a-wikening among your ex-apps, right? They'll give you like labs, you'll see like a low white, and you're like, hmm, this person's white has like a thousand, right? And then they may describe like left upper quadrant fullness or something like that to tell you that is spleenomegaly, right? So they just basically use code words to describe the classic findings, and then you make the, you kind of make the diagnosis, right? So that's why I try to talk people through our exam scenarios whenever I'm making a, making these podcasts because at the end of the day, that's what ultimately counts, right? And remember rheumatoid arthritis can cause many other things, it can cause myocarditis, it can cause pleural effusions, it can be a presentation of carpal tonal syndrome. Remember anything that makes you a demeris, increases your risk of carpal tonal syndrome, right? So like rheumatoid arthritis being pregnant, right?

Those are all classics things that can increase your risk of a, of a carpal tonal syndrome. Also don't forget patients with rheumatoid arthritis, they actually have a pretty high risk of lymphoma. Lymphoma is actually a relatively common complication in people that have a rheumatoid arthritis. So it's just one of those weird questions I want to keep at the back of your mind that most people for some reason keep getting wrong. And also, right, again, you can get like, you can say like pleural effusions in patients with rheumatoid arthritis, right? So what are some high yield, or the high yield things as I begin to round up the podcast? Some high yield things about rheumatoid arthritis is the pharmacology, right? And this thing is incredibly frustrating for many people. The thing is rheumatoid arthritis from a ecology, I'll encourage you to learn it in the context of scenarios, okay? That is how they usually present these things on the exams, right? So let's sort of talk, sort of talk through those. Now, the thing is if a person has like, oh, like they're, they have like a cute like worsening of their symptoms, joints are hurting a ton, they're having significant symptoms, right? You can go ahead and give those people NSAI Ds, right? In the like in the acute phase, right? Just to sort of like calm down your symptoms, we'll remember NSAI Ds do not modify the disease course, right?

If a patient has rheumatoid arthritis and you want to go ahead and study them on a medication on your exam, go ahead and study them on methyl trexit, okay? Go ahead and study them on methyl trexit. Now, if methyl trexit doesn't work, those incontrolate symptoms appropriately, then just go ahead and move to like a biologic, right? And I'll talk about that in a bit. But so let's assume you start a patient on methyl trexit, right? And then they tell you that this patient over the last like week or two, they're having like this cough that is like non-productive, they're having fever, they're having shortness of breath, you probably want to go ahead and consider stopping the drug, right? Because remember, methyl trexit can cause like a kind of like hypersensitivity on immunitis, right? And remember that it can also subtle its hepato toxic, right? So you can raise your, can raise your LF Ts, remember? Methotrexit can actually cause intestinal long disease, right? So you can cause a pulmonary fibrosis, right? So if they give you a question about a patient, has a history of rheumatoid arthritis or studying on methyl trexit? And then they give you PF Ts and you see like the FVV1 to ABC ratio being normal or elevated, right? So like greater than 0.8 and they have like a reduced DLCL, right? Don't forget methyl trexit, long toxicity. Also don't forget your other drugs, right? That can cause pulmonary fibrosis, anitrofyrantoin, right? So microbit can cause a pulmonary fibrosis.

What's the name of this other drug that's an anti cancer agent? Blomising, Blomising can also cause pulmonary fibrosis. And then also don't forget a mutorin, remember a mutorin is a class 3. Anti-rhythmic, it's a potassium channel blocker. It also does have the ability to cause intestinal long disease. Okay, now what if they can give you a question about a patient that they give you labs and you're like, man, all this person's blood cell counts, like the white count everything is all low. And let's assume it's a person that's being treated for rheumatoid arthritis and then they have like some kind of like skin and soft tissue infection or UTI and you're giving them like trimethylprame, so-for-methoxazole for that. Remember that methotrexate inhibits the fully pathway, right? Well, TMPSMX also inhibits the fully pathway. For those of you that are taking step 3, remember that the TMP part trimethylprame inhibits dihydrofolio reductase, just like methotrexate. And then the SMX part, right? So the so-for-methoxazole inhibits dihydrofatory synthetase. So those both inhibit the fully pathway. So you can have like an additive effect, so you can get like a profound bone marrow suppression. If a patient is taking like methotrexate and another anti-foolite agent, right? So like trimethylprame, soft-for-methoxazole, a pure methamine even, right? Again, those things can all cause a profound bone marrow suppression, right? So how do you rescue the bone marrow under those circumstances?

I hope you're thinking about the full leneck acid analog, a look of worrying, right? It can basically like bypass the pathway and rescue the bone marrow under those circumstances. So again, don't forget that the treatxate can also raise your, it can also raise your LF Ts, right? And the thing is methotrexate is a teradogin. It is pregnant and she has run a third arthritis, bypass methotrexate, okay? bypass methotrexate. Basically, you cannot use methotrexate and you cannot use this other drug, Leflonomite. It's another demart. You cannot use those agents in the setting of pregnancy. Now, another demart that can be used on exempties is a soft-for-salicyme, right? Soft-for-salicyme actually works pretty well, but me, you can already begin to see the problems with it, right? It has a soft-for-in the name. Soft-for-salicyme has a soft-for-in the name, right? It can cause, it has an association like soft-for-alleges. So if they give you a question about a patient that you know has rheumatoid arthritis, you start a new medication, and then they have like a rash and their skin begins to like fall off and all that crap. Maybe think about Stephen's Johnson syndrome. So, fo-salicyme actually has that pretty, a pretty strong association there. And so, fo-salicyme is actually one of those demarts that are actually safe in pregnancy. I'll just tell you this. The two demarts that are safe in pregnancy that show up all the time on exams. So, fo-salicyme and hydroxychloroquine, okay?

So, fo-salicyme and hydroxychloroquine, the two demarts that are on safe in pregnancy are methotrexate and Leflonomite, okay? Leflonomite. So, other things to sort of kind of keep at the back of your mind, right? So, the thing is hydroxychloroquine, right? I mean, it's, for the most part on exams, you use it for lupus. It's actually one of those drugs that has been shown to decrease mortality. That's very high you to know. It has been shown to decrease mortality in the setting of lupus. You can also use it as a demart in the setting of rheumatoid arthritis. Most times you don't use hydroxychloroquine as monotherapy and you can, but most rheumatologists actually do something called a triple therapy where they give your combination of methotrexate, sulfacylizine and hydroxychloroquine, right? So, they give you those three drugs. Actually, combining those three drugs has actually been shown to be more effective than using either of those drugs individually as monotherapy or even as bi-therapy, okay? So, that triple therapy actually works. The triple therapy of methotrexate, sulfacylizine and hydroxychloroquine are being shown to work out pretty well better than those other agents by many studies. But what are some key things you want to remember with hydroxychloroquine, right? So, don't forget hydroxychloroquine. It can cause issues with the retina, right? It can cause retina, retina issues. That's like the big, big, big, big side effect. You want to remember your exam.

And it's again, it's also safe in pregnancy. And then, the flutomide, literally all I've not bothered about it if I were you is you cannot use it in pregnancy. It's a teradogen. But I know the series of drugs you want to keep in mind that your TNF inhibitors, right? Usually if your demyldosin work, you can, I mean if your methotrexate doesn't work, you can proceed to a TNF inhibitor, right? So, your TNF inhibitors like you infleximap, adalimiumap, golimiumap and all that crap, right? And then there's one that's known as a etanerset. Etanerset actually sort of deserves special mention because it presents with certain scenarios on the exam, right? So, like etanerset, remember it, yes, it has an association with a with a drug induced lupus, right? So, don't forget your classic anti-histona antibodies with that. And the way etanerset works is it's a TNF inhibitor, but it's actually not a monoclonal antibody. It's actually like a decoy TNF receptor. So, it's like kind of hangs around in the circulation, you know, moves around. And TNF is like, oh, look at my and then it binds to it, but it's a decoy receptor. So, it basically activates a TNF that way. Don't forget the actual drug induced lupus, but actually this is one of those weird points that people will see on the exam and they're like, huh? What am I supposed to do with this? You need to remember this, this is Florida high-yout 4, the ABI exam. Etanerset has less risk of infection compared to the other TNF inhibitors, right?

Remember, etanerset is like the decoy receptor most of pretty much every other TNF inhibitor is a monoclonal antibody, okay? Etanerset actually has less risk of infection because remember, these are essentially aminousin presence, right? Etanerset has less risk of infection compared to the monoclonal TNF inhibitors, okay? And other scenarios they can give you, right? So, what if they give you a question about a patient, you know, resistance decid treatment for, for rheumatoid arthritis and then they tell you that the person has like rapidly progressive weakness and you perform brain imaging and you see like extensive demyelination, what are you think? Old drug did they recently start, right? They just started on retoximab, right? Remember, retoximab has a stronger association with a progressive multi-focular lucansephalopathy, right? Although it's a very rare association, but it's just one of those annoying things that pops up on tests. Remember, right? That's from like reactivation of the GC virus. Another drug that classically on these exams that's associated with a PML, GC virus reactivation is this drug that's used for MS, not a LISU map, right? It's an alpha-point ingredient inhibitor. It's using a treatment of MS. It can basically also, it actually has that pretty strong association with a PML. Okay, and your TNF inhibitors, right? Obviously, before you start your TNF inhibitors, you want to make sure that you check for TB, right? Don't miss that question on the test.

It shows up way too often, right? So check, go ahead and check for TB. If the patient has latent TB, you actually have to treat that latent TB before you start a TNF, before you start a TNF inhibitor. And then, what if they give you a question about a patient, you know, there's been threaded for rheumatoid arthritis. He started on new drug and let's say he has a history of COPD and then his COPD symptoms get worse. What drug are you thinking about? I hope you're thinking about a bata sept. That's probably all you need to know about a bata sept. A bata sept, I believe it, like inhibits one of the genus kinases like Jaq 3 or something like that if I'm not mistaken. But basically, it can exacerbate a COPD. So that's probably the only thing you need to know, you need to know about it. I guess, I'm talking about Jaq. What is the hematologic issue that's associated with like Jaq's stat mutations? I hope you're thinking about your your polycythemia vera, right? Your polycythemia vera. Basically, those are myeloprolyphritiva issues like your polycythemia vera, your essential thromocythemia and crap like that. Those are all associated with like the Jaq commutations. There's just one of those things that again, I promise you shows up quite commonly on these examples. And then there's this drug that you may see on the test. It's called a Tousselizumab.

Literally, all you need to know about this is you probably want to get a lipid panel before you start the drug because from a this drug can actually like scrub your lipids, it can cause, it can like raise your LDL for example. So that's pretty much all you need kind of need to know about like the pharmacology associated with the rheumatoid arthritis. So I think I'm going to go ahead and stop here. As I always do before in every podcast, I do want to want you to learn for the USML Step 1, 2 CK, 2 CS, Step 3 exams. And then the ABIM board exam, I do tutor people for those, the medicine training exam, what else do I tutor? So, preclirical exams in med school, shelf exams, right? So like all the shelf exams. And then for college students, if you have a college student of Quintins that needs to learn in general chemistry or gynechemistry, biochemistry, physiology, physics, histology, I do offer one and one tutoring for all those subjects. And then if you're a med student applying to residency, so like an ERAS app or a college student applying to med school, so an AMCA app, I do offer consulting and like one-on-one application advising, right? So like personal statements, preparing for interviews, like mock interviews, putting the application together to make it top-notch. Those are things I always say, I've been on the admissions committee of a top-to-med school for a year, sifted through thousands of super high-quality applications.

So I know the things to kind of look out for that can make you stand out as an applicant. So if you need consulting with any of those things, feel free to reach out, either through the website, so you can send me an email at Divine Innovention, podcasts with an S.A.D. End at gmail.com. So, have a wonderful rest of the night. I am super happy that the raptors beat the warriors. I know I've probably completed a small army of enemies that are warriors fans, but I want someone else to win this year. So, have a good night, sleep well, and I will see you in our next episode. Thank you and God bless you.

DI Ps (distal interphalangeal joints), first CMC joint, and PI Ps (proximal interphalangeal joints).

OA has short-lived stiffness (< 1 hour); RA has prolonged stiffness (> 1 hour).

Boutonnière deformity (flexed PIP, extended DIP) and Swan neck deformity (extended PIP, flexed DIP).

RA, Ankylosing Spondylitis, Juvenile Idiopathic Arthritis (JIA), and Down syndrome.

Septic arthritis has a high WBC count (> 50,000) and neutrophil percentage (> 75%); OA has a low WBC count (< 2,000) and low neutrophil percentage (< 25%).

R-A-N-S (RA, Neutropenia, Splenomegaly).

Anti-CCP (anti-cyclic citrullinated peptide) antibody is more specific.

Marginal erosions and parahiapatellar osteopenia.

They usually grow off to the side of the joints (e.g., Bouchard's nodes at PI Ps; Heberden's nodes at DI Ps).

It inhibits dihydrofolate reductase.

Hydroxychloroquine and Sulfasalazine.

General risk of infection; Etanercept is associated with Drug-Induced Lupus (DIL).

Anti-CCP (anti-cyclic citrullinated peptide) antibody is more specific.

Marginal erosions and parahiapatellar osteopenia.

They usually grow off to the side of the joints (e.g., Bouchard's nodes at PI Ps; Heberden's nodes at DI Ps).

It inhibits dihydrofolate reductase.

Hydroxychloroquine and Sulfasalazine.

General risk of infection; Etanercept is associated with Drug-Induced Lupus (DIL).