DIP Episode 320 - USMLE Step 2CK Rapid Review Series 59 (and 20hr 2CK/3 course reminder 6/18-19)

Okay welcome, I'm Steve Vine. This is episode 320 of the Divine Intervention Podcast. I'm in this podcast. I'll be continuing the Rapid Review series for the USMD Step 2 CK exam. As a reminder, if you're taking the Step 2 CK Step 3 exam any time within the next few days or weeks, I would encourage you to sign up for the comprehensive review course taking place on Friday and Saturday this week. It's 10 hours each day, so 12 to 20 hours. And then the MBME Test Ticking Strategy Scores from 3 to 5 30 p.m. Pacific Standard Time this Thursday. Again, both a pretty high-level courses. There's been tons and tons and tons of people that have taken the courses that have done extremely well on the exams. I've had people have like really big scoring improvements between the pair just before they took the course and the pair just after they took the course. Again, we basically visit about 1500 or most scenarios. That touch occurs like Neural, I am surgery, Peds will be going psych, internal medicine. I think I mentioned that already. And the Step 1 material that has made its way to the exam. We also spend a lot of time on bio stats, on ethics, on healthcare systems. We really break those things down. And again, lots and lots of people have found out to be extremely helpful. So if that's something you're interested in, feel free to reach out to me through the website and I will give you some more information on how to sign up. Okay, so let's just go ahead and jump right into it.

So what if they give you a question about a person, they give you a question about like a 42 year old female, and they tell you that for the past two weeks or less two months, she's been having a lot of parrides, and then they give you labs. And you notice that our alkaline phosphatizes elevated and she has a direct type of inner bignini. If you see that, what are you thinking about? I hope you're saying old wine. I think this person has a PBC, right? So primary, belirical angitis. And many of us know that PBC has an association with anti-midocondrial antibodies, right? Remember a very key thing to keep at the back of your mind with regards to PBC is that PBC tends to affect women for the most part, and it tends to affect the intra-hypatic bowel dots. Okay, it doesn't really do much with the extra-hypatic bowel dots. The inflammation is almost exclusively limited to the intra-hypatic bowel dots. So what do we do for these people? Well, we're going to give them also dial. Remember also dial on exams can also be known as orso-deoxy-colic acid, right? It can also be known as orso-deoxy-colic acid, or so-deoxy-colic acid. And the thing is, what are the things we use orso-dial for on ambient exams? Besides PBC. Or remember, we can also use orso-dial to treat intra-hypatic holostasis of pregnancy, right? That's a pretty common use on ambient exams. They want to keep at the back of your mind. Orso-dial is actually used for intra-hypatic holostasis of pregnancy, right?

And since we're on this PBC train, we know that obviously PFC is an analogous disorder. It's usually going to be in a person that has a history of um, it's usually going to be in a person that has some kind of history of ulcerative colitis. Well, we know that if people have ulcerative colitis, they'll have a chronic histral bloody diarrhea. And then in addition to having that chronic histral bloody diarrhea, they would also have, you know, just the involvement of the colon for the most part. It'll be a younger male. It'd be like a guy that's like in his, no, probably no more than 40 years old on a test. It's usually people that are under 40 on an exam. Well, we know that on like PBC that affects only the intra-hypatic bowel ducts, PFC affects both the intra and extra-hypatic bowel ducts, right? And the thing with PFC is, orso-dial does not really do much for people that have PFC. We'll say that again. Orso-dial actually doesn't do anything. Let me put it that way. For people that have PFC, right? So, what can we do for people that have PFC? Well, the thing is like PBC, the only way you can actually cure PFC is with a liver transplant. With PFC, one thing you may see, if it don't see liver transplant as an answer, is that for those people, you could consider performing an ER, CPM, plecinstense, right? Just to help the abiliary system drain.

This is actually something that's also usually done with people that have pancreatic cancer, especially when a person has like inoperable pancreatic cancer. When people have inoperable pancreatic cancer and MBA means, right? And yet each and a lot, and you know, they're not necessarily getting better. Then one thing you can actually do on an exam is, you know, it's inoperable because many times it's pancreatic cancer that involves the head of the pancreas. Obviously, if it involves the head of the pancreas, it's going to be really hard for you to, it's going to be really hard for you to do much of anything for those people, right? I mean, you're going to give them pain control to help them. And by the way, let me just say this because these some of the many med students get wrong. When a person has metastatic malignancy, that is not getting better, that they're going to die from, go ahead and give them as much. Like if for example, they give you an MBA question where their symptoms are currently not being well controlled. If for those people, go ahead and give them more opioid, right? Again, these people are unfortunately going to die, right? Might as well just meet the alastias on earth as pleasant as possible. Again, that's what, again, none of this podcast is given for medical advice, right? But I'm saying for MBA exam purposes, right? Just something you want to give the back of your mind for tests, right?

So again, if a person has pancreatic cancer and they have a lot of parietas, have a lot of jaundice, one thing you can definitely do to help these folks, right? Is to endoscopically place some stents. And then those stents will pretty much open up their pancreatic ducts and their battery tree. And that will help their battery tree during that something that's actually very high up to keep in mind for your exams. Now, what if they give you a question about a 67 year old male? And they tell you, they show you, you notice that, wow, this guy has like an anemia, like he's in multiple buildings like seven. I noticed that his MCV is like 84, right? So he's an anemone. So he canemia. And then you notice that he's his creatinine is like 3.5. So you're like, man, this guy's creatinine is is elevated, right? And then they tell you that he has been prescribed that he had to go to the emergency room, like three weeks ago because he had like ultra mental status. I was having like another abdominal pain and that he improved very well after they gave him like three liters of normal saline and they gave him like IV zone adronic acid, right? If you see stuff like that that tells you that obviously this guy likely has multiple myeloma, right? Again, you see the way I just, again, the thing is the MBME, they're not just going to spell out crap symptoms for these days. No, they're not going to do that, right? What do you do these days is the basically describing of the findings, right?

So remember in multiple myeloma, those people tend to have crap symptoms, right? So the C stands for hypercalcemia, right? Because remember, those myeloma cells, those plasma cells, they're releasing to look in one. By releasing that into looking one, you're going to basically activate osteoclasts and your resort bone and cause hypercalcemia, right? And then ours for redophilia, right? Remember, the redophilia is usually from light chains, right? Those bands, Jones proteins, the positive in the kidneys and cause an amyloidosis, right? So they have like renal amyloidosis, right? So they get renal failure. And then there is frenemia, right? Because again, those plasma cells have taken over the bone marrow. So those people have like ineffective production of red blood cells and then the bees for bone pain again, if your osteoclasts are going like going berserk, they're going to basically be reserving, reserving, reserving bone, right? So that's going to cause some bone pain. Remember, those people tend to have like osteolytic lesions on imaging, right? So many times when people have multiple myeloma, it's usually going to be a normal acidic amynea, something you actually keep in mind, keep in mind, for exams, right? So again, the reason behind the kidney damages is amyloid, essentially, right? And remember, they can even give you a question about a person that has multiple myeloma and the person has heart failure, right? What kind of heart failure would you see they have?

I would hope you are saying, oh, divine. I think they have a restrictive cardiomyopathy. Remember, whenever something ends in osis, usually causes restrictive disease of the respective organ, right? So like in the case of multiple myeloma, right? That amyloid, if it begins to deposit in the person's heart, it'll begin to have heart failure, right? You have a restrictive cardiomyopathy. And remember, when people have amyloidosis, right? That restrictive cardiomyopathy, right? That infiltrating the walls of the heart can actually present as a low voltage EKG on an ambiemia. I'll say it again, those infiltrating the walls of the person's heart can produce like a low voltage EKG picture on ambiemia exams. And actually, the drug of choice for treating multiple myeloma on ambiemia is bortezomib. That's very high, you know, the drug of choice for treating multiple myeloma on ambiemies is is bortezomib, right? It's bortezomib. Remember, bortezomib is a pretty zoom in inhibitor, right? So maybe like, okay, why do we need to care about that? You do certainly need to care. And the reason you need to care is in multiple myeloma, they have accelerated destruction of things that cause apoptosis of those myeloma cells. I'll say it again. In multiple myeloma, they have accelerated destruction of proteins that help in apoptosis of those myeloma cells. Obviously, that's a good thing, right? Because the thing is like, sorry, let me pack track a bit. Obviously, that's a bad thing, right?

Because the thing is, myeloma cell is a cancer cell. You want those cells to undergo apoptosis. You don't want to be destroying those things that will cause apoptosis of those cells. And unfortunately, the thing that causes apoptosis of those cells is actually the thing that destroys those proteins that cause apoptosis is the pretty zoom, right? So the reason in there is if you give a person bortezomib, bortezomib is a pretty zoom inhibitor. By inhibiting pretty zoms, then those myeloma cells will then begin to die faster because those proteins that were previously destroyed by the pretty zoom, they persist for longer. So they actually cause apoptosis of those myeloma cells, right? So if you see stuff like that, right? That's why bortezomib is the drug of choice for which really multiple myeloma is. Just one of those things that many people don't really think about, right? But it's actually high-o to no, right? Especially step three, step two, CK, they love to test multiple myeloma and mechanism of action of bortezomib. Now, what if they give you a question about a patient and they tell you that this patient was in a one-of-a-eco accident and his blood pressure is like 60 over 40, you know, he's not doing well, right? And they tell you that you see like a big fluid collection in his pelvis on imaging, right? Obviously this person has high-povalymiq shock, right? And whenever a person has high-povalymiq shock, well, what are you supposed to do?

I would hope that you'll be like, hmm, okay, let's, let's give them fluids, right? That's usually his first smart thing to do, right? Just go ahead and give those people fluids. That's usually a smart thing to do initially, right? Now, the thing is when people are high-povalymiq, your friends at VMA, they like to make all these integrations as to, oh, high-povalymiq, if you can make certain key deductions on some findings in these people, right? So, we know that first and first, if these people's creatinine is elevated, well, what's causing the creatinine elevation? Well, I hope you're saying volume depletion, right? These people basically will have some kind of periodal isotemia because if you think about it, if your volume down, well, you're going to be profusing the afraid materials very well so the kidneys are going to start filling those effects, right? Because if you think about it, if you don't profuse the afraid material as well, I don't know how you're going to be creating hydrostatic pressures in your glomerular capillaries. If you don't create hydrostatic pressures, you know, glomerular capillaries, you glomerular capillaries, I'm not going to be feeling for any stuff out, right? So, because your GFR is going to be down, right? The pressure screening is going to go up, right? So, that's the mechanism behind the creatinine elevation and a person that has periodal isotemia, right?

And in fact, if a person has been hypoverlimic for a while, right, that can actually cause hyponychromia in those people, right? And it'd be like, oh, divine. How exactly does that cause hyponychromia? Well, the way that causes hyponychromia is if you think about it, if you get volume down, your afraid material is not being perfused well, your GG cells, your juxtaglomerular cells, this that freaking out, right? So, this that, you know, we can turn our reigning, again, that reigning will cause angiotensinogen to be converted to angiotensin-1. Remember, angiotensinogen comes from the lever, right? angiotensinogen comes from the lever, right? So, angiotensinogen, you know, it's converted to angiotensin-1 and then angiotensin-1, it's converted to angiotensin-2. Remember, angiotensin-2 is a very powerful visual constrictor. If I, this is one of the reasons why people that have an stage lever disease, they tend to have low blood pressures because they essentially have an angiotensin-2 deficiency, because the feedstock material angiotensinogen is not there, right? If you have an angiotensinogen, well, I don't know, you're not going to have angiotensin-1, you're also not going to have angiotensin-2, right? So, you're not going to have good visual constriction, right? So, those people tend to be very visual, visual dilated. Yeah, taking care of lever disease patients is an exercising just understanding physiology.

So, something that's always usually pretty good for residents, you can learn a lot from taking care of lever patients. They are very complex to manage, but that's a different conversation. So, getting back on angiotensin-2 train, right? So, that angiotensin-2, remember, it does a bunch of things, right? One thing it does is it goes to the posterior pituitary, right? And tells you to secret EVH. And then, the other thing it does is it goes to your zonal glomerulosa of your zonal cortex so they can make out a duster. Remember, our duster is a mineral aquatic void. So, the thing is, our duster's job is to go to the principal cell of the connecting duct and cause you to reabsorb most sodium. If you reabsorb more sodium, well, water is going to follow, right? Remember, through that image channel, that epithelial sodium channel that's on the surface on the urine side of the principal cell. So, sodium goes in water follows, right? But remember, I said one of the action of angiotensin-2 is that it increases EDH secretion. Well, EDH's job is literally to reabsorb just free water, right? So, if you notice, if you're comparing our duster and EDH which are both increasing hypervolemia, the auduster is causing more sodium reabsorption and more water reabsorption. The EDH is causing more water reabsorption. So, you have one factor, excuse me, you have one factor, fevering sodium reabsorption and two factors, fevering water reabsorption.

If that happens, obviously it's going to be hyponytremic, right? Because you're absorbing a lot of water, not as much sodium in response, right? So, that's how people get hypervolemic hyponytremia, right? That's the mechanism behind the hyponytremia, right? And remember, these people as well, if you were to check the urine, what do you think will be true of the urine sodium? I hope you're saying, oh, the urine sodium will be low, right? Because again, think about it, our duster is literally doing its job, right? If our duster is doing its job, it's going to be reabsorbing a ton of ton of sodium from the urine, ton, ton of sodium from the urine. So, you can maintain volume because sodium is a relatively active substance. So, in those circumstances, the thing that's going to happen is the urine sodium will be low. I mean, if one of these people's fractional expression of sodium is also going to be really low, it's going to be less than 2 percent on an exam, because again, the area of sodium is a ton of sodium from the urine, right? And then, remember, since it's a pretty little isotemia picture that you have, the buien to creatinine ratio will be elevated, right? The buien will be elevated, the creatinine will also be elevated. But the thing is, the buien is rising faster than the creatinine. Again, for many reasons, right? One is that your kidneys, you know, when you're having an isotemia, your buien, your creatinine is rising.

But remember, again, this is something for whatever bizarre reason, I feel like they don't teach many med schools, they don't find many resources, but it's actually kind of high up to now, because it explains a lot of pathophysiology is. EDH's job is not just to reabsorb free water. EDH also helps to reabsorb your ear in the kidneys, right? Because if you think about it, that medallery comes in trading gradient to learn about in med school. It's created not just by ions, but it's also created by your ear. And we know that EDH's job description in life is to one of its major job descriptions, is to make your reabsorb water. Well, you need a medallery concentrate ingredient for that to actually happen, right? So it should make sense that EDH increases the medallery concentration gradient by making your reabsorb your ear. So when a presence hype over limit again, I said on the reaction of angiotensin too. EDH levels go up. If your EDH levels go up, right? That's going to increase your area absorption. That's why your buien rises faster, your blood, your ear, your buien rises a lot faster than your creatinine. That's why imperializotemia, the buien to creatinine ratio, is usually going to be more than 20 on an embankment exam, right? Now what kind of potassium abnormality would you expect in a person that has hypovolemia? Well, again, if a hypovolemic, your renal angiotensin aldosterone system gets revved up.

So you're going to make a ton of aldosterone, 300 tens, into as I described. That aldosterone, its job is to make your reabsorb sodium in the inect channel of the principal cell of the collecting duct. And it also makes you pee potassium. So if you're reabsorb in sodium and pee in potassium, then you put more potassium in your urine, right? So that means that potassium is living in your body. So guess what? You're going to have, you're very likely going to have hypochyline, right? And again, you're also going to have a metabolic alkalosis, right? Because again, remember our dostorone, one of its job is to make your pee protons into your urine. So if your pee protons into your urine, you're literally losing acid, so you're going to become alkalotic. So again, if you notice, hypovolemia actually has a concept, it's just very high yield to know for example, in fact many times, if you're taking a USMEL exam, you've done all the questions on set exam. And you don't see a single concept on hypovolemia, something has probably gone horribly wrong on that test you just took, right? It's something you just definitely want to make sure that you know and understand, right? Because if you notice, I can literally write probably like 15 to 20 different USMEL equations. And you know, I love writing questions because it's something I'm thinkfully pretty good at. So there are just many questions they can write on this stuff.

So just make sure you understand all this physiology that I was kind of like navigating, navigating, navigating through. Okay. Now what if they give you a question about a patient and they tell you that you know, this patient for the last three months, he has been having shortness or breath. And then they tell you that at birth, he had a large murmur that was on physical exam. So he could hear Holus' stomach moment at the left, stomach, bladder. But then over the last three months, he needs to have been short of breath. And then they give you a lapse. I noticed that this person's hemoglobin is 17. And then you're like, what question can my friends at the MBM test here? Right? And of course, they produce a question and say, what's the mechanism behind the person's polycyphemia? Or they can see what's the diagnosis, right? Again, there are many different questions they can make up here. If you see this, I really hope you're saying, oh, divine, this person has isomangers. I also want you to listen to this maybe like, okay, divine. What exactly do you mean by isomangers? So why is isomangers? How are you able to make that deduction based on the information given? Well, the thing is this person has a hemoglobin of 17. This person has a profound polycythemia. Well, if you have a polycythemia, I mean, if you don't have polycythemia vera, then you probably have your polycythemia from elvededipo production.

Well, in the person that has had a large phesid for a long time, why would he make a ton of epoch? Well, that's because they've started becoming cyanotic, right? Because remember, when a person has a phesid initially, it's going to be a left to right a cyanotic shot. But again, the right side of the heart, the pulmonary circulation, not built for handling those elevated, a left and true blood blood, like those pressures, you know, elevated pressures from left and true blood blood. So over time, those people can get pulmonary hypertension. Then if a person gets pulmonary hypertension, something that will happen is the pressures on the right side of the heart in the bulmonary system will much higher than the pressures on the left side of the heart. So that would then reverse that left to right and make it a right to left shot. Remember, those right to left shots are cyanotic shots. Now, once you become cyanotic, well, you're going to become chronically hypoxic, so the thing that's going to happen in response is that your body is going to start making epoch, right? Because if you make more epoch, you make more red blood cells, and that will improve the oxygen carrying capacity of the blood. Because yes, the amount of oxygen around is low, but if you put more buses in circulation, maybe that will increase the oxygenation of the body's tissues. So that person essentially have some kind of a reactive polycythemia. So the epoch will be elevated.

Remember, the polycythemia, that's a such a low epoch on embhemic exams. It's going to be polycythemia there, right? Because they have that jack-to-mutation, right? With that jack-to-mutation, their ribylosyl precursors proliferate like a ton, and if that happens, then you're going to see, you're going to see elevations in their ribylosyl count, right? But the epoch is actually going to be suppressed, almost like negative feedback from their ribylosyls. Okay? So since this is a rapid review podcast, I think I'm going to go ahead and stop here. As I do at the end of every podcast, I do offer courses again for the USML exams, especially step 2, seek hands, step 3, and I also help people with applications, personal statements, recommendation letters, reviewing errors, applications, mock interviews. Again, I've done this with tons of people. People that have had many red flags on the applications, many tricky parts of the applications, and they are now residents. So if that's something you're interested in, just shoot me an email through the website, and I'll be happy to give you some more information. And then I also have a new podcast I started. Actually, also has a website called Divine Intervention Life Lessons, because I've got in emails from like more people than I can remember that like, oh, Divine, you know what I've been really blessed by your life lessons that you put at the end of your podcasts.

So I have a podcast that's again, it's a lot of Bible-based teaching, they're very short podcasts, most of them are like five to seven minutes long on a life lesson. That you know, applies to a lot of people that I medicine, right? So I've put up two episodes so far. I put the first one was on focus, second was on diligence, I'll try to put up a few every week, right? So again, the podcast is actually now live on Apple podcasts. So if that's something you're looking for, just feel free to kind of sign up and again, whenever I make a new podcast, you'll get you'll be able to review it. And then again, I have a website again, Divine Intervention Podcast.com. That's where I have all my podcasts from episode one all the way to this episode, I believe is episode 320. Again, on the podcast apps, especially on Apple podcasts, you can only put the most recent 150. It's a road that I literally have like zero control over. It's not much I can do about it. But if you want all the podcasts from episode one, go on the website. It's there, right? And then I also have a You Tube channel, Divine Intervention, USMLE podcast and videos. That's where I put the videos that I make, although if you want the slides that go with those videos again, check on the respective episode on the website. And the thing is if you subscribe to the website, you'll get an email notification whenever I make a new podcast. So thank you for listening. I do hope you have a wonderful day.

I'll see you in the next podcast. Thank you. God bless you.

Positive Anti-Mitochondrial Antibodies (AMA) and inflammation limited to the intrahepatic bile ducts.

Ulcerative Colitis (UC). PSC affects both intra- and extrahepatic bile ducts.

Amyloid deposition, specifically from light chains (Bence Jones proteins), leading to renal failure.

Activation of RAAS leads to increased aldosterone secretion, which promotes H+ excretion into the urine, causing systemic alkalosis.

Initial left-to-right shunt; if pulmonary hypertension develops, the shunt reverses to right-to-left, causing cyanosis and chronic hypoxia.

Bortezomib (a proteasome inhibitor). It works by preventing the degradation of proteins necessary for apoptosis, thus allowing the myeloma cells to undergo programmed cell death.

Hypercalcemia, Renal failure (due to amyloidosis), Anemia, and Bone pain/osteolytic lesions.

Intrahepatic bile ducts only.

Treating PBC and intrahepatic cholestasis of pregnancy.

Hypokalemia and Metabolic Alkalosis.

Antidiuretic Hormone (ADH) or Vasopressin.

Low Urine Sodium and a low Fractional Excretion of Sodium (<2%).

Decreased Angiotensinogen production leads to reduced Angiotensin II levels, resulting in systemic vasodilation and hypotension.

Hypercalcemia, Renal failure (due to amyloidosis), Anemia, and Bone pain/osteolytic lesions.

Intrahepatic bile ducts only.

Treating PBC and intrahepatic cholestasis of pregnancy.

Hypokalemia and Metabolic Alkalosis.

Antidiuretic Hormone (ADH) or Vasopressin.

Low Urine Sodium and a low Fractional Excretion of Sodium (<2%).

Decreased Angiotensinogen production leads to reduced Angiotensin II levels, resulting in systemic vasodilation and hypotension.