DIP Episode 344 - USMLE Step 2CK/3 Rapid Review Series 65 (+10/4-8 2CK/3 Course Reminder)

All right, welcome. My name is Divine. This is episode 344 of the Divine Intervention Podcasts and I'm going to be giving a review on the given or rapid review for the Step 2 CK exam. This is going to be Series 65, but again this is episode 344. As a quick reminder, if you're taking the USML Es any time this month or early next month, especially Step 2 CK Step 3, I will encourage you significantly to attend the MBA Me Testicking Strategy scores that I'm holding tomorrow. It's from 2 to 4.30pm Pacific Standard Time. That's 5 to 7.30pm Eastern Standard Time. And then I also have a review course for the Step 2 CK Step 3 exams. It's also relevant to the complex level 2 and 3 exams. And it's going to be on from Tuesday to Friday of this coming week from 10am to 4pm Pacific Standard Time. So that's basically 1pm to 7pm Eastern Standard Time. Again, we're going to use about 2,000 different scenarios to discuss like Peds, Surgery, OBE Guy, Psych, Neuro, Internal Medicine, Ethics, Biostatistics, Multisystem Processes and Disorders. Psychiatry just many, many different things. Patho and the thing is, again, at least you've listened to my podcast, you know what I mean? I'm not a very big proponent of just giving people facts without context. No, I will give you a context and I will explain Patho fits. Again, I've had many people that have taken this course, that I've had like 40-point jumps on the exams, that I've done extremely well.

So again, if you're interested, shoot me an email and I'll give you some more information on registration. So what if they give you a question about a patient? And this patient, you know, they tell you that on his face, he has these very tender, very erythematous lesion that is raised and well demarcated. Well, what is the thing you're supposed to think about on those circumstances? Well, I would really, really hope that you see, oh, this person likely has erycipilates. Now remember, erycipilates classically will be described on in-bim exams and I'm going somewhere here. There'll be a circular lesion, right? There'll be well demarcated, there'll be raised and there'll be extremely tender. Many times these people have like a mild fever, right? That's erycipilates and the thing is on in-bim exams, what is the most common cause of erycipilates? Well, really hope you're saying, oh, divine, erycipilates are classically caused by a group A-strip, right? Strip to cocospiatginis. But then, what if they didn't ask you a question because again, this is something our friends at the in-bim really love with the more recent exams they can see? Which of the following represents a likely sequelae of this infection, so the thing is if they ask you for the most likely, so pay attention here, if they ask you for the most likely sequelae is going to be resolution with no future symptoms, that's it, that's it.

But if they ask you which of the following is a potential sequelae and they don't put like resolution, right? Unless they put dramatic fever as an answer, unless they put post-infections glomerulon and fridis as an answer, which one should you pick? I would really hope that you pick the answer that says post-infections glomerulon and fridis. This is a classic time-honored thing that our friends at the in-bim is love to test. Let me tell you this, there are two major kinds of problems you can get with group A-strip. You can get a skin infection or you can get faring jidis, right? The thing is if you have a group A-strip skin infection like erycipilates in this case, you can go on to have only post-infections glomerulon and fridis. As a sequelae, you cannot get dramatic fever after getting a strep skin infection. If you have a group A-strip skin infection, this is very high yield. You cannot get dramatic fever afterwards. The thing you can get is post-infections glomerulon and fridis. But if you have strep faring jidis, you can get dramatic fever as a sequelae and you can also get post-infections glomerulon and fridis as a sequelae. That's very, very important. That is very, very important. Again, strep faring jidis, potential sequelae could include dramatic fever or post-infections glomerulon and fridis. But a strep skin infection like erycipilates, the only thing you can get as a sequelae of that is post-infections glomerulon and fridis. That's it. That's literally it.

That's very important to keep at the back of your mind, right? And remember, you know, post-infections glomerulon and fridis, right? Remember it's a kind of nephritic syndrome. So obviously those people have red blood cell casts on a, on a urinalysis. Remember, those red blood cell casts are friends at the MDM Es can also call them the smurfy carry-throcytes. Right? You can call them the smurfy carry-throcytes. And remember the classic auto-antibodies you may find, right? So you may find like anti-DN As B antibodies, those ones especially tend to be associated with groupase strep skin infections, right? Anti-DN As B, right? Antibodies, right? And remember again, just other ones, right? Like ASO titers, you may have anti-striptolizing, O being positive, right? And most times when people have post-infections glomerulon and fridis, it's very important to remember that the thing that happens is, you know, they'll have an respiratory infection and then like two to six weeks afterwards, they'll start having hematuria, right? They'll start having periododolidema, they'll start having the antisidens of an ephritic syndrome that tells you they're dealing with post-infectious glomerulon fridis. And don't forget the histological correlate, or I guess the electro-microscopic correlate of sub-epithelial humps in people that have post-infectious glomerulon fridis. Now, what if they give you a question about a patient and they tell you that, oh, this patient, you know, is a HIV patient.

And for the last two weeks, he has been having a lot of a DMA. And then he presents today with like severe shortness of breath that's studied about two hours ago, like severe shortness of breath, and they give you some AB Gs and you notice that his PL2 is really low. So he's hypoxic and he's tacky cardic, he's the kipnic, right? What are we thinking about in this person? Well, I would really hope you're saying, oh, this person likely has a pulmonary embolus, right? This person likely has a pulmonary embolus. So, well, what's going on? What's the underlying pathophysiology behind this person's PE? Well, the underlying pathophysiology here is that this person essentially, this person has an ephrodix syndrome, right? Because remember, poor, they have HIV, they tend to get focal segmental glomerulus sclerosis. Most specifically, they get the collapsing variant, right? The collapsing variant of FSGS. And because they have that collapsing variant, the thing that ultimately happens is that, you know, they have nephrodix syndrome, they're losing many proteins in their urine. And one of the key proteins they lose, right? I mean, is albumin first off, right? By losing albumin, if you think about it, you have no more oncotic pressure in your blood. And if you don't have adequate amounts of oncotic pressures in your blood, then you cannot hold fluid in your vascular tree. You're going to have fluid extravasation. You're going to get in hot water. You're going to have a dima, right?

And also, these people, right? Because they don't have albumin, you know, they have a dima, I will explain one more sequelae of that. But why does this person have the PE? Well, another protein they lose is antithromin 3. And if you lose antithromin 3 in your urine, you have nothing to help you inhibit factors 2 and factor 10. Because you cannot inhibit factor 2 and factor 10, you're going to be in deep trouble, right? What is that deep trouble you could potentially be in? Well, the deep trouble you could potentially be in is the fact that sadly, you may have problems with stopping the coagulation cascade. So actually, having nephrodix syndrome is a hypercoglubal state. Because again, you are losing an anticoagulant in your urine. You're losing antithromin 3. Remember, antithromin 3 is what heprin acts on to increase its activity significantly so that you can inhibit factors 10 and factor 2, right? So if you don't have that protection, you can get in trouble with PE, right? Or strokes or dv Ts or things of that nature. Now, one thing that your friends at the MBME could take as an out-shoot of this nephrodix syndrome is, let me see. Oh, they can give you these arrow questions. Again, let me tell you this news to ask for those of you that are taking stucygase 3, they still give arrow questions. So what can they do with these arrow questions?

What they can do is they can see, which of the following will be expected raining, angiotensin 1, angiotensin 2 and our industrial levels in this person? Well, think about it. These people, you may look at them and say, oh, divine. Wow. This person has nephrodix syndrome. They're demodus. So their volume status must be great, you know. So their raining system must be turned off. No, it is not, right? The thing is, the fact that you have a lot of volume in your body doesn't mean that that blood volume is effective, right? So they are really going to try to, in the course of this rapid review, try to emphasize just some very salient physiological points that treat people a lot on exams. So the thing is, the fact that you have volume on board does not mean that it is effective, right? Like, for example, let me just give an analogy in real life. Let's say you have an inheritance like a trust fund, but your parents put some significant covenants on either you cannot tap into that trust fund, and that trust fund is not effective to you. You may have like 10 million dollars heating in some trust fund, but let's say you're still driving like a, like a, you're still bicycling around, you're still taking the bus because you have no access to that money. That's the exact same thing that happens when a person has nephrodix syndrome, right? When a person has nephrodix syndrome, they don't have an oboe mean. So they have a lot of a demon because fluid is not in their vascular tree.

So if any, if you look at them, they are all a demodus and stuff. Their preload is actually not good. There is in their preload is not good. It's because that blood, that fluid is not in the blood vessel. It's outside the blood vessel. It's the classic thing that many people say, oh, third space in third space in third space in third space in, right? It's extra vascular, right? So because those people are not profusing their hearts properly, right? Then they're not sending that blood not being in the vascular tree is not able to go towards the afrin material properly. So because the afrin material is not seen at a liquid amount of blood, it's like, not seen at a liquid amount of blood, oh, man, this prison blood pressure must be really, really low, right? So these people make a ton of ringing. So they are ringing levels actually be high. And then obviously that ringing is going to convert angiotensinogen to angiotensin 1. So the angiotensin 1 levels are also going to be high. And then that angiotensin 1 travels to the pulmonary arteries as it goes through the pulmonary capillaries is going to be converted by angiotensin convertin enzyme to angiotensin 2. And then that angiotensin 2 that is coming out of the pulmonary capillaries towards the pulmonary veins would then begin to go do things in the body. Like for example, it can go to the zona glomerulosa of your adrenal cortex and it will help you make ourosterone.

So these people are ringing angiotensin 1 and angiotensin 2 and our osterone are all elevated, right? They are all elevated. And again, you also see similar values in a person that has cardiogenic shock. Because again, for persons in cardiogenic shock or a person is in a heart failure, their hearts are not able to pump fluid forward. So even if they have a demon, that fluid is not effective. It's not effective because it's not being pumped forward towards the afrin materials, right? So again, that's very high yield to know for the purposes of exams. Now, what if they give you a question about a child that has like a demon like 1 to 6 days, after an upper respiratory infection? Or if you see this, I would really hope you're thinking about like IgN Fropathy. Remember IgN Fropathy? It shows a profit 1 to 6 days after an upper respiratory infection. Again, sometimes on exams, they call it a sin firing gyric nephropathy, right? Because it happens synonymously right around the same time as you have the upper respiratory infection. Again, remember, if it's less than 7 days off from a URI and you're seeing like a demon stuff like that, think of IgN Fropathy. Remember, even if it has the term IgN Fropathy, it's actually a nephritic syndrome. But if you see it more than a week out from that upper respiratory infection, they want to think more along the lines of post-infectious, merulonophritis. That is a nephritic syndrome, right?

So remember, IgN Fropathy and post-infectious, merulonophritis. Those are both examples of nephritic syndromes, right? Nephritic syndromes, right? So you have less than 3.5 grams per day of proteinuria. Again, that's very important to keep in mind. And then, what if they give you a question about a person and they tell you that this person's blood pressure is extremely high, right? It's like 250 over 140 and the person has like ultra-adventual status, right? And then they tell you that they see schistocytes on a blood smear. If you see that, what should you be thinking about? Well, I'll really hope you're thinking and you know, they can see what is the most likely diagnosis. And the thing is, we know our friends at the NBA, they're very, they're very wise, right? So in those moments, you may be like, hmm, okay, I'm looking for the answer that says hypertensive emergency, right? Because that's an answer that makes sense, right? The person's blood, I mean, it's actually correct in this case. The person has a high blood pressure. They have ultra-adventual status, right? So they have signs of end-organ dysfunction. Now, tells you, okay, okay, okay. This person's got hypertensive emergency. Makes sense, right? But the thing is our friends at the NBA, there is a unique distinct thing that they do these days, right? In fact, this is something that I address very specifically during my NBA me testing and strategy scores.

And also during my review, my 24 hours step to secure review course, step to seek is step three and you know, the complexes of review course. I tell people this, one thing the NBA me does these days is they were right a question. As you're reading it, you're like, I know exactly what is being tested here. I know exactly what is going on here. But then you look at the answer choices and none of them reflect what you think is going on, right? Again, those questions are called, I think I've mentioned this in a previous podcast, but those questions are what are called derivative questions. What in the world do I mean by the term derivative question? It's a question where they give you an answer that is based on something, but it's not that actual thing, so for example, in this question, instead of putting hypertensive emergency, do you know what they can put? They can put thrombotic micro angiopathy, right? They can put thrombotic micro angiopathy, right? We know that there are certain conditions that can cause a person to form schistocytes, right? In their blood smear, right? Many times it's when you have a thrombotic micro angiopathy. Well, one thing that can cause that is if you have like really, really bad hypertension, that can cause a thrombotic micro angiopathy, right? So, see, for example, if people have like malignant hypertension, like malignant hypertension, that can cause thrombotic micro angiopathy.

If people have like a sclerogram or a renal crisis, that can cause a thrombotic micro angiopathy, right? So the theme is in the process because these people's blood pressures are so high, right? They are damaging endothelial cells. As you damage endothelial cells, you're going to express sub, you're going to basically expose sub endothelial collagen. If you expose sub endothelial collagen, well, guess what? You're going to start making these peraps between vomulibran factor and GP1 B. And once vomulibran factor and GP1 B joined together, you've essentially kick-started primary hemostasis, right? With the formation of those are completely thrombi. And those places thrombi that begin to form in your blood stream, the thing that can happen is as red blood cells go past them, they're going to shed those red blood cells. As you shed those red blood cells, you're going to form schistocytes, right? So these people will have hematuria, right? They will have hemoglobin in their urine. Again, that's very, very important to keep at the back of your mind, for example, right? So these are all things that can cause thrombotic micro angiopathy, right? So again, the classic thing and the thing is that the pathway to thrombotic micro angiopathy can be diverse, right? I just talked about like the malignant hypothermia pathway, the sclerodamerino crisis pathway. Well, another way you can get to thrombotic micro angiopathy is DIC, right? It's DIC.

If you get into DIC, you can have a thrombotic micro angiopathy. If you have help syndrome, right? Remember, that's an OB-GYN concept. Himaluses, elevated liver enzymes, and low platelets. These people can have schistocytes, right? They can have a thrombotic micro angiopathy, right? Or if you think of people that have hemolytic uremic syndrome, you know, remember, HUS is usually caused by Ihec. Ihec, Ihec, enterohemoragic, Icoly is the most common cause, very high of this, the most common cause of HUS, right? You know, she gets like a very distant second, right? These things can cause thrombotic micro angiopathy. So these people can have schistocytes on a blood smear. Another classic thing that causes schistocytes on a blood smear is TTP, right? Thrombotic thrombocytopenic prepare. Right? If you think about it, in TTP, the problem is you have a deficiency of Adam T. S13. Remember, another name for Adam T. S13, on NBME exams, is Von Willibrand factor metalloprotees. If you lack Von Willibrand factor metalloprotees, then you're not going to be able to chew like, like degrade your Von Willibrand factor. So they're going to hang out a lot in your bloodstream, kickstart the primary hemostasis cascade. And if that happens, again, as your red blood cells are going past, you're going to be sharing them, right?

Again, you're going to get a thrombotic micro angiopathy, to be honest, with you, thrombotic micro angiopathy is a very high yield concept to keep at the back of your mind for NBME exams. Now, what if they give you a question about a patient and they tell you that, you know, this patient has a history of like diabetes or like sickle cell disease. And then they tell you that this patient, you know, for the past few weeks, right? Has been having like, like, cost of a tuberal angula tenderness, has been having, and that, you know, many times this person has been treated for UT Is and in those days, to be recovering or whatever, right? And then they give you like a histological image. So let me tell you this, whether you like it or not, unfortunately, on step 2, CK, especially these days, they love to give certain questions. It's not a ton, but they certainly love to give certain questions where you see histological images, right? So if, for example, they tell you that, oh, kidney biopsy, they give you like a kidney biopsy specimen, right? And you notice that the person's kidneys looks like the thyroid gland, right? So you'll mostly like this pinkish material. And then you see like these renal tuberous cells kind of surrounding it like, like a thyroid gland almost. Whenever you see something like that, I really want you to think of the diagnosis of chronic pylon arthritis. I want you to think of the diagnosis of chronic pylon arthritis, right?

The classic histological finding in those circumstances is thyroidization of the kidneys, right? Thyroidization of the kidneys, thyroidization of the kidneys. Again, it may sound like a trifle point, but it's not. It's a point that is very high yield to know for the purposes of endemic exams, right? So again, don't forget, you'll see thyroidization of the kidneys on exams. Now, what if they give you a question about like, you know, 55-year-old guy, and they tell you that, oh, you know, in his right foot, he has been having like just very, very severe pain for the last like 12 hours, right? And then, you know, they tell you that they did not seem to be any trigger. The person did not have any trauma or anything like that. But they tell you that, oh, this person, you know, consumes alcohol, right? And they tell you that, oh, you know, the extremity looks red, warm, tender, right? And, you know, you aspirate. And let's say this person has no fever, right? Well, that extremity, right? That foot, right? Looks red, warm, tender, things like that. But what is the first thing you're supposed to do? Well, hopefully you're like, okay, let's go ahead and perform a through synthesis. So let's say you perform the a through synthesis and you notice that, oh, wow, you check the joint fluid, you notice that the white count in the joint fluid is like 20,000, right? And you notice that you see like, you know, like 90% neutrophils and you see these rhomboid shaped crystals.

Well, what should you be thinking about in those circumstances? Well, I really hope you're saying, oh, divine, this person likely has pseudo-gout, right? This person has pseudo-gout. Remember, what causes pseudo-gout? Well, remember, pseudo-gout, classically is caused by the deposition of these calcium pyrophosphate crystals, right? In joint spaces, right? And again, the thing is many times, you know, there may be no triggers, right? But they potentially could be triggers for these things. Well, what are some of these triggers? Well, some of these triggers could be things like, let's say, you know, you've had like resentsurgery or let's see, you studied like a new workout program. That's a pretty classic one on exams, right? And the thing is, once those crystals deposit in your joint spaces, your immune system goes nuts, especially your neutrophils, right? So those neutrophils, they bring an inflammatory response, right? So that's why these people have all these symptoms, right? And sometimes they can even ask you this question, like, what is the most common location? What is the most common joint that is affected in pseudo-gout? You want to go ahead and pick the knee joint, right? The knee joints are the most commonly, so I use the foot, but the knee joints are the most commonly affected joints in pseudo-gout. That's actually something that's high you to know, for example, right? So again, don't forget, you're going to find rhomboid-shaped crystals.

Remember, when people have, remember, these are rhomboid-shaped positively bi-referringent crystals, unlike regular gout, where we have needle-shaped. So, pseudo-gout is rhomboid-shaped positively bi-referringent crystals. Gout itself is needle-shaped negatively bi-referringent crystals, right? And again, one thing I will say is sometimes one very good hint or tip off to pseudo-gout on imbim exams is that the person has a history of hemochromatosis. Hemochromatosis has a very well-established association with pseudo-gout on imbim exams. Another metabolic disease that has a well-established association with pseudo-gout on imbim exams, right, is going to be Giddoman syndrome. Remember, Giddoman syndrome is an Orozomer recessive disorder where you have messed up the sodium chloride-symporter that we find at the level of the distal-convoluted tubule, right? Remember, when you have Giddoman syndrome, it's almost like you're taking a thiazideioretic, right? Remember, thiazideioretics can cause hypercalcemia, right? Because they cause you to reabsorb calcium from your urine, right? So, if you reabsorb in that excess calcium because you have Giddoman syndrome, that calcium could potentially begin to deposit in joints and show up as condrocalcynosis from these calcium pyrophosphate crystals that can trigger an immune response, right? And cause pseudo-gout, right?

So, it's very high yield to know that pseudo-gout is associated with hemochromatosis, is associated with Giddoman syndrome, right? And again, one other thing they can just tell you again, I just pretty much explained the pathophys. You're going to see condrocalcynosis. That's a classic extra term. If you detail you that, oh, you notice that while a person has like signs of like, you know, inflammation in a joint, and you also see condrocalcynosis, you absolutely want to think, that's just like a classic tip of an embankment exams to pseudo-gout. Now, the thing is, how do we, how do we manage pseudo-gout? Well, remember, the first line treatment for pseudo-gout is an n-set, right? So, like, Kittorolac, ibuprofen, right? And the proxene, things like that, right? That's how you manage pseudo-gout, right? So, pseudo-gout first line is an n-set, right? Second line is a steroid. Third line is, is coacheset, right? Third line is coacheset, right? And again, many times, if you're giving steroids, you can just give an oral steroid. You can give an oral steroid. So, again, that's very high your true notes. So, I think I'm going to go ahead and pause here. Again, as I do at the end of every podcast, again, I do offer one or one to do it for many exams, step one, step 2 CK, step 3, complex level one, two, and three, preclinical med school exams, 30th shelf exams, the only thing I don't really do for is OMM.

So, for the people that are, you know, deals with students that don't really do to OMM, but they do to all those things. And then, I'm not going to say as many people, they say, oh, divine, I really love the life lessons you put at the end of your podcast. So, the thing is, I've got all emails that I can remember from people that say, oh, divine, I'm really blessed by these life lessons. So, I decided to start a website. It's called divine intervention life lessons.com. If you go on that website, you'll see a bunch of life lessons, right? You're all like, you know, very short and sweet podcasts, just Bible based teaching, many of you know, I'm a Christian. And in those podcasts, I just detail a life lesson or something that I know that is especially pertinent to people. Like, for example, this morning, I made a piece of 26 on godly parenting, right? So, the thing is, these are just all things because, again, parenting is getting more and more challenging as the days go by, especially in the world we live in these days, right? So, like, you know, things like humility, the tone, these are all examples of topics I've explored. So, just go to divineinterventionlifelessens.com, and you can get those podcasts. Again, most of them are around 10, 10-ish or there about, in terms of minutes. And, you know, I'm going to be putting a few in every week, you know, God willing. And I even have the podcast on Apple Podcasts, right?

So, if you just go on Apple Podcasts and search for divine intervention life lessons, you'll see a podcast and that, you know, it will give you all those episodes as well. It's on Apple Podcasts. And then I do, you know, have my, you know, have a You Tube channel, divine intervention podcasts and videos, uh, USM, divine intervention, USM, podcast and videos. That's where I post the videos that I make. And obviously, the podcast for, you know, this, uh, this specific podcast is on Apple Podcasts, is on Google Podcasts, is on Spotify. And again, I also offer these review courses for the USM, really exams. Again, step two, seek is step three, complex level two and three. I'm coming out with some new step one content, right? In terms of a step one class, very soon. So just teaching for announcements on that, uh, that's going to be coming very soon, actually. And then, um, I also have the website, divineinterventionpodcast.com. If you go and click on that website, if you go there, you'll see every episode from episode one, all the way to this present episode, episode 344. The thing is, on the podcast apps, you can only see the most recent 150 episodes, right? So let's say you probably caught off by like episode 200 or thereabouts, uh, if you're using these podcast apps, especially like Apple Podcasts, for example, uh, it's a Word Press role. There's not really nothing I can do to circumvent that role.

So if you want everything from episode one, if you want the slides that I my You Tube videos, go on to those respective episodes on, on the website. And the life lesson, I want to share today is, is about the importance of not being intimidated. So this is something that I actually learned in, uh, we've actually been exploring my church, you know, in a youth program, we have at my church, uh, about intimidation, right? So intimidation is just being afraid, right? Being afraid, being fearful, um, and, you know, essentially having that prevent you from doing what is right. So the thing is, some of us may say, oh, no, I'm not intimidated. I'm a very bold person. Think about it. If there's something you know, you're supposed to be doing in your life that you're not doing, um, you're pretty much under intimidation. And the thing is, intimidation can come from many areas, right? Many times the primary sources of intimidation are, human beings themselves, like us, right? So say, for example, if you know that, wow, there's this wonderful thing I can do, but you are afraid, oh, what do people think about you or you're insecure? I don't think I'm the person that is suited for the job. I don't think I, I don't think I can hack this. I don't think I have what it takes all those fears, those doubts that unbelief, uh, mindset, right? That's intimidation. That is you literally being intimidated, right?

Like, you see certain meds today, see, oh, I have imposed, imposed your syndrome to be honest with you, I absolutely hit that term. Oh, imposed your syndrome. I think I'm in the midst of people that are way smarter than I am. No, you go into med school because you're smart. You go into med school because you have something to contribute to the world, right? So sub sub sub du getting yourself from the outset, right? If you think, if you look at a biblical example, like Moses, when God was calling him to one, you know, deliver the people of Israel, Moses kept saying, Oh, but I starter, I this, I that, I this, I that, I this, I that. The thing is, instead of looking for the 10 reasons why you cannot achieve something, where can you not look for that one reason, why you can accomplish that thing? The thing is many of us as humans, we're very used to just focusing on the negatives, focusing on the negatives, focusing on all your disabilities, focusing on all your defects, focusing on your background. Again, to be honest with you, because again, you know, again, I'll say many of you know this, but I'm black, right? I'm African American. Let me tell you this, to be honest with you, even if there is truth, I'm not saying there's no truth, there is truth to it. Absolutely. Trust me, I'm quite well versed in African American history, right?

But to be honest with you, these terms, like when I moved to the US for the first time, I just kept hearing these buzzwords every day or divine your, your disadvantage, your, your dissent franchise, using all these terms, almost like a badge of honor. The thing is, I mean, encouraging the African American people listening to this podcast, don't take on those badges of honor. The fact that you're African American, doesn't mean you can not accomplish great things, right? So because the thing is, the Bible says as a man thinks in his heart, so he is. Those thoughts that you keep entertaining, that you keep agreeing with in your mind will one day become your reality, right? So the thing is, even if there is truth, you can break through that and be different. You can be a different example, you can be wow, this African American that is succeeding, this African American, even if there is again a disadvantage, again, I'm sure many of you have heard me say this statement on this podcast over and over again, I learned this when I was in Nigeria, you know, maybe when I just moved not too long into the US, that don't let your background keep your back to the ground, right? Don't let that keep your back to the ground. You see many people, they hang on to their deficiencies, they hang on to their disabilities, they're like, oh, I have this problem, so because of this problem, I cannot achieve XYZ. And no, that is not supposed to be the case, that is not supposed to be the case.

Watch the Paralympics. These people have big time disabilities, but they are still representing their countries with honor. They are still bringing great almighty things. The thing is many times in life, the thing that prevents people from achieving their destiny is because they've lost the battle already in their minds. They already believed that they are disadvantaged, they already believed they are dissent franchise. And again, I know that I'll probably ruffle a few feathers as a result of what I'm saying here, but to be honest with you, I'm not going to be intimidated. I'm going to speak up and see the truth. So I'm telling you, as an African American, if you're a parent, especially tell your kids, you are not at a disadvantage. You are an advantaged child, you're a special child, right? Moses, he's parents saw that there was something special in him. That's why they did not kill him when there was this edict that went out in the land of Egypt and all every kid, I think, under the age of two years old or whatever should be killed. His parents were like, hmm, there's something unique about this child, right? They did not look at Moses as a disadvantaged child. They did not look at Moses as a person that was supposed to be on the back burner. No, they were like, hmm, there's something unique about this child. And because there was something unique about him, they were willing to take risks, right?

So the thing is, as an African American, as a person that has a disability or something, look beyond that disability, look beyond that problem. There are many people that have taken that same thing, you call it disability, I mean, great things of their lives as a result of it. So I'm just trying to use this to motivate you today. Even if you had a medical school, where you come from a place where you know, like I remember, like where I went to med school, there were many smart people like my med school, wow, people from like Harvard, Stanford, UCLA, UCSF, all the big, big, big, big brand new schools, right? And yes, I went to a state school and again, my state school was amazing, by the way, right? I went to University of Louisville, I'm Kentucky, Go Cardinals. It was a great, great, great institution, right? But it maybe did not have as much clout as many of the people that I was amongst. But did that mean that when I was at Hopkins, I performed poorly? No, no, right? Because again, that thing is sometimes people just have these mental models that they just use to put themselves down. No, don't put yourself down. Don't put yourself down. Don't put yourself down. The fact that you're a black person, the fact that you're Hispanic, the fact that you're a minority doesn't mean that you cannot make something great of your life, right?

For every person that is, oh, I'm disadvantaged or whatever, there are people that had even worse backgrounds that have made great things of their lives and they have changed agents in the world we live in today. So again, I know this is a very long life lesson, but please I'm begging you, please I'm begging you, don't let these internal enemies intimidate you and don't let external enemies intimidate you either. All these friends that are downstairs that keep putting you down, that keeps saying, oh man, wow, like for example, to be honest with you, just looking for the USML Es, are you hanging around Debbie Downers? You are inflicting injury on yourself. These people that are like, wow, this test is so hard. There is no way I'm going to be able to succeed on this test. Do you know what, if you keep exposing yourself to that mindset, that will become your reality after a while. Don't have those people for friends, cut them off. I'm telling you this, cut them off. If you have these people that are just always good at busting your verbal and putting you down, don't hang out with them. Those people are not helping you, they intimidate you, they are unlocking your destiny. You don't want anything related to that in your life. So please I'm begging you, right? Don't be intimidated. Don't get me wrong. Don't get me wrong. Fearful circumstances are going to arise in your life.

If anyone tells you that you are going to achieve greatness without going through fearful circumstances, they are lying to you. You're going to go through fearful circumstances, but you need to take that white man, or force you to use this term, step of faith. Step of faith. You need to take that step of faith. When you take that step of faith, then you notice that things begin to break apart before you and you begin to break through. You begin to break forth. You begin to succeed. So again, don't be intimidated. If there is this wonderful dream you have, pursue that dream. Don't be afraid. Don't look at your background. Even if they say no one has ever achieved it before, well you can be the first person to achieve that thing, right? Again, if you want to achieve something that has never been achieved before, you must be willing to do things. You must be willing to break barriers that have never been broken before. So thank you for listening to me. I'll see you in the next podcast. Have a wonderful day. God bless you. Thank you.

Circular, well demarcated, raised, and extremely tender erythematous lesions on the face/skin.

Post-infectious glomerulonephritis (PIGN). Crucially, they cannot get rheumatic fever.

Antithrombin III. Loss impairs coagulation factor inhibition, creating a hypercoagulable state.

Calcium pyrophosphate dihydrate (CPPD) crystals; rhomboid-shaped and positively birefringent.

Thyroidization of the kidneys.

IgA Nephropathy (IgAN).

IgAN occurs within 1-6 days of URI; PIGN occurs 1-3 weeks after infection.

Post-infectious Glomerulonephritis (PIGN).

Giddan syndrome.

Antithrombin III.

Exposure of subendothelial collagen (leading to platelet activation).

Gout = Needle-shaped, negatively birefringent; Pseudogout = Rhomboid-shaped, positively birefringent.

IgAN occurs within 1-6 days of URI; PIGN occurs 1-3 weeks after infection.

Post-infectious Glomerulonephritis (PIGN).

Giddan syndrome.

Antithrombin III.

Exposure of subendothelial collagen (leading to platelet activation).

Gout = Needle-shaped, negatively birefringent; Pseudogout = Rhomboid-shaped, positively birefringent.