DIP Episode 210 - USMLE Step 2CK Rapid Review Series 31

Okay, welcome. My name is Divine, I'm a resident. This is episode 210 of the Divine Intervention Podcast. And in this podcast I'll be talking about the USMLSTEP2 C key rapid review. This will be Series 31. So let's go ahead and jump right into it. What if they give you a question about a patient? And this patient is like this patient has like a menstrual cycle that is 40 days long. What would the length of the person's follicular phase be? This is one of those things that's like a basic science concept, but it's something that people actually don't under. Like that classically shows up quite commonly on the USMLSTEP2 C key exam. So I think maybe before I answer the question, let me go ahead and discuss the phases of the menstrual cycle. So the first thing with mentees is that when a person, you know, after you have your mentees, right, after that you rest out the follicular phase. The thing in the follicular phase, the big time hormone is estrogen. Estrogen is released by the dominant follicle. So the dominant follicle is making, making, making estrogen. And that estrogen is causing proliferation of the person's endometriol. So the endometrial layer is proliferating. I'll see that again. The endometrial layer is proliferating. So the follicular phase of the menstrual cycle has proliferative endometrial. But the thing is, over time you will then have an LH search. You have an LH search. You then have ovulation. Ovulation is where you literally release the egg.

And then after you release the egg, you form a remnant of the follicle that is essentially not the egg is formed that's known as the corpus lurium. The job of the corpus lurium is to produce progesterone. It's to produce progesterone. Progesterone is something that stabilizes the endometrium. It stabilizes the endometrium because it's trying to, I mean, look at the name progesterone. It means that it is progestational. It tries to stabilize the endometrium. It converts it from a proliferative endometrium to a secretory endometrium so that you can support pregnancy. So if by some chance, right, that egg that was released gets fertilized by sperm and you form like a like a zygote. Right? And that zygote will implant in the uterine cavity like in the endometrial one. And when it implants, it begins to release beta-hicigi. And that will keep the corpus lurium living for much longer than its natural lifespan, which is 14 days. Okay? But if for whatever reason you don't have any fertilization, right, then you don't form a zygote, then you won't form a placenta, then you won't make beta-hicigi. So those survival signals that are sent by beta-hicigi to the corpus lurium will not be there. And the corpus lurium will die after 14 days. When the corpus lurium dies after 14 days, the source of progesting to stabilize the endometrium to keep it in that secretory phase will be gone. And the person will essentially bleed. Okay? The person will essentially bleed.

That's what's known as, that's essentially what happens in the menstrual cycle. Right? So notice what I said, I said that the length of the secretory phase of menstruation is 14 days. That's it's 14, it's a fixed number of 14 days because that's the let like the lifespan of the corpus lurium without survival signals. Right? So if a person has a 40-dimensional cycle, that means their follicular phase is going to be 26 days. Okay? The reason I'm going over this is your friends at the MBM, the affund of writing questions where an individual, you know, they will tell you that this person has menstrual cycle that is this long and then they'll say on the X, what phase is this person? And then they'll, it's literally like a basic science question, making its way to a step to seek exam. So that's something you want to keep at the back of your mind for tests. And that also kind of explains why if for example, a person has a detail you that, oh, they give a person projecting. Let's say this person has not had me since for like four or five six months. Right? And then they tell you that you do a projecting withdrawal test. You administer projecting to the person and then you withdraw from you. Notice the person bleeds. That means you supplied progester, right? The person bled. So that means a deficiency of progestin must have been the problem that was making them immunoric, right?

And if a progestin deficiency was the problem, that means the corpus luteum never formed in the first place. Because if the corpus luteum formed, then the person would have me projected. So it's like almost like a working your way backwards kind of deal. So you're like, I give this person projecting the how do we draw bleed? That means projecting deficiency was the problem. If projecting deficiency was the problem, that means the acroprosyluteum did not form. Well, if the acroprosyluteum did not form, that means they did not ovulate, right? So that person probably has an ovulation as the cause of the amenory. And most commonly on MBME exams, when a person has an ovulation, you absolutely want to think about PCOS on that those circumstances. You want to think about PCOS on that those circumstances. Now, one other thing I want to talk about here is differentiating a lesion in the medial longitudinal fasciculus from a lesion with the paramedian pontine reticular formation. That's one of those like questions that essentially like you take a USMLE exam, pretty much everyone taking that exam ultimately gets the question wrong, right? So let's kind of talk about it so that you don't get it wrong on a test, right? So the thing is the MLF is known as the medial longitudinal fasciculus, right? The MLF is known as the medial longitudinal fasciculus. It is classically impaired in a person that has internally a pharma pleasier, right?

That's almost always people that have multiple sclerosis on an MBME exam. So the thing is when a person has an MLF lesion, right? Because the thing is the MLF, we find it for the most part in the ponts and its job is to con, like it serves in making horizontal conjugate gaze work, right? It serves in making horizontal conjugate gaze work, right? So work with me here for a second. This is one of those areas of this podcast where you may want to pause and listen again, pause and listen again. But basically if you think about this, if you're trying to look to the right without turning your head, right? Your right eye has to AB docked, so abs like abs like AB docked. And then your left eye has to AD docked. I'll say that again. If you want to look to the right, your right eye needs to AB docked and your left eye needs to AD docked, as in like, AD as in addition, right? AD docked. So the thing is that means your right lateral rectus muscle needs to work and your left midiorectus muscle needs to work. So if you work your way backwards even more with that, it means your right cranial sex has to work and your left cranial three needs to work at the same time. I'll say that again, they need to work at the same time. So for them to work at the same time, it should make sense that there is a structure that serves as an intermediary between the cranial six nucleus on the right and the cranial three nucleus on the left.

And that structure that acts as the intermediary is known as the medial longitudinal faciculus. And it is found for the most part for all intents and purposes in the point. Okay? That's a high-yield thing to know, right? That's a high-yield thing to know. Now, the thing is if, for example, a person and basically the way the signal starts is it starts at the cranial six nucleus and then he hits the MLF and then he hits that cranial three nucleus. Right? So the thing is if a person has an MLF lesion, it's the cranial three nucleus that will be affected, not the cranial six nucleus. Right? And essentially that person on horizontal conjugate gaze, they will not be able to AD-duct the eye that needs to AD-duct. So in this case, for example, saying, oh, the person should look to the right, right? The right cranial six will work, you know, they'll AB-duct the right eye, but the left cranial three will not work, right? They will not be able to AD-duct the left eye. So they'll have an estagmas in the AD-ducting eye, right? Whenever you see that, right, that person has an intonucle of thymoplesia, right? And the thing is if you want to know the right side of the MLF that's affected, it's always going to be the same side as the eye that has problems with adduction, with AWD-oxion, okay? Adduction problems, right? So in this case of looking to the right, you'll be the left MLF that'll be affected. That's a high old thing to know.

So notice when a person has an MLF lesion, it is only one eye that'll be affected, you'll be the adducting eye. Now, let's contrast that with something called the PPRF. The PPRF is what's known as the paramedian point in reticular formation. I'll say that again, the PPRF is known as the paramedian point in reticular formation. The thing is when a person has a PPRF lesion, the PPRF is found in the and its job is again, it's used in horizontal conjugate gaze, right? It's job. So I think of it as, you know, when I say that, oh, cranial six drives the medial longitudinal for circulus, and then the medial longitudinal for circulus drives cranial three. Think of the PPRF as being a driver of cranial six itself, so being like the manager of everything. There is even a bigger super boss on top of that, like the frontal eye fields, but I talk about that in my neurology podcasts, right? So basically think of the PPRF as the thing driving cranial six, and then that will then enable cranial six to drive the MLF, and then that will then enable the MLF to drive the cranial three nucleus, right? So the thing is, if a person has a PPRF lesion, it means that the, so say for example, a person has like, because, oh, let me describe what a right, like one normal PPRF does, right? So let's say a person has like the right, let's say, oh, you activate the right paramedian point in reticle formation.

When you activate the right PPRF, though, activate the cranial six nucleus on the same side, on the epsilon side, right? So if you activate the right PPRF, though, activate the right cranial six, and after you activate the right cranial six, though, activate the left, though, activate the left MLF, and then after you activate the left MLF, though, activate the left cranial three, right? So that means if you activate the right PPRF, it means that eyes will look towards the right, okay? Because again, you AB docked in the right eye, and you're AD docked in the left eye. That's a very high, I know some of you may be saying divine, this is low yield step one crap that you're trying to force us to memorize. I promise you, just take enough NV Me exams over the course of third year and take your step two CK exam, and then come back and report to me when you finish taking those exams. I promise you this thing is floorily high yield to know for the neurology shelf and for step two CK itself, right? I promise you a very, very important one. Actually, understand this stuff that I'm taking my sweet, sweet time to explain, right? So the thing is if you activate the right PPRF, the eyes will deviate to the right, right? So a corollary to that would be that, oh, if you activated the left PPRF, the eyes will deviate to the left. By again, just the same identical mechanism I just described. So the thing is whenever a person has a PPRF lesion, right?

The eye will actually deviate, because think about it if the right PPRF, for example, stops working. Then that means the left PPRF will act on a post, and if the left PPRF is acting on a post is like you are activating the left PPRF. So the eyes will deviate towards the left. I'll say that again, the eyes will deviate towards the left. So whenever a person has a PPRF lesion, both eyes will deviate away from the side of the lesion. That's very high yield. Both eyes will deviate away from the side of the lesion. That's what happens when you have a PPRF error, right? So again, it's something I'm really hoping and praying that you really try to understand, right? So if you want to differentiate an MLF lesion from a PPRF lesion, when a person has an MLF lesion, it is only one eye that will be affected, the AD-doctin-ide, the addoctin-ide. But if a person has a PPRF lesion, it will be both eyes that will be affected, because the MLF, it's just again, think of it as a pathway from PPRF to cranial six on the pseudo lateral side to MLF on the control lateral side to cranial three nucleus on the control lateral side, right? Basically, if you damage the MLF well, you only kill the thing that comes afterwards, which is the cranial three nucleus. But if you damage the PPRF, you will kill everything that comes distal to it. You'll kill the cranial six nucleus, you'll kill the MLF, you'll kill the cranial three nucleus that comes after the MLF.

So whenever a person has a PPR lesion, that I will deviate away from the side of the lesion. And many times, the MBM, when they're writing questions that test this factoid, they'll write it like in the middle of a question, right? So that is like you're reading the question and you don't even realize that, oh, this is a PPRF question to start with, right? Easily writing with all these are stroke problems when a person has like brainstem is scheming. And then the, so MLF lesion effects one ID, I that has adopting production problems. And then the PPRF lesion effects both eyes, right? And again, I've explained why that's the case. Now, another thing that's useful to be able to differentiate on an MBM exam is being able to differentiate between an MLF lesion and a cranial three lesion, right? Because I just described that, oh, if a person has an MLF lesion, if they are trying to perform horizontal conjugate gaze, or they'll have problems with, problems with adopting one of the eyes, right? So the thing is to the only initiated, right? For a person sticking an MBM exam and they're like, hmm, a person has trouble with adduction. Ah, well, I know adduction is controlled by the media directors. So that means it's got to be a cranial three deficit. That is not always true. An adduction problem in an eye is not always a cranial three deficit, right? It's not always a cranial three deficit. An adduction problem in an eye literally could be caused by an MLF problem.

And I've already described the potential mechanism behind that, right? So the grand question here is divine. How am I going to be able to differentiate between an MLF lesion and a straight-up cranial three lesion? The thing is, if a person has a straight-up cranial three lesion, then they will not be able to have adduction of that eye when you test the convergence response, right? You can even look up a video of this, right? If you're trying to, so I mean, you can even do this on your own, stand in front of a mirror, put your index finger away from your eye, and then bring your index finger towards your eye, right? If you look at your eyes in the mirror, you'll notice that both of your eyes are almost like converging, right? For both of your eyes to convert, you need your medial recti on both sides to work, right? So you'll bring both together, right? So the thing is, if a person has a straight-up cranial three lesion, that convergence response will not work, right? One of the like the affected eye will not be able to adopt in the convergence response, right? But if a person has an MLF lesion, right? When you try horizontal conjugate gaze, they will have adduction problems, but if you actually try convergence, they will actually have no adduction problems. You may be like, wait, have I healed this person adduction problem? You've not necessarily healed it, right? The thing that just happened is you've used another pathway that does not take advantage of the MLF, right?

The MLF has no role in the convergent bilateral eye adduction response, okay? So that's how you tell, so if you want, like if for example, like they give you an adduction problem in the in an MVM question, and then they tell you that, oh, this person has a normal convergence response, they unite an MLF lesion. But if a person has like an eye adduction problem, and they have an abnormal convergence response, that person has like a legit cranial three lesion. And I mean, what are some things that can cause a cranial three lesion? If a person has like a p-com aneurysm, right? A posterior communicative aneurysm, that can cause a compressed cranial three, you can get into trouble with that. So please, make sure if you need to go back and listen to this, I mean, I know this probably where I'm going to have lyrics, probably spend like eight minutes just describing these two phenomena, but again, it's super, super high to know this stuff, right? If we're pressing, make sure you can differentiate between an MLF lesion, which is one eye affected, and a PPR lesion, which is both eyes affected, and then also make sure you can differentiate between an MLF lesion, right? Which can cause an adduction problem, but will have a normal convergence response, and a cranial three problem where you have like adduction issues, and you have an abnormal convergence response.

Okay, now, what if they give you a question about a patient, and they tell you that this patient has like what is like the, you know, let's see, describe a patient, and this patient has like, like, nephrologythesis, right? And you know, they show you like a picture of the urine sediment on the microscopy, and you see like, like kidney stones shaped like benzene rings, and then they say which of the following best represents the most likely psychiatric comorbidity in this patient, right? No, no, no, no, no, no, no, sorry, sorry, sorry, scrub the question I just gave you. Let me make this an easier question, I think I was getting a little too smart for myself there, so because I was thinking of something completely different, my apologies there. I was thinking of like cola, like the cola disease, where you have trouble reabsorbing, cysteine or anything like that, and arginine, scratch that, that's not going to apply to this thing I want to ask you. Okay, so let me ask you this question, in a person that has heart-nob disease, right? So they can give you a question about a person with like heart-nob disease, and then they can ask, what is the most likely psychiatric comorbidity that'll be present in a person that has heart-nob disease? I would really hope you're telling me that that person will likely have depression, so you may say, well, divine, why is that? Think about it, when people have heart-nob disease, right?

It's a, it's a defect in a transporter that helps with reabsorbing neutral amino acids, right? And one of those neutral amino acids, surprise, surprise is triptophan, right? So the thing is, if you're not able to reabsorb triptophan, well, for starters, you'll not be able to make niacin because niacin is a derivative of triptophan, so you can get pelagra, right? But I don't think that can also happen. Remember, serotonin, serotonin is known as 5-HT, 5-hydroxy triptophan, right? So the thing is, if you lack triptophan, then you're not going to be able to make serotonin, right? And if you remember the mono-amine theory of depression, right? Where if you have low levels of like serotonin, noripinephrine, dopamine, right? That can trigger depression like symptoms, right? So people that have heart-nob disease, they ask you like the most likely psychiatric comorbidity, you want to think about depression under those circumstances because essentially, by being unable to reabsorb triptophan at the level of the proximal convoluted tubule and also in the GI tract, they are certainly going to have problems making serotonin. And if you have issues making serotonin, you can bet that they're going to have problems with depression, right? So that's one of, like it's, again, it's one of those, like because the MBME these days, right? They're getting pretty good at like bizarre questions that just require pretty extensive integration of concepts across multiple fields, right?

So that's one of those annoying things you want to keep at the back of your mind, for example. Now, one thing I want you to be able to differentiate between is a cardiac contusion and a pulmonary contusion, right? So that's something that your friends at the MBME love to test all the time. They love to test this stuff on medicine shelf exams, on surgery shelf exams, and they also love to test it on e-made shelf exams and on step two, CK and on step three, right? And if you're medicine resident, believe it or not, they also love to test this stuff as well, right? So let's talk about this. So the thing is the way a contusion will present is the patient will be in some kind of trauma. 95 to 97% of the time on MBME exams, the trauma is almost always some kind of motovicul accident, okay? So if they give you a question about a person that's in a motovicul accident and then the person starts having like a lot of pulmonary symptoms, right? Like they may have like bilateral and testicially infiltrates on a chest x-ray, they'll have like signs and symptoms of like hypoxia and you have like a low oxygen saturation, right? If you see that, think about a pulmonary contusion, okay? But on the flip side, if a person is like in a motovicul accident, right?

And then they start having like cardiac symptoms like some chest pain, they may have like an elevated pulmonary capillary wedge pressure, they may have like, remember a pulmonary capillary wedge pressure is a surrogate for lefty troprasia, right? Or they may have like an elevated central venous pressure, right? Which is a surrogate for righty troprasia, right? Or they may tell you that oh, this person has like mildly elevated troponines, again, after a motovicul accident, if you see stuff like that, you absolutely want to think about a myocardial contusion under those circumstances, right? So a pulmonary contusion is a person that has predominantly pulmonary symptoms after a motovicul accident with again bilateral and testicially infiltrates on imaging. A myocardial contusion is a person that has cardiac-like problems, right? Like signs of like fluid overload or signs of elevated cardiac pressures like elevated PCWP, elevated CVP, right? After a motovicul accident. That's the classic way pulmonary contusions and myocardial contusions present on MBM exams. And then I also want to go over like an algorithm that again, the MBM seems to care about these days and that's the algorithm for managing like blunt force trauma to the kidneys, right? So the thing is if a person suffers, you know, blunt force trauma to the kidney, your first step in diagnosis is always to get a urinalysis, okay?

Very high you to know that if a person has blunt force trauma to the kidneys, first thing you absolutely want to do, you absolutely want to do, go ahead and obtain a urinalysis and look for hematuria, right? If the person has blood in the urine, right? Then your next step in diagnosis will be to obtain a CT scan of the abdomen, okay? I'll see that again. So blunt force trauma to the kidneys get a urinalysis first. If the urinalysis is positive, proceed to getting a CT scan. If the urinalysis negative, your diagnosis stops there, you don't need to obtain a CT scan. It's just one of those easy, pz diagnoses algorithms that they love to test that many people are not aware of and you don't find in many resources. Now what if they give you a question about and they tell you like, oh, which, like they give you a question and then they mention all these risk factors and then they say which of the following historic factors is the biggest risk factor for C diff in this patient, right? Let's say like you have a patient with C diff. Well, I really hope you are going after the answer that says to, I really hope you are going after the answer that says to, like, says like recent antibiotic use, right? Or like recent hospitalization, right? Those are like the two biggest risk factors for getting a C diff infection, right? Those are the two biggest risk factors for getting a C diff infection. And then if for example, a person has an elevated alkaline phosphatids, right?

What are things that can cause an elevation in a patient's elk force? Well, I hope you're telling me that the, I mean, probably the most common cause on in-beaming exams is like an obstructive biliary process, right? So if a person has like colidocolithiasis, for example, or a primary biliary colonjitis, or a person has like primary sclerosing colonjitis, or ascending colonjitis, right? Those obstructive biliary pathologies can certainly cause an elevated elk force. Remember elk force can also be elevated in things like Pajet's disease, for example, right? So there are many things that can cause an elevated elk force, right? So if you want to be absolutely certain that a person's elevated elk force is from a biliary pathology, one smart thing to check on an ambient exam is the GGT, okay? GGT stands for gamma glutamil, gamma glutamil transfer is, okay? If your elk force is elevated and your GGT is elevated, you can almost say with like, I mean, you can say with 100% certainty, where you can say with a pretty high degree of confidence that this person has an obstructive biliary process going on, right? Because the thing is occasionally, your friends at the MDM meeting, right? Questions where a person will have an elevated elk force and they will try to trick you into picking a biliary process as the answer, but they will write like, oh, GGT is normal or something like that, right? So don't fall for those kinds of things on your exam, right?

So and remember that GGT, like an elevated GGT is also pretty classic for chronic alcoholism or even acute alcoholism on an ambient exam, right? So just an elevated GGT can also mean alcoholism on a test. So there are some other things I want to talk about, but they will require lengthy explanations that will take this far past 30 minutes, so I'm going to go ahead and pause here. As I do at the end of every podcast, I do offer one or one to learn from many exams, right? So step one, step two CK, step two CS, step three, preclinical medical exams, 30-ish-off exams, if you're a medicine resident, I need to learn for like the intruding exam or the ABIM board exam, offer to learn for all those things. And also if you have college student, I need to learn for the MCAT, or for like general chemistry, organic chemistry, physics, biochem, histology, physiology, offer to learn for all those things. And then I also offer these booster courses. It's 15 hours for step two CK and step three is 20 hours for step one. And basically, I review the most notes that you need for those exams. Again, I've done this stuff with tons of people and the vast majority of people have done this with. They found it to be extremely helpful and extremely high yield for the exams they ultimately ended up taking. And then I also, like again, probably studying something like next week or later this week, I plan to start offering something I call like an online private study group.

It'll basically be for like an hour, it'll be for about two hours, and there'll be like a theme, it could be like a cardiology themed study group or a histology themed study group or a GI themed study group. The theme is, it'll essentially be like a subscription basis for that session and it'll be like for small nominal fee. So I will send out more information on that. You know, probably have like a couple tens of people. I will go over like a ton of high yield content relating to that system as it turns to like either step one or step two CK or whatever. Right. So I will give our send out some more information on that as soon. And if you interest, they just reach out to me. You'll be again, a very small fee, you'll be like two hours, you'll be like over zoom. And again, I suspect that many of you will find it to be extremely helpful, extremely high yield, especially when you have a particular weakness for an exam. This is something I've actually done like in person before, like tons and tons of times. And people always found it to be like floridly high yield from any of these exams. Right. So that's something to watch out for in the next few days. And then I also offer like one-on-one coaching. So if you're a medicine applying to residency, so like an like an era's application or a college student applying to a med school, right. So like an Amca's application.

I do offer one-on-one coaching with like personal statement editing, editing applications, rec letters, mock interviews. Again, the vast majority of people have worked with have all much that their first choices. And I've also have like very valuable admissions community experience. I mean, I've been on the admissions community of a top two med school for like a year. Right. So again, I've had tons of time reviewing high quality applications. And I can give you tips that can essentially set you up for success on these exams. So if that's something you're interested in, reach out to me through the website or send me an email at divine intervention podcasts with an srbend at gmail.com. And I'll see you in the next podcast. Please subscribe to the You Tube channel. I also have this stuff on on Apple podcasts on Spotify on Google Play, right. So please subscribe every useful comment or feedback helps. So have a wonderful rest of your day. Thank you for being with me today. God bless you. I'll see you next time. Thank you.

Estrogen.

The corpus luteum; its job is to produce progesterone.

Only the adducting (adducting) eye.

An MLF lesion patient will have normal convergence response; a CN III deficit patient will have an abnormal/absent convergence response.

After 14 days.

PPRF lesion causes deviation of both eyes away from the side of the lesion; MLF lesion affects only one eye (the adducting eye).

The follicular phase.

The developing zygote releases beta-hCG, which maintains the corpus luteum beyond its natural 14-day lifespan.

Both eyes deviate away from the side of the lesion (e.g., right PPRF damage causes deviation to the left).

1) Urinalysis for hematuria; 2) CT scan of the abdomen (only if urinalysis is positive).

Serotonin (due to impaired Tryptophan reabsorption).

Elevated GGT (Gamma-glutamyl transferase).

The follicular phase.

The developing zygote releases beta-hCG, which maintains the corpus luteum beyond its natural 14-day lifespan.

Both eyes deviate away from the side of the lesion (e.g., right PPRF damage causes deviation to the left).

1) Urinalysis for hematuria; 2) CT scan of the abdomen (only if urinalysis is positive).

Serotonin (due to impaired Tryptophan reabsorption).

Elevated GGT (Gamma-glutamyl transferase).