DIP Episode 527 - USMLE Step 2/3 Rapid Review Series 113

Welcome, my name is Divine. This is episode 527 of the Divine Intervention Podcasts. Into these podcasts we're going to be continuing the Rapid Review series for the USMLSTP2 CKNSTP3 exams. It's going to be series 113. Let's jump right into it. So what if they give you a question about an African American female? And they tell you that this lady has over the last three months stopped going to the beach because whenever she goes, she has this rush that breaks out on the skin, especially on her face. And then you're giving some labs and you notice that at ESR and CRP are markedly elevated. And you notice that a humano-credits decreased and her white blood cell count is decreased. What should you be thinking about? I hope you're saying, oh, Divine, this is Lupus. I just want to maybe like, wait, what? Lupus? Yeah, that's precisely what this person has. And again, I think as I've said so many times on this podcast, the USMLSTP2 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 CKNSTP3 Again, our friends at the MVM is not going to always come out and say, Mela Rash Mela Rash Mela Rash again. If they see Mela Rash, everyone will get a 270. Well, obviously that does not happen. So again, they have very big descriptions. They can just see photosensitivity or the insidupercians that are worse than with sun exposure.

You see all those things, think about lupus. And you may also wonder, why did the low hematocrate and the low-y blood cell count come from? Again, it's from an autoimmune cytopenia. So the thing is, people that have lupus, they have this nasty habit of making autoantibodies against their blood elements. They basically make autoantibodies against blood elements. So, white blood cells, red blood cells, bleaklets. Obviously, if you make autoantibodies against your white blood cells, that's an autoimmune lupus. If you make autoantibodies against your red blood cells, that's going to be an autoimmune hemolytic anemia. That's going to be comspositive. That's a nice way to think about that. Remember, whenever you have comspositivity, it means that you have hemolytic anemia from an immune-based origin. Antibodies are messing up your cells. And then, these people also tend to have an autoimmune thrombocytopenia. That's going to be ITP, immune thrombocytopenia. Many times you make autoantibodies against GP2 B3 A. So, those are some key components of those autoimmune cytopenia. Again, you can mention immune thrombocytopenia on your exam and satisfy everyone that has memorized stuff. Or you can see an autoimmune thrombocytopenia. You'll be like, wait, what? Or they can just put anti-GP2 B3 A antibodies as an answer instead of putting immune thrombocytopenia. Again, these are the ways you need to be thinking about your exams. So, again, what are a few high-yield things to know about lupus?

Again, I will say critical things you want to know about lupus for exam, because honestly, I could probably even make a lupus podcast if I've not made one already. But there are so many things to know about lupus for the exam. There are so many ways they can go after it. Lupus is like the prototypical, okay, let me backtrack here. Whenever you see divine mentioning multi-systems processes and disorders, or the USML is mentioning, multi-systems processes and disorders, lupus is the classic, classic, classic example of something like that. So, what are the key things to know about lupus, for example? One, the asymptoms are very periodic. They don't usually have constant symptoms. They will have chronic symptoms for their periodic. There is a periodic density to the asymptoms. Number two, lupus is way more common in women on the USM Ls. Can you get a male having lupus question who you exam absolutely? But who is it going to be like 90% of the time? It's going to be females. What race typically gets lupus on the USM Ls? African Americans, right? Especially African American women. Again, it's usually rare for them to give lupus to a Caucasian on the exam. So, this extra bit of information will be surprised, and I will help you very quickly get rid of setting answers on your test. And then, what's the pathophage behind lupus?

Honestly, if you really think about it, because there's a reason why you learn anti-double-stranded DNA antibodies, anti-smith antibodies, ANA blah, blah, blah, blah. Basically, it's from immune complex deposition. Many of these diseases where you have this immune complex deposition, you have an antigen and an antibody, I just like to think of it this way. You know some people that just always seem to carry trouble with them. Wherever they go, the carry issues with them. And actually, I'm going to make a life lesson on that at the end of this podcast. I'm going to discuss a quick life lesson at the end of this podcast on just that concept. But there are some people that just seem to carry trouble anywhere they go. They're like partners in crime. They show up somewhere if there was peace, chaos breaks out. That's literally what you see with lupus. You basically from this anti-double-stranded body complexes, and then they just go to different places in the body. They can go to your joints, they can cause joint disease, they can go to your skin, they can cause skin disease, they can go to your kidneys, they can cause kidney disease, right? Lupus nephritis, they can go to the person's plural surface, they can cause like pleuritis, they can cause pleuricy. They can cause many, many different problems, right? So again, it's from immune complex, the position. That's the big battlefield phase you want to know, right? And again, you're used to the male rush.

Again, they're not going to use the term male rush on your exams. If they do, that's the envy me giving you a freebie. They're going to describe it. They're going to basically discuss a rush around the nasal, you know, around the nose, around the cheeks, things like that, right? Think of that. Sometimes you see the term, discoid rush, kind of looks circular in a sense, right? And what if they give you a question about a person that has lupus, and they tell you that, ooh, this person, I don't know this kind of turned into a loop, let's say my lupus podcast, but anyhow, they give you a question, and they tell you, basically I want you to get every lupus question right after this video. So they tell you that, ooh, this person that has lupus has been having shortness or breath, and she has pain with the breath, so whatever. And they tell you that you have like somewhat decreased breath sounds on that same side, want to think about serocytes, right? Serocytes, serocytes. Lupus likes to waft her like serosal surfaces, right? It can go the classic one on the examinal, waft is your plural surface. So you can cause a paritis. It's going to hurt as you breathe. Those people, they don't like taking deep breaths because whenever they take that deep breath, they kind of feel this almost like a splamet, like someone is like injecting something to the buro cavity. That's going to hurt. And many times those people will have a concomitant plural, a fusion, right?

Or they tell you that a person has lupus and man, they're cracking his eyes and a what not. You obviously want to think about lupus and the frights. One thing about lupus and frights is usually for that, you're going to go ahead and get a renal biopsy of some sort, right? And again, don't forget photo sensitivity with lupus, photo sensitivity, photo sensitivity, photo sensitivity, right? And remember, most people would have lupus, they're any positive. Any is very sensitive for lupus, okay? Any is very, very, very sensitive for lupus, right? So it has a very high negative predictive value for lupus. You probably noticed this in recent times, I've been trying to bring some bio-stats integrations with some of the concepts I discussed because that's how they do it these days. Bio-stats is not about memorizing the formulas about like, oh wait, how can we present this, right? Like they can give you a lupus question, any positivity, or they can give you a lupus question, give you a bunch of labs. And then they ask, which of the following has the highest negative predictive value for diagnosing lupus? I hope you're going to go ahead and pick out. You're going to go ahead and pick any any is very, very sensitive for lupus, right? If something is sensitive, it means it has a high negative predictive value, right? How about specificity? Let's look at things from the other end of the coin.

Well, things like anti double-stranded DNA and anti-smith antibodies, those are very, very specific for lupus. When you see those, there's not many other things that cause those things, right? So make sure you understand the difference between sensitivity and specificity. Almost everyone that has lupus will have a positive A&A, but there are many things that can cause a positive A&A. So any sensitive for lupus, but it's not specific for lupus, it's one of these things that people, you'd be surprised by how far people will go and didn't have a true understanding of what sensitivity and specificity means, right? So I'm going to repeat that statement again, make sure you kind of think about it. Almost everyone that has lupus will have a positive A&A, but there are many causes of a positive A&A that are not lupus. That's very important to keep at the back of your mind, for example. So any sensitive for lupus has a high negative predictive value for lupus, but it's not specific for lupus. But if we think I don't know why this is kind of beginning my mind, I divide this cause this concept, it will help someone on their exams. When anti-double-stranded DNA antibodies, anti-smeafantybodies, they have very, very specific for lupus, they have very, very specific for lupus. So they have a high positive predictive value, right? So anti-double-stranded DNA antibodies, anti-smeafantybodies, you don't find them in many other conditions besides lupus, so they're pretty specific.

They have a very high positive predictive value for lupus. I don't know. So remember, if they give you a question about a lupus patient that has a lot of venostromobolic disease or they've lost many pregnancies, like, you know, spontaneous abortions, think of antifosful lipid syndrome. Think of antifosful lipid syndrome. Remember, we would have antifosful lipid syndrome. Typically, they're going to have venostromobolic disease, you're going to see these people having all these issues, P Es, DV Ts, strokes, and they tend to lose pregnancies on a somewhat recurring basis. Remember, those people, they are one of those folks where a mixing study would not correct the PTT, right? So remember, it's kind of weird, anti-fosful lipid syndrome. These people will have a high PTT, right? Many times you think that, oh, gee, if I have a high PTT, you know, I should not have, I should not be hyperquaglable. But an antifosful lipid syndrome, probably something I can discuss, although I've probably discussed it actually in a previous podcast, like Gone Deep into Pathofence. But they have a high PTT, but they're hyperquaglable. And one of the things they love with these antifosful lipid syndrome is to test the mixing study. And typically, the mixing study is where you take normal serum that contains clotting factors and put it in mixing with a serum of a person that has high PTT and see if okay, with the PTT normalize.

Well, the thing is, in a disease like hemophilia, where you have a factor eight or factor nine deficiency, that's hemophilia A or B respectively. If you mix in normal serum, you're pretty much giving them the clotting factors that are deficient in. Then obviously, the PTT is going to normalize because you're pretty much giving them what they're missing. But in a person that has antifosful lipid syndrome, mixing study will not correct the PTT elevation. Why? Because antifosful lipid syndrome, those people, they have a clotting factor inhibitor disorder. You pretty much make autoantibodies against the clotting factors. So you're like, okay, this person's PTT is elevated. But the thing is, if you were to do a mixing study and give normal serum that contains clotting factors, those autoantibodies that are the pathophase behind antifosful lipid syndrome will gobble up those clotting factors so the PTT will not correct. That's actually one of those mice ways that they test antifosful lipid syndrome on your exams. They'll give you a question about a person that has a high PTT that does not correct with a mixing study. Slam long, that's antifosful lipid syndrome. Although believe it or not, you can also find those same labs in hemophilia if they develop autoantibodies against factor 8 or factor 9. That's actually something that over time happens in people that have hemophilia.

Because obviously, if you have hemophilia and you're lacking clotting factors, we give you those clotting factors back. We can give, you know, recombinant clotting factors and even get transitions of some stuff that contains clotting factors. The only problem is that over time, because those proteins are not needed to your body, your immune system will start making autoantibodies against those things. That's why people that have hemophilia after a while, at least some people, they stop being responsive to infusions of like factor 8 or factor 9 concentrate because they develop autoantibodies. So how do you know that a person that has hemophilia has developed autoantibodies against their clotting factors? Simple, just do a mixing study and you'll notice that that PTT that previously corrected with a mixing study will no longer correct because those autoantibodies have come into view. That's almost like they're tendin towards antifosful lipid syndrome in a sense. Different disease but somewhat similar pathophysiology. Okay, let's continue. Spent a week more time on that. Okay, so what are some other things you'll find in lupus? Well, again, remember I said with the autoimmune leukemia, the comstest is going to be positive. It's going to be the direct comstest that's going to be positive. Many people stress out about like, oh, divine, I got to know direct comst, indirect comst.

Honestly, I don't really care about knowing the difference because I know that in generally my experience on the USML Es, there's generally one thing that they almost ever use the indirect comstest for. What is it used for? It's for the origin compatibility. So figure out a woman's antibody status to see if she has from antiretron antibodies or not. That's it. Most other cases of comst anything on the USML Es, like autoimmune hemolytic anemia or what else do they use the stuff for? So autoimmune hemolytic anemia or you know, I guess that's the only big thing that comes to mind. But yeah, I will say most cases of comst testing, oh, another one can be a transition reaction. Exactly. That's the other thing I was thinking about. Like, I could hemolytic transition reaction. Those are the direct comst testing, that circumstance. But indirect comst is usually going to be origin compatibility country. Pretty much every other thing is usually going to be direct comst. That's just a nice way to pass all things out on my exams. And again, remember, one kind of weird, bizarre, strange question that they can give you exams is they can give you a question about a person going through a loopless flare. And then they'll make a table out of it. They'll say which of the following will be found on further analysis of this patient's cell. And then they'll put a table that has two rows. One row is going to talk about antibody titers. Another is going to talk about complement levels.

One row will talk about antibody titers. Another row will talk about complement levels. What's going to be true of there? And they'll put in his decres, decres, decres, decres, you know, they'll put out the different permutations. Well, what should you know here? When people are going through a loopless flare, the antibody titers are going to go up. That's super high, you know, for exams. Right? So all these things like the antismith antibodies, the antidobbles trended DNA antibodies, those titers will rise with a loopless flare. But what's going to happen to their complement levels? Their complement levels are going to go down. Right? So they're going to have low levels of C3, low levels of C4. One of the weird things they do is kind of like a throwback from step one is CH50. CH50 is just like an orthodox measurement of how your complement levels are. Right? It's going to be decres, they're going to have decres, CH50. Okay? So can I keep that at the back of your mind? I mean, I want to divide. Okay, the antibody titers make sense, you know, more inflammation or whatever. But why do the complement levels go down? Well, here's the thing. Those antigen antibody complexes. And then you kind of want to keep at the back of your mind with those. Is that the actually trigger or activate complement? If you trigger an activated complement, they're going to be using up your complement proteins. That's something that's super, super high you to know for your exams. Okay?

So again, just to summarize, make sure you know this. You're going to see an increase during a loopless flare. You're going to see an increase in their antibody titers and a decrease in their complement levels. Now, what's another thing you love to test? There's actually something that really pops up or when it pops up, pretty much everybody gets this stuff wrong. Right? So I would hope you're not one of those people. What is this thing I'm talking about is they will ask what arm of the immune system is all messed up in a person that has loopess? Well, you want to think about aberrant in need immune activation. It's going to be a problem with your innate immune system. Not your adaptive immune system. Please keep that in mind. I know you may be like divine antibodies against this and that and this and that. But again, when you exams, I'm not going to go into the details of it. We don't, this is a rapid review series. But I was strongly encouraged to think about problems with the innate immune system. Okay? Problems with the innate immune system. That's please that's very, very high up to know for your exams. Right? But again, if they give you a question about again, any of these problems like lupus nephritis or arthritis and lupus or whatever, again, always think about immune complex deposition. Does the pathophys behind those symptoms, those immune complexes, the deposited in those different areas of the body and then they cause problems.

Remember, we're going to manage lupus with a hydroxychloroquine. Obviously, if you have a flare, we're going to give you steroids. We're going to give you steroids. We're going to give you steroids. We're going to give you steroids. Right? And don't forget, every now and then they can actually throw a question on your exams. I'm pretty sure not. We're going to give you a lupus patient, the person has anti-rural and anti-la antibodies. Remember, it's not only show grints that has anti-ra and anti-la. Lupus is also a source of positive anti-ra and anti-la antibodies. Remember, anti-rural, those are the anti-SSA antibodies, anti-la. Those are the anti-SSB antibodies. All right. Now, what if they give you a question about like a 63-year-old male? And they tell you that, you know, for the past six months, he has been having pain in his, in his, in both knees, but that it's worse in the right knee, and that he has a little bit of stiffness in the morning. What should you be thinking about? I'll probably say in the vine, this is osteoarthritis. I know, right? I think that stiffness, I'm sure some of you, you see stiffness, you're like, ooh, divine. Room-athoid arthritis. No, come on, that's not smart. Right? 63-year-old, you're not gonna wait till age 63. Just like getting a room-athoid arthritis. That doesn't make any sense, right? So, this person has osteoarthritis. And remember, osteoarthritis, what other term could he use for it on the exam?

Why put osteoarthritis as an answer when you can put something like a non-inflammatory arthritis as an answer? Right? Again, I'm telling you this, you may not believe me, but when you take your real exam, you'll come back and say, hmm, divine was right on this, then I kid you not. The USM and these, they don't give straight answers anymore. They give derivative answers. Is that also an osteoarthritis? You know, they can put degenerative joint disease, they can put non-inflammatory, athropathy, as the answer. Remember, what are some key things to know about osteoarthritis for your exams? Right? It's gonna be more common than room-athoid arthritis. Right? It's gonna be more common. I'm gonna see it in older people. In fact, let me ask you this. What is the biggest risk factor? What is the strongest risk factor? What is the most important risk factor for osteoarthritis is gonna be age? It's gonna be what? Age? Age is the biggest risk factor in your exams for osteoarthritis. And let me ask you this. Who tells you get osteoarthritis more? Is it men or women? It's gonna be women. OA is more common in women. Although, if you look at hipathritis on the exams, whatever bizarre reason, hipathritis is usually more common in men. Actually, in the real world, hipathritis is also more common in men. Right? And again, what are some things you're gonna see in osteoarthritis? It's gonna work in with you. As they use that joint, it hurts more.

As they rest that joint, the pain kinda goes down. And they can have stiffness on your exam. Stiffness does not always mean R-A. Stiffness can also be found in OA. It's just that the stiffness in OA tends to be briefer than the stiffness in R-A. It's not as long-lasting. And sometimes they will even tell you that, oh, that Wendy used that joint in the morning. You can hear a grading sound, GR-AT-I-N-G, a grading sound. You hear creptis. Right? You hear creptis. So what are you gonna see on the image? This is a flurry high autonome for your exams. You're also gonna see asymmetric joint space narrowing. That's very, very high autonome for your exams. In osteoarthritis or degenerative joint disease or non-inflammatory, a thropathy, you're gonna see asymmetric joint space narrowing. But in rheumatoid arthritis, you're gonna see symmetric joint space narrowing. Right? And then in osteoarthritis, you're also gonna see loss of the atyclo cartilage. Right? So that atyclo cartilage is gonna be lost. Let's see, for example, look at the knee. If you lose that atyclo cartilage, you're basically rubbing bone on bone. That's gonna hurt. That's literally gonna hurt. That's literally gonna hurt. Right? Because you've lost that atyclo cartilage. You've lost that atyclo cartilage. Right? You're gonna see osteophytes. Like literally, these things I'm saying, you should be able to identify them on imaging on your exams. You should be able to identify them on imaging on your exams.

The asymmetric joint space narrowing, the loss of atyclo cartilage, osteophytes. Those are like bone overhangs. You find around the joint. You should be able to identify those on your exams. And then you should also be able to identify a sub-chondrosist. A sub-chondrosist is very prototypical of osteoarthritis on the exams. Now, one weird thing that they love to do on the USML Is is again to make an arrow question. To make an arrow question. To make an arrow question. You can ask about these weird enzymes. You can ask about these weird enzymes. Because you may wonder, what in the world are they gonna be tested in terms of enzyme activity with osteoarthritis? Well, let me show you. One classic thing that they love to test is which of the following enzymes will record increase the activity in a person who has osteoarthritis. And they'll put a bunch of different enzymes that people are familiar with. They'll say, glucose, sex phosphate, dehydrogenase, alkaline phosphatase, blah, blah, blah, blah, blah, blah. They'll put a bunch of bone related enzymes. Here's the one you want to pick. You want to pick increased metalloproteinase activity. Wait, what? Yes. I kid you not. You may see, the vine is messing around. I promise you with these rapid review series or any of my podcasts, I'm certainly not messing around. You're gonna have increased metalloproteinase activity. You're gonna have increased what? Metalloproteinase activity.

If those metalloproteinase is that literally will chew up your particular cartilage. They'll literally do what? Chew up your particular cartilage. That's why you have the loss. That's why you have that loss of the particular cartilage in osteoarthritis. So again, please keep that at the back of your mind for your exams. Now, what are some classic people that they love to settle for osteoarthritis on the test? Well, the classic person is the old individual. Old people tend to be the ones that get osteoarthritis. But obesity is also a risk factor for osteoarthritis. I mean, think about it. If you obese, you're gonna be heavily, heavily weight-bearing. That's gonna mess up your joints. That's gonna raise your risk of osteoarthritis. And also, if a person has joint injury very early in life, joint injury very early in life. So see, for example, a person has trauma to a bone very early in life. Or the person has some kind of accident that damages their joint. That's gonna cause problems. Or let's say, for example, the person has one of those pediatric orthopedic disorders. One of those pediatric orthopedic disorders, like juvenile rheumatoid arthritis, for example, that can raise the person's risk of osteoarthritis down the line. Those people tend to have osteoarthritis a little bit earlier than the normal person. Then the normal person. And again, remember, how do we treat osteoarthritis? You should be gonna start with exercises.

Sometimes you can try to strengthen the muscles around the joint that can help. You can just do walking. Just general exercise really helps weight loss if you're obese. That's gonna help. Usually, for osteoarthritis, we try to recommend lifestyle interventions to start. But if that does not work, then you need to go for a set of menophanes. A menophanes the first life pharmacotherapy for osteoarthritis. If that doesn't work, you'll talk on an insane. If that doesn't work, you're gonna start popping steroids into that joint. If that doesn't work, then you're gonna go ahead and replace that joint. That's what you're gonna do. I think this podcast is gonna, I don't wanna go from another round to another topic. So I think I should go ahead and stop here. Again, I have a bunch of classes for the USM Ls in the month of April. For step one, two, three, have a test taking class, have a bio-stats class that's four hours long, have a social science and ethics healthcare system quality improvement class that's five hours long. And then for step two, step three, have a 20 hour course, and then have a three hour last meeting review. It's like a very quick high-old review. It doesn't go into as much depth as a 20 hour class as it's not possible. 20 hours or three hours make a difference. But again, many people, I suspect, will find the course to be extremely helpful. So I think there's a lot of integrative scenarios. Again, these courses are not lectures.

They're pretty much all key scenarios, like NV Me style questions. And again, I try to really help you understand pathologies and make integrations. And then I'll throw on one tutorial for all the USM Ls and complex exams and medical exams. And then I also help with ERAS applications and personal statements and rec letters and all those things. And then I have this podcast on Apple, Google and Spotify. And again, remember, I have a You Tube channel where I post the videos that I make. And remember, you can literally just go to my website, devaninterventionpodcast.com. No logins, nothing. You can listen to and download podcasts from there for free. And then I also have another website called devaninterventionlifelessons.com. Every week from a biblical perspective, I post two podcasts. They usually about 10 minutes long and I address a life lesson. There's actually an Apple podcast associated with that. Again, devaninterventionlifelessons.com. Now, the quick life lesson I want to give today is just the importance of what do you do wherever you go? What do you do wherever you go? Are you like these anti-chenanty body complexes that cause problems everywhere they go? Are you the kind of person that wherever you go, you spread positivity, you spread good? Right? Because you'd be amazed that people, when they shop to a place, the piece that was there is gone. You don't want to be that kind of person.

Honestly, it's really hard to hang around such kind of people, really hard to have relationships with those kinds of people. So I'm just going to try to encourage you today. Be the kind of person that spreads peace. Wherever you go, spread peace, spread good. When you're leaving, let people be like, oh, really? Are you leaving this place? That should be the kind of testimony you want. You don't want people to be like, this person is finally gone. Thank God. No, you don't want that kind of testimony. Because you see some people, they are very ruthless. They don't care about, they're just so self-focused, so self-absorbed that they don't care what happens to others. They just care about themselves. Let me tell you this. If you're living that kind of life, your life is very, very empty. That's the truth. I don't mean to sound harsh, but that life is one of the MTS lives there is. You don't want to have that kind of life. You've been perfectly honest with you. Right? Just because, again, like for example, could I just focus on my own thing? No, but I love making this podcast. I feel like if it feels some good, some good in the community, some good in the medical world, and I just love doing it. Teaching is my passion. I've thought for pretty much all my life. I love teaching in church, in school, in many different settings, even at home. So, again, I'll just encourage you, just be the person that makes positive impact everywhere you go.

Make that your goal that, oh, whenever I'm living a place, I'm going to leave it a lot better than I got there. Don't go and tear something down. Don't go and build things up. Build people up. That's just that notcharing characteristic is very good for a person's life. Well, I'm going to get off my soapbox now. Well, thank you for listening to me today. I'll see you in the episode 528. Have a wonderful rest of your day. God bless you and bye for now. Thank you.

African American women.

Immune complex deposition in various tissues (joints, skin, kidneys).

The PTT fails to correct after performing a mixing study.

OA shows asymmetric joint space narrowing; RA shows symmetric joint space narrowing.

They decrease due to consumption by immune complexes.

ANA (Antinuclear Antibody).

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

Metalloproteinase activity.

Direct Coombs Test (or Indirect if screening for Rh antibodies).

Lifestyle modifications/exercise; pharmacologically, NSAI Ds or menochondanes.

An inhibitor disorder (e.g., Antiphospholipid Syndrome).

Aberrant innate immune activation.

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

Metalloproteinase activity.

Direct Coombs Test (or Indirect if screening for Rh antibodies).

Lifestyle modifications/exercise; pharmacologically, NSAI Ds or menochondanes.

An inhibitor disorder (e.g., Antiphospholipid Syndrome).

Aberrant innate immune activation.