DIP Episode 589 - 2025 USMLE Step 1 Free 120 Discussion Part 7 (Q61-70, super helpful for Step 2 and 3!)

Alright, welcome. My name is Divine. This is episode 589 of the Divine Intervention Podcast. And in today's podcast, we're going to be continuing the series on the Step 1, 3, 1, 20. This is going to be Series 7. So if don't, questions 1 to 60. So we're going to pick on from 61. 61 says 78-year-old woman is admitted to the hospital. Because of a one-week history of John Des, CT scan of the abdomen shows a mass, suggestive of pancreatic cancer. Three hours later, the uncle physician enters the patient's room to discuss the prognosis. And obtain consent for a biopsy scheduled for the next morning. On entering the room, the physician grids the patient on her husband. The physician then learns that the patient only speaks mandarin. Her husband is fluent in mandarin and English. The hospital interpreter is not available until tomorrow morning. The patient's husband appears anxious and insists that the physician speaks to him and allows him to serve as an interpreter for his wife. Which of the following is the most appropriate next step in management? Right? So this is pretty straightforward. In general, you always want to use a certified medical interpreter or translator. If the only time we should use another person that is not certified is if it's an emergency, and a certified person is not available. This is not an emergency. So we need to find some answer that involves getting an interpreter. So option A says allow the patient's husband that's wrong.

Option B says consult the hospital's ethics committee. Don't do that. Option C says explain to the husband that information cannot be provided until the interpreter arrives in the morning. That may be reasonable. Let's keep that option D says user telephone interpreter service. Yeah, you know, their telephone interpreter service says you don't want the patient just stay anxious for no reason when you can get someone over the phone that can do correct interpretation. So I'm going to go with option D for that one. Pretty straightforward question there. All right. Question 62 results of a study that examined the impact of risk factors on cardiovascular health being evaluated in the study. Serum LD alcohol is concentration is found to have a correlation of 0.6 with serum high sensitivity serious active protein concentration, which of the following statements best describes the relationship between LDO concentration and high sensitivity serious protein concentration based on this find it. So we're seeing that this is a correlation right. So you know usually you get these from scatter plots, you know, these correlation analyses. Now remember your your correlation analysis give you an R and you are can range from negative one to positive one. Right. If you have a negative R, it means you have a negative correlation. What's a negative correlation? It means as basically the two things the two variables going opposite directions.

But if you are as positive it means you have a positive correlation. It means that the two variables you're dealing with going the same direction. They both go up or they both go down. So since there are here is positive it means that the things both go up or both go down. Right. And we're told that in the study serum LD alcohol cholesterol concentration is found to have a correlation of 0.6 with serum high sensitivity serious active protein. So it's either both are going up or both are going down. Right. Again, I can tell you right off the bat. We can probably get rid of C and D. Those make no sense. Again, you can not just establish position from a correlation analysis. So that's wrong. Right. So option A says higher LDL concentrations that are treated with higher high sensitivity serious active protein concentrations. Okay. That's same direction. So that's right. Option B says higher LDL concentrations that are lower high sensitivity serious active protein concentrations. Well, that's opposite directions that they'll give you an R that's negative. That doesn't feel with the data we have. So the answer is a right. And you know, just something to know higher levels of high sensitivity serious active protein tend to be a kind of straight up people having kind of like just not great health outcomes. Just something to keep in mind. Me kind of pop up on an exam. All right.

So going to question 63 says a 45 year old man comes to the physician because of a 10 year history of heartburn that occurs after he eats late at night to consume spicy food. He has had no week loss or difficulty swallowing. He takes over the counter-enter sits as needed. But they relieve his discomfort only temporarily. Physical examination shows not normalities and endoscopy is done. The distance of the disease shown in the micro photograph, which of the following is the most likely cause of this patient symptoms. Right. So again, I told you whenever he's images on your exams, don't panic. Don't freak out. Just read the question carefully. Many times you can figure out what it should be the right answer just based on the strength of that. But this person probably just from the question without looking at the image sounds like they have good. Right. And it sounds like antices are not working. Right. But or at least working kind of temporary. This person is probably going to need a proton pump inhibitor at some point. So this person has a gird and again, if you look at the image, right, you can see the subjunctive cause it just looks red and inflamed. It's probably gird. Right. It's probably gird. I'm not going to think too hard about this one. Okay. So he says what's causing it? So option A says defect in secret in production. That's wrong. Um, secret in doesn't really have much of, um, don't get me wrong. There is some kind of link.

You know, especially I'm sure you can think of the secret in stimulation test. That's one of the ways you can confirm the diagnosis of gastrinoma, um, especially when you the gastrin levels are equivocal. But again, I wouldn't, I wouldn't worry about that. Now there's like gird is not caused by people having secret in problems. Right. No. Right. Gerdy is a pretty common disorder. Option B says, uh, excessive gastrin production. That's going to be a gastrinoma. Right. You make a ton of gastrin. It's going to make you make a lot of gastric acid and getting trouble. Uh, that's wrong. Right. This person, if you have a gastrinoma, you have a ton of ulcers. Right. This problem seems to be localized to the esophagus. So that's wrong. Option C says excessive transient lures of a jaw relaxations. That's correct. Right. Like whenever your esophagus is too relaxed, then acid can reflux from the stomach and cons gird. Uh, I bet that that's why it affects the distal esophagus when people have gird. So the answer is C. Remember, if you have excessive, uh, you know, failure of relaxation. So like almost like the opposite, failure of relaxation of the lures of a jaw's fincter. That's going to be collisia. Just something you want to keep in mind there. Option D says, uh, failure of primary esophagella, uh, peristalsis. Um, no, that's, that's wrong. Right. Uh, that's more than a esophageal motility problem. And people that have gird is not an esophageal motility problem.

And then option E says failure of saliva production. That's, that's ridiculous. Right. So we're not going to pick that. All right. Question 64. A 72 year old man comes to the physician for health maintenance examination. He has no personal or family history of major medical illnesses. He has never smoked cigarettes. Post-oxymetrion rumours shows an auto-sad of 98%. Physical examination shows plethorax skin and spino-megaly. Laps to this show. So this hemoglobin is 21.1. Uh, that's pretty high. Uh, hemoglobin is pretty high as well. White count is pretty high. Um, a lot of neutrophils, you know, it's fine. Whatever. Plytile count is pretty high as well. And local cell alkaline phosphatesis increase, right? So a peripheral bloodstream shows occasional giant pletilets. Uh, the primary hematologic defect, defect in this patient most likely according to which of the fluins cells. Right. So, uh, again, let's work this out first. That's a kind of pretty start nausea in this podcast. But we see this person seems to have, um, pretty high hematocrate, pretty high pletile count, right? Has plethorax skin, has plethorax skin, so we're seeing like, antecedents of a polycythemia vera, right? P vera. I remember p vera. But we also seen that the pletile count is also pretty high. So it's like, hmm, does this person have essential thrombocytosis? Right. Although, if you notice, so much of the question is focused on the spino-megaly, the plethorax skin, the high hematocrate.

So I'm going to vote more for a polycythemia vera. Right. So this person has p vera. Now, remember, p vera, um, is one of these myeloproliferative disorders, where you have this jaqtumitation. And because of the jaqtumitation, you produce tons of cells, right? And the thing is, many times on the USML Es, it will affect multiple cell lines. It can affect your white blood cells. It can affect your pletlets. It can affect your red blood cells, right? It affects multiple cell lines. So the fact that it affects multiple cell lines, you kind of tell you something, right? That maybe it's not just one distinct kind of cell, like not just like red cells alone. No, right? Because if it's only like a red cell line, it affects, then why would this person split, let it come be elevated? Why would this person's white come be elevated? That doesn't make any sense. So the thing is, it's actually a common progenitor that's affected. That's why you can have multiple cell lines affected. It's just that typically we name the myeloproliferative disorder for the cell type that just seems to be increased the most, right? So it's like this person's hematocrate is pretty high. So we're probably going to call this polycythemia vera. So let's look at the answer choices here. So option A says a rethroid progenitor. Again, that would only raise your red cell count and do nothing with the white cells and the platelets. So that's wrong. Option B says hematopoelic stem.

Let's keep that that's probably going to be right. Because again, we're seeing the red cells, white cells and platelets are affected here. Option C says lymphatic progenitor. Again, that will only raise your white cell count. That's not what we see. That's not the date. That's not consistent with the data we have in this question. D says mega-carriers type progenitor. Again, that's not consistent with the data we have here. Because the platelets are elevated. Don't get me wrong. But the red cells are also elevated as well. And then peripotent stem. Peripotent is going to affect so many different cell lines. Like, no, that's not what's going on here. This is a hematopoelic stem cell problem. Not a peripotent stem cell problem. Peripotent, a cell that is peripotent has like amazing abundant potential. It can form more than just blood cells. It can form so many things. So if you're a peripotent, it means you can form many, many, many, many different cell types. No, this is just focused on like red cells, white cells, platelets. So honestly, I'm going to go with option B for this one. Right? And again, this person, what would you expect this person's equal to look like? Well, this person's equal, I hope you're saying, oh, the vine there, equal is going to be low. Right? Because the body sees that, gee, this person's red cell count is too much. So that's going to lower the presence of erythropoietin. Right? But remember, you can have polycythemia because you have like hypoxia.

Right? You know, let's say you have COPD or cystic fibrosis. That's going to cause a person to have polycythemia. But that polycythemia will be a pseudo elevated epoch because the hypoxia elevates your epoch and that causes you to have polycythemia. But again, this person doesn't have hypoxia, though, too sad is 98%. All right, let's go to question 65. A 35-year-old man is brought to the ED 30 minutes after he's sustained the cord on his hand while loading cargo at his job. He leaves alone and takes most of his meals at a local restaurant. He eats mostly snack foods at the bar and fast food. He drinks four to six, 12 ounce beers, daily and double that amount on weekends. He takes no medications. Physical examination shows a three-centimeter elaceration on the right hand that is bleeding steadily. Lab studies show a hemoglobin concentration of 11. Logosite count of 4,000, and plecite count of 150,000 per millimeter cubed. A photomicrograph of a peripheral bloodstream is shown on the efficiency of which of the following is the most likely cause of dyspacines and inemies. All right, so let's ask ourselves, again, keep the image for now. Let's focus on the question. If you notice, this question is showing that this person has anemia. Okay, and this person is an alcoholic. Again, let's try to work with that information and see if that can guide us in some direction. The thing is, alcoholics, what would be probably like a pretty common issue with alcoholics?

Alcoholism has a stronger, so it's a fully deficiency. Because alcohol inhibits certain enzymes that helps, that help with fully triabsorption in the GI tract. So that can cause a fully deficiency, and that can cause anemia. Remember, fully deficiency is going to cause a megaloblastic anemia because you're going to have impaired DNA synthesis. All right, so that's probably what's going on here. So let's look at this image, though, to see if it gives us any credence. And it kind of looks like it does, right? Many times when the USML is want to show you a relevant finding with an image, they will put it in the center of the image, or roughly in the center. We can see these big, ginormous neutrophils, right? Because again, they put all these red cells that I almost look like. You're like, ooh, these hypochromic red cells, right? Just to see if they can kind of throw in, wrenching your thinking. But again, just kind of look at the, look at these white cells. Look at these neutrophils. You can see like multiple lobes, right? Those are hypersegmented neutrophils. Those are hypersegmented neutrophils, right? So whenever a person has hypersegmented neutrophils, again, that's pretty consistent megaloblastic anemia from fully to B12 deficiency. So I'm going to go with option A here. I'll go six plus three dehydrogenase deficiency. I will cause anemia, right? But it will cause, you're going to see more hind's bodies and bite cells on a photo micrograph, right?

Because remember, those hind's bodies oxidize red cell elements, the bite cells or splinic microphiges haven't taken a bite out of the red cell to remove those hind's bodies, right? So that's wrong. Iron deficiency anemia will cause hypochromic microcetic anemia, right? And the cells will usually be small, right? These red cells look fairly big. They look almost as big as the white blood cells that we're seeing here. So it's probably not microcetic. Probably not microcetic. And again, we would not be seen hypersegmented neutrophils under those circumstances. Option D says vitamin B1 thiaming. Thiaming deficiency generally causes heteroblastic anemia. Actually, let me think about that for a second. Let me think about that for a second. Actually, you know what? I take that back. Whoops, sorry about that. Thinking of option E, vitamin B6 pyreducts in deficiency will cause heteroblastic anemia, right? Think of isonize it. Isonize it inhibits the activation of thiaming of pyreducts in vitamin B6, right? Whenever you have a B6 deficiency, then the first step of him synthesis, where delta amino level inic acid is made will not work very well. So if that happens, you won't be able to make him, and if you cannot make him, you cannot make himoglobin. So that's going to cause microcetic anemia, but that's going to cause more of a heteroblastic anemia, right?

Whenever you have him synthesis pathway problems, that tends to cause more of a heteroblastic anemia with those ring-ceteroblastic. That's what we don't see that here. So option E is wrong. So please, I mean, spoke option D, thiaming deficiency causes more of a wernic acid course of coffe syndrome, okay? It doesn't typically cause anemia. So that D is wrong. So the answer here is definitely option A. All right, question 66 says, at 3800 grams, so 8 pounds, six ounce newborn is delivered vaginally at 39 weeks gestation. After a non-complicated pregnancy, abscribes are 9 and 9 and 1 and 5 minutes respectively. The newborn is crying, haspink skin, and appears vigorous. Physical examination shows of a vagina and also a structure that appears to be a penis. With the urethra located at the base, near the opening of the vagina. Okay, at the base, urethra at the base kind of looks like a hypospedia. All right, now, chromosome analysis is ordered. Which of the following is the most likely cause of the intersex findings in this newborn? If the chirootype is found to be 46xx, right? So let's again, kind of work out what we got here, right? So if the chirootype is 46xx, that means genotypically the child is female. But we see this child has female reproductive organs and this child has also seems to have what appears to be a penis, right? So we're kind of seeing like, it's kind of like a big genitalia here.

All right, so the thing is, usually when you get these questions, you should probably go through every single answer and try to kind of cross things off, right? Try to cross things off. That's usually the smart play, right? But this child genotypically is female. So normally, phenotypically, this child should be female as well. But we see like a penis. So what may be causing that? All right, so let's go through these one by one. So option A says, 17 alpha hydroxyprogesterone deficiency. Well, if you have a deficiency of that, if you're thinking of the, and again, this is something that I think may be potentially helpful for you to learn for your exams. But if you have an issue with 17 alpha hydroxyprogesterone, the thing is, it's actually part of that synthesis pathway in the adrenal cortex for making like sex steroids and glucocorticoids and our dosteroid. Right, if you have a deficiency of that, you will have issues making, you'll actually have issues making up. Parties all, you'll have issues making our dosteroid. So typically for these kids, we're gonna expect to see a lot of electrolyte abnormalities, right? So you should expect, because you're not making our dosteroid, you should expect like hyponitremia, because you cannot excrete acid, you should expect metabolic acid doses, you should expect hyperchilemia. The child will be very hypotensive, right?

The child may even have skin hyper, actually, the child will have skin hyperpigmentation because they're not making cordies also, there's no negative feedback, so their ACT is high. And because ACT comes from POMC, their MSH is also gonna be high as well. That doesn't really feed the data that we have here. So I'm gonna go ahead and say that that's wrong, right? That's wrong, right? That's gonna give more of like a congenital adrenal hyperplasia picture. That doesn't really feed what we have here, so that's wrong. Option B says increase concentration of moliran inhibiting substance. Well, moliran inhibiting substance, if you have an increased concentration of that, then that's gonna shut down the production of female reproductive structures. So you shouldn't really be seeing a lot of female reproductive structures in this person. Well, this person appears to have female reproductive structures, right? This person has a vagina, right? And this person, we're not told like, oh, no uterus, no fallopian tubes, no this, no that. We're not told that, right? We're not told that the lack derivatives of the molirion duct, we don't have that information. So we cannot jump to those conclusions. So option B is definitely wrong. Option C says maternal angrigin exposure. Well, if you're supposed to angrigin, then that can make some of your outward sex organs look male. So that's probably right. But let's keep that.

Option D says presence of the sex determining region on the Y, that doesn't make any sense. Again, this child is 46 XX, right? And if you have the sex determining region of the Y chromosome, then you're gonna make, you're gonna have a lot of derivatives of the wolfian duct, right? So you're gonna have a lot of male structures, right? A lot of male reproductive structures. We don't see that here. The only thing we see is what appears to be a penis. It's not even like it appears to be a penis, right? I'm not gonna jump on that there, that's one. And then two, also, if you have the sex determining region on the Y, again, it means you probably have testes. And if you have testes, then you're gonna be making a lot of molirion inhibiting factor. So you will not have derivatives of the molirion duct. Like again, the fallopian tubes, the uterus, the upper vagina and things like that. Again, we don't really see that here. That's not really consistent with what we have here, right? So we're not gonna pick that option. E says five alpha reductase deficiency. Those are, people that have five alpha reductase deficiency, genetically, they're male, they're 46 XY, but on the outside, they're gonna look female, although that's gonna change during puberty, right? Because if you have a five alpha reductase deficiency, you're not making DHT. And if you can not make DHT, your outwardly male sex organs will not look outwardly male until you hit puberty.

And then those region hormones just take over. And they make a ton of testosterone because you know, you've hit puberty. And that forces that realization. We don't see that presentation here, so that will be wrong. Personally, like a lot of the answers here don't make sense. The only thing that makes any kind of sense is option C. You know, this child is crying, has pink skin, appears vigorous. This child doesn't have electrolyte problems. This child is not profoundly hypotensive, like you see in congenital adrenal hyperplasia from like 21 hydroxylist deficiency. So it is wrong. B doesn't make sense with the data we have. D and E don't make sense. Even just giving the genotype, right? This child is 46 XX. You know, so options D and E just make no sense because generally those tend to be found if people that are 46 XY, right? So again, whenever you get these disorders of sexual differentiation questions, it's always helpful to finish the block first and leave them for last because they can really eat up a lot of time. And then when you're done with the block, come back, work through them by crossing of answers based on data you will have, right? If you don't have data on something, cross it off, right? Cross it off. And many times have noticed that it's helpful to ask yourself, what will be the classic presentation of this answer? If that classic presentation is not there, cross off that answer as well. All right, let's go to question 67.

An 80 year old woman is brought to the ED 30 minutes after she fell out of her wheelchair home. This is the second visit to the ED for her fall during the past three months. Oh no, she lives with her daughter and son-in-law. Who say they do the best we can? Patient has dementia, coronary artery disease, type 2 diabetes hypertension. As she's on a low-deepena spring, at over-starting to Nepezile, insulin and lysinopropyl. Five years ago she went bilateral below the knee amputations because of infected ulcers of the feet. She uses a wheelchair for emboleation. Ten years ago she went three vessel cabbage. She has smoked one half pack of cigarettes daily for 60 years, drinks the shot of whiskey nightly, thin appears, ill and disheveled. Her vitals look pretty good. Her auto sat on two liters is 95%. She has temporal wasting on physical exam. There's scutted echimoses over the abdomen and all extremities, no other abnormalities are noted. I wish I was following the most appropriate initial history to obtain from the speech. This is a pretty classic question. This person has so many risk factors for being abused. Looks like she's being abused, right? You see all these echimoses, abdomen, all extremities. You know, the daughter and son-in-law, like, hey, we do the best we can. And this person has so many risk factors, right? She's demented. She is immobile because, you know, bilateral below the knee and putations, right? This person just has poor functional status.

This is like a prime, prime, prime example. And she looks disheveled. Looks like these people are not taking care of. You're doing the best you can. And your mom looks disheveled and stuff like that, right? She's not been taking care of. This is elderly abuse. You need to contact the non-protective services. So let's see the answer choice. That makes sense here. That relates to the best to elderly abuse. So option A says, ascribed out of normal bleeding, nah, that doesn't make any sense. Option B says, dire, nah. Option C says, relationship with our family. I'm gonna pick that one. This person is literally being abused. Option D says, respiratory symptoms. Nope. Option E says, urinary symptoms. Nope. Right? This is elderly abuse again. Your life just gets a lot easier when you try to work out what's going on in a, in a queue stem. So the answer here is clearly, clearly see. If you pick anything other than see you, you, you should, that one of your wise life decisions. All right. So question 16 says, a healthy 26 year old man with red, green, red, green color blindness. Where is a woman whose father? Where is a woman whose father? Also has red, green color blindness. Pedigree is shown. Which of the fully imbest predicts the risk than a son of this cop will be affected? Mm. All right. So the man has red, green color blindness, right? So he's like generation two, person number two, right? His wife, you know, is a generation two person number one.

And we see the, it looks like the wife's dad, that's person two, generation number one. We see the wife's dad also has red, green color blindness. Well, what do we know about red, green color blindness? Let's try to work this out for us. Well, we know that red, green color blindness has excellent recessive inheritance, right? So it's going to be more commonly males. It's probably going to show up more in males, right? And maybe like divine, what if I didn't know that off the top of my head? Well, if you didn't know that off the top of your head, well, you can read a pedigree, right? We can see that in generation one, the male has the problem. Generation two, the male seems to have the problem. This problem just seems to show up only males. It's almost like the females are just like, we don't want this problem. Whenever you see something just predominantly showing up in males, think of an excellent recessive disorder, right? That's like a just a common sense thing to keep in mind here, right? So we know that, okay, we're asking like, hey, best predicts the risk that a son of this couple will be affected. Well, the thing is, look at this, the man has it, right? The man has the problem, right? But the woman has a dad that has the issue. So because it's excellent recessive, right? And this one, the, you know, generation two number one, this man's wife is unaffected. She's probably a carrier because her dad has the issue, right?

Because remember, if you're a woman, your ex ex, you got one ex chromosome from that, one ex from mom, right? One ex chromosome from that one ex from mom, right? So since her dad has it, she for sure got one bad ex chromosome from dad. But she probably has a good ex chromosome from mom because, you know, you know, she is unaffected, right? For an excellent recessive disorder, if you have two bad ex chromosomes, then you're getting trouble, right? She must have one bad and one good because she's unaffected. She for sure has one bad because her dad has a bad ex chromosome. That's why her dad has the problem, right? So she has one bad one good. So she's a carrier. I think we can definitively say that she's a carrier, right? And her husband is affected. And then he says, risk that the son, well, their son is gonna be XY, right? You're gonna get your, and if you're XY, right? You can only get your Y chromosome from a man. So this son's Y chromosome must be from dad. The son will not get an X chromosome from that. So this son is actually not getting the bad ex chromosome that dad has. So the son's X chromosome must come from mom. And we know that mom is a carrier. Mom has one good ex and has one bad ex. Well, the child has a 50, 50 chance of getting the good ex or the bad ex, right? So this son has a 50% chance of getting this red-green color blindness, right? Remember the drugs that can cause coloblin is like a thambutol, right? Like a thambutol.

And remember, dejoxing can also cause like yellow vision problems, right? So this question is not where I'm gonna go through all the answers. Like this is something that you either know it or you don't. And again, I think I've walked you through my logical thought process as to why option C is the right answer, right? The son will get a Y chromosome from dad, will get an X chromosome from mom. Mom is a carrier. She has one good ex, one good, one bad ex, right? 50, 50 probability that you will get either the good or the bad ex chromosome. So the answer has to be option C, right? So let's go to question number 69. 25 year old woman comes to the physician because of a long history of pain with men's teeth. The pain occurs on the first day of her five day menstrual period and last all day. She is the pain as a 10 on a 10 point scale. The most appropriate initial pharmacotherapy to relieve this patient's pain has which of the fully mechanisms of action, right? So again, what does she have? This person has primary dysmene rare, right? Painful men's teeth. And again, what causes it? What's the pathophysiology? Well, it's because of, it's because you have like pretty violent myometrial contractions. And those violent contractions happen because of prostaglandins. That's why for primary dysmene rare, NSAIDS are amazing, right? Because NSAIDS, they are reversible inhibitors of coxone and cox 2. They will decrease prostaglandins synthesis.

That will shut down those violent myometrial contractions and that's gonna help the person, right? So we're gonna give this person an NSAID, right? So option A says inhibition of estrogen synthesis. And that's wrong. That's gonna be more like an aromatis inhibitor, right? Like an astrosol, electrosol, exymestine or four vestrant. We use those for like breast cancer, chemotherapy, relaxes, that's wrong. Option B says inhibition of 11 beta hydroxylase activity. That's wrong, right? There is no high yield drug that typically works on that. That is usually US military testing. So that's wrong. Option C says inhibition of prostaglandins synthesis. That's clearly right. So C is the right answer. Option D says stimulation of FSH synthesis. No. Option E says stimulation of LH synthesis. No, right? Remember your FSH and your LH no rise. If you have like a streak ovaries, like primary hypogonadism where your gonad is not working. So there's no negative feedback. Because there's no negative feedback your gonadotropians will rise like FSH and LH, right? So the answer is C, this is a pretty straightforward question. Okay, question 70 says. A 56 year old woman comes to the physician because of a two year history of recurring UT Is accompanied by left flank pain. Physical examination shows no abnormalities. Renal autosanography shows, left-sided hydronephrosis. A T2-witter coroner MRI of the abdomen is shown. The arrow indicates the hydronephrosis.

The left renal collecting system is most likely obstructed and which of the following anatomic locations in this patient, right? So of course they give you an MRI and I know somewhere like shoddering like, oh no, MRI, oh no, what do I do? I don't know, what the life's an MRI. Calm down, chill out. Again, I told you, most times images do not absolutely matter to you answering questions correctly, right? So it's like you're not a radiologist. The USM is you're not stupid, they know, right? They know you're not a radiologist, right? Again, depend on the question. This is one of those, this is one of those like pretty straightforward things, right? So like whenever there is obstructing the urinary tract, what is the most common location of a urinary obstruction? Literally, what is the most common location? It's gonna be the uretereopelvic junction. That's a factoid you should know, right? This MRI, you literally don't need it at all. I'm not even gonna waste time on the MRI, right? This is again, something you should know, right? So the answer is option D. Again, these anatomy questions, anatomy is usually one of those things where you cannot kind of rationalize your way to the right answer, you don't know it or you don't know it. So the right answer is option D, right? The right answer is option D. Remember your option A relates to a person that has more like a BPH, you know, has more like a BPH, right?

You know, option E, something you may find in a person that has like vesico-urotereo reflux, option E, vesico-urotereo reflux. So again, the right answer is D, right? The most common location of obstruction in the urinary tract is usually gonna be the uretereopelvic junction. All right, so I'm gonna go ahead and stop here. Again, if you love the way I teach, again, I have a bunch of classes you may find to be helpful. I have actually a step one class taking place in the first week of May. You can still sign up for it actually. So pretty, it's 25 hour class, very good for step one, level one. I've had many people take the class and pass the exams. And also, because there is a lot of basic science making it to step two, step three, a lot of step two, step three takeers are beginning to take that class as well. And then I have a bunch of other classes, you know, for step one to step three, you know, test taking class, biostat class, social science class. Those are taking place about two, about 10 days from now, starting about 10 days from now. And then I have a 20 hour step two, step three review and I have a last minute review. That's all those last two I just mentioned as specifically for step two and step three. And then I have a 50 hour class taking place in the first two weeks of June, just for step two, step three. That class is going to be amazing. But again, I meet separate podcasts where I talk about those classes.

I'm also offering one to you during for all the USME Lian complex exams. And I have these podcasts on Apple Google and Spotify. And then I also have a You Tube channel, you know, Divine Intervention USME Ly Podcasts and Videos where I post the videos that I make. And then I also help with ERA's applications, personal statements, mock interviews and things like that. So if you need any of those help, just shoot me an email through the website or you want to sign up for my class. It should be an email and I can give you some more information. And then finally, I have another website called Divine Intervention Lifelessens.com. Divine Intervention Lifelessens.com. Pretty much every week I post like two to three podcasts where from a biblical perspective, address a life lesson. There's actually an Apple podcast associated with that, you know, many of you know I'm a Christian. So I release these life lessons podcasts every week where I try to just use the Bible to educate people on life lessons. So thank you for listening to me today. I will see you in a episode 590. Have a wonderful day. God bless you and bye for now. Thank you.

The two variables move in the same direction (both increase or both decrease).

The ureteropelvic junction (UPJ).

Prostaglandins.

Cobalamin (Vitamin B12) deficiency.

X-linked recessive inheritance.

The underlying defect affects a common hematopoietic progenitor stem cell.

Inhibition of prostaglandin synthesis, reducing uterine contractility.

The common hematopoietic progenitor stem cell (affecting multiple lineages).

Hypersegmented neutrophils.

50% chance of being affected (due to inheriting the mother's bad X chromosome).

Hyponatremia, metabolic acidosis, and hyperchloremia.

Hematopoietic stem cell problem.

Inhibition of prostaglandin synthesis, reducing uterine contractility.

The common hematopoietic progenitor stem cell (affecting multiple lineages).

Hypersegmented neutrophils.

50% chance of being affected (due to inheriting the mother's bad X chromosome).

Hyponatremia, metabolic acidosis, and hyperchloremia.

Hematopoietic stem cell problem.