DIP Episode 291 - USMLE Step 2CK Rapid Review Series 51 (+ USMLE Step 2CK/3 Course Reminders)

Okay, welcome. My name is Divine. This is episode 291 of the Divine Intervention Podcasts. In this podcast, I'll be continuing the rapid review series for the US Emily Stepjusica exam. This will be series 51. Okay, so let's get right into it. So what if they give you a question about a person that comes in and they tell you that they have like hard burn that is really bad at night? What should you be thinking about? Or you know, they may tell you that they have like a cough that's really worse at night? What should you be thinking about? We're thinking of those who potentially having dirt, although that can also be a presentation of asthma on your exam, right? But this person likely has dirt, right? And for person who has just regular guardian, your IT, what are you supposed to do for them? Well, I hope you're telling me that you're going to give those people PPI's, right? PPI's are the first thing you do for people that have dirt. You do like a six week trial, but you know, let's assume you've tried it and that's not caught in it. Then, sadly, you have to proceed to operating doskopee, right? So you're going to do an EGD, right? The term for that is esophago gastro-doa-denoscopy, right? So you go ahead and push right straight to the EGD. And then remember, there are some situations, let me call them maybe like almost like derivative situations where you may do things a little different, right?

So if for example, a person comes in with dirt symptoms, and they have like alarm symptoms in addition to that, right? So what are alarm symptoms? It can be that, you know, they are more than the age of 50. It can also be that they're having like dysphysia or dynophysia. Basically, whenever you see things that you're like, hmm, this person seems to have more than guarding variety dirt or like extremely severe dirt, they want to go ahead and do an EGD in those circumstances, right? And then don't forget, there are other people that can also get PPI's on your test, right? Remember, PPI's can be given to people that have hot severe burns, right? Remember those curly noses that they can get in the stomach and also people that have increased intracurricular pressures. In fact, they can make this a strong question on your exam, right? Like, you can tell you all brain imaging shows like global cerebral edema, yada, yada, yada, and then they'll ask for your next best step and they'll be to give a PPI, right? And then remember, so if a person is going to be placed on a bisfoss fan heat for a prolonged period of time, they also need to be placed on a PPI at the same time, right? So that again, you can protect the airsofagil, mucosa in a sense. And also, if you're going to be taking, oh, sorry, not bisfoss fan heat steroids, for a person is going to be taking steroids for a long period of time, steroids can cause peptic ulcer disease, those people need to be placed on PPI's, right?

And then remember, right? Again, if a person had ecalysia, right? Remember, you don't go straight to the EGD, right? I'm kind of talking around this EGD business, right? Remember, you do the barium, you do the barium studies first, you do the barium swallow. And then after that, you do the monometry, right? And then after you do the monometry, you go ahead and perform the EGD, right? Barium swallow will show you that bird's beak sign, right? And then the monometry will show you that or they have like, like a pair of stalses, right? Of the, especially of the mid-esophagus, right? And then the EGD, right, is to roll out surgery callicia because sometimes what do you think is bird's beak is actually cancer, right? So an EGD helps you kind of roll that out. And again, please don't forget that ecalysia, right? Increases the presence risk of having a scrimousal cancer of the esophagus. Okay. And then what if they give you a question about a patient that has zenkers? Should you do an EGD with those people? Again, I would hope you don't do an EGD, right? Because again, in zenkers, you can go ahead and perf the esophagus. And then you have a whole new set of problems, right? So typically when a person has zenkers, you don't, you don't do an EGD. When a person has zenkers, what are you supposed to do is do the biome swallow, right? You'll see the problem around the crackle thyroid membrane, right? And then you go ahead and fix it with a divertic elective, right?

Remember, those are people, you'll be an old person, right? Zenkers is not a young person's disease, typically on imbibing exams. It's going to be an old person that, you know, they have environmental problems because the guy's mouth is usually meant for whatever bizarre reason. The guy's mouth, you know, stinks up every, every time. And then he tells you that, oh, sometimes you know, like some undigested food comes out in the morning from his mouth, right? If you see stuff like that, you want to think about zenkers. Just do the barrier. That's pretty much all you need to do, right? And you go ahead and fix the problem with surgery. You do a divertic elective, you'll do remember, zenkers, that particular again, is another risk factor for esophageal squamous cell carcinoma, right? The biggest risk factor for a squamous cell cancer of the esophagus is smoking, okay? I'll say that again, the biggest risk factor for a squamous cell cancer of the esophagus is smoking. Just, you know, something to keep in mind. Well, the biggest risk factor for a so-called zenocarcinoma is going to be baritone esophagus, right? Because you know, get it from dirt and all that fun stuff. Okay, what if they give you a question about a patient and they tell you that the patient is taking like two or three different anti-hypertensive drugs. And then they tell you that all those person has peripheral edema, like squilling of the legs, right?

What anti-hypertensive is going to be causing that peripheral edema? Well, I would hope you're telling me that, oh, it's going to be like some kind of dihydropyredine-concimensional blocker, right? So something like amlodipine, phyloepine, right? Those dihydropyredine-concimensional blockers, remember, they all cause peripheral edema, right? And the thing is, your friends at the MBM actually expect you to know the mechanism behind set edema, right? So remember, the thing that happens is these drugs, they have the dilute materials, right? The dilute pre-capillary materials. So if you dilute those pre-capillary materials, remember, we have materials, then capillaries, then venules, right? So relative to the capillaries, the materials are pre relative to the capillaries, the venules are post, right? So those pre-capillary materials are diluted very powerfully by these dihydropyredine-concimensional blockers, right? Again, like my phyloepine, amlodipine, right? So because they dilute those pre-capillary materials, they send more blood to the capillaries, right? So that will increase the hydrostatic pressures within capillaries. Well, when you increase hydrostatic pressures within capillaries, sadly, the thing that's going to happen is you're going to have more fluid extroversation. That's good because they're peripheral edema. So your friends at the MBM may sometimes can ask you, how can you prevent the sedema or treat the sedema?

Well, it's actually kind of high up to know that you give those people an isin inhibitor, right? So remember, isin inhibitor is they are very powerful, post-capillary venule dilators, right? So remember, it's almost like a concept. Isin inhibitor is a very good at dilating blood vessels that come after capillary beds, right? So they dilute these post-capillary venules. If you do that, you take away more blood from these capillaries, right? So you decrease the hydrostatic pressures in those capillaries and that would ultimately help help the patient. If you're thinking in terms of that post-capillary whatever dilation, also thinking in terms of the kidneys, right? Remember, we have the glomerular capillaries. The capillary system that comes comes right after it. That's the e-friend material. The e-friend material is preferentially dilated by isin inhibitors and AR Bs, right? So again, just very high up to know that. Now, what did they give you a question about a person? That has a history of a Crohn's disease. And then the person over the last two, three days has been having a lot of vomiting, a lot of nausea, not able to keep any food down. Person hasn't had any bowel movements. If you see that, what do you want to think about? Well, I hope you're thinking about like strictures, right? From the Crohn's disease. Remember, Crohn's loves, loves, loves to constructors. And those strictures, right? He can cause a small bowel obstruction, right?

So whenever you see a person with an inflammatory bowel disease, especially Crohn's, like almost like 99% of the time when he being exempt is going to be Crohn's. And then they have like small bowel obstruction symptoms, think about strictures as the cause, right? And then remember, people that have Crohn's, if they ask you about the nephrolethyases they have, what should you be thinking of? Well, I'll hope you think about like calcium oxaline, nephrolethyases, right? Again, remember, the terminal really, I don't work. So if it doesn't work, you're going to raise a ton of oxalate, you're going to get those oxalic crystals. Remember, oxalic crystals are actually the most common kind of of nephrolethyases, at least that pops up on exams and actually also in the real world as well, right? And then what if they give you a question about a patient that has pneumonia and they tell you that all this patient is a big time smoking, you know, two packs per day for like 40 years or something ridiculous, and they have pneumonia. And usually when they do this for whatever bizarre reason, they love to make these questions like super non-specific, right? They don't give any clues, they won't give you any spirit of culture any fit, right? And they are supposed to figure it out. Well, what I'll just say is if you ever see a person that has COPD on your exam, and they have pneumonia, always think about Hachian fluenza.

Hemofluosin fluenza is actually one of the most common causes, especially on MBMS of pneumonia in patients that have that have COPD, right? And remember, if it's Hach flu, you're going to go ahead and treat that with with a safe track. So you're going to use a third generation of cell flu sparring like safe tracks on a cephaltoxy. Now, I think one other thing that maybe bears mentioned here is just going to talk about some of the classic MBMS scenarios where safe tracks on a cephaltoxy, you know, these third generation cephalosporins are the right answer. If we're still thinking in terms of pneumonia, for sure, they are definitely the right answer in the person that has a pneumococcal pneumonia, safe tracks on works like a charm in those circumstances. That's one. Another important one is if you see a person that has SBP, right? Again, it would be an alcoholic and an alcoholic who are a person that has like liver issues, right? They'll have like this fluid wave, they'll have mild abdominal tenderness, they'll have all treatment of status. Well, what are you supposed to do for those folks? Well, I hope you'll tell me that, oh, you know, let's do a parsing thesis, right? Again, read your questions carefully. The MBMS fund of doing this when you're asking about SBP, they'll put parsing thesis as an answer. But then you'll put many other kinds of synthesis for us and thesis, pericardial synthesis, right?

In fact, for sure, they love that pericardial synthesis because the piece kind of match, see kind of looks a lot like, oh, especially in the heat of an exam, you know, you're kind of all emotional, right? So pericardial synthesis, parsing thesis, right? So just make sure doing the parsing thesis, right? That's where you would draw fluid from from the abdomen, right? So remember, what you're looking for is not even the bugs that will tell you anything. You're looking for more than 200 or more. So if you, I mean, sorry, 250 or more neutrophils, right? If you find 250 or more neutrophils, right? That tells you all you need. Person has their SBP and then you go ahead and and give them a third gen sephalosparring for those purposes. Okay. Now, what if they give you a question about a patient that has celiac disease? How can you differentiate on MBMS? How can you differentiate celiac disease from lactase deficiency? This is a common mistake many met students make, right? So what's the big, what are the big differences? Here's what I'll tell you. If you see the person having any lab or physical exam abnormalities is going to be celiac disease, right? If you see any lab or physical exam abnormalities like vitamin G deficiency or iron deficiency anemia or anything of that sort or the person has lost like precipitose amounts of weight seems malmourished, always think about celiac disease.

People that have lactase deficiency, they almost never on MBMS lose like tons of weight or have lab abnormalities or anything like that, right? So I think that's something that can actually help you pretty significantly on exams, right? And again, remember people that have celiac disease, they can actually make an endocrine question of it, right? So these people if the celiac disease involves their terminal area, right? Remember, they can have like B12 deficiency as a result of that, they can get a vitamin D deficiency, right? Because they're not going to be able to reabsorb these fat soluble vitamins, right? So they can get a vitamin D deficiency so they can have like low calcium, right? And because they're not reabsorbinated in the gut and if that's the case, the NPTG is going to rise, right? And that PTG, remember we call it the phosphate, trash in hormone. So it's going to, you know, trash the phosphate. So the phosphate will be low, right? The phosphate is going to be low, right? So because the acnes actually work, right? So just something to kind of keep at the back of your mind on on the example, right? And then another classic thing that the NBN is test a lot is at this, you know, they can give you a question about about a child that has ADHD and they tell you that, you know, he has like very, a very long face, very big testicles. What should you be thinking about? Well, I hope you're thinking about a fragile X syndrome, right?

Remember fragile X syndrome is one of these high yield trying to have repeated disorders to know for exams. I remember it's in Herithidian and X-link dominant fashion. Remember, it's one of two high yield X-link dominant diseases you need to know for your NBN exams. The other one, if I'm not mistaken, is going to be, come on, divine, thank you. Outports, right? Outports syndrome. Outports syndrome is X-link dominant. Frigial X syndrome is also X-link dominant. Outports syndrome, remember, right? It's the C-O-L-4-A-5 gene mutation, right? So the alpha-5 gene of typhal collagen has issues, it's just so happened that typhal collagen, we express it a lot in basement membranes, so that's why the kidneys are screwed. You also express it in the eyes, right? So that's why they have eye problems and also hearing problems as well. So X-link dominant, right? And again, fragile X is also X-link dominant, right? But let's get back to what I really wanted to talk about, right? The the Chinese flu-thedrup-repeat disorders. Remember, the Chinese flu-thedrup-repeat disorders, we have fragile X, right? Remember, it's those CGG Chinese flu-thedrup-repeats, right? And then another classic one is going to be fridrixy-taxia. Fridrixy-taxia is kind of unique. It doesn't have any kind of dominant inheritance. The inheritance pattern is actually a little more recessive, right? And those are GAA-Trenic-reuthed repeats, right? GAA-Trenic-reuthed repeats.

So just something to keep at the back of your mind for, for exams, right? And then don't forget that the other ones have got those almost dominant inheritance, right? You know, like contentants, you'll be a person like choriform movements and you know, they do inappropriate things, scene-appropriate things. It's going to be a person in their 40s or early 50s or late 30s, right? So if you see that think about contentants disease, I remember it's a chromosome 4 problem, right? So they'll have like atrophy of the chordate and you have those C-A-G, triangle-thedrup-repeats. And don't forget that people that have haunting tins, right? Especially these autosomal dominant disorders, just in general, right? They can begin to reflect like genetic principles, like anticipation, right? Where, you know, they start having symptoms earlier and they have like a very, worse phenotype as you go across generations, right? And then remember that the last, the last, what is it called? The last writing-clothed repeats, the order to know about. Don't forget your myotonic dystrophy, right? So you'll be a person that has trouble, the physician has trouble releasing his grip from sed patient, or it can be a patient that has trouble opening doors, right? Or it can give you like a guy in his 20s, very young, and he's already bald. Whenever you see stuff like that, you want to think about myotonic dystrophy. And I remember myotonic dystrophy actually involves CTG, triangle-thedrup-repeats, right?

And the actual gene that's all messed up, right? It's like a kind of, if a numb is speaking, it's like the DMP-KG, right? So the DMP-KG doesn't work very well in people that have that have a myotonic dystrophy, right? So those are your 4-trenifithytherapeutic disorders. So I'm just going to summarize them real quick, right? So remember, haunting disease, C-A-G triangle-thedrup-repeats, or the zomodominant inheritance, biotonic dystrophy, CTG triangle-thedrup-repeats, or the zomodominant inheritance, fragile X syndrome, C-G-G triangle-thedrup-repeats, excellent dominant inheritance, and then for G-Cataxia, G-A-A triangle-thedrup-repeats, so G-A-A triangle-thedrup-repeats, and autosumor recessive inheritance, right? And then, what if they give you a question about a patient, and you know, they tell you that this patient says, oh, whenever he's going up and down stairs, he has double vision, right? So this person almost has like vertical deplopia, right? Like, if you see that, what should you be thinking about? Well, I would hope you're thinking about parynotes syndrome, right? I hope you're thinking about parynotes syndrome, right? It's a problem with the superior colliculus on MBM exams, right? So remember, your superior colliculus is your vertical geyser, so if it doesn't work, you're going to get in a lot of trouble, right? So, what are the things that can cause a problem with the superior colliculus?

Well, there's one that many people know, and then there's one that is unusual, but is tested, so you want to know about it, right? It's kind of unusual, it's not many resources, but it's really high-youtuna, right? So, remember, one is a panyloma, because remember, the panyl gland is superior to the superior colliculus, right? The panyl gland, I'll say that again, is superior to the superior colliculus. So, the parynotes syndrome has a panyloma that's going to compress the superior colliculus, right? And that's going to cause parynotes syndrome. Another thing that can also cause parynotes syndrome, if you remember your circle of willis, right? Remember your bazzlar artery, you know, it gives off AIK first, the anterior and fiorosarabella arteries, right? And then after that, it gives off the parymidian pontine arteries, right? We supply the medial ponds. Remember, AIK applies the lateral ponds, but then if you're going more terminal for the bazzlar artery, it gives off the superior cerebral artery. The superior cerebral artery is the principal arterial supply to the superior colliculus, right? So, it's easier, remember, superior cerebral artery supplies the superior colliculus. If a paryson has a stroke or an infarct or whatever of the superior cerebral artery, that's going to cause problems with the superior colliculus, right? That's going to call definitely cause problems with the superior colliculus.

Now, there are three things I want to, there are three drugs I almost want to compare and compare and contrast. So, these are things that, because many people know, the friends at the end of the end of the end of the end of the end of the end of these things, where they test some step one from a collager and again, many people, you know, usually forget this stuff, right? So, let's kind of talk about this. I want to compare and contrast three antiplitlid drugs, right? Although the first thing I'll establish remember, antiplitlid drugs, and not the symptoms as anti-coagulants, right? Anti-coagulants work on secondary, the inhibit secondary hemostasis, antiplitlid drugs inhibit primary hemostasis, right? So, what do I want to make a big force about here? Well, the big force I want to make here is that it's actually very high yields to know that aspirin, right? Inhibit cycloxygenings. I know maybe like, oh, to find that makes sense, kind of obvious. But let me explain what I mean, right? So, those aspirin cause a net viso-constriction or a net viso-dilation. Well, I hope you're telling me that it actually causes a net viso-constriction, right? Because remember, aspirin is a cox inhibitor, so it would decrease the synthesis of first-aglandins. If you decrease the synthesis of first-aglandins, right, you're going to get less viso-dilation, more viso-constriction. This is one of the reasons why aspirin can cause renophilia, right?

Because essentially, it's an insect, you know, inhibit cox, you make less-per-staglandins, right? So, you're going to constrict the afrin material. And if you do that, that's going to, that's going to raise your raining levels and all those things, right? And again, if you also constrict your afrin material, you're not going to be profusing your kidneys very well, your brumelic capillaries. So, that's going to cause a decrease in GFR, so your creatinine is going to go up, right? So, that's one end of the spectrum where we have an anti-plit lead agent, that is a viso, that is, it's anti-plit lead, but it's a viso-constrictor, right? But the thing is, there is also an anti-plit lead agent that on the flip side is a viso-diliter, right? So, you're thinking more along the lines of those, uh, edi, not, not, uh, those phosphodistories inhibitors. So, drugs like selloztosol and diperidomol, right? So, selloztosol and diperidomol, are the way they work is the, the inhibit phosphodistories, and that's going to raise the person's levels of cyclic AMP. The thing is, high levels of cyclic AMP actually inhibit the function of platelets, right? So, whenever your cyclic AMP is high, you're not going to be able to express GP2 B3 A on the surface of a platelet, right? If you cannot express GP2 B3 on the surface of a platelet, then you cannot have the aggregation step of primary hemostasis, right? So, that's how those drugs like selloztosol and diperidomol work.

I mean, that's why selloztosol is used to trip peripheral arterial disease after you've tried the 30 minutes of, you know, so, provides walking and it doesn't work. So, you can do selloztosol, it's an anti-plit lead drug, right? But it's also a very powerful visual dilator. And then, remember, diperidomol is another one, right? But diperidomol is no useful PED. Diperidomol can be used as like a third-line agent. If a person has like carotid stenosis, as from a psychological therapy, remember, first line, you're going to use aspirin, second line is Lupito Gryl, third line is diperidomol. But if none of those work, if, you know, if aspirin is not an ancestral NBM Es, that's first line, if Lupito Gryl is not, is not around, right? That's second line. Then you can go to diperidomol. Remember, also use diperidomol to, in the coronary steel principle, when we're doing these pharmacological stress tests, I've talked about this coronary steel principle in multiple podcasts in the past, right? So, again, remember, aspirin is on one end of the spectrum. It's anti-plit lead with a visual constrictor. And then diperidomol selloztosol, those phosphodistrius inhibitors. They are on another end of the spectrum. They are anti-plit lead agents for their visual dilators, okay? They are visual dilators. So, I'm going to go ahead and pause here as I do.

Again, if you're interested in the step one or step two CK courses, or the MDME test-taking strategy course, just shoot me an email through the website. I'll be more than happy to point you in the right direction. Remember, the step one course, I stay in place from the fifth to the ninth of April. It's five days, it's 40 hours total. And we're going to be reviewing about 4,000 concepts from all the MDME disciplines. And again, a lot of these things, I'm going to go over them with Viniets, right? I'm going to do a lot of integration. So, I may be covering Europe or any at the same time, be covering biochem and hemonc and pathology. So, I'm just going to move around a lot. But at the end, you will learn a ton from the course. It's going to be from, you know, again, from the fifth to the ninth of April, from 7 to 10 EM, noon to 3 PM and 4 to 6 PM. This is all Pacific Standard Time. So, there'll be three hours behind a Eastern Standard Time. And then from a step two CK perspective, I'm having a step two CK actually step three. So, this course is combined as step two CK step three course. Going to be doing that from the 25th to the 27th of April, it's going to be from, it's going to be 16 and a half hours, right? So, it's from 11 to 4, 11 EM to 4 30 PM, Pacific Standard Time on, on all three days. And then I have an MDME Testikin Strategies class. Again, this is more for people taking step two CK step three.

It's going to be on the 24th of April from 2 to 4 30 PM, Pacific Standard Time. Again, all these classes are over Zoom. Tons of people have taken these classes. They've done extremely well on the exams. I mean, I will say probably the highest score I've gotten from my courses for a person that attended. This person, I'm not going to say the exact score because it can be personally identifying. But I'm pretty sure this person got just a few points on their, a 280, right? So, again, if you're interested in these courses, again, hundreds of people have taken them, especially the step two CK step three course. So, if you're interested, shoot me an email through the website and I'll give you some more details on registering. So, thank you for listening to the podcast. Please subscribe to the website, divininginterventionpodcast.com. And then I have this podcast, an Apple podcast, Google podcast, Spotify. So, please subscribe. And then I have a You Tube channel, diviningintervention, you're seemingly podcasts and videos. That's where I put my, that's where I put my videos, right? So, thank you for listening to this. I wish you a wonderful weekend. God bless you. See you next time. Thank you.

Barium swallow $\rightarrow$ Manometry $\rightarrow$ EGD (Esophagogastroduodenoscopy).

If there are alarm features, such as age >50, dysphagia, or extremely severe/persistent reflux.

The "bird's beak" sign at the gastroesophageal junction.

Calcium oxalate stones, due to fat malabsorption leading to increased oxalate excretion.

Haemophilus influenzae.

Cilostazol and Dipyridamole.

A pair of simultaneous, diminished peristaltic waves in the mid-esophagus (aperistalsis).

Fragile X syndrome and Outfield's syndrome.

Smoking.

$>250$ neutrophils/mm$^3$.

CTG trinucleotide repeats (DMPK gene).

Weight loss, iron deficiency anemia, or fat-soluble vitamin deficiencies ($\text{Vit D} \downarrow$, low Calcium, high PTH).

Angiotensin II Inhibitors (AC Ei) or AR Bs.

A pair of simultaneous, diminished peristaltic waves in the mid-esophagus (aperistalsis).

Fragile X syndrome and Outfield's syndrome.

Smoking.

$>250$ neutrophils/mm$^3$.

CTG trinucleotide repeats (DMPK gene).

Weight loss, iron deficiency anemia, or fat-soluble vitamin deficiencies ($\text{Vit D} \downarrow$, low Calcium, high PTH).

Angiotensin II Inhibitors (AC Ei) or AR Bs.