DIP Episode 307 - USMLE Step 2CK Rapid Review Series 55

Okay, welcome. My name is Divine. This is episode 307 of the Divine Intervention Podcast. And then this podcast will be continuing our Rapid Review series for the USMELY Step 2 CK exam. Again, this Rapid Review is also relevant for a presence on the first step 3. Again, for those that are taking the step 2 CK step 3 examini times soon, I do have a 20-hour comprehensive course is starting next week Wednesday. It's green all the way from Wednesday to Saturday. It's 5 hours each day. And yes, 5 hours a day for 4 days. Super comprehensive will be covering peeds, surgery, OBGYN, internal medicine, neuro, psych, ethics, bio stats, and many of those changes that crept up in November of 2020 last year. And also the step 1 material that is my greeting to the Step 2 CK exam and step 3 exams. So we're going to be talking about those things. So it's super comprehensive. It will cover about 1500 scenarios across the four days. Again, it's something you should find to be floridae high for your exams. Many people have taking these courses and found them to be helpful. So it's going to be taking place from 11 a.m. to 4 p.m. Pacific Standard Time on all four of those days. And then the day before on Tuesday, we're going to be having the Testikin Strategy Scores is 2 and a half hours. So again, if you're interested in any of these things, it's from like 2 to 4 30 p.m. Pacific Standard Time. If you're interested in any of these courses, just shoot me an email through the website.

And I'll be happy to give you some more information. Okay, so let's just go ahead and jump right into it. So one scenario I want to discuss this morning is how do you distinguish between over production versus an enzyme defect as the calls for an indirect type of aloeurobeen email? See that again. How do you differentiate between over production versus an enzyme defect as the calls for a person's indirect hyperberebenemia? Right. So let's think about this for a second, because the thing is, if you really think about it, there are two ways you, well, there are many ways, but let's maybe talk about like the two major ways people get indirect hyperberebenemia, namely, exams. They either get them because they're overproducing an indirect bilirubin. Right. So let's say a person has some kind of hemolytic anemia, like hair distracers, cytosis or sickle cell disease or autoimmune hemolytic anemia, just or g-sex pd deficiency. Right. If you have any of those problems, right, like you're going to be overproducing, because you're going to be breaking down your red blood cells, your red blood cells are not going to be living for very long. So the person will be overproducing an indirect bilirubin. Right. And that will cause an indirect type of aloeurobeenemia. But that's not the only cause of an indirect type of aloeurobeenemia. Right. If a person has an enzyme defect in UDP, look for an orcial transferase. Right. So let's say a person has a gyober syndrome.

Remember the way that classically presents is as an individual that has had like a major medical illness or just underwent some kind of surgery or went through some kind of trauma. And then they have a mild indirect type of aloeurobeenemia. Right. Those people have like decreased activity of UDP GT. Right. So gyober syndrome, although remember, gyober syndrome is not treated. But also other disorders like regular and a heart syndrome, right, type one type two, and the type one, you have like no activity of UDP GT type two, you have inducible activity of UDP GT. Right. So like if you have an enzyme defect, right, like you're not going to be able to conjugate indirect bilirubin. So that's going to cause an indirect type of aloeurobeenemia. Right. So you may say, okay, so divine. How do I tell about how do I tell these two causes of indirect type of aloeurobeenemia, part of an embankment exam? Let me tell you this. It's actually in the direct bilirubin. Whenever a person has an enzyme defect as the cause of their indirect type of aloeurobeenemia. So let's see, they have like crickland a heart, for example, right. They will have very little if any direct bilirubin on an embankment exam, but the angri bilirubin will be very high. Right. Because the problem is at the level of the enzyme, they're not able to take that indirect bilirubin and make it into the regular bilirubin. Right.

But if it's an overproduction problem, right, they will have both an indirect and a direct type of aloeurobeenemia. Right. Because the thing is, the enzyme is working. So they're just finishing that enzyme with lots of indirect bilirubin. And because they are finishing it with lots of indirect bilirubin, then they're going to be making lots of direct bilirubin. The key that I'll just see though is that the nominal amount, the nominal amount of the indirect bilirubin must exceed the nominal amount of the direct bilirubin in the Q step. Right. So you'll be like, okay, divine. Why does a person that has indirect type of aloeurobeenemia from overproduction have direct type of aloeurobeenemia as well? Well, again, the thing is, if the enzyme is working, you're finishing the enzyme with a lot of indirect bilirubin, it's going to make direct bilirubin. Right. But essentially, the reason you have the direct type of aloeurobeenemia is that the enzyme is working, working, working. So it's turning that stuff out. Right. But remember, that enzyme is such a variable, right? UDPGT, also called UDP, Glucorodosyl transfer rates, does not have unlimited capacity. So because it does not have unlimited capacity, it's going to get saturated at some point. So at some point, the person is in direct bilirubin will step building up. But the person is direct bilirubin will also step building up as well. Right.

So again, your friends at the NBMED like to write some of these tricky questions where they try to see, oh, can you tease apart the cause of the indirect type of aloeurobeenemia? Again, look at the person's direct bilirubin. The direct bilirubin is also like marketly elevated, but you know, just under the person's indirect bilirubin, you know, that this person likely has some non enzyme problem. The person has an overproduction problem that's giving rise to the issue. Right. But again, if it's an enzyme problem, then the direct bilirubin will be very, very low, but the indirect bilirubin will be very, very high. Right. And again, some people may ask me this, I've had this for many people have worked you one on one. Like, the way, how do I know what kind of hyperbilarubinemia is being posed in the question? The way you know the primary bilirubin problem is ask yourself, which kind of bilirubin is higher? If the indirect bilirubin is higher, then it's an indirect type of bilirubinemia. If the direct bilirubin is higher, then it's a direct type of bilirubinemia. Right. I'll encourage you if you want more details on this bilirubin problems, consider listening to my clutch bilirubin podcast. I believe it's episode 257, but I'm not 100% sure. Just go on my website in the search box, type in bilirubin, being good shape. And by the way, I want to say something, some people actually emailed me.

So thank you to those people that did that of some podcasts not showing up in the podcast apps. So I've corrected whatever may have been causing those problems. So now everything should be updated. Okay. Now, what if they give you a question about a patient? And you tell you that, oh, this patient has been comes to the emergency room. So they tell you that, oh, this patient comes to the emergency room. Because for the last three days, he has no been able to poop, right? And he has not been able to pass gas. Well, maybe he has been passing. So the person has not been able to poop, right? And they tell you that, oh, you get the image of the abdomen. And you see, you know, like the standard abdomen throughout, including the colon, right? And you notice that, oh, there's like, you know, these are Earth-fluid levels. And they tell you that, oh, this person has never had any kind of abdominal surgery. But in the telling the question that the person was recently started on some kind of cough suppressant, what should you be thinking about? And I hope you're thinking about like opioid-induced GI dysfunction, right? Remember opioids, you can find some of them, especially co-dean in some of these cough suppressants. And we know that opioids, they really, really hamper a person's GI motility, right? So they can cause like a functional obstruction of the person's GI tract, right? So you should kind of keep that at the back of your mind, for example, right?

So again, in some situations, especially when you're dealing with an old person that may have like diabetes on your upper, you'll be pretty supposed to gastroparesis and stuff like that. Whenever you're putting them on any opioid-containing compound, it's typically not about ideal NBM Es, that also in the real world, to put them on a stool softener or a promotility agent, right? Like, colis, like, center, things of that nature. Now, what if they give you a question about a patient and they tell you that she's 32-year-old female, she has been pregnant, you know, she's pregnant, she's at 33-weeks gestation, and then they tell you that, you know, she comes for one of her pre-delivery visits or whatever. And then they tell you that, oh, the amniotic fluid index is two, right? And let's say they give you like a normal empiricist, they say, oh, normally it's between like five to seven or whatever. I don't know what the normal is, right? But it will give you the normal. You don't have to memorize anything like that. And then they can tell you that, oh, she has been having low back pain for the last, you know, two months as, you know, as part of this pregnancy. And then they ask, what's the mechanism behind the abnormalities that you're observing with the amniotic fluid index? Well, the way you should answer this question is, think about it, right?

So again, the NBA needs is about being able to meet these connections, being able to meet these integrations, kind of put things together, right? So the low back pain that this woman has, you know, is probably from the pregnancy right again, if a woman is carrying a gravitiate virus, right? That's going to put some stress on the person's back. That's why usually when a person is pregnant, it's maybe not the worst idea in the world to exercise, do some of these strengthening exercises. And also, you know, use like a good chair and stuff at home, you know, but that's a different conversation. But let's see, maybe for those low back pain, maybe she has been taking an NSAD. Well, why will an NSAD kill the amniotic fluid index? Well, if you think about it, NSAD's just like they can cause renal dysfunction in like human beings, they can also cause a renal dysfunction in the in the feeders, right? And if they cause renal dysfunction in the feeders, then the feeders is not going to be able to produce urine, right? Remember, the amniotic fluid that surrounds the feeders is basically the amniotic, the feeders is pee, right? So in the feeders, pee, you know, urinates, does the amniotic fluid is swallows it, and then it pees again, swallows it, that's basically the amniotic fluid cycle. So if the feeders in utero has renal dysfunction, then the feeders is not going to be able to make urine. So the feeders is going to have oligohydramneus.

And we know that oligohydramneus can present as border sequence in a newborn, right? So again, they can even extend this question a little bit more. I'm talking about a baby being born. And this baby has like abnormal feces, limb problems, and all those things, right? And the creatinine of the baby is like super, super innovative, right? And then they tell you that oh, mom has had low back pain for many points during her pregnancy, which was taking NSA Ds, right? You want to be able to put one two together, right? You'll have like pulmonary hypoplesia and all those problems as well, right? So again, remember NSA Ds in general is something that you try to not take on NBM exams, past 20 weeks gestation, right? Because again, it can cause renal dysfunction in the feeders. And you especially want to be careful about NSA Ds in the third trimester of pregnancy, because it can lead to a premature closure of the doctor's arteriosus, right? And again, think about this, right? This should make sense. Think about this. If you give NSA Ds, NSA Ds in Hibit cyclocigenis, by Hibit encyclocigenis, you're going to increase, you're going to sorry, decrease the production of prostaglandins. When you decrease the production of prostaglandins, you're decreasing the production of a visodilitary agent, right? If you decrease the production of a visodilitary agent, it will then make sense that the doctor's arteriosus, which is a blood vessel, whether or not, will close.

And if you close this, the baby is not going to do well. The baby is probably going to die, right? And you clearly don't want that. So after 20 weeks gestation, a woman should not take an NSAD in general. If you're taking an NSAD while you're pregnant, you can't play with fire at that point. But the guidelines, if you're more than 20 weeks, you should definitely not be taking NSA Ds during pregnancy, right? Now, what if they give you a question about a patient and they tell you that, oh, this newborn, if I let me just maybe explain this, what should happen to a VSD, the loudness of a VSD as a baby progresses through life? Let's say from when the baby was born to like three weeks, four weeks, two months, three months afterwards, what should happen to the loudness of the VSD? I hope you're saying, oh, divine, the VSD is supposed to get louder. Well, why is that the case? Well, let's walk with me here for a second, right? So remember in utero, the fiddle lungs don't work, right? So because the fiddle lungs don't work, there is like profound pulmonary viso-construction, right? So there's almost no venus return for the left side of the heart in the fidus. So in general, in utero, the right side of the heart has way higher pressures than the left side of the heart, right? And this relationship of the right side of the heart having way higher pressures than the left side of the heart also obtains for like the first few minutes after the baby is born.

So if you think about this, if that relationship holds where, oh, the right side of the heart has pressures that are higher than the left side of the heart, or you know, after the baby is born, maybe the left side of the heart pressures start rising a bit, right? You'll see that there's not much difference in pressure between the right and the left side. So because there's not much in the way of differences in pressures, then there's no gradient for flow. And if there's no gradient for flow, then you won't have much flow across the VSD. So it will not be very loud. What as time goes on, you know, the baby is taking a many deep breaths, the poner vessels, vessels are visual dilating, right? There'll be more venous return to the left side of the heart. The left side of the heart pressures will then become markedly higher than the right side of heart pressures. And if that happens, the gradient of flow, right, then becomes even stronger from the left ventricle to the right ventricle. So there'll be more flow across that VSD. And if there is more flow across that VSD, the VSD will sound louder, right? So VSD should sound louder as you go farther and farther from a child's birth. Again, this is very, very high you to know for purposes of the USMN. Exams. Now, what else? Because you know, I feel like I've been talking about cox inhibitors a lot today. What else can we keep in mind with cox inhibitors for OBGYN? Well, think about aspirin specifically.

Aspirin, you can actually give it to a woman that has had preeclumsia or eclumsia in a prior pregnancy, right? You can give her that aspirin to lower her risk of preeclumsia slash eclumsia in future pregnancies, right? Again, you may see it would divide what's the potential mechanism behind that? Well, the potential mechanism behind that is that this, we know that I mean, for the most part, preeclumsia, eclumsia, people don't totally understand the mechanisms of disease or pathophysiology. One thing we don't understand is that there's potentially problems with some of the spiral arteries, right? In the uterus and there's all this inflammation that goes on that causes some of the, you know, that is implicated in some of the pathophysiology of the disease. So the thought process is if we give aspirin, which is a cycloxygen, is inhibitor, we will decrease the inflammation, right? Because we're making less of those inflammatory molecules like prostaglandins and stuff like that, right? That thromboccin, right? But you're also making less thromboccin, A2. And remember, thromboccin A2 is one of the most powerful natural activators of platelet aggregation. So if we shut that down, then those blood vessels that feed the uterine, like the endometrial wall, may probably work better and the person will not have that much in the wheel of problems, right?

So, classically, your name-be-me-examts, you actually want to keep in mind that aspirin can be used to prevent preclamsia, slasheclamsia in future pregnancies. And then, what if they give you a question about a person? And you tell you that, oh, this individual is like a foyer baby and this baby is at the 99th percentile for head circumference, which is pretty high, obviously, right? And then you tell you that, oh, this baby also has paralysis of upward gaze. This baby also has paralysis of upward gaze. What should you be thinking about on MB-me-examts in relation to this? Well, if you see a person having paralysis of upward gaze, the first thing you should ask yourself is, oh, where's the upward g-center in the brain? Well, I would hope you're saying, oh, divine, this is the superior colliculus, right? Remember, the superior colliculus is the upward g-center, is the vertical conjugate g-center in the brain, right? So the thing is, people, this person obviously has parinote syndrome. Remember, parinote syndrome is when, for some reason, the superior colliculus doesn't work, right? And usually on MB-me-examts, it doesn't work because it's being compressed by some mass, by some tumor, right? Usually, it's going to be a tiny loma, right? So that tiny loma is compressing the superior colliculus. Well, if you compress the superior colliculus, right? And then you have that paralysis of upward gaze on a MB-me-examts.

But the more important question here is, oh, why does this child, so the more important question is, why does this child have, why is this child in the 99th percentile for hits or conference? In this question, well, that tells you that, okay, the child has hydrocephalus. Again, the MB-me-me-me is not going to come out and tell you, oh, the child has hydrocephalus, right? You just describe it. Again, that's the thing you've heard me harping about for a long time that people say that, oh, wow, divine, these neuro-USM and exams are hard. The reason they are hard is because it's not like they're, yes, they have some new things they're testing, don't get me wrong. But many times, it's the same old stuff they're testing, they're just being more descriptive, they're just using different words to describe those things, right? So why does this child have hydrocephalus? Well, if you're asking you about that on your exam, I would hope you're telling me that, oh, I'm going to pick the answer that says cerebral aqueduct obstruction. Because if you remember, right in front of the superior colliculus is the cerebral aqueduct of Sylvia's, right? So remember, the cerebral aqueduct is the thing that drains CSF from the third ventricle and gets it into the fourth ventricle. So these people, they will have hydrocephalus, right? And on imaging, you expected finding will be enlargement of the lateral ventricles and the third ventricle, right?

Again, sometimes they'll give you some of these questions and it's almost like they want you to localize the neurologic lesion in terms of where the obstruction is, right? Again, just come on simple thinking here, don't overthink this stuff. Whenever you have an obstruction somewhere, right? You have dilution of the things that are proximal to the obstruction, but you will not have dilution of the things distal to the obstruction. So remember, if a person has a cerebral aqueduct of Sylvia's obstruction, then the things that are proximal to it like the third ventricle and the lateral ventricles will be distended, but the fourth ventricle will be fine, right? If you was an obstruction where you notice that, oh, wow, the lateral ventricles are distended, but the third and fourth ventricles are normal. Then it was very likely a problem at the level of the interventricle of foremen of monorail, right? The person has some kind of phyrraminal stenosis that's causing that person's hydrocephalus, right? And these types of hydrocephalus I've talked about, right? These are examples of an obstructive or non-communicating hydrocephalus, right? These are examples of an obstructive or a non-communicating hydrocephalus. Remember, when a person has a communicating hydrocephalus, it's a problem that they have at the level of the arachnoid granulations, right? Where they wrap, so it's CSF into the superior sagittal sinus, right?

So just something to keep at the back of your mind, for example, right? So since we're still talking about this pyrrinoid syndrome business, right? So it's the pinyloma that may have grown big enough to obstruct the cerebral acroduct of sylvios that's also causing this child's hydrocephalus. Now, quick question here is a pinyloma the only potential cause of pyrrinoid syndrome on an MBM exam? And I'll hope you're saying no, right? Because remember, what's the blood vessel that supplies the superior coliculus? What is the blood vessel that supplies the superior coliculus? Well, I hope you're saying, oh, divine, the blood vessel that supplies the superior coliculus is the superior cerebellar artery. Remember, that's one of those terminal branches of the of the basilar artery, right? The superior cerebellar artery, the superior cerebellar artery supplies the superior coliculus, right? So you see superior in their names, so you should hopefully be easier to keep strict. So if a person has an infarction, the person can actually infarct their superior coliculus if they have a superior cerebellar artery stroke or aneurysm or rupture or something like that, right? In that case, that will be a vascular cause of pyrrinoid syndrome for purposes of the USML exam, right? That'll be a vascular cause of pyrrinoid syndrome for purposes of the USML exams.

Okay, and then maybe the last we need to talk about here, what if they give you a question about an alcoholic on an MBM exam, and you know, this person, this alcoholic, they tell you that that he has an etoxic gate, right? They tell you, he has an etoxic gate, and then they also tell you that this alcoholic has like a positive Babinski sign, and they tell you that, oh, Romburg test is positive, right? So the thing is, if they give you a question like this, your friends at the MBM, they are very smart, here is one thing they will do, I mean, I totally do this, but this is something I can definitely almost promise you, your friends at the MBM will do, they'll put an answer that says Wainiki Corsica of syndrome, many people will pick that, and then they will be wrong, and then I know some of you may be raising your hands right now in operar, but divine, etoxic gates, come on man, that looks a lot like Wainiki's, well, did you consider the rest of the question? Did you consider that maybe it's not the person's alcoholism that is causing their, their etoxic gate? Because look at the other things I said, the person has a Babinski sign, that's an opa moron your own lesion, right? And then the person's Romburg test is positive, right? So the person has like decreased vibration and perceptive sense, they are those old columns and are working. If you track all those things together, those remember those old column dysfunction can definitely also cause itaxia, right?

If you put all those together, this person actually has subacute combined degeneration of the spinal cord, right? Subacute combined degeneration of the spinal cord, remember in subacute combined degeneration it's a combined degeneration, so that means there are two problems at play, there are two pathways that are not working, the lateral corricus spinal tract and the doso column medium, medial and niscos pathway, right? So remember, doso column dysfunction can also cause itaxia, so don't always just make it like a reflex, ooh, itaxia and alcoholic equals when it keeps low. That's not a smart way to take exams, I can pretty much promise you that. So just something to keep in mind there, right? So again, that's why you should read your questions carefully on these USML exams, right? Really your questions carefully on these, on these USML exams. So again, if you see opa moron your own lesions in an alcoholic and you also notice a lot of doso column dysfunction, think about subacute combined degeneration of the cord, remember that's usually associated with a vitamin B12 deficiency, right? That's usually associated with a B12 deficiency, again, alcoholics they don't usually get the best nutrition, right? So because they don't get the best nutrition where you can potentially see them having having these kinds of problems and I will encourage you if you want to be like an alcoholism expert for purposes of the USML exams, listen to my alcoholism podcast.

Again, just go on my website in the search box type in alcoholism. I kind of remember the specific podcast episode of the top of my head, but that's probably probably one of my top, I don't know, I feel like in general, my podcast is pretty high, that's probably one of my top 10 highest yield podcasts of all time, right? It's a super high yield podcast. It's just one of those things you know if you listen to it and master it, you're going to get certain questions right on your exam. So I think I'm going to go ahead and pause here. Again, as I do at the end of every podcast, I do offer one or one children for many exams, step one, step two, CK, step three preclinical exams and third year shelf exams. And then if you're applying for the ERAS cycle, I do offer consulting for that, advising with students. You're going to have worked with tons of students that are now residents in many specialties all over the country like neurosurgery residents, plastic surgery residents, dermatology residents, internal medicine residents, family medicine residents, obi-gui residents, right? So I've worked with lots and lots of people all over the country. Again, if you even have a tricky application like you feel the USM in exam or you graduated 10 years ago or you have no research, right? Or you have just a very complicated story.

Again, just reach out to me, I have a lot of experience in this, I've successfully helped people navigate through these tricky circumstances and now these people are residents. I know a lot of residents all over the country in very diverse area of disciplines. So if that's something you're interested in, just shoot me an email through the website. If you also want to sign up for one or one children or for these courses I offer, again, remember that step two, CK step three course, sticking please next week. Just shoot me an email through the website and I'll point you in the right direction. And please subscribe to the website, divineinterventionpodcast.com whenever I make a new podcast you'll get an email notification. And then also I have these podcasts on the podcast apps, on Apple podcasts, on Google podcasts, on Spotify. You can subscribe to those podcasts and again, any feedback or anything differently helps. And again, remember these podcasts apps can only take the most recent 150 podcasts, right? It's a Word Press role is something that is like this little, at least as far as I know, there's literally no work around around it. So if you want all the podcasts from episode one, all the way to episode three or seven, just go on the website. And some people say that oh divine, sometimes it's really hard for me to like how do I know what podcasts to listen to again. There's this big ready post, especially for step two, CK step three folks.

There's this big ready post I made about a month or maybe six weeks ago. It's on the other R step two sub. It's a pinned post. You'll see it's probably like the first thing you see in the R step two, whatever sub. And it's like, oh, how to study for the newer MBM exams. And it's like a guide I updated for 2021. I write these guides every now and then. Usually it takes a pretty long time to write. So if you read that guide, it'll tell you exactly what you're supposed to do for step two, CK step three, right? It'll just get really guided in the right direction. And then if you go on my website, if you click on exam topics list or exam topic lists, I think that's how I put it there. It's a header on my website. You'll lead it to a Google Doc, a Google sheets document. No one can edit it. It's only me that can edit it because again, I've learned well enough how, you know, people are always willing to screw up something that they get access to. So it's only me that can edit and basically whatever and make a new podcast, I file it on that different folders, right? So say, for example, if you go and click on the step one part of it, you'll see for the different step one discipline is like pharmacology or GI or hemo or whatever. I tell you the podcasts and you listen to that are relevant to those things. So all you then have to do is take this specific episode number, type it into the search box on my website.

And I'll just take it directly to to the specific podcast you're supposed to listen to, right? And then, so I have that for step one and for step two, see, step three, right? So that should help in that regard. And then I do have a You Tube channel, divide intervention, USMLE podcast and videos. So please subscribe when I post a video, I posted there. Okay. Now, today's life lesson is going to be extremely short, extremely extremely short. And it's just a thought, I think I want to live with you. Many people say they never want problems. One thing I think this is actually something I learned in church yesterday is I want you to consider the fact that the problem you may be going through now, maybe a problem that you're supposed to solve, right? Because I feel like people run away from problems because the thing is many times they actually grow by going through certain challenges of life, right? I mean, the reason by the grace of God, why I can tutor people extensively for the USMLE exams. Again, I'm not saying that, thankfully, things be to God, I've crossed my exams. But I've just had a lot of experience working with a lot of challenging students that I've just had a lot of USMLE challenges. So I'll see most problems that people face on the USMLE exams have successfully helped people deal with those problems. So I have a lot of experience in those things, right?

So in dealing with those problems, in solving those problems, I've accumulated experiences that has allowed me to be able to help a lot of people down the line, right? So the thing is sometimes, I will just encourage you to embrace challenges. And instead of looking at the challenge as a problem that, oh wow, this thing is going to put me down, this thing is going to destroy me, this thing is going to for close my future. Have a somewhat different perspective ask yourself, oh, how can I conquer this challenge? How can I overcome this challenge? I mean, there's this part of the Bible that says that we are more than conquerors, right? Through him that loved us and gave himself for us, right? It not give, give himself for us, right? So the thing is, you are more than a conqueror, you have the ability to conquer that challenge, you have the ability to conquer that problem, right? That problem is not going to destroy you, right? And the thing is once you solve that problem, then you'll come out from the other end of it stronger. And then you then have the fortitude to help another person that we experience a similar challenge in the future, right? Again, experience is the best teacher, although I'll add the schoolery. The experiences of other people sometimes is the best teacher, right? Obviously, if you can avoid a problem, try to avoid it, like for example, you don't want to feel like, I mean, can you come back from it if you feel a USML exam? Absolutely, right?

But it's better to not have failed the USML exam in the first place, right? So I think the thing I will tell you is, if you can learn from the experiences of other people, so you don't make the same mistakes they need, that's obviously a smarter thing to do, right? Even a part of the Bible says that, you know, a simple person just walks through trouble and falls for it, but a righteous person sees trouble ahead and takes cover, right? So, you know, I'm not saying you should just like walk into problems just for fun, it's no, right? If you can learn from the experiences of others and not make the same mistakes they need, that's a good thing, right? That's one thing with me. I'm a very big consumer of the experiences of others, of books and stuff, right? I seek mentorship, I ask people for advice, because again, if I see that you've successfully over a concert in challenges, why do I have to go through those challenges as well? I'd rather just learn from their experiences and not make the same mistakes. So thank you for listening to this podcast. I'll see you in the next episode. God bless you. Have a wonderful week. Thank you.

Check the direct bilirubin level. If it's an enzyme defect (e.g., Gilbert's), the direct bilirubin will be very low/near normal, but the indirect is high. If it's overproduction, both indirect and direct bilirubin may be elevated.

Very high indirect bilirubin coupled with very low or absent direct bilirubin (indicating failure to conjugate).

Fetal renal dysfunction/oligohydramnios, and premature closure of the ductus arteriosus due to prostaglandin inhibition.

Because pulmonary vascular resistance drops, increasing venous return and raising left-sided heart pressures relative to the right side, thus increasing the pressure gradient (L $\rightarrow$ R).

It is the vertical conjugate gaze center. It is supplied by the Superior Cerebellar Artery.

At the interventricular foramen of Monro (Interventricle stenosis).

Gilbert syndrome.

Superior cerebellar artery (SCA).

Inhibition of prostaglandins, leading to decreased renal perfusion/urine output.

Optic atrophy lesion + positive Babinski sign (UMN) + impaired vibration sense (Dorsal column dysfunction).

Obstructive/Non-communicating shows dilation proximal to the blockage; Communicating shows generalized ventricular enlargement due to failure of arachnoid granulations.

Vitamin B12 deficiency (Cobalamin).

Gilbert syndrome.

Superior cerebellar artery (SCA).

Inhibition of prostaglandins, leading to decreased renal perfusion/urine output.

Optic atrophy lesion + positive Babinski sign (UMN) + impaired vibration sense (Dorsal column dysfunction).

Obstructive/Non-communicating shows dilation proximal to the blockage; Communicating shows generalized ventricular enlargement due to failure of arachnoid granulations.

Vitamin B12 deficiency (Cobalamin).