DIP Episode 405 - USMLE Step 2/3 Rapid Review Series 80

Okay, welcome. My name is Divine. This is episode 405 of the Divine Intervention Podcasts. Into these podcasts we're going to be continuing our Rapid Review Series for the USML Step 2 C Can Step 3 exams. Obviously this also works for Complex Level 2 and 3. We're going to be doing series ED. Just as a reminder, if you're taking the USML Step 2 C, you'll step 3 exams or Complex Level 2 or 3 exams anytime soon. Have a 20 hour review course. It's going to be taking place from the eighth to the 13th of August. It's going to be from 5 to 9 p.m. Pacific Standard Time. So we'll meet from one day to Saturday, although we will moment on Wednesday. So it's five days four hours each day. Again, tons of people have taken the scores. Found it to be super helpful. Then if you're taking step 2 or step 3, we have the MB Me Test Against Strategy scores. That's going to be on the 5th of August from 5 to 7 30 p.m. Pacific Standard Time. Again, I literally get emails from people that, oh, while my Q Bunk percentages have gone up like 20, 30 percent, my scores have gone up 30, 40 points. Just from taking this Test Against Strategy's class. Then I have an MB Me Bio Statistics Board Camp. It's going to be taking place on the 18th of August. That's a Thursday from 5 to 9 p.m. Pacific Standard Time. So if you interested in any of these courses, just shoot me an email and I'll give you some more information. The courses are all held over Zoom. Now, what if they give you a question about 67 year old male?

His daughter tells you that over the last six months, he has been very forgetful. He has been having a lot of issues with remembering to pay his bills and getting back home on time from the store because he loses his way. Then they tell you that he was recently prescribed the wheelchair because he keeps falling over. He keeps falling over, keeps falling over. Then they tell you that he has had a lot of urinary accidents that has led him to have some of these pressure ulcers and sores and whatnot. If you see something like this, what do you want to think about? Well, I really hope you're saying, oh, divine, this sounds a lot like normal pressure hydrocephalus. This is like wacky wet and wobbly. The person is wacky, your wet and their wobbly. So they have eutaxia, that's the wet. I mean, that's the wobbly. They have the wacky, that's the dementia. Then they have the wet and that's the urinary incontinence. That's normal pressure hydrocephalus. Remember, typically these people, again, you know the NBA means they're pretty smart. They know that most people that have the job description met so they don't have memory. Wacky wet and wobbly and I'm not playing hydrocephalus. They've memorized all that stuff. So what do they do? Again, it's the same pathology. Just hey, how can we test it in a different way? So they will say which of the following would be the most likely finding on a lumber puncture in this species.

It's very, very high yield to know that these people, the problem they have is that they have CSA free absorption issues. But if you do a lumber puncture, the CSA for being pressure is are normal. That's very important. I think that's kind of like the big thing I want to get out here. The CSA for being pressure is normal. That's why it's called normal pressure hydrocephalus. It's a simple question, but I can imagine something like that just throwing someone for a loop on an exam. So they have normal pressure hydrocephalus. This hydrocephalus is actually an example of non-obstructive, we can call it a communicating hydrocephalus. So there's no problem with CSA flow. It's just a CSA free absorption issue. At the level of the arachnoid granulations, that's how those people get in trouble. So it's a non-obstructive or we can say communicating hydrocephalus. The same pathophysiology actually is what you find in a pseudo-tomar cerebride. We'll talk about that in a bit. But how do we trade this normal pressure hydrocephalus? Well the way we're going to trade this is we're going to place a VB shot. You're going to place a ventriculu peritoneal shot. You're going to drain some of that CSA and the person is going to hopefully be okay. It's one of those potential irreversible causes of dementia. Then the second thing you want to keep in mind. Again, the close causing idiopathic intra-cranial hypertension.

The way you make that differentiation is that in I-I-H, in I-I-H, which we used to call pseudo-tomar cerebride before. When you do a lumper puncture on these people, the CSA opening pressures are going to be high. Usually it's going to be over 200 on an NV Me exam. That's actually pretty high yield to know for for tests. So remember, pseudo-tomar cerebride, a friend of the NV Me is kind of want you knowing the risk factors. So if you take vitamin A, so let's say for example, a person is taking a vitamin A related compound because they have acne. Usually acne or they have acute promylocytic leukemia with that 15-17 translocation. Because remember, all trans retinoic acid, it's a vitamin A derivative. So those things are all risk factors, tetracycline, and risk factors. Those are things that can all increase your risk of getting pseudo-tomar cerebride. So how do we diagnose it? Well, it depends on how they present. So if the person presents with like blurry vision, they have like papilladema in the eyes because that's usually the way we present. They'll have like blurry vision problems, they'll have headaches, they'll usually be an obese woman, and they'll be a chronic issue. They'll have all these problems, you're like, hmm, okay, well, the thing is if they present with those symptoms, they present with the papilladema in the headaches, that kind of makes you worried about increasing your cranial pressures.

So you're going to freak out, you're going to get a CT of the head, you're going to get a non-contrast head CT. That's what you do first, right? But then, if the non-contrast head CT is fine, then the next step will then be a lumbar puncture. You'll notice that they will have increased CSA-phopin pressures. So what do we do for these people in terms of treatment? Well, one thing you can do is you can do serial lumbar punctures. Many of these people are coming to like a radiology department and they just get the CSA-drained periodically, like once a month or something like that, that actually helps a lot of these people. Or, alternatively, you can also give them a sedazolomide. Remember, a sedazolomide is a carbonic and hydraise inhibitor. So because it's a carbonic and hydraise inhibitor, it decreases CSF production. Because remember, carbonic and hydraise is actually one of the enzymes that are necessary for CSF production. So you don't make CSF, and that's going to help, right? That's going to help. But if, for example, you know, all these things are not helping and having like profound visual problems, one thing you can consider is a kind of surgery known as optic nerve sheath, finistration, optic nerve sheath, sheath finistration. That's something that can help these people that have pseudo tumor cerebride. So that's something you kind of want to keep on the back of your mind, for example.

And since I'm talking about a sedazolomide, what are the uses of a sedazolomide, or name gamemies? Well, there are a few classic uses, right? As we've said already, you can use it for pseudo tumor cerebride. That's one. Secondly, you can use it for treating open angublochoma. Because again, carbonic and hydraise is a pretty ubiquitous enzyme. It's one of these enzymes that are also necessary for the production of ekeosumer. We know that in glaucoma, you have increasing chocolate pressures. So you're like, hmm, how can I fix this in chocolate pressure issue that I have? Well, one of the ways you can accomplish that goal pretty easily is by just going ahead and decreasing its production. So you can give a sedazolomide, or a hippocabonic and hydraise, and that'll be helpful in those circumstances. So those are probably like the two big things, you know, every now and then, you know, you hear about how is a sedazolomide can be used to reducing trocranial pressures. But really, for pressing has increasing trocranial pressures, you know, as evidenced by them having like hypertension, so their blood pressure is really high, but it'll be pretty cardiac, right? So they're partly really low, right? And you'll notice that they have, you know, they'll have that cluster of bradycardia hypertension, and there'll be many times altered. That's increased ICP.

Yes, you can give a sedazolomide, but the thing you want to consider first, the quickest way to lower a presence in trocranial pressure is to go ahead and give those people a hyperventilation, right? Go ahead and interpret them, hook them up to a ventilator, and just to resolve that rate, right? Hyperventilite those people, you know, through way a lot of CO2, and that'll cause a cerebral viso-construction, and that can lower their intra-cranial pressures. I'll say that again, the fastest means of lower intra-cranial pressures is to give hyperventilation, is to hyperventilite the patient. You can also give hypertonic saline, but again, that's really the correct answer on in-game, means many times it's going to be hyperventilation, right? But some auxiliary methods you can use, if hyperventilition is not an answer, you can try to elevate the head of the bed. I mean, sorry, not elevate the head of the bed. You'll try to, right? You try to, essentially, elevate the head of the bed, right? So you basically put your head, you'll basically be above your heart, essentially, right? In the horizontal plane, that can help. But again, those things are not going to be as helpful as hyperventilating the patient. You can give hypertonic saline, you can give us a zolomide, but again, hyperventilition should be like the first thing you go after an exam. Giving normal hypertonic saline, or giving us a zolomide should be much lower on your ladder on NBMI exams.

And I guess, remember what I said, a zolomide, friends at the NBMI sometimes expect you to know the electrolyte anomalies you can get with a zolomide. So what are the electrolyte anomalies? We remember it's a carbonic and hydrogene inhibitor. So what does carbonic and hydrogene do to even start? Well, the thing it does is it combines carbon dioxide and water to make carbonic acid. And then, that carbonic acid that is formed in a different environment, be it the intracellular, extracellular environment, it converts that carbonic acid to hydrogen ions and bicarb. Right? So the thing is, in general, if it does not work, if you're in inhibitor enzyme, you can actually build up a lot of bicarb, depending on the direction of the arodye inhibitor. But the key critical thing I'll say is just, if you're thinking about it from the kidney perspective, because really, it's the kidney that's ultimately going to control many of the outcomes you get with a zolomide. If you inhibit carbonic and hydrogene in the kidneys, there'll be more bicarb in your urine. You're going to be wasting a lot of bicarb, wasting a lot of bicarb. Right? So your in-page obviously is going to be high. So you're going to waste a lot of bicarb, going to waste a lot of bicarb. Well, if you think about it, if you're wasting a lot of bicarb, the key critical thing I would encourage you to keep in mind is that you could develop a metabolic acid doses. I said, a zolomide can absolutely cause a metabolic acid doses.

Right? But remember, because it's causing you to lose bicarb in your urine, that bicarb that is showing up in your urine is going to automatically attract water. So you're going to become fully depleted. If you become fully depleted, well, what do you think you're reading and you're tensing out those urine system does? It gets revved up. If you get revved up, you'll basically make a ton of our dose turn. What does our dose turn do? Our dose turn makes you dump potassium in your urine. It makes you people potassium, pea protons, and reabsorbed sodium. So if you have high our dose turn, your pea potassium, so you develop hypochyline. Right? You develop hypochyline as a result of that. Some people may say, divine, but since you're peeing protons, wouldn't that reverse the acid doses that you get with acid doses? No. The thing is, acid doses, in the use of acid-isolate, the predominant effect is that bicarb loss. So you're going to have a net metabolic acid doses. Okay? You're going to get a metabolic acid dose with hypochyline. That's very important to know because most of the diuretics cause a combination of a metabolic alkalosis with hypochyline. So because acid-isolate is kind of weird in that way, that's why the NBN is the law of testing the electrolyte anomaly. Right? It causes metabolic acid doses, but with hypochyline. It causes metabolic acid doses just because of its mechanism of action.

It prevents you from reabsorbing bicarb essentially in the proximal tubule because it's a carbonic and hydrism inhibitor. But it makes you volume depleted because it's a diuretic. That's going to cause hyper-auto-steroanism. Right? That's going to cause a secondary hyper-auto-steroanism and that's going to cause you to lose potassium in your urine. So that's going to cause you to be hypochyline. So it causes a metabolic acid dose and hypochyline. On like the other diuretic, say for example, like a lube diuretic, lube diuretics, they're going to inhibit the sodium potassium-tucloride transporter that you find at the level of the thick ascending length of the lube of Henley. So that's going to make you super volume depleted. When you get super volume depleted, your reigning and trotensing our dose-steroan system is going to get revved up. You're going to make a ton of our dose turn. That our dose turn is going to make you to pee protons in your urine. So you're going to develop a metabolic alkalosis because you're losing protons. And then it's also going to make you pee potassium in your urine. So you're going to develop a hypochyline. You're going to develop a hypochyline and a metabolic alkalosis. So again, just make sure when you're dealing with these things, make sure you know your arrows and your electrolyte abnormalities and whatnot. The MV is the kind of like stuff, stuff like that. Okay.

And then if you really think about it, friends at the MV is I don't know, I'm really hidden at this acetyzolomy. It's just something that they love to test on exams. Remember I said acetyzolomy. The police who works in the kidney is the proximal tubule. So basically by inhibiting biocarbonyl absorption at the proximal tubule, by inhibiting carbonyl and hydrates, is essentially causing you to have a type 2 renal tubular acidosis. It causes a type 2 RTA. Acetyzolomy is a cause of a type 2 RTA. Right. So now one conundrum, if you're following along with this podcast, one conundrum, some of you may get into his, hmm, divine. You just said that acetyzolomy causes you to dump by carb in your urine. Hmm. Okay. So it's going to dump by carb in your urine. Aren't you going to have a basic urine? Isn't your urine pee is going to be really high? Is it not, is that not what you see in a type 1 RTA? Yes. So let me explain. Now the thing is in a type 2 RTA involving the proximal tubule. Right. More by carb is showing up in your urine. But the thing is that by carb is going to encounter the alpha and the beta intercalated cells that are more distal in your nephro. Those things are one of the primary regulators of your urine pee.

So as long as those cells are working, as long as you're, especially like your alpha and beta intercalated cells, more especially the alpha intercalated cells, if those are working, that by carb that you've dumped from the proximal tubule, you're going to deal with that problem down the line in the nephro. So ultimately, your urine pee is not going to be more than 5.5. But when you have an actual alpha intercalated cell problem, which is exactly what happens in a type 1 RTA. If your alpha intercalated cells don't work, then you cannot regulate your urine pee. You can not regulate your urine pee. You cannot acetypile your urine. So your urine pee is going to be over the magic number, I believe it's 5.5. So again, make sure you keep that in mind. A type 2 RTA, even if you're putting more bicarbonate in your urine, there are just other cells that can help you deal with that extra bicarbonate thrown in the urine and can help you out there. But in a type 1 RTA, your alpha intercalated cells for sure for sure do not work. So since the for sure for sure do not work, then you're not going to be able to acetypile your urine. So your urine pee is going to be high. It's going to be more than 5.5. Really, there are two major things that can cause you to have a higher in pH on NBM Es. One is if you have a type 1 RTA, which is a problem the alpha intercalated cells.

And two, if you get a UTA with a urese positive bug, stuff like prettiest merubles, for example, it's going to make your urine super-bizic. You're going to form those as trovide stones. Sometimes you call them the magnesium and monium phosphate stones. So you can cause all those problems. Okay, so I think that's going to be my entire sermon on acetyzolomide. Okay, that's going to be my sermon on acetyzolomide. So hopefully you'll find that to be helpful. Now, I talked about hypertonic saline and I get this question from many people all the time. I divine. When would I use hypertonic saline on an NBME exam? To be honest with you, yes, you can lower intracranial pressures. I'm not going to argue with that. But the primary use, I will say probably one of the only times that hypertonic saline is classically correct on NBM Es. Is when a person has hyponitremia? But the hyponitremia is severe. What do I mean by severe? The sodium is on the 120 and they are having seizures. When you see a person that is has a sodium on the 120 and they're seasoned, they have seizures, then those people will have prime candidates for hypertonic saline on NBME exams. Okay, those people have prime candidates for hypertonic saline on NBME exams. Again, hypertonic saline, you can use it to lower acp's. But that's certainly not a first line measure. That's something you need to keep at the back of your mind for, for example.

That is something you absolutely need to keep at the back of your mind, for example. Now, one other thing I want to mention here is what if they give you a question about a patient and they tell you that this patient has this, has had a brain tumor is sected. They had this brain tumor is sected when they were kids. And then, now they're in their 30s and they were getting a CT of the other name pelvis for screening. And you notice like a mass like at the renal pelvis or something like that or like on the renal cortex. Just somewhere in the kidneys. If you see something like that, what should you be thinking about? I really hope you're saying divine. This person has VHL. This person has one hiphole in the mouth. They're probably have VHL. They have a lot of problems. They can have renal cell carcinomas. So if you may even be wondering divine, what in the world was the brain tumor? Well, the brain tumor is that one of those things that can cause you to have polycythemia. That's a hemantium blastomer. Hemantium blastomas, you pump out a ton of erythropoetit. That hiphole can cause your hematocrate and your hemoglobin to go up. And that can cause you to have a polycythemia. Okay. Usually it's going to be a mass that shows up in the cerebellum. Usually like in the cerebellum, it usually contains calcifications and it produces a ton of ipo. Right? It produces a ton of ipo. Right? So that's one hiphole in that. So don't forget the findings.

These people can get renal cell carcinomas. They can get bilateral renal cell carcinomas. They can get hemantium blastomas in the brain, which contain calcifications and make ipo. They can have a lot of fulcrumus like tumors. So they can give you a question about this same brain tumor person that then has like episodic headache and hypertension with an epidemic and effrints. Again, think about VHL. VHL, right? Remember it's an Orozomo dominant disorder. Essentially the thing that happens is you have a deletion of the VHL gene on chromosome three and that's how you're getting trouble. Okay? That's how you're getting trouble. Now this renal cell carcinoma, how do we work up renal cell carcinomas? Obviously again, if you suspect that a person has renal cell carcinoma, the first thing you want to do is you want to go ahead and do a CT of the abdomen and pelvis with IV contrast. Right? A CT of the abdomen and pelvis with IV contrast. When you see the mass, what's going to be your next step? Again, our friends at the MBM is they're very good at making you go and do a biopsy, don't do a biopsy. You don't buy, there are certain cancers that are not biopsyde, right? There are certain cancers that are not biopsyde and one of the easiest ways to remember them is just remember the things along the urinary slasher productive tract. We rarely biopsy those malignancies. The exceptions, right? Well, those exceptions are not very common, right? But what are the cancers you don't biopsy?

You don't biopsy testicular cancer. Well, what's analogous to the testicles in women is the ovary. You don't biopsy ovarian cancer. You don't biopsy testicular cancer. You don't biopsy ovarian cancer. You don't biopsy renal cancers. And you almost never biopsy adrenal cancers, okay? So testicular ovarian renal and adrenal. You do not, okay? You do not, you do not biopsy those are malignancies, right? Those malignancies when you suspect them and you see them on imaging, your next step is to take out the entire organ. So for example, this person will renal so of course, you know, you need to do an effectomy. The nephrectomy is your biopsy, okay? Do the entire nephrectomy, cut out that entire kidney, send it off of pathological analysis, ovarian cancer, same deal. Do not overreact to me. Just cut out that entire ovary, send it off analysis. Testicular cancer, you don't biopsy testicular cancer. You literally cut out the entire testicle ovarian and send it off for pathological analysis, same deal with adrenal, cut out the adrenal on that side. That's pretty high eoltonone, right? Those are pretty high eoltonone, right? So renal so of course, you know, my again, don't forget, you're doing an effectomy, that's how you work it up. Renewal so of course, you know, my tends to have like pretty bad outcomes because you love to spread to the bone, it can cause like these lytic bone lesions, right? And remember, your kidneys, right?

The cycle a lot of blood in your body, so you can already see that how malignancies can be easily disseminated all around the body, right? And if you're looking for a way to treat renal so of course, you know, my again, you can do an effectomy. One thing you should maybe keep in mind, this is more for step one. So for people who listen to this podcast, probably doesn't really matter much to you, but interlooking to analogs are quite helpful in the management of renal cell carcinoma, okay? They're quite helpful in the management of renal cell carcinoma. Okay, so I've kind of hit 20 minutes, that's kind of my quarter four. These are rapid review series. So I'm going to go ahead and stop here. I do offer one on one tutoring for all the USML exams. Step one, step two, three, preclinical, medical exams, 30-year-clutch, research exams. I also help with the complex level one, two, and three exams. The only things I don't do for I don't do for I don't do the OMM, that's something I don't, I don't classically do. And then I have to get my 20-hour review course for step two and step three on complex level two and three, my MBA Me testing strategy is class four. Step two, CKAN, step three. And then my biostatistics bootcamp that applies to step one to step three, complex level one to three.

In fact, if you're an internal, if you're a resident and your board exam involves biostatistics, which a lot of board exams involve, then my biostatistics book camp is something you're going to find to be profoundly helpful. I also help with ERAS applications, recommendation letters, personal statements, supplemental applications, the ERAS application itself. Again, I've worked with tons of people, some of them are attendants now, many of them are residents, all over the country, specialties from or thought to dermatology, to internal medicine, to peed, to gen-search, to ENT. I've worked with tons and tons of people. I have a lot of experience with this process, especially if you have like a tricky application and many times able to help you wiggle out of those situations. Again, if you play your cards right, after all is said and done. And I love to give people honest advice. So if you interested in any of these things, just shoot me an email through the website and I'll give you some more information. So thank you for listening to me today. I also have these podcasts on Apple Podcasts, Google Podcasts and Spotify, at least the most recent 150. If you want everything from episode one, episode 405, go on the website, divineinterventionpodcast.com. If you have a Word Press account and you subscribe, you will actually get an email notification whenever I make a new podcast. I also have a You Tube channel, Divine Intervention, USMLE podcast and videos.

Again, in the final stages of making a change to that You Tube channel. So again, if you're interested, just subscribe. Just go there, divineintervention, USMLE podcast and videos. Subscribe and you'll see those updates as they happen. And then also have a new website called divineinterventionlifelessons.com. Many people told me, oh divine, I love your life lessons. And you know, I'm still going to be putting life lessons at the end of some of these podcasts. But I said I started a whole new website. Even has a podcast associated with it. I make about two every week. I have more than a hundred right now. They're about 10 to 20 minutes long. And you know, I use the Bible to discuss a life lesson that is pertinent to humanity. So if that's something that you're interested in, again, just check it out. I have the podcast on Apple Podcasts. It's called Divine Intervention Life Lessons Podcast. So thank you for listening to me today. Have a wonderful rest of your day. God bless you. I'll see you in the next podcast. Thank you.

Gait ataxia/difficulty walking, urinary incontinence, and dementia ("wacky wet wobbly").

Elevated, typically over 200 mm H₂O.

Use of Vitamin A derivatives (e.g., retinoids) or tetracycline antibiotics; and obesity.

Carbonic Anhydrase Inhibitor (CAI); it decreases CSF production by inhibiting the enzyme necessary for CSF formation.

Metabolic alkalosis and hypokalemia.

Type 1 RTA.

Testicular, Ovarian, Renal, and Adrenal glands.

Wacky (dementia), Wet (incontinence), and Wobbly (gait ataxia).

It inhibits carbonic anhydrase in the proximal tubule, leading to bicarbonate wasting in the urine.

Treating severe hyponatremia (Sodium < 120 mEq/L) accompanied by seizures.

Hemangioblastomas (usually found in the cerebellum).

Type 1 RTA has a high urine pH (>5.5) because the alpha intercalated cells fail; Type 2 RTA maintains a normal, acidic urine pH (<5.5) due to distal compensation.

Loop diuretics cause metabolic alkalosis and hypokalemia (due to Na-K-2 Cl inhibition); Acetazolamide causes metabolic acidosis and hypokalemia (due to HCO₃⁻ wasting).

Wacky (dementia), Wet (incontinence), and Wobbly (gait ataxia).

It inhibits carbonic anhydrase in the proximal tubule, leading to bicarbonate wasting in the urine.

Treating severe hyponatremia (Sodium < 120 mEq/L) accompanied by seizures.

Hemangioblastomas (usually found in the cerebellum).

Type 1 RTA has a high urine pH (>5.5) because the alpha intercalated cells fail; Type 2 RTA maintains a normal, acidic urine pH (<5.5) due to distal compensation.

Loop diuretics cause metabolic alkalosis and hypokalemia (due to Na-K-2 Cl inhibition); Acetazolamide causes metabolic acidosis and hypokalemia (due to HCO₃⁻ wasting).