DIP Episode 99 - USMLE Step 1 Rheumatology Review (Part 1)

Okay, welcome. My name is Divine. I am a PGY1 transitional year resident that's going into a biology. This will be the 99th episode of the Divine Intervention Podcasts. And in this podcast, I'll be studying the USML review of of rheumatology. This will probably be a two-part podcast and we'll be done with that. Again, I apologize. You've probably not seen podcasts for me in a while. I've just been on my 10th ICO rotation that kind of makes it difficult because it's the intensive care unit. It's called intensive care unit for a reason. But without much ado, let's go ahead and jump into it. So what if you get a question about a patient that has, let's assume they have a recent history of like a gastric cancer. And then they tell you that this patient is now having like a muscle weakness. She has like difficulty rising from a chair. And they tell you that it's mostly the proximal muscles that are weak on both upper extremities. And then let's say you do some studies and the serum creating kinase is like, I don't know, like a thousand, right? And then they tell you that the patient has like this weird rash on their fingers and rash like on their trunk. What disease are you thinking about? I really hope you're thinking about dermatomyositis. So if you notice in this case scenario, it just brought up, right? This patient has like some kind of visceral malignancy, right? In this case, a gastric cancer.

It could be any other kind of visceral cancer like it could be like a cancer of the bladder or whatever, right? Some G-U cancer, or like cancer of the colon or like lung cancer. People that have those cancers, they can actually have a dermatomyositis. So they're showing up as a perneoplastic phenomenon. Polymyositis, little less so, but polymyositis can also show up as a perneoplastic phenomenon, usually like in the realm of lung cancer. But really any kind of like visceral malignancy like lung cancer and stuff like that can present as perneoplastic phenomena in the setting of basically like with polymyositis or dermatomyositis, right? And really the hallmarks of these diseases, these two diseases, right? Basically that the person has proximal muscle weakness, okay? So like your shoulder girdles, so your limb girdles, a week, right? So like your shoulders. So the person may have like difficulty rising from a chair, difficulty coming their hair, stuff like that, things that you require your proximal muscles for, okay? And there's two types of those problems, right? So there's polymyositis, dermat, there's dermatomyositis. The key thing, right? dermatomyositis has derm in the name. So that already tells you right off the bat that it's a disease that should affect the skin in addition to affecting your muscles, right? So and again, because it's a noteworthy problem, shows up in women, more than men. That's kind of like the way to remember that. And again, right?

So dermatomyositis also affects the skin addition to the muscle polymer ositis. It's just muscle problems. There is no skin involved. And really one high-yielding, you kind of want to keep at the back of your mind is, right before, right? You'll say that you need to do a muscle biopsy to make the diagnosis of polyodermatomyositis. That's no longer true. These these you can actually make the diagnosis of these disorders by doing an MRI. The MRI of the muscle is not diagnostic. Then you can go ahead and pursue a muscle biopsy, right? So I say that really the key differentiating thing here is like if you see skin problems, think about dermatomyositis. And the skin problems, right? You can have like a rash on the on like the knuckles, right? That's what's known as the classic gotrons papillons. So you can basically see like it's kind of like a rash, like you can look up pictures of this online. But like a rash on like your PI Ps, your DI Ps, your MCP stuff like that. Think about dermatomyositis with that, right? And then, right? Heliotroporusher. That's another classic association where you see like redness or like blue around the person's eyes. That's one of the things you can see classically in patients with a dermatomyositis, right? Sometimes they can actually also have like lesions on their on their nose, right? So I know that in in lupus, right? You guys have probably learned that, oh, lupus can cause a Miller rash that spares the nisolibial folds.

Believe it or not on NBM Es, they have actually been no locationally to present dermatomyositis questions as a patient that has a Miller rash. But the key thing here is that the Miller rash in in dermatopolymiositis does not spare the nisolibial folds. That's actually a very high-yoda differentiating factor. You want to keep at the back of your mind, for example, right? And then other kind of like key things to keep in mind, right? So you see the, you can see like the shell sign. Basically, you can have like a like a red discoloration of your skin either like in front of your body or the back. If it's at the back, that's where you wear a shot, right? So it's called a shell sign. If it's in front, that's like the V-neck sign, stuff like that. And again, like I said, right? You do a muscle MRI. MRI can make the diagnosis pretty well. But you can also do a muscle biopsy. But that muscle biopsy, you do it when the results of the muscle MRI are equivocal. And there are certain things I kind of want you to keep at the back of your mind in terms of the histologic findings. The thing is, these histologic findings, they are tested very classically on the USML step one, right? So the thing is in dermatomyocytes versus polymyocytes, you need to know the kinds of cells that mediate the damage. And the easy way to remember that is that dermatomyocytes starts with a D, polymyocytes starts with starts with a P, right? And D comes before P in the alphabet.

So that means CD4 cells, cells with a lower number can cause the symptoms in dermatomyocytes versus CD8 cells, cells with a higher number that cause the symptoms and polymyocytes, right? So you basically have like CD4 positive T cells in dermatomyocytes, right? Remember, those are like the one of the sources of your helper T cells. So you can already envisage that this will be some kind of antibody problem, right? So your antibody is basically like Nucleoblod vessels. So you may see like blood, and these are like blood vessels that you find in the connective tissue around muscle, right? So the classic buzzword, you won't remember for the USML exam, says something called like perimiceal, perimiceal or like perifacicular inflammation. If you see that, you can pretty much stop reading the question, that's a dermatomyocytes. Contrast that with polymyocytes where it CD8 positive T cells that mediate the damage, but they actually attack the muscle directly, right? So selmedia that you're trying to attack the cell itself, not the connective tissue surrounding it. So if you attack the muscle itself, right? You get like inflammation of the muscle itself, right? So like the endomycem. So endomycyl inflammation think about polymyocytes, perimiceal inflammation, think about perimiceal or like perifacicular inflammation, think about your dermatomyocytes, right?

And again, because you have a strain muscle, anything that you find a ton in muscle will sort of spill into the circulation, right? So like you'll see kill be high, you're lactate, dehydrogenase, your LD to be high, all the leaves, all the leaves is an enzyme in glycolysis, right? Basically like many of those non-specific things, the big one you want to remember is like CK and the LDH and all the leaves. So the other is like basically anything that you find your muscle will be elevated, right? So those are not super-specific, super-specific for disease. Now, some things I guess I want you to also keep in mind for the USML Es and sorry with the arms and arms, right? Again, I have topics in my mind that I choose to discuss and then whenever I have free time, I just sort of sit down and just try to record stuff on my phone for memory. So you just kind of want to remember like the antibodies, right? So she did with polyandromatomyocytes, right? So for example, there's like the anti-SRP antibody. So like the anti-signal recognition particle antibody. I believe I may have talked about this in a prior podcast, probably like myself, physiology podcasts, where I talk about how remember, right? They're bound ribosomes, right? So ribosomes that are sort of like bound to like endoplasmic reticulum. So I guess in that case, you'll be the rough endoplasmic reticulum.

As those ribosomes are making proteins, those proteins, the sort of like the guide that sort of threads them into the endoplasmic reticulum is the signal recognition particle, right? So if you make auto antibodies against the signal recognition particle, that's one of the antibodies that's found in the myocities, if you, if there's such a term as that. And then there's like your anti-jou one antibody. It's like an antibody against a, it's a kind of TRN synthesis of remembering correctly, I mean, TRN synthetase. If I remember correctly, it's like a histidyl, TRN synthetase, right? Remember, you amino-acyl, TRN synthesis enzymes that help you basically co-join TRNA, right? I believe it's like the three prime end to, to the amino acid that you want to incorporate into the green or polypeptide, okay? So histidyl, TRN synthetase, if you make auto antibodies against that, those are the auto antibodies that are made in, that are made in, in, in the myocities, right? So that's the anti-jou one antibody. And then there's another one kind of weird, it's called like the anti-MI2. So anti like me, 20-body, it's just a non-antibody against like helicase, right? Remember, helicase, right? It's the thing that's, if you want to make DNA, you need to separate the double strand first, right? So to separate those double strands, you kind of need a, you need an enzyme to make that happen. And in this case, it's a helicase.

So if you make auto antibodies against helicase, those are the anti-MI2 antibodies that characterize, that also characterize polyendromato myocytes, right? And really like again, muscle MRI, you do the biosephids, if it's not very, if you're not getting like convincing results. And really for the most part, the way you treat polyendromato myocytes, you can just sort of treat with like steroids, right? You can give like all these immunosuppressants like your methyl trexate, remember methyl trexate, inhibits thyhydrofolid reductates, I've talked about that extensively in my biochem podcasts, or video, I guess. And you can also use pretty much like your immunosuppressant, any immunosuppressant therapy should be able to work pretty well for polyendromato myocytes. And personally, I think that's all I want to say about those conditions, pretty straightforward. Don't get any of those things wrong, I believe I've, unless if I'm sort of running through my mental game or whatever, I believe I've discussed pretty much everything you can see that is testable on those two topics. So let's sort of go ahead to the next topic, I have at the back of my mind. Let's see. So how do I present this to you? Okay, let's assume you get a question about a patient that says, Doc, it's kind of hard for me to true crackers anymore. And I always have like this feeling like there is sand in my eye.

If you see that, and let's say like you do a physical exam and they're, you sort of see the amount sort of swollen like they have mumps, what disease are you thinking about? And again, think this is a rheumatology podcast. So what do you think I'm going after here? Going after show green syndrome, right? Show green syndrome. Basically, the key thing you want to remember or show green syndrome is you essentially destroying glandular structures, okay? glandular structures, especially like the salivary glands and like the lacrimal glands, right? So if you destroy the lacrimal glands, you will make tears. So you have like that feeling like they're sending the eye. If you destroy your salivary glands, right? Those people can have like really bad dental care so they have trouble like swallowing stuff because they don't like, kind of like softening the foot enough with, with, with saliva. So the path, the thing is, unfortunately, many of these rheumatologic problems, no one really knows the path of face. But I mean from some of the diggers I've done, some people actually believe that what may trigger show green is that these people may actually have like some kind of like viral infection of, of like the salivary glands or like they're lacrimal glands. And then when do you have that viral infection? Some of those viral antigens or some antigens that are previously like hidden from your immune system become expressed.

And then when that happens, your body is like, oh, crap, let me go ahead and have t-cells that are sort of reactive against, I mean like you presents some of these antigens to t-cells and then your t-cells sort of go nuts and decide to react against these, these are glandular organs like your salivary or your lacrimal glands and then the person gets into trouble. One high-yield thing you actually kind of want to remember with that for show green is that it's actually a kind of a type four hypersensitivity reaction. That's something that actually shows up quite commonly on the exams. And again, it's an autoimmune disease so who should get it? So woman, right, very unlikely to be a man on an envy any. It's likely going to be a problem with a woman. And they're just certain, I guess Latin terms or Latin terms or whatever, but certain like terms you misuse you exempt, right? That's like the presentations, right? So I talked about like the dry eye, right? The boss freeze for that is, is a kerado conjunctivitis as Sika, right? And then I talked about the dry mouth. Sometimes you can see that it referred to as a stormy. The thing is, if you actually just have the dry mouth dry eyes and that's all you have, and you got nothing else, that's actually what's known as a Sika syndrome. But if you have the dry eyes, the dry mouth, and then you have joint pain, then that is what actually constitutes show green syndrome, okay?

So it's one of those rare things you want to keep at the back of your mind. And to be honest, I don't want to forget this, you just sort of popped into my mind right now. But don't forget that show green syndrome can be associated with with renal tuberculosis, okay? That's a very high yield renal association. So that's one thing you sort of want to keep at the back of your at the back of your mind. And really again, like every other autoimmune disease, you definitely want to know your auto antibodies, right? So remember your anti-SSA, those are like your anti-iron antibodies. And then you have like your anti-SSB, those are your anti-lach antibodies, right? They are basically antibodies against like some ribonial pleoprotines. Those are like the big ones you definitely want to remember. Although many people with show green have like their A and E is like positive, right? So remember, A and E is very sensitive for like lupus, but it's not specific for lupus, A and E is elevated in like many other things. So the anti-iron anti-lach, right? So those are things you kind of want to keep at the back of your mind. They are your anti-SSA, anti-SB antibodies. The key things you won't remember is that these antibodies, if a pregnant woman has them in high enough a tighter, those things can actually go ahead and cross the placenta and destroy the conducting system of the heart. So the kid can basically, the child of that mom can basically get like a third degree, right?

So like a complete heart block. So those kids can get a complete heart block, right? So that's one thing you want to keep at the back of your mind with that. And really you may ask, okay, so how do we treat type show greens, right? So you can actually treat show greens by remember, acetylcholine is the thin, I mean I've talked about this extensively multiple podcasts. Acetylcholine is the thin that stimulates your glands, right? So like your salivary glands, your lacrimal glands. So if you give a maceramic receptor agonist like pylocarpine, for example, that can help to increase secretions and that can decrease some of the symptoms that are found in show greens syndrome. So pylocarpine, there's another drug that's beginning to make it sweet to the MBM is known as a seven melons, like C-E-V-I-M-E-L-I-N-E. It's also a maceramic agonist that can be used to treat the symptoms of our show greens. And the thing you want to remember, I guess one thing, in fact it's probably the one of the most common, if not the most common cause of death in our patient with show greens is that they can, right? Remember if you take like a biopsy for example of the salivary glands, you see like a lot of like lymphocyte, like lymphoid follicles, those people wherever lymphocytes are rapidly proliferating, that can lead to a lymphoma, right? So like a marginal zone lymphoma is actually one of the most common causes of death in patients with a show greens syndrome.

So that's something you definitely want to keep at the back of your mind for exams. And one other thing you see on the exam is like, oh, how can you check to see if this person has like dry eyes? You can actually put like filter paper in their eyes. And then if the, if it doesn't get wet to a certain depth or whatever, you'll sort of like, that's almost like a screener for like lacrimogland dysfunctions, calling the Schirmer, there's like SCHIR-MER, like the Schirmer's test. It's a test for the diagnosis of of our show greens. And again, really if you take a biopsy of their glands, you'll see like a lot of lymphocytes and lymphoid follicles. So personally, I think that's all I'm going to say about about our show greens. And I'm going to kind of leave it at that. And I guess with that I can guess talk about some other topic. So let's see, how do I want to present this topic? Obviously, I don't want to tell you the topic without giving the clinical presentation first. Okay, so yeah, I think that's it for for Schirmer's. So what if you get a question about a 30 year old guy, presents with like, sodium onset, severe chest pain, like tear and chest pain, redempting to the back. And they tell you that this patient has a history of, let's see, low back pain, right? And like morning stiffness, that sort of gets better as they sort of go about their day. What are you thinking about? I really hope you're thinking about an kilosin spondylitis, right?

Ankilosin spondylitis is obviously one of your seronegative spondylathropathetes, right? And this question I just gave you sort of talks about some high old associations with an kilosin spondylitis. The thing is, angspond, one of its, I guess, extra joint manifestations are the present can have like inflammation of the order. So you can get like an eurtidase and it can ultimately end up causing like an euric regurgert, right? And you can get like heart failure from that. So they will get more of like a systolic heart failure because they are getting like volume overload in the heart. Another thing you want to keep in mind with an kilosin spondylitis is it's also associated with like inflammation of the uvea, right? So they can get like an anterior uveitis. They can even get like a kind of like restrictive lung disease because when they get like chai forces, right? Like fusion of the spine, like the bambu spine. And that can sort of prevent along from expandant appropriately, right? So they can have like a kind of restrictive lung disease. They'll have like the low lung volumes, but the DLCO for those people will actually be normal, right? So if you get like a restrictive pattern, right? So the FFV1 to FVC ratio is normal elevated, but the DLCO is normal. You want to think of some kind of like neuromuscular or like structural disease that's giving rise to that person's or restrictive physiology. Thank you, Lusin spondylitis could be one of them on an exam.

So again, if you notice from my podcast, it's not just about like take this concept, take this concept. At the end of the day, I sort of want you to understand how these things will be tested, right? And the thing is your friends at the NBME, their geniuses at integrating concepts together across multiple disciplines. That's kind of like the best way to learn in the first place. So that's an Kilosin spondylitis, right? And again, classic presentation, low back pain, because you tend to have like involvement of the secret iliac joints, right? So secret lightest, once you see that word on an NBM exam, it can pretty much stop reading the question. They are basically talking about an Kilosin spondylitis. And Kilosin spondylitis, we're not sure if in a guy that's in his 60s on an NBME, if you see it present that, or there's not an Kilosin spondylitis, it's like a young man's problem, right? So it's like a guy in his 20s, 30s, right? So they're having like the low back pain. With that thing more about them, and Kilosin, a spondylitis. And the thing is, there are just some buzz phrases you want to be able to remember with angospond. And one of them is like the term synovitis. It's basically like an inflammation of the joint, right? Like your synovium is one of the epithelium that basically produces like things that nourish your joints, right? So you can have like synovitis. Another term you mission on an NBM is like entercytis.

Basically whenever like like a ligament attaches to bone, you can actually have inflammation of that region, right? That's what's known as the entercytis. And then another thing you mission on an NBME is something called a syndesmophyte. Basically, it's again, it's right around like that tendon ligament area. And you begin to have like spinal fusion and all that crap happening. But just sort of keep that at the back of it. Keep these buzz words like entercytis, synovitis, endesmophytes. Keep them at the back of your mind when you're talking about angospondylitis. And classically, right? These patients on NBME is like a bamboo spine. That's part of what like restricts causes like restrictive problems with their with their lungs. And one thing I guess I want to mention that you want to keep in mind, but this is more for step two CK. But it may be one of those like 270 sort of questions on step one. If a person has a history of angulosine spondylitis and let's say they want to start participating in sports or they want to get like some kind of surgery where you need to manipulate their necks. And then the NBME says what is the next best step in management? For those people, you want to go ahead and get a lateral neck x-ray, okay? The reason you want to do that is you want to roll out atlantoaxial instability.

It's actually a phenomenon that has been described in patients that have a history of angulosine spondylitis because you don't want to have like spinal injury and then they become permanently quadriplegic if you over manipulate their cervical spine. So those people, you need to go ahead and perform a lateral neck x-ray, roll out atlantoaxial instability. To other classic patient populations where this similar concept is tested is like Down syndrome, right? So Down syndrome before the step participating in sports, again, roll out A in stability. Another classic presentation is patients with rheumatoid arthritis, right? Those people are also at high risk for atlantoaxial instability. So that's something I want to keep at the back of your mind for the USMLE exams. And personally, to be honest, I think that's all I'm going to say about angulosine spondylitis. Again, it's a seronegative spondylopathy. So obviously those people will be HLB27 positive. Rheumatoid factor will obviously be negative for these people. And really, angulosine spondylitis is people tend to have like a mom-old life expectancy. It's not like they die earlier, like somewhere at crop. No, they actually have pretty young, but they, I mean, live to be pretty old, but they can just have like joint problems and like they may be bedbound at some point, but they actually live pretty young. I mean, pretty, they live pretty long. It doesn't like reduce their life expectancy.

They live as, especially if they treated, they live about as long as the next man is standing next to them. And really the treatment is you can give like indomethasine, like any insect, ketoro lock, whatever. If that's not cutting it, then you can go for like the big guns, right? Like your TNF inhibitors, like your adalimium app, infleximab, etanerset, that's more of the decoy receptor. Although remember, before you start these drugs, right? You want to go ahead and check those people for like TB. And you also want to check them for hip B, right? Again, you want to check for these bugs before you start treating these people. So they don't get issues and like die or something. And then you, all the seronegative are spondylathropathes, right? So don't forget your, there's a psoriatic arthritis, right? So obviously this will be found in a person that has a psoriasis. Remember psoriasis classically presents as like the like the rash on the extensor surfaces with a silvery scale. These people, for the most part, they tend to get a lot of like finger problems on NV Mes, right? So they can have pitting of their nails. I would encourage you to look up an x-ray picture of this, the pencil and cup deformity, where basically like their middle phalanx, sort of like jabs into the DIP of the approximate phalanx. That's what sort of produces the pencil and cup deformity. They may have like the sausage shaped fingers, right?

Like the mechanics hands, those are all classic presentations of psoriatic arthritis. You want to keep at the back of your mind for NV Mes. And again, same treatment as ankylosein spondylitis, you give in seds, you give like your methotrexid, whatever, and that sort of helps with the, helps with the disease. And then there's your reactive arthritis. I believe back in the day, it was called like Rider syndrome. Basically, what do I want to go ahead and say here? The thing you want to keep in mind is these people, they have reactive arthritis, right? So reactive arthritis means that they're having a reaction to something that happened earlier, right? So the thing that usually happens earlier is either like a GI infection or some kind of sexual infection, right? Sorry, I shouldn't use the word sexual infection. SDI, sexually transmitted infection. The sexually transmitted infection is usually from like Clamedia on NV Me exams. So that's the one I will keep at the back of my mind. I really would not think about gonorrhea. Gonorrhea is very unusual as a cause of reactive arthritis. Okay, think more about Clamedia. Another one that me show up is this bug that produces a UR Is. You're a plasma, you're a liturant. That's another one that shows up on NV Me exams. So think about like the ST Is and think about the GI infections.

And in terms of GI infections, the easy way to remember the bugs that are associated with like GI infections that may ultimately lead to like a reactive arthritis is something called basically the, the GI bugs that cause bloodied diarrhea, right? So like salmonella or like Campilo Bacter di Junai. Remember that is also associated with Guillembrace syndrome, Shigella, right? Remember Shigella can cause bloodied diarrhea and also like your senior that then that classically causes like the sudu up in the side is. And if you see those things, you really want to think about about reactive arthritis. Sorry, I'm just drinking some water. So you see those things, think about a reactive arthritis with that on NV Me. And really the only time you give antibiotics to these patients is if they have like you like actually like detect infection, then you can treat them. But if not, you don't necessarily need to you don't necessarily need to treat these people. You can like give them and say just like again, you do for any other seronegative and spondylothropathy. I mean the inflammatory disease has a third-edithritis. There's really not much to see there. You just have inflammatory bowel disease. So you don't have Crohn's or you have, I don't know what's it called, or three of colitis and then get arthritis. But let me say a few more things about this reactive arthritis, right?

So some of you, I mean probably from your preclinical studies, you probably heard of this nomonic where they say, oh, can see, can pee, can't, can't climb a tree, right? So can see is these people tend to get like a conjunctivitis, right? The can pee, they tend to get like urinary issue, like inflammation of the urethra. So they get like a urethritis and then they give you arthritis, they are thritis, right? So that means they cannot climb a tree. And some other things they may have. So they may use these words to bamboozle you on NV Me exams. But basically some people with a reactive arthritis, they can actually on their penis, you might really see things that kind of look like ulcers, they kind of like round, they sort of look like tinia, it's like tinia of the penis. If you see that, it's like red, it's like like playing the middle, but it's like a ring. Think about something known as a sercinator balamitis, okay? It's kind of like an inflammation around the penis. If you see that, or if they give you like a penis picture in your NV Me exam, you see like round things, just and the person has like joint pain, you can pretty more stop reading the question. That's a that's a sercinator balamitis, that's a reactive arthritis. Another thing you may see on an NV Me exam is, they may show you like something like on the, it's like a almost like a lesion on the palms and soles. It kind of looks like, I was just in the, it looks like HIV, HHVH, right? So like the cuposes, whatever.

It kind of looks like that. I will encourage you to look up pictures of this, but it's something known as a carotiderma, blanoragica. It's like a, like just red, like they're just like tiny lesions, they're like kind of like raised, they kind of look like blue red. You find them on the palms and soles. That's a big thing you want to remember. That's also pathonomonic for, for a reactive arthritis on NV Me's. So those are the things I would strongly recommend, remembering about the seronegative and spondylathropathes. And again, don't forget the HLEB27 positive for the aromatheroid factor negative. And personally, I think that is all I'm going to say about these seronegative spondylothropathes. Now, one other thing I want to talk about. So what if you get a question about a patient that, you know, let's say they're 21 years old, and they tell you that they have like very severe joint pain and they tell you that they sort of started in their elbows. And then today it has sort of moved to their knees and then it has moved to their foot. And then they show you a picture of their skin and they have like postions or they have like a pepper on their skin. What are you thinking about under those circumstances? I really, really hope you're thinking about like a gonococcal arthritis, right? Remember my seronegorea, it's a remnegative and diplococcus. It tends to show up as a migratory polyathritis, right? So migratory, it sort of jumps from one area to the other, right?

From one joint to the next. And then if you have like pinning the fingers, that's what's known as like a tenocinovitis. So if you see arthritis, no skin findings, the first thing that should come to your mind on NBME exams is gonococcal arthritis, especially in a young person, not a young person. All people don't do risky things on NBM Es. It's young people that do risky stuff on NBM Es. If you see those things, you really want to think about them, about gonococcal arthritis, right? And really the way you treat it is, you can go ahead and give like sef-traxone. Remember sef-traxone is a third generation of sefinal spore. Although you want to avoid a sef-traxone in like neonates, right? Because that can cause like hepatic acolystasis, which is not an ideal outcome for those kids. And also don't forget, I mean, I've mentioned this in many, many podcasts, right? But if you have like a terminal complement component deficiency, so like from C5 to C9, that also increases your risk of recurring glycerial infections, right? And then I also mentioned this case scenario where if a person is on aculesumab, right? Remember aculesumab is one of those treatments for paroxysmal and nocturnal hemoglobinuria. If a person is on aculesumab, that aculesumab is a C5 inhibitor, it's a monoclonal antibody against C5. You're basically using pharmacology to induce a terminal complement component deficiency. And that can also again increase your risk of recurring glycerial infections.

Although there is no vaccine against glyceric gonorrhea, unlike a glyceric aminegitis. But if a person has arthritis, right? Like an infectious arthritis, and they don't give you like those specific scenarios. You want to think more about stuff for you as the bug that may be causing it. And I mean, you hopefully know the bugs that all the drugs that cover stuff, right? Especially like mercer, like vancomycin, daptomycin, linesolate, clendomycin, doxiacycline, right? Your tigiacycline, right? Those are like your advanced tetracycline, those are all cover mercer. Your strep species, right? They can actually also cause like an infectious arthritis. But they tend to be less common on an endgame, is I'll say like really think more about stuff for you. And I mean, don't forget your Lyme disease, right? Your Lyme disease can cause like a chronic arthritis. The thing is, just go ahead and tell you this. If you see a person that has a thritis and has been going on for a long time and it's a multiple joints, think more about Lyme disease versus if you see a person suffering from arthritis in one joint and you're thinking about infectious arthritis, think more about like gonorrhea or like stuff or else. But if you see like multiple joints involved, right? So like a chronic poly, so not mono, poly arthritis, you really want to think about Lyme disease on NVME exams. And then don't forget, right? That Lyme disease is caused by Boralia Bocdo for remembering to spirochete, right?

Those are just those weird annoying things you want to know for NVM Es. So it's like a spirochete. And remember, it's carried by the x-adestic, right? So that's a classic thing that shows up on exams. And the thing is, don't forget TB, right? I'm POTS disease. Remember TB can cause an infection of vertebral bodies. That's what's known as POTS disease. If you do like a joint tap of whatever, right? You see like the acid faster, the acid faster organisms. So personally, I think that's what I'm going to say about the infectious arthritis. Yeah, I think those are the big things there. And I guess I can talk about joint findings, right? So just some key things you want to keep at the back of your mind. If a person has like a red, painful tender joint, blah, blah, blah, and it's like you're on set on an NVME, you want to tap the joint, right? So the boss phrase you're looking for in an exam as your next step in diagnosis is an atheroscent thesis. Now, if the white count from that joint fluid, or from the joint aspect is less than 2000, you can pretty much stop reading the question, that patient has also a thread. So it'll be an old person on an NVME, right? And then, if for example, you, you tap the joint and you see like a white congregate than 50,000, that's an infectious arthritis. That's a, that's a septic joint. That's a septic arthritis. All right, so you want to be thinking about your stuff, or yours, your nice cereal, going to rean all that crap.

But if it's in the tens of thousands, let's say like 10 to 30,000, you want to think more about some kind of inflammatory arthritis, especially if you see lymphocytes, right? So you want to think more about rheumatoid arthritis, or the crystalline arthritis, right? So like CPPD, or like GALT. Remember GALT is where you see the needle shaped negatively by refringent. Yeah, wait, yeah, needle shaped negatively by refringent crystals versus CPPD where it's like the positively by refringent rhomboid shaped crystals, okay? So those are kind of like ballpark numbers, they are not hard and fast, but they're ballpark and they're like almost like 99% accurate on NVME exams. So I'd keep those at the back of your mind if I were you. Now, let's see, because I also don't want this podcast to run for too long. Let's see, I'm trying to see if I should feed in this topic. You know what, let's go ahead and talk about a one more topic, why not? Might as well do it. Okay, so what if you get a question about a patient that is brought to the hospital because they have like, you know, like a severe headache and you measure the blood pressure and it's like 250 over 180, right? So it's like super crazy high. And you try to like obtain a physical exam on this patient. I noticed that this person's body basically has like no wrinkles, like their faces like very like straight, they can't smile nothing. What generalized rheumatologic disorder are you thinking about?

I really hope you think about scleroderma, right? Scleroderma. Remember that scleroderma, right? It can cause like a renal crisis because they can have like microvascular damage to like their kidneys and then they get into trouble, right? So like scleroderma renal crisis, it causes, it can cause like profound hypertension in these patients. So that's one thing you want to keep at the back of your mind and really the way you treat a scleroderma, renal problems is with like ACE inhibitors, okay? So that's one thing you kind of want to keep at the back of your mind because ACE inhibitors decrease intraglomerula hypertension so that you don't get like, I sort of talked about that, I believe in my renal, my renal video. So basically this question I just brought up right, it's about scleroderma. Scleroderma, right? The big things you want to know are like the two major types, right? So there's like the limited scleroderma. In fact, people prefer to call it like unlimited systemic sclerosis and then there's the diffuse scleroderma which is the one that's like super bad. Just like the diffusers scleroderma, the diffuser systemic sclerosis.

Now in terms of pathophysiology again, like most rheumatologic disease, no one really knows the pathophys, but the thing is at least from the papers and stuff I've read, if you want like the cleaves notes version, basically what the people think the pathophysiology represents is that you essentially have exposure to like some weird unknown antigen and when you're exposed to that weird unknown antigen, your immune system sort of says, hmm, okay, let's go ahead and have some of ourselves like lymphocytes for example, begin to make certain cytokines like TGF beta. That TGF beta, one of the evil things it does is that it tells fibroblasts to go make collagen and as you tell your fibroblasts to go make collagen, well, badness happens. They begin to like deposit collagen like in your lungs, in your skin, in your syphagylamus cells, right? So if you deposit like fibro collagen in your lungs, right? You can get like in testicio-long disease. If you deposit that in your skin, you can get like the sclerodactyl right? If you deposit that in your like a syphagylamus cells, right? You can basically get like incompetence of the Lewis of a Joes finger. So you can basically get like really nasty like gird slash, I guess, baritone, syphagos with that. If you deposit those in your the collagen, like in your blood vessels, you can begin to have like ischemic events, right? So you can have like re-node phenomenon.

You can have, because really if you're you can have pulmonary hypertension, right? That's another thing that can arise. In fact, the most common cause of death is very high you to know the most common cause of death in patients that have that have scleroderma, especially like the diffuse scleroderma is actually like respiratory failure, because they get like just bad, bad, bad like pulmonary hypertension, like pulmonary fibrosis, right? So like in testicio-long disease from all that collagen deposition and then they die, right? So that's the most common cause of death. Very high you to know that, especially for step two and step three, in patients with with like diffuser systemic sclerosis, right? So those are the big things you kind of want to keep at the back of your mind with a scleroderma, right? But obviously that's not all you, unfortunately, you need to know for mbim exams, right? So the key things you want to keep in mind, you want to know your antibodies, right? So like the diffuser scleroderma, in fact let me talk about the easy one first, the limited scleroderma, also called limited systemic sclerosis. That one basically tends to affect three areas in the body. It affects the hands, it affects the forearm, so any part of your upper extremity that is distal to your elbow, so it affects the hands, the forearm and the face. Those are the three big areas it affects. And for the most part, that's all it affects.

So those people tend to have like you know pretty decent life expectancy. But by definition limited systemic sclerosis are like the limited scleroderma can also involve like visceral organs, but visceral organ involvement is usually like super super super super lead in disease. It's not something that sort of happens like early in disease. So that's one thing you want to keep at the back of your mind. And that's this limited scleroderma is the one that says really the crest syndrome, right? So like the calcium noces. So when you have like calcium deposits on the skin and then like the renown phenomenon where you get like visospasm, right, of your like your digital vessels, especially when you come out into like cold weather or whatever. And then you can also have something called so that's the hour they can have a suffigility, right? So that can cause like bird, that can cause parrots as suffigus. They can have like the sclerodactyl that's like the thick, like the thick, tot-tight skin, right? And then they can get like the lactic tissues, they can get like these riblovisals on their skin. But in addition to that, the limited scleroderma, right? The crest scleroderma is also associated with anti-scentromere antibodies. That's when you definitely want to remember. Now contrast this with like the diffuse scleroderma, right?

So the diffuse systemic sclerosis where these people tend to have like like they will have like involvement of like their skin, everything, but they can also get involvement of like their visceral organ, right? So they can have like involvement of the lungs, of the kidneys, of the heart. And these people tend to get like a rapidly like these people die relatively quickly, because those organs stop functioning, especially the lungs, right? They get pulmonary fibrosis, getting this shell on disease and then they're kind of screwed. And the key things you want to remember are the auto-antibodies, right? For like the systemic sclerosis, like the diffuse systemic sclerosis, so the diffuse scleroderma, that one is a serial like anti-SEL, 70 antibodies. So those are like antibodies against like two pysemeres, one. They also make antibodies against like RNA pull three, okay? Those are the big ones you want to keep at the back of your might. And again, like I said, pulmonary fibrosis, pulmonary hypertension, they can get those with scleroderma, especially like the systemic sclerosis. These people are right again if they fibrosis like their kidneys and like the vessels that feed their kidneys, they can get like a very bad like renal crisis that again you treat with an ACE inhibitor. On MBMI exams is very high you to know that. And some other things you also want to keep at the back of your mind with scleroderma is like the renalz phenomenon.

They can actually integrate this with pharmacology really nicely on the MBM Is because if you think about it, right? Like if a person has renalz phenomenon repeated this among across multiple podcasts, those people should not be giving drugs that can cause visospousen, right? Classic ones are like your drugs for migraines, like your sumatriptan, those people with a history of scleroderma should not get those drugs. Other drugs will also be your like ergot compound, right? Like your goddameans, like dihydro, goddameans, those like visospastic agents, you don't want to give those to people with renalz phenomena. And that also kind of explains why you can give like a dihydroperidine calcium channel blocker as treatment for renalz phenomena because it causes those agents to cause a visodilation. So those are things you all want to keep at the back of your mind with a scleroderma. I mean like scleroderma, these people can also get like like my absorption because again if you fibros, your GI tract bacterial be able to overgrow and that can begin to cause a lot of problems. Alternatively as well as you fibros, the blood vessels that feed your GI tract epithelial, right? You don't have like enough surface here for absorption of stuff so you can have like fat malabsorption. So those people can have like stiadoria and whatnot, right? So that's why patients with scleroderma can have like malabsorptiva symptoms. So I think that's all I really want to say with the scleroderma.

I think that's probably more than enough. I will pick up, I promise. Like I said, I will pick up from here in the next podcast. We'll keep talking about our rheumatology. And as I round up, as I always mentioned, I do offer one of one tier in for all the USMEL exams. Step one, two CK, two CSTEP three. And then also for like the pre-clinical exams you take in medical and the third year of exams. And then if you're a med student applying to residency, so like Amcass apps or I mean, ERAS apps and if you're college student applying to med school like Amcass apps, I do offer like one on one like consulting and whatnot for those, right? So like prep for interviews, clinical personal statements and applications. So basically like presenting you in the best possible lighting and application, I can help with those things. I mean, I've been on the admissions committee of a top two medical school for about a year. So I have a lot of experience of sifting through applications. Now, other things I also offer tutoring for like organic chemistry, biochem, physiology, astrology, or if you're preparing for like the internal medicine board exam, so the entry in the exam for internal medicine, I do offer one on one tutoring for those.

So yeah, so those are all the things I offer like I guess outside services, I guess if you can think of them as related to the podcast website, I'm really excited that I'll be getting to episode 100 at the next podcast and I will try to hopefully give that done a relatively soon. I just I'm just kind of sad with the slow pace of our podcast website because I've just not had the time. It's just been really hard, especially when I see it's just just terrible, terrible, terrible work life balance. So you just really don't have time to make as many podcasts because trust me like my brain is chock full of stuff, I want to make podcasts for, but just literally there's literally no time to make these podcasts. But hopefully as this IC rotation winds down, there'll be like a pretty good increase in the number of podcasts I make. So I wish you all the best. I really hope that someone other than the Gooding State Warriors wins the Western Conference this year, but I'll see you in the next podcast. Have a wonderful weekend and God bless you. Thank you.

Dermatomyositis involves skin findings (rash), while Polymyositis primarily affects only the muscles.

Gottron's papules (a rash over the MCP/PIP joints).

Anti-Ro (anti-SSA) and Anti-La (anti-SSB).

Sjogren's Syndrome.

Respiratory failure due to pulmonary fibrosis/pulmonary hypertension.

Gonococcal Arthritis (or other septic/infectious arthritides).

Nail pitting, "pencil and cup" deformity, and sausage-shaped fingers (dactylitis).

Anti-Mi-2 antibodies.

Perifascicular or perimysial inflammation (connective tissue surrounding muscle).

Anti-centromere antibodies.

White blood cell count between 10,000–30,000 cells/mm³ (with lymphocytes).

Atlantoaxial instability.

Clostridium difficile (C. diff) and Shigella.

ACE inhibitors (Angiotensin-Converting Enzyme Inhibitors).

Anti-Mi-2 antibodies.

Perifascicular or perimysial inflammation (connective tissue surrounding muscle).

Anti-centromere antibodies.

White blood cell count between 10,000–30,000 cells/mm³ (with lymphocytes).

Atlantoaxial instability.

Clostridium difficile (C. diff) and Shigella.

ACE inhibitors (Angiotensin-Converting Enzyme Inhibitors).