DIP Episode 219 - USMLE Step 2CK Rapid Review Series 33

Okay, good morning. Welcome. My name is Divine. This is episode 219 of the Divine Intervention Podcast. In this podcast I'm going to be continuing our rapid review series for the USM Listep 2 CK exam. This will be episode 33. This will be a short and sweet one. But I'll talk about a bunch of high-yield concepts that people tend to not really understand or tend to pop up quite frequently on exams. So what if they give you a question about a patient that has, you know, like they make it one of these physio style questions on the exam, right? They will tell you that this patient has hepatic congestion and the patients, hepatic venous pressures are elevated, the right atrial pressures are elevated, both the right ventricular pressures are normal. What's your diagnosis? I'll really hope you're thinking more in terms of try to cause pit stenosis, right? Because you have to have got pit stenosis, you have elevated rectal short pressures and then you have like that pressure will be transmitted equally all the way back to the liver, right? So you have hepatic venous congestion, right? But compared to the patients, this is the person that has hepatic congestion as a result of botchiaris syndrome. Botchiaris syndrome, right? Arraises from hepatic vein thrombosis, right? Usually you may find that in a person that's taking OC Ps on an embankment exam, or you may find that in a person that has polycyphemia there, right? That's a classic presentation.

So you won't see the person that has one of these hyperquagulable disorders. If you see that clearly in those circumstances the right atrial pressures, the right ventricular pressures will be fine, but the hepatic venous pressures will be elevated, right? So that's one of those weird things you want to keep at the back of your mind, right? Remember botchiaris syndrome is a thrombosis of the hepatic vein, right? So the person will have elevated portal pressures and all that stuff, but it will be from a blockade of the hepatic vein, right? The thing is whenever you get these pressure questions, it's always important to localize where's the primary problem and then you can work your way backwards from there, right? Like for example, if a person has like left heart failure, right? Their pulmonary capillary which pressures will be elevated, right? Because remember the PCWP is a surrogate for left-titre pressures and then the central venous pressures will also be elevated because remember the CBP is a surrogate for right-itre pressures and then in addition to that they may also have like elevated hepatic venous pressures depending on how severe the symptoms are, right? And then what if they give you a question about a patient?

Let's say it's like a two-year-old girl, you know, she's February and they tell you that you hear crackles on the scotation of the lungs and they tell you that all like two weeks ago, you know, she had like these respiratory symptoms and they tell you that oh, you know, they get like an echocardiogram of the chest or they get like a chest x-ray and it shows like global ventricular dilation, like global like dilation of the heart. What kind of disorder are you thinking about? I would really hope you're thinking about a diluted cardiomyopathy or myocarditis. Basically myocarditis always causes diluted cardiomyopathy and in this case I would really hope you're seeing it from coxacub virus, right? Remember coxacub is the most common viral cause or even infectious cause of myocarditis. On MBME exams, right? So the classic presentation will be where a person will have like respiratory symptoms and then weeks later or these later, they'll start having like signs and symptoms of like heart failure, they'll have a new S3 heart sound. That's a classic thing to put on exams. And one thing I will say is the MBME is becoming a little more more creative with edges of things, right? So what do I need by that? So you may see a loop of question in a five-year-old, right? It will still be the same classic presentation, it's just the edges that change, right? So again stick with the classics on these MBME exams when you're taking these tests.

And then what if they give you a question about a patient? And you know, this patient has like, it's like a young, let's say it's like a young 23-year-old guy, let's say this person just got a kidney transplant, right? Like you know like six months ago and this person has like really bad soul throat posturesis, colin, phatomapathy, right? And this person has Plino Megaly. And then they tell you that the monospot test is negative. What bug would you want to consider on your test? I really hope you're thinking about CMV, right? CMV, especially with this person being a post transplant person, right? Post transplant recipients, right? Those people tend to have a lot of immunosuppression on board, right? And CMV loves to affect people that have immunosuppressive problems, right? So they'll remember CMV can cause like colitis, it can also cause right colitis, but it can also cause a mononuclosis like syndrome that is monospot negative, right? And obviously for person has CMV, you want to treat them with guns like clover, right? You remember guns like clover, you can build up resistance with a mutation in the kinase that's supposed to activity before it's incorporated into DNA. It so happens that that kinase is known as a UL, 97 kinase, right? Obviously the person has like, guns like clover resistance and you want to give false carnage on those circumstances, right? And that false carnage essentially is a pyrophosphate analog, right?

So the thing is this podcast specifically, I'm going to kind of be touching on basic science topics that tend to show quite frequently on step 2 CK. So let me say define, oh, this is really basic science. Again, I promise I'm doing it with a specific kind of intent, okay? So pardon me, but obviously the monospot test is positive, I've got to be going with EBV, right? EBV that's herpes number three, right? So EBV, the Epstein bar virus. So you know, that's just something, sorry, that's herpes number four, that's HHGV4. HHGV3 is a VZV, oops, sorry about that. So EBV, right? Again, it was a monospot positive monoclosis syndrome. And the thing is again, don't always rely on that posterior cervical lymphatic empathy, right? People can have anterior cervical lymphatic empathy and still have EBV. There's just something I want to commit to memory on your test, right? And one thing that your friends at the NBM also care about are the kinds of infiltrates you're finding organs in some select diseases, right? So let's kind of talk about those things for a second here, right? So if for example, they give you a question and they tell you that you see a lymphocytic infiltrate in a person's like small intestines and this person has like Fatmonellabserption, has like a vitamin D deficiency or has like a microcytic anemia. You want to think about CDIAC disease, right? CDIAC disease has an association with lymphocytic infiltrates in a person's small intestine, right?

Alternatively, they give you a question about a person that has period of idema, right? This person is Breedy Cardiac, has gained weight, right? And this person, you know, like has like a neck mass detected on physical exam. You want to think about Hashimoto's thyroiditis, right? Classically, you'll also see again a lymphocytic infiltrate in that person's thyroid gland. You'll see like lymphoid follicles. In fact, that's one of the reasons why having a history of Hashimoto's increases a person's risk of thyroid lymphoma. That's a high young thing to keep in mind on exams. And then this viral myocarditis business I kind of talked about earlier, right? Typically, you'll see like infiltrates of lymphocytes as well in that person's myocardium, right? You'll see like a diffuse infiltrate of lymphocytes in the presence of myocardium. And then finally, one thing I would also say is if a person, if they tell you that, oh, like you take a person's thyroid gland, you see like upper grain birefringents on Congolite staining. I would really hope you're thinking about medallary thyroid cancer, right? Remember, medallary thyroid cancer, pathonomonically, you'll find amyloid in the thyroid, right? Remember, essentially, those people, calcytonin is a tumor marker. So that calcytonin is the thing that ultimately forms amyloid, right? But if you see upper grain birefringents in a person's pancreas on an MBMI exam, what disease you want to think about?

Well, I hope you're thinking about type 2 diabetes under those circumstances, right? Remember type 2 diabetes. You have like, as you are over-secreting insulin because you have like insulin resistance, you're also secreting a compound known as amylin at the same time, AMYLIN. That amylin can certainly form amyloid on tests, right? So that's something to keep in mind, right? And then if you tell you something about using like, world's of calcified bodies in some kind of lesion, right? So world's, so WHORLS. So world's of calcified bodies, you want to think about some momobodies, right? And remember, some momobodies, you can find those in misotheliuma, right? So that'll be an asbestosis person, so that has worked in a sheepyard or whatever. And you can also find some momobodies in meningiomas, remember meningiomas on MBMI's will present us parastagetomasis, right? You know, they actually like jokers the post to some kind of dural food, like the cerebrum, like the fork cerebrite, for example. Although you can also find meningiomas at the cerebralopontinangle, although the most common mass that shows up at the cerebralopontinine is going to be an acoustic neuroma, right? Usually in a person that has neurofibromatosis type 2, on MBMI's at least, right? And then another thing that contains some momobodies is papillary thyroid cancer, right? Remember, papillary thyroid cancer is the most common kind of thyroid cancer, right? Remember, papillary thyroid cancer is papular, right?

And remember, there are some histologic things you see, right? Like these some momobodies, again, I call them, sometimes the MBMI's called in laminated calcifications. And remember that papillary thyroid cancer, the biggest risk factor, right, is exposure to headache radiation and in addition, papillary thyroid cancer also tends to have those anti-offend and in-eye nuclei, right? And it spreads through lymph nodes, right? It doesn't spread in my togeon, in my togeonously, like follicular thyroid cancer. So those are all high old things to keep in mind there. And then the final thing that contains some momobodies are the cirrhosis that no cross-numbers of the ovary, right? So you just want to keep those things in mind, right? And then if they tell you that a person has like a tennis-shaped rackets on his stology that you see and this person has like some red malignancy, think about Lunga Hanselle histiosytosis, right? That's a classic thing again that should come to expect on MBMI exams. And then what if they give you a question about a patient that's, you know, going through like a measles episode and the ask which of the following would improve morbidity and more like morbidity in this, like, you know, like because measles obviously there's no cure, there's nothing can do, right? But what can you give to improve morbidity when a person is going through like a measles attack? I would hope you're thinking about vitamin A, right?

Or sometimes instead of putting in vitamin A, give me put a recnoic acid derivative as an answer choice, right? That's something you want to keep at the back of your mind on exams. Now, one of the weird basic science things that tends to pop up on exams are things that are released to oxygen delivery to organs, right? Because I know some of you may not believe me, but if you have any experience taking the shelf exams in third year or taking step two practice exams or taking step two CK itself like myself, you'll see that there are some questions where you're like, this thing the last time I learned this stuff was when I was studying for step one, right? So the thing is this stuff again, like on physiology and oxygen delivery is one of those classic physiological scenarios that you'd likely see on a test, right? So for example, if a person has like if for example, they give you like a set of like labs, right? Or physiological measures and they tell you that oh, this person's arterial oxygen content is decreased, but the partial pressure of oxygen so the p little EO2 is normal and the oxygen saturation the S EO2 is normal, but the oxygen content is decreased. What diagnosis should you entertain on your exam? I would really hope you're thinking more along the lines of anemia, right?

Because remember in the oxygen content equation, the key things that are important there, I mean there's all these numbers, but I feel like the things that are most important to remember are that hemoglobin is part of it and then the S EO2 is part of it. Remember hemoglobin can hold for oxygen, so the S EO2 is just what percent of that hemoglobin is saturated and then the p little EO2 is also important, right? It deals with the amount of oxygen that's dissolved in the plasma, right? And obviously if oxygen dissolved like oxygen can not just get on hemoglobin, it needs to dissolve in the plasma first and then after that you'll then dissolve in hemoglobin, right? So if you notice that the presence oxygen content is decreased, what the p little EO2 is normal and the S EO2 is normal, then you know that they likely have anemia as the cause of their squibbles, right? Now what if they give you a question about a patient, the arterial oxygen content is decreased, but they tell you that the p little EO2 is normal, you notice that the hemoglobin is like 14, so it's normal, or you notice that the S EO2 is decreased, what are you thinking about under those circumstances? Well I would really hope you're thinking about like carbon monoxide poisoning or like cyanide poisoning, right? Because remember carbon monoxide and cyanide, they love to binds to hemoglobin and when they bind to hemoglobin they prevent oxygen from being able to bind, right?

So carbon monoxide poisoning is probably the classic one you see on a test, right? Because again it has like a 244 more affinity for oxygen compared to, I mean for hemoglobin compared to oxygen, right? So oxygen is affinity for hemoglobin, carbon monoxide exceeds that by a factor of 240, right? So the S EO2 will be down in a patient that has carbon monoxide poisoning, but the P EO2 will actually be normal, right? So this thing may sound a little confusing, but let me give you one rule, your S E O 2 being low does not always mean your P E O 2 has to be low, but if your P E O 2 is low your S E O 2 always has to be low because your P E O 2 is literally what creates your S E O 2. Well there are some special or let me say specific chemical properties of carbon monoxide that make that rule sort of kind of not apply, right? It relates to some stuff from step one that's kind of hairy if you're interested in it, reach out to me I'll be happy to explain, but for probably since this is a rapid review podcast I'm going to keep going from that. And then what if they give you a question about a person, the person's oxygen content is decreased, right? Atheroloxygen content is decreased, the hemoglobin is 14 so it's normal, but it tells you that the P O 2 is decreased and the S E O 2 is decreased. What are some potential causes on an MBM exam? Well I hope you're thinking about along the lines of like hypoventilation, right?

If you're hypoventilating your Atherol CO2 will go up, if that goes up right then your Atheroloxygen will go down and if your P B little E O 2 goes down your S little E O 2 will go down, now another thing that could cause that is if a person you know is like overdose on opioids, that's essentially hypoventilation right there, right? Or if a person has like ARDS, right? Or if it's a kid question like a pediatric question like new needle respiratory distress syndrome, right? The P little E O 2 will be low, the S little E O 2 will be low as well, right? Even if the hemoglobin is normal and I mean the way your body will kind of respond is your body will be all crap, I'm not seeing enough oxygen, right? Chronic hypoxia, so with that hypoxia your body will ward, you know, there's this transcription factor called HIF1 alpha that will be activated, right? And then your kidneys, right, will begin to make a ton of Epo and as you make that ton of Epo, you will essentially begin to increase your hemoglobin number, I mean that's why people that have chronic COPD or CISIFI broses, they tend to be like super super super polycyphemic, right? Another thing that can also cause this low P little E O 2 to low S E O 2 and the levied hemoglobin business and that thing that can actually cause that is if a person has if a person goes to like higher elevations, right? So let's say you go to Colorado for example, that'll be the mechanism behind the hypoxia in those people, right?

And then don't forget that if a person has you want to be able to differentiate between a shunt and dead space, right? For step 2 CK, again, I know, so and that's why I'm going to specifically make this podcast very short because I know I'm discussing a lot of technical things that kind of like requires a person to think, right? I'm just trying to dust off those physiological cobwebs in your mind, but essentially that space, right? Means that a person's like dead space essentially means that a given piece of long is being ventilated, but it's not being perfused. That's something that typically happens at the apex of the locks, right? If a person has like a PE, like a pulmonary embolose, that'll be like a very good pathological cause of an increase in dead space because you literally have an obstruction of the pulmonary vasculature. So blood is not getting to certain regions of long, and if blood is not getting to certain regions of long, those regions are not being perfused, even if they are being ventilated, right? Now a shunt on the and but the thing is if a person has dead space, right? If you increase, if you increase the, so that's essentially like a VQ mismatch, and with that VQ mismatch, you'll have an increased AA gradient obviously, right? And the thing is when a person has dead space, if you give them 100% oxygen, it should increase the oxygenation status, right?

But a shunt on the flip side means you have a given region of long that is being perfused, but it's not being ventilated. I mean, think of the easiest shunt, like the easiest to understand 100% shunt. If a person has like is a manger syndrome, where blood is traveling across a VSD straight from the right heart to the left heart, you are completely skipping the longs entirely, right? So you're skipping that ventilation that comes with the longs, that's what's known as a shunt. So a shunt refers to physiology where a person has a person has like you know like regions of long that have been perfused, but don't have a ventilation. If a person has a 100% shunt, so notice I didn't see 90% shunt. If you have a 90% shunt, if you give the person's supplemental oxygen, the auto-sats will go up, not so for a 100% shunt. If you have a 100% shunt, if you give supplemental oxygen, the oxygen saturation will not go up. For obvious reasons, because that 100% oxygen is not getting access to that blood that's going through the longs, right? So again, it's just one of those weird high yield things you won't keep at the back of your for example. And then with regards to A-agridients, one thing I'll just go ahead and say is if you have problems within the long parenthesis itself, that would increase your A-agridients, right? So like, let's say for example, you have pulmonary fibrosis, right? Obviously that increases the diffusion distance, right?

So the DLC will be decreased under those circumstances, but that's an intra-parence how long problem the A-agridients will be up. If a person has pulmonary edema, right? Again, if you put that fluid, that essentially like increases the distance that oxygen will have to traverse for a person, for the blood moving through the pulmonary vessels to capture that oxygen, right? That will increase A-agridients, right? But if a person has like a neuromuscular disease, one anatomic problem like pectosexcavado, or kyphosis, or scoliosis, or myostenia graph is that torches your diaphragm, or ALS, right? Those things are a guion-berre syndrome, right? Those things that extra parankoma problems, there's nothing wrong with the lungs, but it's either like some anatomical problem that exists, or some neuromuscular problem that exists, that makes it impossible for the person's lungs to expand and relax as he should, so the person has hypoxemia under those circumstances. So those would be examples of hypoxemia with a normal E-agridient. And then one of the classics in the area that tends to pop open exams is, it may tell you a question about a person that is, you know, started on Proprienolol, and then he asked like, oh, which, what would the hemodynamic effects of taking this medication look like? Well, the hemodynamic effects of taking Proprienolol, remember, Proprienolol is a beta blocker that comes past the letter M, right?

Remember, so all the beta blockers that go from E, like a tenelol to M, like metoprolol, those are beta-one selective, those are beta-one blockers. But Proprienolol, right, is a, because anything that goes from N going forward, so like the letter N, like N, C going forward to like Z, those are non-selective beta blockers, right? Like the classic post-so child one on M-MIM exams is Proprienolol. Well, the thing is, if you block beta-one receptors, where do we find beta-one receptors? We find beta-one receptors on the heart, and we also find them at the level of the afraid material. So if you give a person Proprienolol and you block those beta-one receptors, the person's cardiac output will go down, because the force of contractivity is going down, right? And the heart rate is also going down. I remember the cardiac output is heart rate times stroke volume, right? So the presence cardiac output will go down, right? And also from those beta-one blockade effects, the reigning will go down as well, because activating beta-one receptors is actually one of those things that can increase the production of reigning. So if you block those beta-one receptors, the reigning will go down, the angeotensin one, angeotensin two, an autostron will all go down as well. And also E, yeah, let me not, yeah, let me stop talking here, because I feel like if I mentioned the last one I want to mention, that would confuse people, because it's not always true.

Now, by blocking those beta-one receptors, remember, beta-one receptors cause dilation, right? Because the beta-one receptor is a dilating receptor, right? Like it causes, if you give a beta-two-agonist, for example, for asthma, you get like bronchodilation, beta-one receptors, you also find them on your blood vessels, so if you give them, that will cause a visodilation, right? So the thing is when a person is given a beta-blocker, like propanolone, right? You block the beta-two receptors, that will actually increase, the systemic vascular resistance. So the presence of the astolic blood pressures will actually go up on that those circumstances, right? Because remember, the astolic blood pressures are closely fed to your systemic vascular resistance, right? And again, that's the reason why you don't give propanolone to people that have a history of asthma, or like very severe reactive airway disease, because that bronchospastic effect can cause them to go into respiratory failure, right? So I think I'm going to go ahead and stop here, as I do before, at the end of every podcast, like I said, I want to start talking about like some kind of life lesson. The life lesson, I think, I want to talk about today is the value of being locked in and being focused, right? The thing is, if any of, I mean, if you've listened to my podcast for any length of time, you know I'm a Libra James fan, you know I'm a leakers fan. And whenever you see Libra James, right?

Like not coasting, you see him like locked in. And again, the brain James, you can't blame him is, for me, is the best player in the world, right? When you see him not coasting, I mean, like Libra James coasting, he can still drop like 30 points on you, right? But when you see him like super locked in, he's like impossible to stop, right? Because he's like locked in, he's like super focused, right? So I kind of think of it the same way, like if you're locked in, if you're focused on like the goal at hand, like, oh, my step one example coming up, my step two seek exam coming up, right? Even like clinically, if you're locked in when you're talking with your patients, if you're locked in when you're presenting and rocked, it's almost like all your energies are being brought to be on an activity and your chances of failing that activity go down precipitously, right? So always be focused, always be locked in. And what does it mean to be locked in? Being locked in just means giving you all to whatever you are currently involved in, right? Like you are essentially like giving your all and completely tuning your mind off from distractions, right? That is what it means to be locked in when you're participating in an activity. And then like I always do, I do offer one and one to learn for step one, two CK, two CS, step three, pre clinical medical exams, 30-ish off exams. If you're, I do these booster courses for the USML exams as well as like 20 hours for step one.

And for step two CK and step three, I'm actually moving into 20 hours as well because the amount of new material that the NBM is beginning to test is becoming a little excessive. So it's become a little challenging to cover those things in 15 hours. And then if you're a college student that needs to learn for like any of the MCAT subjects or like general chemistry, organic chemistry, physics, biochemistry, physiology, I'd offer one and one to learn for all those exams. And then I do coaching if you're a medicine or a plant like residences or like an ira sap or a college student applying to a medical school or like an MCAT sap. Again, I have like one-on-one experience like with lots of students. The vast majority of students have worked with the whole much that their first choices, right? And I've also been on admissions committee for like a year. So if that's something you're interested in, like personal statements, interview prep, mock interviews, editing applications and all that stuff. Again, that's something I can definitely make a difference for you with. I mean, there are people that have had very bad stories like, you know, low-step scores, not much research, but I've really prepared the applications and it has made a difference for them. Like some of those people are really like residents now in programs all around the country and some very competitive specialties. Right?

And then if you're a medicine resident or a piece resident, I need to do it for like the interesting exam or the board exams. Feel free to reach out to me. So thank you for listening to this podcast. If you're interested in any of these things I'm offering, either send me an email at divineinterventionpodcasts with an SADN at gmail.com or reach out to me directly through the website. So please subscribe to the podcast. It's an Apple podcast. It's on Spotify. It's on Google Play and also subscribe to my Word Press website to the You Tube channel. The You Tube channel is called divineinterventionpodcasts and videos. So thank you for listening to this podcast. God bless you. I'll see you next time. Thank you.

Budd-Chiari syndrome.

Pulmonary capillary wedge pressure (PCWP), as it is a surrogate for left atrial pressures.

Coxsackie B virus.

New S3 heart sound (sign of heart failure).

Hypoventilation (e.g., opioid overdose or ARDS).

Lymphocytic infiltrate in the small intestine.

Amyloid deposits (formed from amylin).

Elevated hepatic venous pressures, but normal right atrial and right ventricular pressures.

Dilated cardiomyopathy/Myocarditis (often Coxsackie virus).

Momobodies (or laminated calcifications).

Intra-parenchymal lung problem.

Upper-gren birefringent calcifications and elevated calcitonin levels.

Non-selective beta-blockers (N to Z).

Elevated hepatic venous pressures, but normal right atrial and right ventricular pressures.

Dilated cardiomyopathy/Myocarditis (often Coxsackie virus).

Momobodies (or laminated calcifications).

Intra-parenchymal lung problem.

Upper-gren birefringent calcifications and elevated calcitonin levels.

Non-selective beta-blockers (N to Z).