DIP Episode 341 - Lupus and The USMLEs

Okay, welcome. My name is Divine. This is a piece of 341 of the Divine Intervention Podcasts. In this podcast I'm going to be talking about Lupus. Lupus and the USM Ls. For those of you who are very taking the USML exams, you know that Lupus is a very well-represented fixture. It's something that just loves, loves, loves, loves, loves to pop up on exams. So it's something that you absolutely sure know as much as this is humanly possible about. So that's why I decided to make a podcast that is entirely focused on Lupus. Now, for those of you that are studying for the USM Ls, step two, CK, or step three exams, or you know, complex level two or three, I do have a review course coming up in about two weeks. It starts with an MBA Me testicking strategy course that's taking place on the 4th of October from 2 to 4 3 PM, Pacific Standard Time. And then I have a review course that goes from the 5th to the 8th of October. It's from 10 AM to 4 PM Pacific Standard Time on all four of those days. Again, I've had tons of people attend these courses, I get emails all the time from people that have attended them and don't really well. And pass the exams, crush the exams, get like really high scores on the exams. So again, if you see that you're struggling with the material, you're struggling to raise your scores, I will strongly encourage you to join the course. So just shoot me an email through the website and I'll give you some more information. You're not going to be getting stock lectures.

You're going to be getting about 2,000 different concepts discussed by primarily by well clinical vignettes. Again, I've had many people attend these courses and do really well with them. Okay, so let's just jump right into it. So, so loopers, right? So we know that, you know, loopers is not great, right? It's not an ideal disease to have. And one of the reasons, in fact, let me tell you this, one thing that people, one nebulos section of the USM in the exams that people struggle to prepare for is the portion that's called multi-system processes and disorders. Right? Look at that term, multi-system processes and disorders. It's basically a part of the exam that focuses on disorders that have like multiple systemic manifestations, right? So loopers is a great, great, great, great, great disease for those kinds of problems, right? So because loopers caught across many body systems. It affects the lungs, it affects the skin, affects your joints, affects your hematologic system, affects your brain, affects just many, many different things, right? So that's just one of those big, high-yield things to keep in mind. That's why they love to test it on the exams, right? And again, remember, most times when you see a person that has, I'm going to basically try to cover loops from every possible angle in this podcast, although it should be a sharp podcast, right?

But the first thing I think I want to emphasize is that when you see loopers on an in-beam exam, it's likely going to be in a female, okay? So the thing is paying attention to demographics helps quite a bit on the USM Ls, right? So if you see a female having problems, right, you're probably thinking more loopers, right? It's very unusual for a guy to have loopers on a USML exam. And remember, most times, the people that have loopers on an in-beam exams tend to not be Caucasians, right, tend to not be white people, right? Tens of people that are like African-American, people that have black heritage, people that are Asian, right? Those are people that tend to have loopers. Loopers, again, is very uncommon in Caucasians. I'm not saying he cannot, right? So that's why you need to consider all the pieces of information given in the question. But loopers, classically, does not affect men, and classically does not affect Caucasians on the USML exams, right? And again, it's kind of important to remember that loopers has certain HLI associations, right? So like HLI A1, HLI DR3, right? Those are kind of like the classic ones. I'm saying that especially for those that are studying for the USM Ls step one exam that are listening to this podcast. Now, the big thing is in terms of loopers pathophysiology is just understanding, why do these people have these systemic problems? Well, they have these systemic problems for, I will say like one primary reason.

So ultimately, there's like two mechanisms that are on the LIE loopers and all the badness that happens, right? But I will say that one of the primary reasons behind the systemic effects, right, is from a type three hypersensitivity reaction. Basically, the thing that happens is that you're forming new complexes, right? So like, for example, many of us have heard of, oh, in loopers, there's like anti-double stranded DNA antibodies, right? So basically that the thing that happens is DNA, right? You make antibodies against it, right? Those are the anti-double stranded DNA antibodies, right? So DNA has antibodies made against it and then they pair up, right? And then when they pair up, they form an immune complex, right? It's an antigen antibody complex. And then they go and start the positive in different parts of the body. And as they deposit in those different parts of the body, they cause a lot of chaos, they cause a lot of inflammation, right? So that's why you see the symptoms are so disparate, right? Like, for example, those things can go to the joint because remember, antibodies, antibodies, especially like IgG and IgM have the ability to activate a complement. So the thing is, they just show up, right? In a part of the body, recruit complement there and just cause a lot of damage. That's why complement is typically low in many antecedents of loopers, right?

So say, for example, if a person has like the fused proliferative glomerulone arthritis, which is like the big NVME, rhino manifestation of loopers, those people will have low complement, right? Those people have low complement. That's actually a very high-yield thing to know, right? The mechanism behind that low complement is from the immune complex, the positive, right? So ultimately, you have a big decrement in your complement, your complement proteins. So those immune complexes, so those immune complexes, they can deposit in your joints, they can cause problems there, they can deposit on serosol surfaces, especially like the surface of like the plurra, right? They can cause like serositis, they can cause a pluritis, they can cause pleuricy, right? They can deposit on your pericardial wall, they can cause a pericarditis, right? They can deposit in the kidneys, they can cause like loopers on the phritis, right? Again, the reason you're hearing all these eyeglasses is because essentially the thing that happens is these things, they show up somewhere, the form of the immune complex cause a lot of complement, recruitment and that causes a lot of damage. But one special branch of loopers, I think I want you to know about are basically the side opinions that accompany loopers, right? So the thing is in loopers, in many cases, you do make autoantibodies against like elements of your hematologic system. So you can make autoantibodies against your red blood cells, right?

There'll be like an autoimmune, chimolytic anemia. Obviously the comstest should be positive in those people. You can make autoantibodies against plecut proteins like GP2 B3 A, that's going to give you immune thrombocytopenia, right? You can make antibodies against your white blood cells, right? You can have an autoimmune loopopenia, right? The thing is in these cases, because you are making autoantibodies against like fixed cells in the body, right? These are examples of type 2 hypersensitivity reactions. I'll say that again, these are examples of type 2 hypersensitivity reactions. So again, the primary pathogenesis behind disease and immune complexes, those are type 3 hypersensitivity reactions. But the side opinions that people getting loopers are actually examples of type 2 hypersensitivity reactions, right? So again, what are the classic findings in loopers on MBM exams? Again, these people have fever, they have a Miller-Rash, right? That's usually, they usually have a rash on their face, right? And obviously we all know the buzzword that you'll spare the nasolibial folds, right? You'll spare the nasolibial folds. And it's very high to know that those dermatologic findings tend to worsen with sun exposure, right? Those dermatologic findings tend to worsen with sun exposure, right? There are just many different things the MBM needs love to put with with loopers, right? Like they can have this Miller-Rash, they can have joint pain, right?

I'll talk about that joint pain in a little bit more detail, right? They can have joint pain, they can have serocytes like pleurcy or paritis, they can have pericarditis, they can have these gloid immune side opinions, they can have many of those different things, right? So I think maybe let's break them down one by one, right? So let's kind of start with the joints, so the thing is it's actually very high to know that loopers can cause a specific kind of arthropathy, right? And the thing is we know our friends at the MBM needs, right? They love to mix and mash things up. The way they love to mix and mash things up is to make you think that, ooh, I'm looking at rheumatoid arthritis, but you're actually not looking at rheumatoid arthritis, so let me explain this, right? So people that have a loopers arthropathy or loopers arthritis, right? They will have morning stiffness just like the regular people that have rheumatoid arthritis, but there are certain key differences that should help you delineate loopers arthritis from rheumatoid arthritis. So we know that in rheumatoid arthritis, the joint's damage is asymmetric, that's very high to know. In rheumatoid arthritis, the damage is usually asymmetric, right? But in loopers, the damage is usually symmetric, although again, let me say this, in certain cases, the damage in rheumatoid arthritis can be symmetric, right? So let me, I guess maybe let me back track a bit.

In rheumatoid arthritis, the joint damage can be asymmetric or asymmetric, when in loopers, it is classically symmetric. Now in rheumatoid arthritis, the joint, the arthritis you have is usually erosive, like you literally have joint damage, you literally have damage to the joints, but in lupus arthritis, the joints actually speak and span, right? The arthritis is completely non erosive, you don't have a region of the joint in lupus arthritis. And then many times, people that have rheumatoid arthritis, they tend to just have joint deformities, again, from all the joint damage. People that have lupus in general, they are joint deformities really non-defforming, right? And the thing is, we know rheumatoid arthritis, you know, affects the hands, affects the knees, affects the hips, affects many parts of the body. People that have lupus arthritis, if almost always on NBM, is just going to be in their hands, right? But again, it will be on their hands in a rheumatoid distribution. Many times, they're going to have problems in the MC Ps, right? Like your knuckles, basically. And also, the PI Ps, right? So the MC Ps and the PI Ps, it kind of, again, looks like a rheumatoid arthritis, a distribution. And then remember, these people, if we're going to the skin findings, right? Many times, they will have this rash, and again, it's going to worsen with some exposure, right? So if on NBM exams, they give you a question about a person that has a rash.

And the rash seems to worsen when they go on the beach, you really, that's like a very specific finding many times on NBM exams in lupus, right? In lupus. Now, they tell you that this person develops this rash after they go on some summer vacation, right? Many times, that should tell you that you're very likely dealing with lupus, especially when the rash is on the face, okay? Especially when the rash is on the face. And I think one thing I want to go ahead and mention here is people that have a male or rash don't always have lupus on NBM exams, right? So again, the NBM is many times they love to conflict lupus and sarcoidosis on an NBM exam, right? So if you see an African-American woman that has many antecedents of sarcoidosis, like the intestinal lung disease, hypercalcine, elevated angiotensin, convertin enzyme levels, hyalurlemphadenopathy, I notice that she has a male or rash. I want you to think of something called lupus perneal, right? Lupus perneal. Perneal is spelled P-E-R-N-I-O, right? Lupus perneal. That's like the male or rash finding in people that have sarcoidosis. Remember, that is not the only dermatologic finding of sarcoidosis, right? In the lower extremities people that have sarcoid, they can have this painful sarcula erythematos rash, right? That's the thing we call erythematosal, right? So those are just two classic dermatologic findings of sarcoidosis, you want to keep in mind for your exam.

Now, what if they give you a question about a patient that has lupus? And you notice that, wow, over a few days that creatinine starts bumping a lot and they have like hematuria. Well, if you see this, I really want you to think of them having lupus nephritis, right? And you know, classically, your NBM exams, sometimes they may not just put lupus nephritis, they may just put the name, they may put like diffuse proliferative glomerulonephritis, right? The diffuse proliferative glomerulonephritis. Now, let me go ahead and see something here. One very high-yield thing to know is whenever you see a person and you suspect they have lupus nephritis, and that's you for your next best step in diagnosis, you always want to get a renal biopsy, you always want to get a renal biopsy, because here's the thing, there's multiple types of lupus nephritis. I remember learning this in medical, there's about five or six types, at least I'm rethought, at Hopkins of lupus nephritis, right? All those different types of lupus nephritis, right? You don't need to know exactly what you're dealing with before you start treatment, right? So I will encourage you in general, don't start impaired treatment of lupus nephritis without having done some kind of renal biopsy, right? You need to do some kind of renal biopsy, right? And back in the day, lupus nephritis was actually the most common cause of death in lupus, but thankfully that's no longer the case.

These days, people that have lupus most typical, you know, most commonly the die of cardiovascular disease. I'll say that right now, actually, the most common cause is very high out. The most common cause of death in patients with lupus is cardiovascular disease. Again, back in the day, it was also like infection, but that is less likely as a cause of death these days. So I'll say it again with confidence. The most common cause of death in people that have lupus is cardiovascular disease, right? It is cardiovascular disease. Remember again, lupus can affect the heart in two big ways, right? On in-beaming exams, right? Remember again, all that inflammation can cause those people to have these, can cause these people to have these, what is it called? Where they have like these sterile vegetations, right? Especially on the mitral valve, many times you'll have the murmur of mitral regurg. That's what we call libman-sax-endocraditis, right? Libman-sax-endocraditis. Again, those immune complexes can cause damage, pretty extensive damage to the mitral valve leaflets, right? So they can get a mitral regurg and they can present as libman-sax-endocraditis. Now, remember lupus, again, those immune complexes can deposit in the walls of the pericardium, right? And those people can get some kind of pericarditis, right? Again, basically, whenever you have any serosal surface in the body, lupus can attack that serosal surface, right?

So they can have like inflammation of the walls of the heart, right? That'll be pericarditis. They can have inflammation of the walls of the lungs. That can be pleuritis. Many times pleuritis, sometimes they may not be pleuritis as an answer, they put pleuracy. But the big thing, right, is it's a it's a it's a serosal surface, pleural surface, pericardial surface that this tends to inflame. And many times those things respond beautifully to NSAI Ds, right? NSAI Ds are the primary treatment. And maybe let me see this because many of us know the way pericarditis presents, you know, chest pain that is worse when you lay back, gets better when you lean forward. But pleuritis, let me tell you this, these are people that have chest pain that varies with respiration, know with the heartbeat, it varies with respiration, right? So when they're taking a deep breath, they almost have to like pause because of the lanceneating pain that they are going through. When you see something like that, I really want you to think of of pleuritis. Again, sometimes they may call that pleuracy on NBMI exams, right? And then don't forget, right? In women that are pregnant, lupus can cause recurring pregnancy losses, right? Because again, that inflammation can begin to cause thrombosis of the utero placental artery. I'll say that again, that inflammation can cause thrombosis of the utero placental artery, right? So that's basically the antiphospholipid antibody syndrome, right?

So you make those, you damage the utero, you cause thrombotic episodes of the utero placental artery. Obviously, the baby is not going to be perfused properly, right? And that baby will likely die, right? And then another thing that can also happen that you should kind of keep in mind is people that have lupus, right? They can make these antibodies, right? The antibodies we find in showrooms, right? So the anti-roantybodies, right? So those are the anti-SSA antibodies, or they can make the anti-lantybodies, those are the anti-SSB antibodies. And those antibodies have the ability to cross the placenta, they are IgG antibodies, right? So since they are IgG antibodies, they can absolutely cross the placenta. When they cross the placenta, they can damage the conductive system in the fetus. And when they damage the conducting system in the fetus, that's going to cause a third degree heart block, not second degree, third degree heart block. Remember, that's also called a complete heart block, right? Those are things that can absolutely happen. Now, what if they give you a question about a patient? And they tell you that, oh, this patient was recently standing on some medication for, you know, like an EVRT, or an EVRT, or like an EV nodal like Reengine, Tachycardia is a young patient. And then they tell you that, huh, this patient starts having like, you know, like pleuricy, having all these astrologers, having these fevers.

If you see this, I absolutely want you to think about drug-induced lupus, right? Drug-induced lupus. Remember, drug-induced lupus associated with anti-histone antibodies, right? The anti-histone antibodies. Many times, right, the drugs that are implicated here are going to be things like hydrozene, right? So they can give you an anti-hypertensive question, sulfonamides, right? So they can give you a question about a person that has HIV, right? And he's being on, he's like on prophylaxis for neurosis, he's juvetsi. Remember, we use sulfonamides there, right? Try metaprims, sulfonethoxazol, right? And if a person is being treated for toxoplasmosis, remember, we treat toxoplasmosis with pyramethamine and sulfonides, and those are examples of sulfonamides, those things can trigger drug-induced lupus. And then don't forget isonides, again, they can make a TB question from this. But forget prokenamide, use it for WPW, right? Remember, WPW is a superventricular tachyroid, right? So all those things, right? A tannercept, right? So they can tell you about a person that was placed on some kind of TNF inhibitor, right? All these things can absolutely, absolutely, absolutely trigger drug-induced lupus, right? And a very happy, I guess, how are you things to know? Because some people ask, oh, divine, how do I differentiate between drug-induced lupus and regular lupus? Well, the thing is, the antibodies will really help you here, right?

So people that have drug-induced lupus, they don't have anti-double stranded DNA antibodies, they don't have low complement, right? They don't have low complement. And many of these, like really bad things that happen with lupus, like lupus affecting the brain or lupus affecting the kidneys, pretty much it does not happen in these people. And for the most part, these people don't need actual treatments. Just stop the offending agent and the problem will disappear, right? That is the primary treatment for drug-induced lupus. Just stop the offending agent problem will go away. That's pretty much it, right? And again, I know I just said that lupus, again, tends to cause these brain findings. Again, many times the brain findings are going to be like strokes, right? They're going to be like, you know, like venostromboembolic disease of the brain, right? Like strokes and things like that. Why? Because again, that inflammation can cause thrombosis, right? That inflammation can cause thrombosis, because remember, whenever you have a lot of inflammation, you can expose subindophilic collagen, and that can trigger the coagulation cascade and ultimately cause problems, right? So in general, I guess, to maybe as I begin to wrap up, how do we diagnose lupus, right? So many times you're going to diagnose lupus by getting the A&E, right? You're going to scream for lupus by getting A&E.

Basically, A&E, remember, in medicine, we're never trying to diagnose some kind of disease, when we start with a screening test, right? The screening test wanted to be a highly sensitive test, right? Because we want to rule out disease, right? But then after that, we need to confirm, right? We do that with a confirmatory test. That's going to be a test of high specificity, right? So like A&E, for example, is very sensitive for lupus, right? It's very sensitive. If a person's A&E is negative, the chances of them having lupus, or an NBM exam, is pretty much zero, right? But the problem, though, is A&E is sensitive. So it's your screening test, but the thing is A&E is positive in many other disorders. A&E is positive in scleroderma, A&E is positive in about 70% of patients that have a showgrain, right? So it's not specific for anything, but it's sensitive. It will help you capture all the people that have lupus. So how do you confirm that a person has lupus? What you're going to confirm by checking the anti-double-stranded DNA or the anti-smith antibodies? This is very high up to now, right? The anti-double-stranded DNA or the anti-smith antibodies, and the anti-double -stranded DNA antibodies are like almost like 100% specific for lupus. The anti-smith antibodies are almost like 100% specific for lupus as well. I think the anti-spith antibodies kind of win out a bit, but for the most part, they are pretty much almost like 100% sensitive, a specific sorry in both cases, right?

So that's why those are your confirmatory tests. And it's very important to know that the antibody that many times tracks along with disease activity are your anti-double-stranded DNA antibodies, right? You anti-double-stranded DNA antibodies. And again, don't forget lupus, you know, we can treat it in a variety of ways, right? So we can treat it like hydroxychloroquine, for example. Hydroxychloroquine is probably like a pretty good drug to use to treat lupus on Mbim exams. Now one thing I want to make you know, slash keep in mind for the USMLE purposes is that hydroxychloroquine is great, but you need to screen those people with like an eye exam every year, right? Because hydroxychloroquine can cause this repnopathy, right? It can damage the retina-pigmented epithelium. So those people in general need anual eye exams. That's a nice, high-eul-preventive medicine question. Our friends are the Mbim in love to test. Another thing you should keep in mind, since I'm just talking about the retina-pigmented epithelium, is actually also high-eul-preventive medicine. People that have, because I remember this from the podcast I made yesterday, for some reason, I just forgot to mention it, but people that have familial adenomatospolyposis, right? familial adenomatospolyposis. One clue, it's an unusual clue, when it shows up, it's very helpful to know.

One clue that can guide you in that direction on Mbim exams is, if you notice a person and they seem to have either born with this, or they seem to have this congenitality, where they have like hypertrophy of the retina-pigmented epithelium. I'll say that again, hypertrophy of the retina-pigmented epithelium. That is a relatively specific finding, and people that have familial adenomatospolyposis. Remember that arises from an APC gene mutation. And then, you know, if, let's say you've tried hydroxychloroquine and it doesn't do squat for the patient, well, what do you need to do? You need to do steroids, right? And remember, steroids, many times you use them to also treat like exacerbations of lupus. Whenever you have an acute worst end of symptoms in an autoimmune disease, any time you want to give like large doses of steroids to kind of calm things down. And then, let's assume those steroids don't work. Well, obviously, the thing you're going to be going to after that is going to be a TNF inhibitor, something like adalineumab, you know, maybe giving those people a tender septus, not the most genius idea in the world, giving us a tender septus also causes a drug induced lupus. So, I think those are kind of like the big things I want to mention, the big things I want to talk about, and hopefully you all find this to be helpful. Again, I'd offer one or one tutoring for all the USMLE exams, step one, just step three, pre-clinical med school exams, 30-ish-off exams.

Even these Caribbean med students that are studying for their complex exams, I'd offer tutoring for those. And then again, I have these review courses for step two, see case step three, complex level two and three that I, you know, happen roughly every month. And then I do help with ERAS applications, personal statements, rec letters, especially with editing those things. So, if that's something you're interested in, just shoot me an email, and I'll be more than happy to give you my list of prices and we can kind of take things from there. And then I also have these podcasts on Apple podcasts, Google podcasts and on Spotify, at least the most recent 150. And then I have a You Tube channel, the Vine Intervention USMLE podcast and videos. If you're going to that You Tube channel, you'd find all the videos that I've made there, they're on there. And then I do have the website, Vine Intervention Podcast.com. Whenever you go on that website, you know, if you subscribe, whenever I make a new podcast, you will get an email notification. And then many people have said that, wow, divine, I really love your life lessons podcasts, right? I really, really love your life lessons podcasts. So, I did actually start a new website like a few weeks ago. It's called divineinterventionlifelessens.com. I actually do, you know, make a podcast like, you know, two podcasts or thereabouts every week. And they're all 10 minutes or less.

And those podcasts, they just emphasize some Bible Bees life lesson, right? That again, I've got any emails from people that like, wow, divine, thank you for making these podcasts. I found them to be helpful. And actually, that podcast is actually an Apple podcast, right? It's called divineintervention life lessons podcast. So, if you look at that, I think you should be able to get some good, good information from there. Now, one thing I guess I want to go ahead and say, maybe like my, my life lesson for today, that I'll just throwing with this podcast is just the importance of service, right? The importance of service. Again, many people just feel that, and I think it's a problem that's especially pervasive with our core in generation that everything must be handed down to them, right? Everything must be done for them, right? Like no personal sense of responsibility, right? And the thing is, when you have no personal sense of responsibility, you're pretty much damaging your life. That's just the truth, right? The thing is, you're not on this earth to be served. No, no, no, you're on this earth to serve other people. The thing is, you'll notice that your life gets a lot cooler, a lot more fulfilling when you actually spend your time serving people, right? If you're always, because life is about give and take, right? And even the Bible says that it is more blessed to give than to receive.

Basically, the Bible there is seen that is more blessed to serve than to be served, right? But the thing is, people have this mindset that no, no, no, no, no, everything must be done for me. This person must do this for me. That person must do this for me. That's why you see many friendships are based on how much you can get from the other member of that friendship, right? The thing is, whenever you have friends like that, those are very shallow friends. I'm not saying those people cannot be your friends, but there's a big difference between having friends and having an inner circle. Those people should absolutely not be of like your close friends. They shouldn't be people you confiding, right? Because the thing is people like that, the moment your wealth or whatever help you are ranging to them goes away. Those people stop being your friends, right? But the Bible says that there is a friend that sticks closer than a brother. This is a friend that is willing to serve, right? So the thing is have that mindset of service, right? Ask yourself, how are you serving the world around you, right? Because the thing is, again, I'm telling you your life just gets like literally from making this podcast alone or from making the videos that I make. I get a lot of fulfillment in my life, right? Again, these podcasts like, you know, is it like a paid service or whatever? No, but do I feel great doing this absolutely, right?

My morning has been bright and literally by just making these podcasts. So again, I'll encourage you, leave a life of service, leave a life of service. Don't be a friend to people because you always want to munch off of them. No, be a friend to people because you want to serve them, right? When you serve people, again, you are creating good networks, good connections, and you're just making the world a better place. So thank you for listening to me. I'll see you in the next episode. God bless you. Thank you.

Type III hypersensitivity reaction, due to immune complex deposition.

Anti-double-stranded DNA (anti-ds DNA) or anti-Smith antibodies.

The malar rash.

Renal biopsy.

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

Lupus pernio and erythema nodosum/erythematosal.

Females, non-Caucasians (e.g., African American or Asian descent).

NSAI Ds are the primary treatment; pleuritic pain varies with respiration.

Type II hypersensitivity reaction.

Cardiovascular disease (previously nephritis/infection).

Hydroxychloroquine.

Drug-Induced Lupus (DIL); Primary treatment is stopping the offending agent.

Females, non-Caucasians (e.g., African American or Asian descent).

NSAI Ds are the primary treatment; pleuritic pain varies with respiration.

Type II hypersensitivity reaction.

Cardiovascular disease (previously nephritis/infection).

Hydroxychloroquine.

Drug-Induced Lupus (DIL); Primary treatment is stopping the offending agent.