DIP Episode 420 - USMLE Step 2/3 Rapid Review Series 85

Okay, welcome. My name is Devine. This is episode 420 of the Divine Intervention Podcasts. I need to do this podcast. I'll be continuing the Rapid Review series for the US Semilistep 2 CK. Has the three exams. This is going to be Series 85. So let's jump right into it. So, what if they give you a question about 70-year-old child? And they tell you that this child has like, for the past three days, has been having like, right knee pain. And you know, the theory that this child has a mouth fever. And then you also tell you that you see like a red circle or a rash on the child's cheeks. What are you thinking about in those circumstances? Well, I really hope you're saying all the Divine. It sounds like this child has a probably 19 infection. Right? Part of a been 19 infection. Remember, a probably 19 is a single stranded in the virus. It's a bug that the MBM is love to test a lot. They love to test it in many different contexts. So what are some of those contexts? Well, the easy context is the slab's cheek rash that is often found in kids. Right? When kids are exposed to probably 19, they'll have a slab's cheek rash. And then they love to also test probably 19 in adults. But testing probably 19 in adults. Our friends at the MBM is love to go after people that work with kids. Because again, kids, right? They're the ones that will probably give it to those adults. So you can be like a kindergarten teacher. It can be a person that works in a daycare.

And you have like these polyathrologists. You see stuff like that. You see a kindergarten teacher with polyathrologists and things like that. The first thing you should be thinking about on your test is powerful being a 19 infection. Simple and straightforward. And then what is the third context in which you would see a powerful being 19 infection? Well, the third context you will see it with is a person that should have a person that should have a reticulositis, not having reticulositis. Right? So say for example, a person that has sickle cell disease or a person that has like hereditary spherositis. Many times these hemolicanemias, the body is like, wow, we're running out of red blood cells pretty quickly here. Okay, fine. Let's try to go ahead and make more red cells, you know, just pump out red cells. The thing is, since your body is working at such a higher age to pump out red cells, the quality control process kind of goes down a little bit. So since the quality control process goes down a little bit, you're just going to be churning out a lot of immature red blood cells. You're going to have a reticulositis. That's like an appropriate response in most, not all, but in most hemolicanemias. So if for some bizarre reason, you know, a person gets a powerful being 19 infection. Remember, powerful being 19 loves to mess up the red blood cell precursors. When it messes up your red blood cell precursors, guess what? You're not going to be able to respond appropriately.

You're not going to have that reticulositis. So that's a very classic common feature of powerful being 19 infection. It causes a plastic crisis, right? A plastic crisis in people that have sickle cell disease or some kind of hemolidic anemia where they're supposed to have reticulositis as a response. So that's just something you want to keep in mind on your exam. Okay, and then what if they give you a question about a patient and they tell you that this patient, you know, has a large tongue. I'm going to tell you that this patient has had imaging before that showed visceromagaly. And that this child had seizures as a newborn, right? And then they also tell you that, you know, four years ago, they tell you that Reno mass was a Reno mass was resected from this person. And then they say that now, you know, the person is having surveillance imaging and a mass having benign features is seen in the right or per quadrant. What should you be thinking about? Well, I really hope you're saying, oh, divine. This sounds an awful lot like a repado blastoma. So if you may be like, okay, divine. Let's what exactly are you getting at here? So let's let's talk about it. Right. So this child has back with with a man syndrome. Right. So back with with a man syndrome. Remember, it has a lot of associations. So let's kind of tease out those associations. Right. And then I'll get to the repado blastoma business. Right. So the very first thing.

And I know so maybe like, no, of course, this is loyal. Okay. I wish you all the best. But basically if you think about it, they go through the ben syndrome, right. It's an overgrowth disorder. That's the first big thing I think I kind of want you to keep in mind. It's an overgrowth disorder. Right. So what are some classic features in this disorder? Well, one classic feature is hemie hypertrophy. Right. Hemie hypertrophy. Literally one side of the body is just going to be bigger than the other side. Right. And you know, one of the things that grew over grows, right, at those pancreatic beta-ilett cells. So in those pancreatic beta-ilett cells over a girl, well, what do those things produce? They produce insulin. So we're going to produce more insulin. And we know that insulin is very good at bringing down your blood glucose level. So you can tank the child's blood glucose and that can cause the child to have high vocal academia. And that can cause seizures, right. And also insulin. I mean, we know insulin is very famous for driving stuff into cells. Insulin, that hyperinsulinemia can drive calcium into the child cells. And if you drive calcium into the cells, then your blood calcium levels are going to be depleted. If your blood calcium is depleted, that can also cause seizures. Hypocol seeming to have absolutely cause seizures. So they can even give you a question about a child with with the syndrome.

And they tell you that this child has like they can tell you that when you tap the child's cheek, you get these facial muscles, pazems, they will basically describe, right. Because the endemic is these days. They are not very big on saying physical exam shows just schmoustic and so side. That's just almost never what you do these days on exams. I mean, that's something that I make pretty clear in my review courses. So you know, just take for so signs and whatnot. And you know, those things when you see them describe, you know, you're dealing with hypothypohypo calcium. Right. In fact, like the endemic is they can go to an extreme and give you a question about a person with big with with the syndrome. And they show you an ekeg and you see a prolonged Qt interval, right. Or the teller that this person is having muscle weakness. What should the cause be that you're thinking about? I'll really hope you're saying, oh, divine. This is hypokillemia, right. Because again, hyperinsulinemia can cause hypokillemia. Maybe like how does that make sense? Well, think about it. When a person has hyperkelimia, right. Symptomatic hyperkelimia, you know, on an ekeg, you're seeing that widening QRS topic, T waves. You see the person, you know, they have in symptoms. The first thing you do right is calcium gluconite. You literally give calcium gluconite to stabilize the myocardium. But what's the second thing you give? The second thing you give is insulin plus glucose.

Why do you give insulin plus glucose? Because insulin increases the activity of the sodium potassium ATP spot. Sodium potassium ATP spot sodium potassium ATP spot. So since it increases the activity of the sodium potassium ATP spot, we got to ask ourselves, what does the sodium potassium ATP spot do? What it does is that it takes three sodiums out of the cell and puts two potassiums into the cell. So if a child has hyperinsulinemia, they have hyper something that is pumping, causing the pumping of more potassium ions into cells. So your blood potassium levels are going to go down. If your blood potassium levels go down, that can cause a lot of problems. That can cause a lot of problems. That can cause hypochylemia. Hypochylemia can cause problems. Many times on NBM is, they like to give the prolonged cutine travel at hypochylemia. But they also love to give this muscle weakness of a thing. When you see a person that has generalized muscle weakness, you notice that they have like resistant hypertension. You really want to think about con syndrome. That's a very classic way the NBM is love to put all those things together. So just going to be mindful of that on your exact right. So becuse with a man syndrome. So we've said that they can have hyperinsulinemia explained why. The hyperinsulinemia, I didn't explain the derivatives. The different things they can go after with hyperinsulinemia. They can go with hypochylcemia. They can go with hypochylcemia.

Those things can both cause seizures. They can go with hypochylemia. So you're beginning to learn the electrolyte anomalies that could be found in a person that is symptomatic and they have becuse with a man syndrome. Now remember becuse with a man syndrome is also associated with WO Ms trimmers. People that have BWS, they can absolutely have WO Ms trimmers. That's the renomast I was resected three years ago in the vineyard that I gave. And then what is this liver mass? This liver mass is a benign liver mass known as a hepato blastoma. It's known as a hepato blastoma. A hepato blastoma. Very classic in kids that have WO Ms trimmers. Very classic in kids that have WO Ms trimmers. Remember hepato blastomas have a phthalo protein as a tumor marker. Okay. So I guess since we're talking about these electrolyte shifts, I kind of feel like it may be helpful to kind of hit on some of these things, some of these select situations that may pop up on an exam. So like for example, the Mbini's one thing they love to do is they'll give you a question about a person that was just placed on an ex inhibitor. And then you start seeing all these electrolyte anomalies. And then you're asking for either the phthalo phase behind the electrolyte anomalies or they're asking for what the electrolyte anomalies will be. Right. So you just want to be careful. And obviously if you're taking an ACE inhibitor, certain things are going to happen.

The first thing that's going to happen is that your creatinine is going to go up, simple and straightforward. Why does your creatinine go up? Well, remember again, an ACE inhibitor literally will prevent the conversion of angeotensin 1 to angeotensin 2. And if you have less than your tensing 2, and you tensing 2 is a constrictor of the efferent arterial. Because remember, your glomerular capillaries are fed by the efferent arterial and they are drained by the efferent arterial. So normally when you have like a low volume state or whatever, your body is going to clamp down on the efferent arterial with angeotensin 2. By clamping down the efferent arterial, the blood is not going to drain from your glomerular capillaries. If blood does not drain from your glomerular capillaries, then the hydrostatic pressure in your glomerular capillaries will go up. If that hydrostatic pressure goes up, then the thing that's going to happen is you're going to have morphio-tration. So your GFR is going to go down. Your GFR is going to be maintained in those circumstances. But if you didn't take an ACE inhibitor, your hydrogensin 2 levels are going down. So your efferent arterial is no longer going to be construed, it's going to be dilated. So if anything, you're going to tank, you're going to bring down the hydrostatic pressures in your glomerular capillaries. When you do that, that's a problem because you're not going to be able to filter things well.

Because remember literally the hydrostatic pressure at your glomerular capillaries is what creates the force that helps you filter things in your kidneys. So if you're not able to do that, then your GFR is going to go up. So that's why GFR has a minor bump when a person is started on an ACE inhibitor. And then, so notice I used the word minor bump. I'm going to get to the word midra bump in a second here. So, I'll in a few here. But what else happens when you take an ACE inhibitor? Nothing that happens is you develop a mild hyperchillinia. You have a minor bump in your potassium. You have a minor bump in your potassium. So, why is that minor bump happening? Again, if you take an ACE inhibitor, you're decreasing an adjutancing too. An adjutancing too is one of the most powerful stimulators of our dose turn releasing the body. So, if you have less adjutancing too, then you have less of a stimulator going to the zonal glomerulosa of your adrenal cortex to cause it to produce our dose turn. So, when you take an ACE inhibitor, you're developing an our dose turn deficiency. You're literally developing an our dose turn deficiency. So, when you develop that our dose turn deficiency, the thing that's going to happen is, what does our dose turn do? Our dose turn makes you reabsorbed sodium in your kidneys and makes you your innate potassium. Well, if you cannot reabsorbed sodium and your innate potassium anymore, that means you're going to be doing the reverse.

You're going to be losing sodium and holding onto potassium. So, since you're holding onto potassium, you're going to have hyperchillinia. Right? You're going to have hyperchillinia. So, don't forget hyperchillinia and hyperchillinia, LVDGFR. Those are very classic features of a person taking an ACE inhibitor. What's another feature of taking an ACE inhibitor? Another feature is that you could also begin to develop metabolic acidosis. You can develop a metabolic acidosis. So, again, you may ask why? Well, one of the other things that our dose turn does is that it makes you your innate protons. It literally makes you your innate protons. So, the thing is, if you take an ACE inhibitor, you have less angiotensin 2. Since you have less angiotensin 2, you have less our dose turn. If you have less our dose turn, then the thing that's going to happen to you is, you're going to be holding onto those protons. You were supposed to your innate. If you hold onto those protons, you develop a metabolic acidosis. You develop a metabolic acidosis. So, again, taking an ACE inhibitor can cause an elevation in your GFR, it can cause a hyperchillinia, it can cause a metabolic acidosis. It causes minor bumps, minor bumps. But if they give you an in-be-in-be-in-be-question, and you see a person in the T can ACE inhibitor and ARB, and ARB is kind of similar to an ACE inhibitor, and notice that you have these massive bumps in your GFR, massive bumps in the potassium.

When you see stuff like that, that's a very classic presentation of renal otter stenosis. Because, again, most people that take ACE inhibitors, they will have these electron anomalies, but they will just have minor bumps. When you see major bumps, that tells you that they have a disproportionate response to that ACE inhibitor. That's one of the roundabout ways our friends at the MDM Es love to test your knowledge of renal otter stenosis. Because if you start an ACE inhibitor, or a LESSI, or an initial GFR was like, like, you know, crabming clearance, let's say for example, it was 1.1. If you start an ACE inhibitor, 1.2, 1.3, not a big deal. When you see a person, they were like 1.1, and then they bumped to like 2.5. That is not normal. That is not normal. That person has renal otter stenosis. And you may be like, divine, why those renal otter stenosis caused this disproportionate bump? Well, think about it. If you have renal otter stenosis, your primary problem is you're not profusing the Afroenaterial. Remember that glomerular capillary business. It is one of the most important vascular relationships to understand in the body. Remember that glomerular capillary business? We said that it was fed by the Afroenaterial and drained by the EFRIENATURE. Literally, your renal otter leads into your Afroenaterial. So if you have renal otter stenosis, your Afroenaterial is not being perfused. So this is not being perfused. You're not sending blood.

Remember the Afroenaterial feeds the glomerular capillaries. You're literally not feeding your glomerular capillaries. If you don't feed your glomerular capillaries, the hydrostatic pressures in those glomerular capillaries will go down. That's going to raise your GFR. So literally from having renal otter stenosis, you have like a risk factor for GFR elevation. Okay. So you may be like, okay, that's not a big deal. And you know, I mean, it's kind of a big deal because you're going to get hypertension and all these problems from it. But then you're like, ooh, let's take a nice inhibitor because your body when you have renal otter stenosis says, okay. Wow, the Afroenaterial is not really helpful here. So we're really going to be working at the EFRIENATURE to maintain GFR. So usually, people that have renal otter stenosis, they have very high levels of 110.01. Because think about it, again, they are not perfusing the Afroenaterial. So those GG cells, they start to freak out. When they freak out, they make a ton of 110.01. ACE will convert 110.01, 110.02. And then you'll have high endosterium. So that high endotencing, too, is going to clump down. It's going to constrict the EFRIENATURE. That's going to raise the hydrostatic pressures in the glomerular capillaries. And that's going to maintain the GFR. So that's almost like a counterbalancing measure. But if you didn't see, ooh, you're offering a renal otter stenosis, let's take an easy inhibitor. And that's a huge problem.

That's a huge problem because that counterbalancing mechanism, you're basically digging it out of the equation. So now your Afroenaterial is not helpful. But then your EFRIENATURE is also not helpful. So since your EFRIENATURE is not helpful, guess what? Your glomerular capillary hydrostatic pressure is really going to tank. And when that really tanks, you're going to get in some real troubles. So the person's GFR, the person is not going to be able to filter out stuff very well. So the GFR is going to go down. They're going to have a decreasing GFR. They're going to have a decreasing GFR. And if your GFR goes down, your creatine care goes up. So just in case, I'm maybe having spoke a few minutes ago about, ooh, if you take an EFRIENATURE, your GFR goes up.

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Slapped cheek rash (erythema infectiosum).

Aplastic crisis. The virus damages erythroid precursors, leading to acute marrow failure.

Hyperkalemia and metabolic acidosis. This results from decreased aldosterone activity.

The GFR will decrease significantly because the counterbalancing mechanism of Angiotensin II is blocked, causing the efferent arteriole to dilate and reducing glomerular hydrostatic pressure.

Hypoglycemia (due to glucose uptake) and hypocalcemia (due to calcium sequestration).

Alpha-fetoprotein (AFP).

Parvovirus B19.

Von Hippel-Lindau syndrome (VHL) or other syndromes involving renal/hepatic masses.

Decreased Angiotensin II leads to decreased aldosterone secretion, resulting in impaired potassium excretion.

Conn's Syndrome (or pseudo-Conn's), indicating mineralocorticoid excess/aldosterone deficiency effects.

The glomerulus is fed by the afferent arteriole and drained by the efferent arteriole; Angiotensin II constricts the efferent arteriole.

Hypoglycemia and hypocalcemia.

Parvovirus B19.

Von Hippel-Lindau syndrome (VHL) or other syndromes involving renal/hepatic masses.

Decreased Angiotensin II leads to decreased aldosterone secretion, resulting in impaired potassium excretion.

Conn's Syndrome (or pseudo-Conn's), indicating mineralocorticoid excess/aldosterone deficiency effects.

The glomerulus is fed by the afferent arteriole and drained by the efferent arteriole; Angiotensin II constricts the efferent arteriole.

Hypoglycemia and hypocalcemia.