DIP Episode 558 - 2024 USMLE Step 3 Free 137 Discussion Part 6a (Q51-54, super helpful for Step 2!)

Welcome to episode 558 of the Divine Intervention Podcast. In today's podcast, we're going to be continuing our series on the USM-LE Step 3, 3137. It's going to be part 6. And again, if you're taking Step 2, highly recommend you listen to this series if you can. It's probably going to help you as well because by the time you take Step 3, they'll probably have released a new 3-3-1-20. Alright, so let's just jump, jump right into it. So question 51 says, 15-year-old boy is brought to the clinic after his father noticed significant swelling of the boy's chest, when he was getting dressed six hours ago. The patient reports a three-month history of gradually worsening, left-sided chest pain and swelling. What he says, he was too embarrassed to tell his parents. He has not had fever, chills, night sweats, loss of appetite, weight loss, or any recent trauma to the chest. Medical history is unremarkable and he takes no medications. The patient is a good student. He does not smoke cigarettes or drink alcoholic beverages. Temperature is 97.5, pulse is 69 per minute. Respirations are 14 per minute and blood pressure is 150 over 70. O2 sat is 100% on rumour. It's 100% on rumour. Examination of the head, neck, and skin discloses no abnormalities. There is a fixed, poppable mass measuring approximately 14 by 12. Centimeters on the left chest wall that is tender to bowel vision. The remainder of the physical exam is discloses no abnormalities.

My up-sale of this mass is most likely to show which of the following. To be honest with you, I absolutely love this question because this is a very good kind of question where I can almost posit that most people studying this have absolutely no idea what this is. When I was looking at this question, I was like, I have no idea what this question is. This is a realistic exam situation. Literally, let's put ourselves in an exam sheet. These are realistic exam situations like, I have no idea what's going on. This question is really, really confusing. I feel completely out of my element here. How do you handle these kinds of things? The way you do it is, again, you do the process of elimination. For example, we see this boy seems to have this chest wall mass that is tender to bowel vision. He is part of the chest wall. It's not a long mass. This has been going on for three months. This is probably not an infection or anything crazy going on. I'm just going to have in this orientation, you can then rule out answers that make no sense. I'm telling you this, I know some people are like, wow, this is you saying this, you teaching all these podcasts seem like you know a lot. I'm teaching this, there's going to be questions you'll see. Nobody knows everything. Even I'm divine, I don't know everything at all. Actually, there's a lot of stuff I don't know. But the thing is, the fact that you see questions like these, it doesn't mean you cannot get them right.

In fact, a pretty decent number of these questions. If you're just a prudent test taker, you should be able to get them right on a test. For example, option A here says acid fast bacilli. Well, what's the classic thing you know about acid fast bacilli? We know that that's TB country. Well, think about this. Does this look like TB? This boy pretty much has almost no symptoms of TB. So I'm not going to pick option A. And then if you go to option B, grand positive coxine clusters, that's usually referring to staff Oreos. Again, it's highly unlikely that you have a staff Oreos infection that is raging for three months. Then option C says infiltrating nests of squamous cells and increased keratin. Again, whenever you see keratin, we're always worried about some kind of squamous cell cancer. Right? Squamous cell cancer. Or even these keratin based things, you know, it can be those Samoma bodies. Right? And what do we know about some of our bodies? Well, we know that we find them in misotheliuma, which this is not. Again, a 15 year old, our hope is not getting misotheliuma. We can see them in jiuma. Well, this says nothing about the brain. We can see them in papillary thyroid cancer. Well, this says nothing about the throat. And we also see this in a serocystadno-customov the ovaries. Well, this is a boy who does not have ovaries. And again, squamous cell cancers, right, of the lungs of the skin.

They don't really give us much of any description that leads us, no alteration or anything that leads along those lines. So option C highly unlikely to be correct. And option D says malignancy and c-sotrophoblasts and cytotrophoblasts. So the thing is, these things, you're going to see this in people that have like something I read from like placenta, like a correocorcinoma. Again, correocorcinoma, your BDACG is going to be very, very high. It can spread to the lungs, but again, many times it's going to be on a very enleisure. They're going to have a lot of morning sickness symptoms. We don't see a lot of those stains here. Do not pick that as an answer. Option D's wrong. Option D's wrong. So honestly, the only answer that makes any sense here is going to be option E. Polydifferentiated and Applastic Spindle cells. Again, honestly, as I was going through this question, I was like, man, I really have no idea what they're talking about here. I did some research. And this child may have a spindle cell sercoma. There's actually like a case report online on this stuff. Again, sometimes on the exams, you just see some of these things that kind of just come out of left failure. Like, where did this come from? So these like a spindle cell sercoma, I believe. I believe that's what it is. But again, this is a very good realistic example of a question where it's like, you mean, no, no, what's going on?

But there's just no good reason why you should not get this right if you're just a decent test taker. If you're just a decent test taker. So we're going to go to question number 52. Okay, so question 52 says, a four-year-old boy is brought to the office by his mother because of a five pound weight loss. Decreased appetite and daily fatigue during the past two months. The mother says the patient's fatigue is limited to his physical activity. The patient's medical history is remarkable for asthma and seasonal allergies. He has had three asthma exacerbations during the past two months that have required treatment or a pregnancy. Routine medications are satirisine, albuterol, and buttesonide. The patient is 99 centimeters. So he's at his 25th percentile for height. Weighs 31 pounds, 25th percentile for weight. And BMI is 14.3, that's the 10th percentile. His temperature is 98, pulse is 70, or his versions are 18 blood pressure is 80 over 50. The patient appears lethargic. Physical exam shows no abnormalities. Results of Lopsidoid is our show. So. Okay. So we see his Lops right. So he is creatinine is fine. Honestly. I mean it's a little high but not too worried about it. But sodium is really low. It's 125. Spotassium is fine. Bicarb is okay. His glucose is at the lower end of normal 60. But honestly, his remaining Lops are pretty okay to me. So he then says which of the following is the most likely on the line cause of this patient's condition. Right. So.

Just to kind of frame this question. So this is a boy. He's been losing weight, having decreased appetite. You know, his feeling fatigued, has hyponitremia. And we see that, you know, he has all this medical history. And you know, he's had three asthma exacerbations. And he has had to take like oral prednisone or whatever. So again, we see hyponitremia. We see all these issues. Kind of sounds like an adrenal issue. And we're going to go through these answers one by one. So option E says decrease the activity of 21 hydroxylates. Again, if you have 21 degrees that's getting a degrees activity of 21 hydroxylates. You're not going to be making cortisol. You're not going to make out dust your. You're going to be making a ton of DTS, right. This is the most common cause of congenital adrenohyperplasia. So they will have hyponitremia, which his guy has. But many times these people are going to have like a frank hypercalemia. This guy does not have it. And they will probably have skin hyperpigmentation. Because if you're not making cortisol, your ACT is going to be. It's going to be pretty, pretty high. Since there's no negative feedback. This guy does not have skin hyperpigmentation. So I'm not going to pick that. Okay, so I'm going to go to option B. Option P says. Decrease production of ACT. Okay, we should keep this one because this guy took oral prednisone. So that can suppress your HP access, right. Because prednisone is a very important thing. So you can suppress your ACTH.

So you won't have ACTH. And if you don't have ACTH, try to your, you know, you won't be making cortisol. And you won't be making, you know, at least you won't be making cortisol. And I know some of you may be like divine. So how does that explain the hyponitremia? Well, the thing is remember cortisol has our dust-erone like properties. So if you're not making cortisol, then you're not getting that. Outdo stereogenic activity of cortisol. So that may actually cause you to have hyponitremia, believe it or not. And also, if you think about it, when you're this hypotensive, this boy's blood pressure is 80 over 50. Because remember, when you're in a state of like adrenal crisis, you can become hypotensive. And when you're hypotensive, you're not going to be profusing your GG cells well. Right. So you're not going to be making. You're going to be making a ton of renein actually. And one of the things that renein does, so you're going to be making a lot of renein. Renein makes you make one of those. And then when you make a lot of our dust-erone, you know, I mean, so let's go through a pathway, right. I don't want to skip steps here. I have a feeling that I'm not going to go out with a question 60 for this one. Because there's kind of a lot of high-yield stuff. So I'm going to go out with a question 60 for this one. And I have a lot of high-yield stuff here that I want to talk about. So I'm not going to rush through this. I'm going to slow down actually a little bit here.

So you make a ton of renein. If you make a lot of renein, you convert angiotensin, or gene 2aniotensin 1. The angiotensin 1 is going to be converted to angiotensin 2. And then angiotensin 2 does a bunch of stuff, right. So it makes you make a lot of our dust-erone, right. And also it makes you make a lot of ADHD, anti-diarrhetic hormone. Now, EDH causes uterine. I was up a lot of free water from you urine. If that happens, that's going to dilute your serum. So you can have hypodytramia. So you can certainly have this from this, right. And again, we see this boy does not have skin hyperpigmentation, which makes sense. Which makes sense. He doesn't have it. He'll not make an ACTH, then you're not making MSH. I'm not making an analisid stimuli tin hormone. So you will not have skin hyperpigmentation. And I know some of you may be like, wow, so divine. You are saying that ACTH is not produced. So since ACTH is not produced, we're not stimulating the adrenal cortex to make cortisol or our dust-erone. So you're just saying this boy has low cortisol. Why you're not saying this boy has low cholesterol? Well, let me tell you this. This boy probably does not have low cholesterol. And here's why. This is one fact that many people forget. And again, this is why basic sciences are so critical for step three. And becoming more and more critical for step two. Here's the thing. Cortisol production is under the control of ACTH. The simple fact.

But our dust-erone production is not under ACTH control. Our dust-erone production is mediated by your reigning angiotensin-erodosterone system. So if we take a small sidebar here, when a person has primary adrenaline sufficiency, so they have like other sense disease, or they have something else that basically explodes your adrenal cortex, like a waterhouse-frideric sense syndrome, then yes, your actual adrenal cortex is dead. The actual site of production of cortisol is gone. Our dust-erone is gone, our DHS is gone. So that's fine. That makes sense. However, so in primary adrenaline sufficiency, you're going to have low cortisol, low cholesterol. But when you have a secondary adrenaline sufficiency, as this boy likely has, because he will stick in oral prednisone, your adrenal cortex is still intact. It's just that the exogenous steroid you're taking is literally suppressing your ACTH. So if your ACTH is being suppressed, you're not going to stimulate the adrenal cortex. You're not going to stimulate the zona fasciculada to make cortisol. But your zona glomerulosa is still going to be stimulated just fine. It's still going to be kicking and screaming just fine, because it's under the control of the renian and your tensin system. So, and this boy especially being hypotensive, because remember, whenever you have an adrenal crisis, that can make you hypotensive. Why? Don't forget that cortisol has a permissive effect on the sympathetic nervous system.

So when you lack cortisol, which this boy lacks, when you lack endogenous cortisol, because your adrenal cortex is not functioning as well, because the fasciculada is not being stimulated properly, then that's going to cause you to get in some hot water. And if your hypotensive and things like that, your GG cells are not seeing enough blood flow. They're going to freak out and make a lot of reigning. That reigning is going to make them make angiotensin-1. That angiotensin-1 is going to make them make angiotensin-2. Remember, the pulmonary endothelium converts angiotensin-1 and to angiotensin-2. Remember, your pulmonary capillaries have a lot of metabolic activity. They have this metabolic activity of also being able to degrade serotonin. That's why the left side of the heart is not affected in carstenoids and rubbed. That's a nice tie in there. So when you see all those things, this child is actually making out those rungos fine. That's why many of those things you would expect with high-poil-dosteronism, like metabolic acidosis or frankhyperchylemia. We don't necessarily see it here. This kid's bicarb is 25, and his potassium is 4.5. So again, just keep that in mind. I think that's a very important thing to keep at the back of your mind. As you prepare for exams. Again, you may be like, wow, divine. This kind of seems like a step one review. No, I'm actually going through a step 3, 3, 1, 37.

Again, I'm telling you, if you struggle basic sciences, you're really going to struggle with step 3. That's the truth. I'm not saying you should go and read all of first date for step 1 again, but honestly, you kind of need to know some basic, basic sciences. You know, in quite a bit of detail, actually. And again, this is becoming a bigger and bigger problem. Because step 3, it's always been the case, right? But step 2 is definitely becoming a bigger and bigger problem. It's becoming a bigger and bigger problem, actually. So it's just something you want to keep at the back of your mind. So honestly, I like option B a lot, because it just kind of integrates everything that this question is about. So I'm going to keep that answer. This question probably has option B as the right answer. And then option C says decrease production of ADHD. Well, we've proven conclusively that that's wrong. Because this boy is hypotensive. So his ring-nang-jutense now, those transistems is working really good. Increased out those trans production. Well, this boy certainly has increased production of our doster. It makes sense. But the fact that the statement is true, does not make it the right answer to a question. That's a test-taking principle right there. I feel like this podcast is almost like a test-taking podcast in a sense, even more so than the knowledge that we're kind of talking about here. But again, this is something I want to drum into your heads on the exams.

This is like a very common pattern over wrong answer choices that people make on exams. The NB Ms will put true statements as answers, but those true statements do not address the problem and the question. Right? So this boy does have increased out those term production. That is true. But that increase out those term production does not explain what's going on. It doesn't explain the weight loss. Does it explain the decreased appetite? Does it explain the daily fatigue? It doesn't explain any of those things. All right? It does not explain any of those things. Keep that in mind. Right? The thing that explains those things is that this guy is in a state of secondary adrenaline sufficiency. All right. So these wrong. And the option E says increase insulin production. Well, I don't know if I'm going to go with that here. I don't know if I'm going to go with that here. I know if I'm going to go with that here. Again, insulin, like an insulinoma. That makes no sense for this question. I'm just going to go with option B actually for question 52. All right. This is going to question 53. So question 53 says. Question 53 says. 38 year old woman is brought to the emergency department because of a four history of confusion and lethargy. Medical history is remarkable for a major depressive disorder and a six month history of moderate low back pain that began after she's lifted heavy boxes during a move.

Have medications are flocks a teen daily and are said to men often with covenants needed. Family history is remarkable for hypertension and CHF and her mother. The patient lives with her husband and her mother. The patient drinks two glasses of wine on the weekends. When I arrived, well, she's some no land, but are also both to strun or rob. Temperature is 97.5. Bosis 32 per minute. That's pretty low. Reservations are 16 per minute and blood pressure is 74 or 36. Again, that's pretty low. Oxygen saturation is 100% on room air. Opials measure 6 millimeters in diameter. Examination shows no other abnormalities. Results of lab studies are shown. So a ALT-ST that can I elevate it? Crap means 2.5. That's kind of high. That's not kind of high. That's actually pretty high. That's really pretty high. You're in toxicology. Opiate positive. And then I can almost promise you the MBM is trying to trip people up with opiates here. But let's continue. Himoglobin is fine. Wicone is so little high. It's not that bad. Plitley count is fine. So he says an overdose of a drug with which of the fully mechanisms of action is the most likely cause of this patient's condition. So option E says agonism of meal opioid receptors. Well, that makes no sense. That's going to be an opioid. But that makes no sense because number one, this person does not have respiratory depression. It's kind of hard to be overdose on opioids and your respiratory is 16. Two, this person doesn't have opioid illnesses.

Again, opioids remember they act on the mu receptor and that is inhibitory, chiepertine coupled receptor. So that's going to prevent you from releasing an open effort at the adrenergic synapse. If that happens, you're actually going to have me use this into my dry asses. That's certainly not what's going on here. So I'm not going to consider option A, option A is wrong. But you see, of course, the MBM is how the embellish that she's on opioid. It's right. I said I'm in a thing with codine. Kind of start getting carried away with that. And you're in toxicology, opi, it's positive. Woo, right. If you just focus on those two things in the question, you get the whole thing wrong. Again, you got to look at the whole thing that you're reading. Option B says inhibition of our dosterion. Well, again, if you have our dosterion inhibition, then you're going to have signs and symptoms of hypodostrbanism. Like hyponitremia, you're going to have metabolic acidosis. You're going to have a hyperchylenia. We don't see any of those here. So that's wrong. And then option C says inhibition of ACE. If you inhibit ACE, you're going to make less than your symptoms, too. That's going to cause you to make less out of those true, less EDH. Again, that doesn't really make any sense here. And this person is not taking an ACE inhibitor. And taking ACE inhibitor is not going to cause you to be confused and lethargic. If anything, it doesn't make any sense for discussion. I'm just going to skip that.

Now, option D says inhibition of Bidowon adrenergic receptors. Well, that actually makes a lot of sense here. Because first thing is first person is pretty cardiac. So if you overdose on a Bidowon blocker, that's going to slow conduction down your EV node. So you're going to have Bidowon adrenergic. That makes a lot of sense. And many people don't think of the aid this way. But believe it or not, you can actually become confused, lethargic, have altered mental status from Bidowon blocker overdose. Because again, you're pretty much suppressing sympathetic activity. You're suppressing sympathetic activity. That can certainly cause this kind of problem. You can even cause a person to start having, believe it or not, respiratory issues. Because when a person takes pretty high doses of a Bidowon blocker, you then begin to actually get some Bidowon effects. So if you're blocking Bidowon receptors in Bidowon concentration, you can start having issues with your airway. And not just that, you can also start having issues with your blood vessels. Because remember, your Bidowon receptors also find them on your blood vessels. But again, this person, I think, I will ask, because you know that Bidowon to effect on blood vessels is kind of mute. The big, big thing causing this low blood pressure, I'm going to say, is a decrease in cardiac output. Because when your cardiac output goes down, your systole blood pressure is going to plummet like crazy.

So it kind of fits with this question a lot. It kind of fits with this question a lot. So let's keep option D. That may be right. And option E says, at least as the first answer I've seen that makes any sense. And option E says, inhibition of CNS system neuron serotonin reoptic. So that's like, overdosing on an SSRI. That doesn't really make any sense, right? Because SSRI, if you have excess of it, you know, you probably have like serotonin syndrome. You have like hyperreflexia, you have myoclonus, you have all those things. We don't really see that here. So I'm not going to go with that. In addition to the glandinin synthesis, that's going to be like what you see with, with NSAI Ds. The hippococs. So that's going to decrease per seglandinin production. But again, if you take a ton of NSAI Ds, you can have bleeding. You may have like peptic ulcer disease. You may have all these problems. But again, that's not what's going on here. And again, I know that our friends at the MVM Es, they'll put this LTST business to kind of mess people up. Again, please, LTST is not the only thing in this question. There's like this whole like series of sentences and stuff, right? Be careful. I'm not going to pick option F. And then option G says, in addition to renal sodium chloride resorption. That kind of sounds like something that a thazide diuretic will do. Remember thazides, they work at the level of the distal-convular tubule. And they prevent you from reabsorbing acetylmancluoride.

So again, that doesn't really fit what's going on here. Right? Thazide overdose. You may have like hypergalicemia, hyperlipidemia, hyperiracemia, you know, hypercalcemia. They may have hyponitremia. Right? Thazides really have a very strong gastrogeonhyponitremia. That's almost going on here. So the only option that makes any sense to me here is going to be option D. So we're going to go with option D for this one. All right. We're going to go to question 54. So 56 year old woman comes to the office because of a one week history of fever and moderate pain and swelling of the left side of her neck. Medical history is remarkable for a four year history of HIV infection. She has declined antiretroviral therapy and takes no medications. BMI is 20. Temperature is 100.9 degrees Fahrenheit. Other vital signs including oxygen saturation on room air within normal limits. Physical examination discloses warmth and moderate tenderness over the swelling shown in the photograph. Alongs that clear those quotation, there is no rash or hipadol, spleen omega. CD4 positive T lymphocyte count is 160 per millimeter cubed. And plasma HIV viral load is 56,000 copies per meal. And this person should take antiretroviral therapy. Okay. So pathological examination of a biopsy specimen of a cervical lymph node shows two plus acid fast but still alive. All right. And results of a nucleic acid amplification test is positive for a drug sensitive micro bacteria.

The infection in this patient most likely reached the cervical lymph nodes through which of the following routes. Right. Rich the cervical lymph nodes through which of the following routes. And before we just answer this question, I just want to see real quick. Remember the pressing from the previous question of the beta block over dose. In that circumstance, what do you want to do for this person? Pretty straightforward. Right. Atropine is a good thing to do. Right. You want to go ahead and give them atropine. It's going to speed up conduction through the AV node. But if that's not working, then you can consider a glucagon. Because remember, glucagon works on G protein coupled receptors. The glucagon receptor is a stimulatory G protein coupled receptor. So, and it just so happens that the beta one receptor is also a stimulatory G protein coupled receptor. Which raises your levels of cyclic AMP, you know, by stimulating a dimilite cyclase. So by using glucagon, you're pretty much using a different receptor that can raise your cyclic AMP within cardiac muscle. But just through kind of like a different receptor compared to the beta one receptor that's blocked with this beta one blocker. So again, just kind of little extra flavor there. All right. So for this person, okay. Let's look at the answer choice this year. So option A says, at direct calculation via the skin, option B says, at direct tissue invasion from the hyalur lymph nodes.

Option C says, hematogen or spread from the lungs. Option D says, lymphatic drainage from pharyngeal tissues. Option E says, trafficking of infected lymphocytes. All right. So for this one, so what do we think this person has? Right. So first things first, we know that this thing is, is acid fast. Right. So it's probably some kind of tuberculosis or, you know, non- tuberculosis micro bacterial species. And we see that it's a skin lesion. And we see that this is in a person that is immunocompromised. Right. A city for counties 160 or less than 200. And a viral load is pretty high. So this is some kind of TB infection. And again, think about it. How do most people get TB infections? Well, most TB infections kind of start in the lungs. And actually know what this is. This is actually something I encountered years ago. I know I wrote up on it. I don't know either years or months back. I will talk about it. But we know that this is a TB infection. And again, on your exams, always think in terms of what is simple and straightforward. Well, what do you know about most TB infections? Most TB infections start in the lungs, right? Most TB infections start in the lungs, right? So let's look for the answer choice that kind of says lungs, right? So option C probably makes the most sense. Option B, you know, from hyalur lymph nodes. But again, direct tissue invasion from hyalur lymph nodes. I don't know like your hyalur nodes are not particularly connected to your neck, right?

That doesn't really make any sense. So I'm going to go ahead and scrape up option B. Directing or collision via the skin. Again, it doesn't really make sense here. Because this person, we're not even told in the question that. We're not even told in question that she had like some skin lesion or whatever or ulcer. That kind of spread and then led to this. We don't see that, right? Directing or collision via the skin can be something you can see from like certain infections, like from a diabetic foot ulcer, getting those to my lightest or from a pressure ulcer, getting those to my lightest, right? That's kind of different. And then or like getting infection from like a burn wound. Again, that's kind of different. And then option D says lymphatic drainage from a pharyngeal tissues. I don't know if that necessarily makes sense, right? Again, TB usually sets up shop in the in the lungs, right? And then option E says trafficking of infected lymphocytes. Again, that's not what's going on here. Again, it just doesn't really make sense for this question. The thing is, there are sometimes you see answers on the examiner like these answers just make absolutely no no sense here. Right? So for this, I'm going to say this is option C. So what does this person actually have? So this person actually believe it or not has a kind of TB infection known as scruffula. You're like, what? Yeah, this person has scruffula.

Scruffula is a kind of TB infection that you know, we treated the same way we treated regular TB. You know, you know, right fan pain, isonize it, pyrozymenomyde, thambiotol. Obviously, you're going to throw in some vitamin B6 with that. Because remember, isonize it can cause B6 deficiency already. It prevents the activation of vitamin B6. And then sometimes you can also add streptomycin to this region. But scruffula basically is a TB infection. And many times it's going to present us like a painful neck mass. Right? Many times going to be on the side of the neck. And it can happen in people that are immunocompetent or very commonly on your exams. You're going to see people that are immunocompromised, people that are heavily immunocompromised, especially people that have HIV. People that have HIV. All right. So I think this is actually a good stopping point. I don't want to speak through because I don't know if you want to 60, just kind of has a bunch of really, really tough, tough questions. So again, if you're interested, I do offer again classes. Have a bunch of classes starting at the end of this month. You know, for step one or the way to step three, have a test taking class. I have a bio stats class. That's four hours long. I have a social sciences and ethics class. That's five hours long. And that's for step one to step three. And then for step two and step three, I have a last minute review. And then I have a 20 hour class that's going to be taking place.

And then I in the month of June, I have a 100 hour, very, very comprehensive step two, step three review. If you're interested in any of that, just shoot me an email and I can give you some more information. Again, many people have attended these classes and found them to be remarkably helpful. I'm going to make a separate podcast where I talk about the 100 hour class, fairly, fairly soon. And then also offer one or one tutoring for all the USML Es, all the complex exams. And I help with errors, applications, more interviews and things of that sort. And also have these podcasts on Apple Google and Spotify. So please go ahead and check those out. And then have another website called a divine intervention life lessons.com, where every week I post one or two podcasts, where from a biblical perspective, address a life lesson. There's actually a lot of people that listen to those podcasts and find them to be really, really helpful. There's actually an Apple podcast associated with that called the divine intervention life lessons podcast. And then I also have a, again, You Tube channel, divine intervention, USMLE podcast and videos, where I post the videos that I make. Thank you for listening to me today. Again, I just want to encourage you. If you're studying for step three, don't deem for size basic sciences. At least try to understand the basics behind most of the disease processes you are learning. So thank you for listening to me today. I will see you in episode 559.

So have a wonderful day. God bless you and our bifurne now. Thank you.

Lack of cortisol's permissive effect on renal function, leading to increased ADH release and free water retention.

Bradycardia or profound hypotension due to blockade of sympathetic stimulation (e.g., slowing AV node conduction).

The lungs.

The Renin-Angiotensin-Aldosterone System (RAAS).

Scrofula.

Glucagon (because it acts via a different G protein coupled receptor than those blocked by $\beta$-blockers).

Primary failure leads to low cortisol AND low aldosterone; Secondary failure maintains normal aldosterone because RAAS is intact.

The Hypothalamic-Pituitary-Adrenal (HPA) axis, specifically suppressing ACTH release.

Renin $\rightarrow$ Angiotensin I $\rightarrow$ Angiotensin II $\rightarrow$ Aldosterone.

Hematogenous spread from primary pulmonary infection.

Polydifferentiated, aplastic spindle cells within mesenchymal tissues.

Secondary adrenal insufficiency due to ACTH suppression.

Primary failure leads to low cortisol AND low aldosterone; Secondary failure maintains normal aldosterone because RAAS is intact.

The Hypothalamic-Pituitary-Adrenal (HPA) axis, specifically suppressing ACTH release.

Renin $\rightarrow$ Angiotensin I $\rightarrow$ Angiotensin II $\rightarrow$ Aldosterone.

Hematogenous spread from primary pulmonary infection.

Polydifferentiated, aplastic spindle cells within mesenchymal tissues.

Secondary adrenal insufficiency due to ACTH suppression.