DIP Episode 532 - USMLE Step 2CK/3 Rapid Review Series 114

Welcome, my name is Divine. This is episode 532 of the Divine Intervention Podcasts. Into this podcast, we're going to be continuing our Rapid Review series for the USMD Step 2, Seek End Step 3 exams. This is going to be series 114. Let's begin. So what if they give you a question about a two-month-old child, the teller that he is brought to the office by his parents for a wellness exam? And you're told that the parents are concerned about a lesion that they find around the child's body. And we're told that, oh, it's a red lesion and it's been growing slowly. And then you're asked, what's the most likely outcome of this lesion? In fact, sometimes they can show you a picture of this lesion. What should you be thinking about? I really hope you're saying oh, Divine, this sounds a lot like strawberry human juma. There are many names they like to use for this on exams. They can call them a strawberry human juma. They can call them a capillary human juma. But this is something that is pretty high to know for your test. And one kind of question I will strongly encourage you to make sure that you're mentally prepared for, as you're taking the USML Is these days, is to ask yourself, what is the likely outcome of this disorder? That's one of the ways they love to test prognosis on the USML Is. Many people ignore it, but trust me, that's a very bad idea. It's a very, very bad idea. So the most likely outcome is it will grow and then it will resolve. It will grow and then it will resolve.

Make sure you know that. These human juma's many times, their vascula is not many times. They're pretty much vasculotumers and it will grow, grow, grow, grow, grow very quickly. You know, many times from angiogenesis. As you see in a bit, they grow rapidly from angiogenesis and then after a while they just regress over a time. So basically, if they were to ask you, what's your next best step in management? Just reassurance. That's pretty much all you need to do for the parents. So again, what are these strawberry human juma's? These things are pretty much vasculotumers. That's why it's even called capillary human juma's because you see a lot of capillaries that are filled with blood and they are mostly separated by, you know, extracellular metrics like connective tissue, for example. So that's something you want to keep at the back of your mind, for example. And usually these things, you don't have to treat them. But if you're kind of concerned, if you're kind of worried, fine. You can give a bit of blocker. If it's like very symptomatic or it's like kind of a tough spot, you can give a bit of blocker because bit of blockers can inhibit angiogenesis. Okay, they can inhibit angiogenesis. So again, remember, these are capillary tumors with a lot of interspersed connective tissue. Very simple. Very, very, very simple. Very, very, very simple.

Again, I will try to emphasize some basic science details because basic science is something our friends at the NBM is, step two, step three are concerned about because that's a way to weed out people that understand from people that are memorizing. All right. Now, what if they give you a question about a woman? You're told that she comes for her 20-week visit and you're told that her amniotic fluid index, you know, she undergoes an ultrasound and an atomic ultrasound and we're told that the fiddle features were told that the fiddle features are well developed but that the amniotic fluid index is decreased. And then we're told that, ooh, that it is noticed on the fiddle ultrasound that one of the fiddle kidneys is significantly larger than the other. What should we be thinking about here? I hope you're saying, hmm, divine. This child has some kind of urinary tract obstruction, urinary tract obstruction. This is something that's pretty high up to no-foot exams. So, what's going on here? What's the pathophase? Well, and let's kind of bring this question together. The first thing I need to understand is that sometimes kids have issues at the level of the ureteru pelvic junction, at the level of the ureteru pelvic junction. What is the ureteru pelvic junction? Well, look at it. Look at these two words smashed together. Ureteru, so it tells you that, ooh, the ureters are involved here somewhere, pelvic. That means the renau pelvic.

So, basically, in a normal situation, there should be appropriate canalization. So that means opening of the tube, the continuous tube, I guess, that is the renau pelvic and the ureter. You know, basically, there should be like a tube that connects both, okay? If that tube is not properly canalized, that's how you get a ureteru pelvic junction obstruction. In fact, this is the most common cause, very, very high up. This is the most common cause of hydro nephrosis in a fetus on the USML Es, especially like a unilateral hydro nephrosis, a unilateral hydro nephrosis. So, make sure it's something that you understand. If you see a unilateral hydro nephrosis in a fetus or in a new born on the USMLE exams and they ask you for the pathophase, they ask you for the mechanism behind it. Think of incomplication of the ureteru pelvic junction, the ureteru pelvic junction. So, it should not come as a surprise to you that, ooh, this child has this woman in a pregnancy, she has decreased amniotic fluid index. Because remember, a lot of amniotic fluid is fetal ureter, at least a constituent of amniotic fluid is fetal ureter. So, if there is an obstruction to the flow of ureter, then that woman's pregnancy is going to be somewhat tenuous. That's why you see the amniotic fluid index is decreased. So, you can already begin to see that our friends at the MBM is can make so many more integrations with this.

They can give you a question involving vesico-irritory flux, and basically give you the same q-stem. They can give you a question that involves posterior uretero valves and essentially give you the exact same q-stem. These people are going to have oligohydramneus because they are literally not producing adequate amounts of ureter. Or, if, for example, a child has runaway genesis, for whatever reason, you know, it can happen because of some problem, organic problem in utero, right? Or remember, there are some teradogins that are nephrotoxic, like ACE inhibitors and AR Bs. Those things are nephrotoxic. Those things can certainly cause problems. So, those things can cause oligohydramneus. But again, it looks like the child in this question has problems with only one kidney. So, at least the other kidney is working. So, we may be hard pressed to see the full-blown border sequence in this kit. Although, say, for example, if both kidneys were not working, or you had like a very crazy significant obstruction, that may cause border sequence. Because essentially, if the child is not, the child obviously is making urine or whatever, but the urine has nowhere to go out, right? You have significant oligohydramneus. Then the child's face will begin to bang into the walls of the uterus so they can have, like, flat, a flat facial profile, right? Their limbs may not be properly developed. And remember, those kids tend to have pulmonary hypoplesia. Why do they have pulmonary hypoplesia?

Or the thing is that amniotic fluid comes into the child's lungs and it expands the fetal lungs. So, that amniotic fluid coming into those airbags, basically, the lungs is what makes it develop properly. So, if amniotic fluid doesn't get in because you have oligohydramneus, then the fetal lungs will not develop. And that's going to cause pulmonary hypoplesia. That's going to cause pulmonary hypoplesia. Those are the critical things you tend to find in powder sequence, in powder sequence. So, please make sure that you know that stuff. Make sure that you know that stuff. So, literally, I just said that, oh, the fetal lungs feel with fluid. Amniotic fluid, that's what makes it develop. So, you can already be in to see that, oh, this may inform some pathophys. I'm just trying to make an integration on another topic. This may inform the pathophysiology behind transient tychipney of the newborn. So, you see a newborn that's born by C-section because the thing is vaginal delivery, there is some benefit to it. Vaginal delivery has some benefit to it. What's that benefit? The benefit is that basically, as the child is going through the woman's vagina, there are a bunch of things that are happening, but at least two major things that examine worthy are happening. Number one, the fluid in the fetal lungs is almost like the woman's vagina is like a laminitine press for that fluid. It squeezes fluid out of the fetal lungs. So, that's helpful.

Two, going through that vagina, look at how small that hole is. You have a fetus going through that. That's going to cause a lot of stress in the fetus. That stress is going to increase fetal cortisol production. That cortisol is going to promote even more lung maturity. But when you're not born by vaginal delivery and you're born by C-section, then you don't have those two things going for you. So, there's still going to be fluid in the fetal lungs, so my mniotic fluid. So, the child is going to be breathing really hard to blow that fluid. Many times, you're going to see fluid in the fissures on radiographic imaging. Those are the classic things in transictic tachypnea of the newborn. All right. Another of integration there, let's go to something else. So, what if they give you a question about a 25-year-old female? We're told that this female, she has been having really bad breath in the morning. So, do you know, use the word bad breath on your ex-apps? You'll call it hallytosis instead. She has been having really bad breath in the morning. And then you're told that sometimes she has noticed undigested food in her mouth in the morning. Wash and you know, she tells you that, you know, she notices that food does not seem to pass down. What is this? When I hope you're saying all divine, this sounds like an awful lot like ecalasia. Ecalasia. Ecalasia, ecalasia, ecalasia. So, what's the pathophage behind ecalasia? Well, a bunch of things you don't need to know.

There's actually many different ways our friends at the Mbimis can take ecalasia. So, what are the different ways they can take ecalasia with on the exams? Well, let's talk about the pathophage. The thing is, people that have ecalasia, they tend to have decreased relaxation of the lower self-adjusted fincter. Okay? So, sometimes on the exams, instead of putting ecalasia on the exam, they'll put a pathophysiological, pathophysiological answer, if you may. They'll just put decreased lexation. That's going to be the right answer. So, why does the lower self-adjusted fincter have decreased relaxation? Well, the thing is, in ecalasia, these are reduced number of these ganglion cells, of inhibitory ganglion cells. You don't have them because those inhibitory ganglion cells, they're supposed to help with your lower esophagus, relax it. But if you have a decreased number of those neurons that inhibit things, then you're going to get in a lot of trouble. You're going to get in a lot of trouble. So, if your lower self-adjusted fincter is not relaxing, then food is not going to pass through. If food does not pass through, then you're going to have this phasia, simple as that. And if the food is not passing through, when you become, when you lay supine, then just probably undergrab you or whatever. So, if that food reflux is back, that's why they have undigested food coming back up in the mornings, you know, overnight. And you'll also notice that these people may have halitosis.

So, remember, halitosis can again be many things on the exams. Halitosis can be what? It can be many things on the exams. Now, younger person may be think of ecalasia as we're describing here. In an older person, you probably want to think about Zenker's diverticulum. Zenker's diverticulum. That's outpouching in the oppressed ophagus, but let's continue here. So, this person has ecalasia. Now, sometimes our friends at the end of the evening, they can give you arrows involving an ecalasia question. They can literally give you what? Arrows involving an ecalasia question. So, for example, what are some classic arrows they love to test? They love to test lower syphagel's finter pressures, like resting pressures. That's one arrow they love to test. Another arrow they love to test is a syphagel mortality, or like a syphagel peristalsis, especially in the middle of a gas. Another arrow they love to test is a distalus of a gel tone. So, what should these arrows look like on your exams? One, number one, let's start with the LES pressures. I've literally just explained that your lower syphagel's finter pressures are going to be elevated. Now, what should be troviar of a gel mortality? Especially your mid-sophageal. Pay attention to that word. Mid-sophageal mortality should be decreased. The mid-sophageal mortality should be what? decreased. Because think about it. Many people don't process ecalasia this way. What ecalasia is a nerve problem. Ecalasia, its root, is a nerve problem.

When you have a nerve problem, then peristalsis will not be good. Peristalsis will not be good. So, you're going to have decreased mid-sophageal mortality. They're going to have decreased as mid-sophageal peristalsis. Now, what's going to be troviar of the lower syphagel's finter tone is going to be increased, is going to be elevated. Right? And again, remember, how do we manage this? Well, the first thing you're going to do is you're going to do the barium swallow. You're going to do that barium swallow. That barium swallow is going to show you the bird-beak sign. Make sure you can identify the bird-beak sign for your exams. After that, you're going to do a syphagel manometry. That is a syphagel manometry. Is what is going to essentially help you look at manometry. Whenever a manometer is used to measure pressures, so this is like manometry of the esophagus. All these arrows that I just discussed, how do you think they get those pieces of information? Very easy. They get them through syphagel manometry. It's going to show you decreased mid-sophageal manometry. I mean, decreased mid-sophageal peristosis, decreased mid-sophageal. So decreased mid-sophageal peristosis, decreased mid-sophageal motility. And it'll show you increased lower-sophageal sphincter tone, increased lower-sophageal sphincter pressures. Because again, they know that people have memorized these algorithms. So our friends at the MDM is what do they do? They just take things as step further.

They just take it as step further. Because everyone I'm sure has memorized. Number one, biome swaddling. Number two, manometry. Number three, EGD with biopsy. That's the workup. And then, ooh, treatment. Well, how do we treat this? Well, you can do all, you can do all my autumn to treat it. Although there are many other things you can do. You can give like my treats, you can give, you can inject the botulinum toxin. Because remember, the botulinum toxin is going to decrease. It's going to decrease the release of acetylcholine at the neuromuscular junction. So that's going to cause muscle relaxation. So it's going to relax the lower-sophageal sphincter. But again, many times you're going to need to get these every six months. I know I had an idea, I was just going to say, I'll get to it in a bit. And another thing can also do is nomadic dilation. But again, that's a horrible idea. Many times, they like to test nomadic dilation on the USML Is as a conduit to a surface of a gel rupture. Because as you're blowing up air in the surface, blowing up air, you can pop the surface of the gas. Those people have subcutaneous infezima. They'll become very, very unstable. That's not a good idea. So the idea will sting is that steediness. Again, check many on key decks. You probably have number one, barum swallow, number two, monometry, number three, eGD with biopsy. If you're testing that on the exams, that makes absolutely no sense. You're not really testing a person's understanding.

So what can you do as the USML Is? Just say, oh, and many times you're reading questions are like, okay, wow, this fact I knew from my own key deck. They've done it already. They've done it already. You're, you're then wonder, hmm, what's the question going to be? And then you start seeing a bunch of arrows and you're like, what? Arrows in ecalasia. So again, that's where the deep understanding comes in. That's where what? The deep understanding comes in. Because you'll say, oh, barum swallow has been done. Issues, I mean, tapered, whatever, distal, suffogous, and they love descriptions, by the way, as well, different story. And then you'll say, oh, so my number three is completed. Which of the fullings, which of the fullings will most likely be obtained from this diagnostic test or whatever, or from this screening test? And of course, they'll give you a bunch of arrows and things all over the place. That's how you test on the standard. That's how the USMEL is looked. And I'll just throw in a word here. If you love the way explained things or you love a person teaching you how the USMEL is love to put things, I'll strongly encourage you to consider the classes I offer. I have a bunch of classes is going to be short. I have a bunch of classes for step one, just step three coming up this month, actually starting this Thursday, I have a test taking class on Thursday, virus that's class on Friday, social sciences, and ethics class on Saturday.

The offer step one, just step three, and then starting next week Monday, I have a 20 hours step, just step three class. And then that's our next week Saturday, actually, I have a last many reviews of three hour class. I have a separate podcast on this. You can listen to and get some information. And then for the step one, takeers, have a 25 hour step one review from me first to me fifth. Although, if you also are taking step two, step three, you have a poor B6 science foundation, that classes are going to be perfect for you. All right, let's go ahead and continue. So what if they give you a question? So please, I guess to read read that point, make sure you're not just memorizing things, make sure you understand pathophase, make sure you see how links can be made between different concepts. All right. Now, what if they give you a question about a patient, your tool that this person has a long history of severe micro stenosis, and that this person had a valve replacement like four weeks ago. And that now this person has been having yellowing of their skin. And they give you some labs. And you notice that man, the indirect bilirubing is markedly elevated. What should you be thinking about here? Well, I hope you're thinking about like a valve you like your molasses. So the prosthetic valve is literally humanizing their red cells. And you can even ask you which of the following will most likely be found on a blood smear.

I hope you're saying divine schistocytes, schistocytes, schistocytes, so let's kind of put everything together here. According to the world is going on. What in the world is going on? Well, this person got a prosthetic valve. The thing is prosthetic valves can some of them can actually begin to liase your red cells. That's actually a known complication of placing a prosthetic valve. Pestetic valves can literally liice red cells. And obviously, if you're lysine red cells, you're going to reduce your, you're causing an hemolysis. You're pretty much causing an hemolysis. That's going to be like essentially like an intravascula hemolysis. Remember, there are two kinds of hemolysis. It's like intravascula hemolysis. There's extravascula hemolysis because this problem is happening with blood flowing through your body. Is intravascula hemolysis. So you're going to see a lot of a schistocytes on a blood smear. Remember our friends at the MDM Es, another name you may see for schistocytes are helmet cells. They may literally call these things helmet cells, helmet cells. Or sometimes on your exams, they can even call them fragmented erythrocytes. So please, what are the three ways you may see schistocytes presented on your exebs number one? It may be called schistocytes. Number two, it may be called fragmented erythrocytes. Number three, it may be called what helmet cells, helmet cells. So those things tell you that a microagentopathic hemolyric anemia is probably going on a maja.

A microagentopathic hemolyric anemia is probably going on or some prosthetic valve is literally showing up your red cells. Well, think about it as you choke your red cells. What's going to happen to your haptoglobin? Your haptoglobin is going to decrease. Your haptoglobin is going to what? It's going to decrease. Your haptoglobin is going to decrease because haptoglobin essentially binds up this broken down red cell fragment. So your haptoglobin is going to decrease. What's going to happen to your indirect bilirubin? Well, your indirect bilirubin is going to skyrocket, right? The indirect bilirubin is going to skyrocket because remember, as you break down your red cells, you know, break down the hemolyubin to human globin, that he might believe is converted to like believe verdin. And then that believe verdin is converted to indirect bilirubin. So you're going to have an increasing your indirect bilirubin. You're going to have an increasing your indirect bilirubin. Now another question I think I want to address here is, will be trove like your LDH? Well, again, a lot of hemolysis is happening. So your LDH is going to go up. Remember, LDH is kind of non-specific. We're just going to be increased in a person that has intravascular hemolysis. Again, you may know that I'm kind of going a lot going a lot with hours and today like you kind of know your hours for your exams, just FYI. So what are some other things that can cause a person to have sheast or sites?

Well, I talked about the prosthetic cardiac valve. Well, think of other things. Think of other causes of mychrobathecimolytic anemia. Like what? You can see this in a person that has DIC, right? In DIC, DIC is a cause of a mychrobathecimolytic anemia. So you may see sheast on a bloodstream. If a person has what else? Divine. Come on. Think. So DIC is one and all the classic one is H2 S. Very good. Right? H2 S. Your olytic uremic syndrome. Eolytic uremic syndrome usually is caused by E coli O5, O7, H7 is going to one of the findings. Remember, those kids tend to have like acuterino failure, mychrobathecimolytic anemia. So you see sheast on a bloodstream. You'll have thrombocytopenia. Those things can be associated with a person having a sheast or sites on a bloodstream. And they're obviously like the oversized brother of H2 S, that's TTP, thrombotic thrombocytopenic paper. Those that can also cause a mychrobathecimolytic anemia. And you can also find mychrobathecimolytic anemia in some people that are septic, especially people that have like very severe sepsis, they can have a maha as a result of their severe sepsis. So just going to keep that at the back of your mind as you're studying for your exams. All right. So I think maybe let me address one more vignette and then we'll kind of call it for for the day. So what if they give you a question about a 71 year old male, you're told that he has a very nasty hypertension and we're told that let's see how do I put this.

So that's very nasty hypertension. I hear you're told that he has flung breweries. So you cannot school teach like a brewery in his right flung or whatever. And then you're asked which of the following is the I know many of you have like go out divine, uncontrolled hypertension flung brewery. Hello, what is hello, whatever disease you know I'm talking about. But then our friends at the inbemies throw curveball. You'll see which of the following will be the most likely finding on abdominal imaging and then you're like, hmm interesting. Well, I'm sure many of you know that I'm clearly talking about in a lot of stenosis, but that's not the entire story here. That's not the entire story here, right. So what are you going to find on your nation? Well, think about it. We have real all other stenosis, right flung breweries and controlled hypertension or person whatever. You're not profusing the kidney's properly. If you're not profusing the kidney's properly, what do you think is going to happen? The kidney is going to be meekly and diamond itself. And if you're and kidney is meekly and diamond itself, it's going to shrink, right. So you're going to see atrophy. You're going to see atrophy of that kidney. That kidney that is affected in a renal outer stenosis is going to atrophy. It's going to what? Atrophy. So what's the pathophase behind renal outer stenosis? Well, it's basically atherosclerosis. It's basically atherosclerosis. Atherosclerosis. So the problem is with the intima.

Remember, blood vessels have three liars. There's the intima. There's the media and there's the adventition. So it's an atherosclerotic problem. It's an atherosclerotic problem. It's literally atherosclerosis. So let's make a few more integrations here. So if you have atherosclerosis and you're not properly perfusing the kidneys, then what do you think is going to happen? Well, your juxtaglimarial cells are going to freak out. They're going to meek tons of reining. That's going to convert angiotensinogen to angiotensin 1. Then that angiotensin 1 in the endothelium of your pulmonary capillaries is going to be converted to angiotensin 2. And angiotensin 2, one of the things it does is that it's going to go to the zone of glomerulosa of the adrenal cortex and cause it to meek. Adostero is also going to go to your pituitary cause it to meek. And angiotensin 2 is also a powerful viso constrictor. So you can see many forces that play. That's because in a person to be hypertensive number one, you have a very powerful viso constriction. That's going to raise your system in facile resistance. That's going to jack up your blood pressure. Adostero remembering the kidneys, it causes you to reabsorb sodium and water. So that's going to raise your blood volume. That's also going to raise your blood pressure. And Adostero is going to make you excrete out potassium. So that's going to cause you to become hypochilimic.

And nothing, Adostero and also it does is to make you excrete hydrogen ions in your kidneys. As you excrete those hydrogen ions, you're going to have a metabolic alkalosis. You're going to have a metabolic alkalosis. So please keep that in mind. Keep that in mind. And again, the more you will mention is a flung brewing on your exams. They need just mention abdominal brewing. They literally need just mention abdominal brewing. And I guess one thing I want to compare and contrast this with is, and usually if you want to diagnose this, you can go a Doppler ultrasound of the renal arteries. Many times what these people get is just blood pressure control. But if the blood pressure control is not working, then you should consider angioplasty, should consider angioplasty of that renal artery. All right. So compare contrast is with fibromuscular dysplasia. Fibromuscular dysplasia is a problem with the media of the artery. The media is the mostly of the artery. Fibromuscular dysplasia is not atherosclerotic disease of the renal arteries. It's not an intimal problem. It's a medial problem. That's something that's lost to many people as they prepare for the exams. The symptoms may be similar, but the puffer phase is different. Renial artery stenosis is an intimal problem. Fibromuscular dysplasia is a medial problem. And I know classically on the exams, fibromuscular dysplasia, they tend to test it in younger females, but I'm going to tell you this actually.

If I'm not mistaken, the most common isch demographic for fibromuscular dysplasia is a middle aged woman. So don't be shocked if they give you a fibromuscular dysplasia question in a middle aged woman. And usually what are you going to find on imaging? You're going to see that string of beads pattern. You're going to see what that string of beads pattern with the renal arteries. That tells you that, oh, this is fibromuscular dysplasia. Remember, what if you see the string of beads pattern with a mesentery vessel? In a person that has high inflammatory labs, what are you thinking about? I hope you're saying, oh divine, this is polyadritis nodosa. This is polyadritis nodosa. What if you see a string of beads pattern? Let's throw in one more integration here. What if you see a string of beads pattern with your blurry tree? That's PSC. That's primary slurs in collagitis. There's many ways they can test those string of beads. They can test those string of beads. Basically, a series of normal or you'll see like ultra-detail normal segments of whatever tube and diluted segments. So let me know your string of beads. Let me describe it. You'll see your ultra-netain. It'll be some tube, whatever tube, ultra-netain normal and diluted. Normal diluted, normal diluted. You just keep that at the back of your mind, for example. I think we're getting close to 30 minutes here. I'm going to go ahead and stop. But again, I encourage you.

If you just any of my classes should be an email through the website. I can email me at Divine Intervention Podcasts with an SIVN Divine Intervention Podcasts at gmail.com. Also, meet a separate podcast where I give some more information on the classes. I offer one on one tutoring for all the US Million complex exams and I tutor from medical exams and shelf exams as well. Then I have this podcast on Apple, Google and Spotify. Please check those out. I have a You Tube channel where I post the videos that I make. Then I have also help with ear-ass applications, more interviews, personal statements and stuff like that. Then both for people trying to get into Med School and people trying to get into residence of fellowship. Then I also have another website called Divine Intervention Lifelesses.com. Divine Intervention Lifelesses.com. Every week I post two podcasts where from a biblical perspective I explain a life lesson. Many people listen to it and find it very helpful. I actually post the podcast on Fridays and Sundays. It's usually about 10 minutes long. It's actually an Apple podcast associated with that called the Divine Intervention Life Lessons podcast. Thank you for joining me today. I hope you find this podcast to be helpful. I'll see you in the next episode. God bless you. Bye for now. Thank you.

Ureteropelvic junction (UPJ) obstruction.

Pulmonary hypoplasia (due to lack of amniotic fluid for lung development).

Decreased relaxation of the lower esophageal sphincter (LES) due to loss of inhibitory ganglion cells.

Low haptoglobin, high indirect bilirubin, and elevated LDH.

RAS is an intimal atherosclerotic problem; FMD is a medial structural defect ("string of beads").

Vaginal delivery, which squeezes fluid out of the fetal lungs and increases cortisol production.

Schistocytes, fragmented erythrocytes, or helmet cells.

Ureteropelvic junction (UPJ) obstruction.

Elevated LES pressure and decreased mid-esophageal peristalsis/motility.

It causes sodium reabsorption (increasing blood volume) and potassium excretion, leading to metabolic alkalosis.

Fibromuscular dysplasia (FMD).

It mechanically squeezes fluid out of the fetal lungs and increases cortisol levels, promoting lung maturity.

Schistocytes, fragmented erythrocytes, or helmet cells.

Ureteropelvic junction (UPJ) obstruction.

Elevated LES pressure and decreased mid-esophageal peristalsis/motility.

It causes sodium reabsorption (increasing blood volume) and potassium excretion, leading to metabolic alkalosis.

Fibromuscular dysplasia (FMD).

It mechanically squeezes fluid out of the fetal lungs and increases cortisol levels, promoting lung maturity.