DIP Episode 355 - USMLE Step 2CK/3 Rapid Review Series 67

Okay, welcome. My name is Divine. This is episode 355 of the Divine Intervention Podcast. And in today's podcast, we're going to be continuing the Rapid Review series for the USMELIS step 2, CK step 3 exams. Obviously, this podcast also applies to the complex level 2 and 3 exams. As a reminder, if you're taking the USMELIS step 2, CK step 3 or complex level 2 or 3 exams in December, so that's this month or January, that's next month. You would want to sign up for the NBME Testicking Strategy Scores that I have. It's going to be taking place next week Monday from 2 to 4 30 PM Mountain Standard Time. That's going to be the same thing as 4 to 6 30 PM Eastern Standard Time. We'll basically review many different approaches to NBME questions. Again, I've had tons of people taking this course. This particular course, and if it's a very good majority of the food that I've attended it, the scores go up, the upper-centage is on Cubans go up, and they end up doing pretty well on the exams. And then, I have a 24-hour review course. It's going to be taking place from 10 PM to 4 PM Mountain Standard Time. So that's noon to 6 PM Eastern Standard Time. From the 7th, that's next week Tuesday to the 10th, that's next week Friday. Essentially, we would go through Peds, Surgery, Internal Medicine, OBEGY, Insight Neural, Ethics, Biostatistics, Multisystem Persises, and Disorders, Professionalism, Communications, and all those things.

Again, I've had many people take this course, and they've done extremely, extremely well on the exams. So if you're interested in signing up, there's still spots. Just shoot me an email through the website. I'll use some more information on payments and things like that, and then your spot will be reserved. Most people will end up having about 130 pages of notes from the course. And again, about, you know, of the 24 hours, about 4 hours total, if you kind of add up everything, is devoted to taking an answering people's questions. So you're going to have your questions answered. We have many different types of questions, multiple choice, a lot of audience response, and things like that. Again, many people have taken this course. They've done really well with it. So if you're interested, shoot me an email, and I'll give you some more information. So, let's just jump right into it. Now, what if they give you a question about like a 62-year-old female? They tell you that, you know, over the last two days, she's been having this burning sensation around her left lower abdomen. And then, you'll notice, you see on physical exam, you'll notice that, wow, this person has these vesicular lesions and the on an erythemisose base. And they tell you that, you know, this person has like very sharp pink as a result of these lesions. If you see that, what should you be thinking about? I really hope you're saying, oh, divine, sounds like this person has shingles, right?

This person has shingles, right? This person has, in effect, you know, the herpes virus, right? So, what are we going to do for these people? Well, I really hope that you're saying, huh, divine, let's go ahead and give this person a cyclover. Remember, a cyclover, how does it work? Again, let me see something here, I guess. Right? For those of you that are taking the USML Step 2 CK Step 3 exams, don't think that pharmacology is just something that if, for God in the sea of Step 1, no. These are things that you're still going to see on Step 2 CK Step 3, right? So, don't forget, we're going to give this cyclover. And again, a cyclover essentially is going to be a false nucleotide and is going to inhibit DNA synthesis. That's a big thing you want to know with this cyclover, right? So, basically, you're not going to be able to meet DNA, right? So, this cyclover works in that format, right? And what are some key high yield things to know with this cyclover on your exam? So, don't forget, this cyclover can cause a no-filia, right? And it can also cause nephrylithiasis. That's a very big one to know, right? So, they can describe the same person, the ontheropie, the symptoms of God in better, and then they start having flanked pain, relating to the growing. When you see stuff like that, you want to think about nephrylithiasis secondary to a cyclover. Right? Remember, a cyclover is not the only drug that causes nephrylithiasis on end genies, right?

If you take a loop diuretic, a loop diuretic can increase your risk of nephrylithiasis. Right? You probably remember the nomonic that, ooh, loops loose calcium. Well, they loose calcium, right? So, they make you put more calcium in your urine. So, because they make you put more calcium in your urine, right? They can increase your risk of precipitating calcium and can get a kidney stone as a result of that, right? Or if you think about the HIV drug in dinner veer, in dinner veer as a HIV drug can absolutely cause nephrylithiasis. And then that's not all. Also, the drug to pyramid. Right? So, if they give you a question about a person that is an antipyletic and they kind of feel slow mentally, right? You're pretty much telling you that it's to pyramids that the person is taking. To pyramids has this predilection for causing a crystalline nephrylathy. Right? So, those are all high-yield things to keep in mind. Right? So, I also want to be like, oh wow, so divine loops, you know, they bring down blood pressure and they can cause nephrylithiasis. Is there some kind of anti-hypertensive that we could give that would help with not causing nephrylithiasis? Well, that's easy. That's going to be a thazideioretic. Right? So, thazideioretics, they actually make you soak up as much calcium as possible from your urine. So, because they make you soak up as much calcium as possible from your urine, especially at the level of the distal-convoluted tubio, right?

So, the DCT, the distal-convoluted tubio, they can actually reduce your risk for nephrylithiasis. Right? So, again, those are all high-yield things you want to keep in the back of your mind for endemic exams. Now, what if they give you a question about a patient and they tell you that this patient is like a 39-year-old male. And, you know, he has tried three different anti-hypertensives. You know, they've put it on an instant inhibitor, hasn't done squat. They've put it on a calcium channel blocker like I'm looting, hasn't done squat. And then, they tell you that this person's hypertension is just not resolving. If you see this, what do you want to think about? Well, I really hope you're saying, oh, divine, this person probably has like a con syndrome. Right? When a patient has resistant hypertension on endemic exams, there are many things that can cause it. One of the big ones I want you to consider is con syndrome. Especially when you notice that that person has hypochylenia and metabolic alkylosis at the same time. So, how do we manage con syndrome? Well, the first thing we're going to do is we're going to check the plasma or dosterone to renean concentration. Right? So, the PEC to PRA ratio. Right? So, again, in con syndrome, you either have an adrenaline in the normal. Or you have a general hyperplegia and you're making a ton of outdosterone. Now, that outdosterone will obviously raise your blood pressure. Right?

And when your blood pressure goes up, your reneanodosterone system is going to be like, what? What is going on? Right? So, those GG cells will freak out and they will make less renean. Right? So, your outdosterone is going to be shooting up. Your renean is going to be shooting down. So, your plasma outdosterone to renean ratio. Your PEC to PRA ratio will be high. It will be greater than 30 on NBM exams. Right? So, obviously, this is a good thing, right? Because if you notice that, wow, this person's PEC to PRA ratio is not high. So, it's like less than 30, right? It's a small number. Then, that will tell you that you're likely dealing with some kind of renal arteries to noses, right? Or fibromuscular dysplasia. Because in those circumstances, you have to noses of the renal arteries, right? And because you have to noses of the renal arteries. And I guess, sorry, let me just say something. Okay, let me continue. And then I'll say something, right? So, because you have stenosis of the renal arteries, your afren material is being hypoperfused. Since it's being hypoperfused, well, your GG cells are going to be like, okay, looks like we don't have much blood pressure going on here. So, you're going to make a ton of renean, right? And as you make a ton of renean, right, that will convert angiotensinogen to angiotensin 1. And then angiotensin 1 will be converted to angiotensin 2. And then angiotensin 2 will go to the zonal glomerulosa of the adrenal cortex.

It's going to make you make a ton of outdosturan. So, your outdosturan and your renean are going up pretty much at the same rate. So, your PC to PRA ratio will be roughly normal, right? It's going to be less than 30. Many times it's going to be less than 20 on your exams. And those people will still have hypochylemia, they will still have ametabolic alcanosis. Because again, outdosturan has certain jobs in life. What are those jobs? Well, those jobs include making you reneit protons. So, if you have a ton of outdosturan, you're going to reneil a lot of protons. So, you're going to get a metabolic alcalosis. And also, it makes you reneit a lot of potassium in your ureth. Especially at the level of the principal cell of the collecting duct. So, you reneil out all those potassium, so you're going to have hypochylemia. Right? So, again, this is one of the reasons why. Because again, like many times I think it's just very beneficial. To not just memorize steps in management or diagnosis, understand why one step comes before the other. The truth is, when you have understanding, you then have predictive ability. I used to tell people this, right, with organic chemistry. If you understand organic chemistry, the mechanisms, you can pretty much predict them. Because they are just certain hours that will make sense. And then certain hours where you'll be like, this thing doesn't make any sense at all. Right? Like many of these diagnostic algorithms that you see.

You see many people, they're like, oh, I'm going to memorize this table, this chart. That this cubanke has given to me. Ask yourself, as you're memorizing the chart. Why is this chart this way? Why are they exploring this first? Like, why does he make any sense? To explore this first step before the second step. When you have that understanding, then your memorization is significantly reduced. Because it's almost like you can see right through whatever question is thrown your way. That is just the truth. Right? But let me get of that so box and continue. Right? So, right? So, that's why whenever you see a person that has resistant hypertension, with hypokillin and metabolic alkalosis, the first thing you should be doing for those people is to check the PAC to PR ratio, the plasma or Dosterone to Renier ratio. If you do those things, then you pretty much help you differentiate between Cons Syndrome, which is a hyper-odosterone state from a problem in the adrenal cortex. Or, fibromuscular dysplasia-renal artery stenosis, which is going to be a hyper-odosterone state. Because you have a hyper-renin state. Because you're hypoprousin, the Afrin material. So, your GG cells make a ton of ringing. Now, that's a small, I'll come back to Cons Syndrome. But the small, off-short thing I wanted to talk about is the importance of understanding that adrenal artery stenosis and fibromuscular dysplasia do not have a similar pathophysiology.

This is a common mistake that many medical students make. Right? They're like, oh, you know, real arteries stenosis, fibromuscular dysplasia, all arises from atherosclerosis. That is not true. That's very important. That is not true. When the thing is, if you look at the layers of the wall of a blood vessel, a blood vessel has an intima as the innermost layer, and then it has a media, that's the smooth muscle layer, and then it has an advantage. Right? Now, in renal artery stenosis, it's the intima that is affected. You have atherosclerosis of the intima of the blood vessel of the renal artery. That's why you have problems. Right? In fibromuscular dysplasia, the intima is perfectly fine. It's the media that is messed up. Right? So remember, in fibromuscular dysplasia, it is the muscle, the media that is messed up, is not there only with intima. Right? Even if the outcome of both the sodders is the same, the pathophysiology behind both the sodders is different. Right? And again, obviously fibromuscular dysplasia will be in a younger person. Right? And renal artery stenosis will be in an older person. Right? Although, believe it or not, our friends at the NBMS, they are very good at also giving renal artery stenosis to kids. Right? That's why many times when you see little children having hypertension, one of the first things you do is you're going to do like a renal Doppler ultrasound. Right? Just to make sure that everything is good with the renal arteries. Right?

Because again, renal artery stenosis don't get me wrong. It's actually pretty common in kids. Especially kids that have problems with other like urinary or reproductive structures. Right? So if you have like a malaria and abnormality, or you have a ureteral abnormality, many times those kids can also have renal artery problems. Right? So let's go back to con syndrome. Right? So we said for con syndrome, the very first thing you're going to do is you're going to check the plasma outdosterium to renal ratio. It's going to be more than 30 on the exam. Okay? If it's more than 30, they're like, hmm, okay. Sounds like this person has got con syndrome. So the thing you're going to then do next is you're going to do something we call a salt suppression test. Right? You're going to do a salt suppression test. Because the thing is if I give you salt, right? Your body is going to retain more water. It's going to raise your blood pressure. So your renal and your dead skin outdosterous system will be like, hmm, okay. This blood pressure is low too high. Let's go ahead and dial down this renal. Right? So you bring down your renal, you bring down your undertense in one and two, and bring down your outdosterium. But if a person has con syndrome, they don't respond to those signals. You give those people an infusion of saline and their outdosterone will not suppress. So the thing you do is you measure the outdosterone before you give them the saline infusion.

And they measure the outdosterone after you've given them the saline infusion. You notice that the outdosterone feels to suppress, right? With saline infusion. That's the thing that I'll tell you, okay, this person has got con syndrome. Actually, the salt suppression test is diagnostic for con syndrome, right? The salt suppression test is diagnostic for con syndrome. Right? But again, you're not done yet, right? Because the thing is sometimes people can have con syndrome because both adrenal glands are messed up. Or they can have con syndrome because only one adrenal gland is messed up. So how do you make those determinations? Well, the way you make those determinations is by doing this fancy schmancy test. We call adrenal vein sampling, right? Adrenal vein sampling. Adrenal vein sampling. Because if you think about it, if one of your adrenal glands is messed up, then you're making a ton of outdosterone from that adrenal cortex. That's zona de l'omerolyssa. That's going to raise your blood pressure. The other adrenal gland that is working just fine is going to be responding to the most signals. It's going to be like, wow, blood pressure is too high. So they're going to have low outdosterone coming from that normal adrenal. But you're having high outdosterone coming from that abnormal adrenal. So you have high outdosterone from one low outdosterone from the other.

So if you check the adrenal veins, and you notice that outdosterone is hiding one and low in the other, then you have con syndrome in just one adrenal. But if you notice that, wow, both adrenal veins have really high levels of outdosterone, then eek, that's bad, right? That's definitely your cause of. That person has bilateral. They have like two adrenal glands messed up causing con syndrome. The reason why you need to know this fact is that it affects treatment. When you have con syndrome in just one adrenal gland, you can take out that adrenal gland. You can perform an unilateral adrenalectomy. But if you have con syndrome in both adrenal glands, then you can not cut out both because that's high morbidity, high mortality. The thing you're going to do in those circumstances is you're going to give medical therapy. Well, what is medical therapy? Well, this medical therapy is going to be an outdosterone. This medical therapy is going to be an outdosterone receptor antagonist. Something like Spirino lactone or Eplereinone. Spirino lactone or Eplereinone. Remember if you're comparing Spirino lactone or Eplereinone, both of those drugs, the outdosterone antagonists, and both of those drugs, the actually high value drugs to know for the exam. Because we use them for a bunch of stuff. We know that Spirino lactone or these outdosterone antagonists, the improved survival in heart failure.

It's one of those drugs that improves survival in heart failure, especially after you've tried a beta blocker and an E-synhibiter. Please don't put people on our dust run antagonists on NV Me exams. If you've not tried beta blockers and E-synhibitors, beta blockers, especially drugs like my toprallol, carvidi-lol, or B-soprolon. You must have given beta blockers and E-synhibitors. Persons E-F must be down bad, usually less than 40% or 30% or whatever. Before you start putting those people on our dust run antagonists. Don't forget that Spirino lactone is a pretty wonderful drug for reducing portal pressures. It's one of these drugs that we can use to reduce portal pressures in people that have cirrhosis. Remember, another drug that also has that claim to fame are your beta blockers, especially like proprylonol and needleol. Those are the two common ones that we love to use on the exams. Remember that with the Treminers practitioner, N-B, needleol and proprylonol. Don't forget that Spirino lactone is a pleridone. Yes, they work the same way, but they have some key differences. One is going to make your breast go grow bigger. That's going to be Spirino lactone. Remember Spirino lactone, in addition to being an aldosterone receptor antagonist, it's also an Androgen receptor antagonist. It can cause gynecomastia. That's something you want to keep at the back of your mind, for example. That's something you want to keep at the back of your mind, for example.

Remember gynecomastia is something that can arise from many different reasons. Spirino lactone can cause gynecomastia. Plera noondas not. What are some other things that would potentially cause gynecomastia on an N-B exam? Don't forget that one thing that can cause gynecomastia can be a person that has a prolactinoma. He has a prolactinoma, so he has a ton of prolactin that can cause gynecomastia. Another way you can see gynecomastia here is that they can give it in a teenage boy. Every other thing will be fine, but this thing, just nobody has his big breasts. Usually it's going to be a boy that is obese. They will try to get you to do these magical therapies. The right answer is supposed to be on your exam is to reassure the parents. Gynecomastia in teenage boys is completely normal. It's completely normal. Or you can give you gynecomastia in a guy that is really tall and has a micro penis. Or they tell you that, oh wow, this boy has like, you know, poppubic and axillary hair. He's really tall. He's really a history of breast cancer and stuff in males. If you see stuff like that, I'll really be thinking about client filters. Thinking about client filters. Remember, client filters syndrome can absolutely positively cause gynecomastia. Gynecomastia is associated with client filters syndrome. It's a serial client filter syndrome. Again, that's actually very high yield to know for purposes of the USMLE exams.

And then remember, people that are serotics, people that have nstagelet liver disease, they can also have gynecomastia on your exam. Well, how those data are right? Well, remember, what's the organ in the body that breaks down estrogen big time? It's going to be a lever, right? So if, for example, your liver doesn't work, right? They are not going to be able to break down estrogen very well. And if you cannot break down estrogen very well, right? You're going to have hyper-estrogenism. Because you have hyper-estrogenism, that can cause gynecomastia. Right? And then don't forget, if a person, they tell you that, they're using a psychiatric history and they're digging some drug for some psych disorder and they have gynecomastia. Well, don't forget your wonderful anti-psychotics. Right? So remember your anti-psychotics like haloparital, quethyapine, closapine, arypipus, all those things, right? Those dopamine receptor antagonists. Well, remember if you're blocking dopamine receptors, there's this pathway that gets a lot a little touchy feeling, right? Your tubero-informed developed pathway. Right? That tubero-informed developed pathway is the pathway of hyper-productinemia. Right? Especially with a respiratory donor of all the anti-psychotics, the big, big, big one that loves, loves, loves to cause hyper-productinemia is respiratory donor. Right?

So the thing that happens is when a person has, is digging an anti-psychotic, their prolactin actually goes up, because you're blocking the dopamine receptors, that hyper-productinemia can absolutely cause gynecomastia. Right? So those are some key things and then don't forget the drug kiloconazole. Right? Kiloconazole can also cause gynecomastia on in-beaming exams. So since we're right at the 20-minute mark, I think I'm going to go ahead and pause here. Again, as I do at the end of every podcast, again, I'll offer these review courses for step 2, CK Step 3, complex level 2 and 3. I'll offer an MDME Testicking Strategy course. I'll throw one on one tutoring for many exams, step 1, step 2, CK Step 3, preclinical medical medical exams, 30-ish-elf exams. And then I have these podcasts on Apple podcasts, on Google podcasts and on Spotify. At least if you want the most recent 150, right? Just go on those things, look for Divine Intervention Podcasts. Please subscribe, any positive feedback you leave is always helpful. And then another thing I will say is if you want everything, though, from episode 1, all the way to this episode, episode 355, then you want to go on the website, Divine Intervention Podcasts with an S.com. And you know, sign up with a Word Press account. Whenever I make a new podcast, you get an email notification. And then I also have a new website. It's called the Divine Intervention Life Lessons Podcast. In fact, it's called Divine Intervention Life Lessons.com.

It has like 41 episodes right now. And basically, I have these short audio podcasts on life lessons that are just relevant for humanity, right? So just something that addresses a specific need, that is common in people's lives. So it consists a lot of very good Bible-based teaching if you're looking for that kind of stuff. And I even have those podcasts on Apple podcasts. It's called the Divine Intervention Life Lessons Podcasts. It's an Apple Podcasts. And then the final thing I will say is I have a You Tube channel. It's called Divine Intervention, USMLE Podcasts and Videos. Right? Divine Intervention, USMLE Podcasts and Videos. If you go there and you subscribe, again, you... That's where I put all my videos. I've been making more videos and recent times. And again, I'm going to be making even more. So thank you for listening to me. I really hope you found this podcast to be helpful. Have a wonderful Friday. God bless you. Thank you. Be well.

Cyclovir (a false nucleotide).

Nephrotoxicity/Nephrolithiasis, and potential myelosuppression.

Loop diuretics (e.g., furosemide).

PAC:PRA ratio > 30.

The plasma aldosterone to plasma renin activity (PAC:PRA) ratio.

Atherosclerosis affects the intima; FMD affects the media.

The salt suppression test (failure to suppress aldosterone after saline infusion).

Primary Aldosteronism (Conn Syndrome).

Thiazide diuretics.

It acts as a false nucleotide, inhibiting DNA synthesis.

Spironolactone (can cause gynecomastia due to anti-androgenic effects); Eplerenone.

Hyperprolactinemia, caused by dopamine receptor blockade.

The intima (inner lining).

Renal Artery Stenosis or Fibromuscular Dysplasia.

Primary Aldosteronism (Conn Syndrome).

Thiazide diuretics.

It acts as a false nucleotide, inhibiting DNA synthesis.

Spironolactone (can cause gynecomastia due to anti-androgenic effects); Eplerenone.

Hyperprolactinemia, caused by dopamine receptor blockade.

The intima (inner lining).

Renal Artery Stenosis or Fibromuscular Dysplasia.