DIP Episode 308 - The Floridly HY NBME Cortisol Podcast (+ 2CK/3 20 hr course reminder)

Okay, welcome. My name is Divine. This is episode 308 of the Divine Intervention podcast. In this podcast, I'm going to be calling this the Clutch cortisol podcast because cortisol problems just pop up on many exams. Many similar exams, step one, step 2, 3, case, step three, shelf exams, right? People pop up all the time and people tend to get these questions wrong, right? So I think if you if you understand these things, I think you should be pretty good from an MBME perspective. And again, it's a high ill topic, right? Just one of these things you know you're going to see on your USMLE exams. So the first thing I think I want to talk about here is talking about what I will call a construct, right? So talking about something I'll call a construct. So what in the world do I mean by a construct? The thing I mean by the word construct is how do these questions classically present on exams, right? So how do these questions classically present on exams, right? So again, I'm dealing just with cortisol today. That's kind of like the big thing I'm thinking about today, right? So the classic construct with these many of these disorders is that if a person, if you're getting up because you can have two kinds of cortisol problems, right? You can have a cortisol excess problem, right? And you can also have a cortisol deficiency problem. Cortisol excess is something you get. If you get a cortisol excess, usually those people have big weights, right?

So they are not going to be normal BMI, right? Usually those people are going to be obese. You may see things like skin hyperpigmentation, but again, as you would hear me say maybe quite a bit today, skin hyperpigmentation should not be your clue that you're banking on to say, oh, this person has hyper cortisolism or hypocortisolism, right? Because skin hyperpigmentation, basically whenever your ACTH is high for any reason, you will have skin hyperpigmentation. As you will see, ACTH can be high in certain cases of adrenaline and sufficiency. And ACTH can also be high in certain cases of adrenal excess, right? So you can get skin hyperpigmentation in any of those disorders. And again, where does the skin hyperpigmentation come from? It comes from POMC, right? Proopiumilano-quartin, right? So it's a compound that is almost like the grandfather of ACTH, right? So proopu, opio, it's a precursor to opio. The opio is an opioid that's being engulfed. Melano, that's melanocystimulating hormone, that's why you get the skin hyperpigmentation. And then quartin, right, is ACTH. So just something to keep at the back of your mind for exams, right? So a person that has cortisol excess, they'll have high weight, right? They will have skin hyperpigmentation, they will have hypochylemia, right? Because remember, quadricosteroids have mild mineral olucodicoid receptor effect, right? So quadricosteroids have the ability to bind mineral olucodicoid receptors.

I mean, that's the reason why in our bodies, we have this enzyme called three beta hydroxy steroid dehydrogenies, too. I'll say that again, three beta hydroxy steroid dehydrogenies, two, three beta hydroxy steroid dehydrogenies, two, is inhibited by something called glyceretic acid. And where do we see glyceretic acid? We get that in, in a, in a lecherish, right? So let's talk about the normal pathway first, right? So that three beta HSD2 has the ability to convert cortisol to cortisol, right? Cortisol is active on mineral olucodicoid receptors. Cortisol is not active on mineral olucodicoid receptors. So your body takes advantage of that pathway to deal with that cortisol problem because you don't want to have a mineral olucodicoid like state when your cortisol is high. So your body has three beta HSD2 to deal with that, right? So that's why when a person consumes a ton of licorice, they can have almost like a con syndrome like presentation where their blood pressure is high, they have hypochylenia, they have metabolic alkalosis. The mechanism behind that there is the hyper cortisolism because those high levels of cortisol are essentially deep, you know, because again, I can say licorice contains a glyceretic acid that inhibits three beta HSD2. So you build up that cortisol and you have that mineral olucodicoid like effect, right? So in general, when people have hyper cortisolism, again, they have skin hyperpigmentation, they have large weights, right?

Because remember steroids, right? They meet people obese, right? It causes insulin resistance, right? So they'll have large weights, they will have skin hyperpigmentation, they can have the buffalo hump, right? They can have a decrease in the abut mineral density, right? So they can have osteoporosis, they can have all these compression fractures, right? So those are all things you'd see. And again, in terms of electrolyte abnormalities, they will throw in this hypochylemia and metabolic alkalosis for reasons. I've already explained. The sodium may not exactly be abnormal. That's something I think I'll throw in there, right? But whenever a person has a cortisol deficiency, right? Again, there are many reasons why which will examine, but the things you would see, you see more hypo nitrimia, right? Because the thing is in general, when you have one thing, many people don't realize this cortisol has a permissive effect on the sympathetic nervous system, right? Especially in terms of like controlling your total peripheral resistance, cortisol has a big effect on your total peripheral resistance. And again, the pathophage here, because this is going to be a short podcast, I'm not going to delve deep into that. But whenever your cortisol is low, your body always accompanies that with very high levels of ADHD. ADHD is secreted in great fashion when your cortisol is low. And again, that will kind of make sense because ADHD will help you retain some fluid.

And if you retain some fluid, at least that can percopy of blood pressure. When your blood pressure is low, because you have a cortisol deficiency, because again, cortisol maintains your total peripheral resistance. When you have a cortisol deficiency, you're not going to be able to maintain your total peripheral resistance. That's why these people tend to have a low blood pressure. People that have a cortisol deficiency, they almost always on MBM exams, will be hypertensive for that precise reason. So whenever cortisol is low, ADHD is high. So when you have high ADHD, you're literally reabsorbing a lot of free water from the nephron, that's going to tank your sodium. Essentially, hypocortisolism is a bona fide cause of SIEDH. I'll say that again, hypocortisolism is a bona fide cause of SIEDH. Again, you have something to do with the battery receptors and creating an operating hotel. But again, that's kind of beyond the scope of what I'm going to be discussing in this podcast. So hypocortisolism causes hyponytremia by way of SIEDH. When a person has cortisol deficiency, they will have hyponytremia, they will have hypotension, they will have hyper-kilemia. Because again, cortisol again works like a mineral aquaticoid. If you have a cortisol deficiency, it's almost like you have like a mild mineral aquaticoid deficiency. So you're not going to be peenoportassium in the nephron. So you're going to have hyper-kilemia.

And usually those people will also have some kind of metabolic acid doses. They'll have some kind of metabolic acid doses. So that's how you tease apart cortisol excess, which we've talked about from cortisol deficiency. And again, please don't confuse this with, and I guess let me see this, when people have cortisol excesses, they have glucose tends to be high. When people have cortisol deficiencies, they have glucose tends to be low. Because again, cortisol is a diabetogenic hormone. So when a person has a cortisol deficiency, they classically will be hypoglycemic on NBM exams. So I know some of you may be like, oh, divine. So if a person has an adrenal crisis, how do I differentiate that from DKA or HHHNS? Because the presentations are very similar. When a person has like an adyssonian crisis, they are hypotensive, and all that stuff. Well, the way you're going to differentiate is by using the person's glucose, right? Because the thing is in DKA, HHNS, those people may have hypercalemia in their labs, although their turbo body potassium is down. But if you have hypercalemia in their labs, they may be hypotensive because they have volume down on everything. But the key differentiating lab on NBM exam is the glucose. The glucose is going to be really high in a person that has DKA and HHNS. The glucose is going to be really low in a person that has, you know, a person that has an adyssonian crisis, because of that cortisol deficiency. Right?

So let's talk about cortisol excess. So what are the things that can cause cortisol excess? Well, there's many things that can cause cortisol excess. I mean, the most common cause is literally people taking a ton of cortisol-based compound, right? Like taking chronic steroids for some autoimmune disease or for chronic asthma management or chronic COPD management, we're taking a lot of steroids, right? That is actually the most common cause of hypercalysolism, a person just taking a ton of steroids, right? But on that thing that can also happen that can cause hypercalysolism is a person can have primary hypercalysolism, right? So primary means the problem is that the adrenal gland, right? So the adrenal gland is probably some adenoma. That's just making a ton of cortisol, right? So that can cause hypercalysolism. Another thing that can cause hypercalysolism can be a secondary adrenal excess, right? So secondary adrenal excess, right? You're making a ton of ECTH, right? So let's say you have some kind of pituitary adenoma. That's just producing a chock full of ACT, right? Again, that's going to stimulate your adrenal cortex, right? Remember, ACTH is a hormone for the adrenal cortex, not the adrenal medulla, right? That's why it's called adrenal corticotropic hormone. It's trophic to the cortex, not the medulla, right? So when people have adesines disease, it's a problem with the adrenal cortex. It's not a problem with the adrenal medulla, right?

Remember, the adrenal cortex is derived from something completely different from a nembrologic perspective compared to the adrenal medulla, which is derived from neurocrest cells, right? So the thing is, so you can have a secondary adrenal excess again from like an ACTH producing pituitary adenoma in that case, right? That's Cushing's disease. Cushing's disease is a cause of Cushing syndrome, right? Cushing syndrome means you have hypercordisolism. Cushing's disease is you have hypercordisolism because of a pituitary adenoma that's making ECTH, right? But remember, you can also make ACTH, not from a pituitary adenoma, you can get that from small cell lung cancer. That's why we have diagnostic steps that we can use to tease those two things apart, right? And then we, person can also have tertiary hypercordisolism, right? Where do you have this is extremely rare, right? Where do you have like some problem in the hypothalamus, maybe like an adenoma or something going on? That's making a ton of corticotropin releasing hormone, right? So the acyriaches like super, super, super, super, super high, right? So that was stimulidia, ACTH, and then that was stimulidia, cortisol production, right? So if you're trying to, if you see all these things, you're like, wow, both a low home, the person is obese, hypercordisolismic, all that stuff, right? How do you, how do you work that on?

Well, the first thing you're going to do is you're going to document that you have hypercordisolism, right? And you can do that in one of three ways, right? You can check the 24-hour urinary cortisol, you'll be elevated, right? Or you can do a late-might salivary cortisol. The thing is late at night, you're supposed to be relaxed, you're supposed to not be worried about much in life, right? So your cortisol is supposed to be low at night. But if your cortisol is high at night, that makes your potential candidate for a person having hypercordisolism, right? A third way you can also scream for hypercordisolism is you can do the low dose dexamethasone suppression test, right? So if you give a person low dose dexamethasone a normal person, the next morning when you measure their cortisol, it should be low, right? But if you give a person low dose dexamethasone, you notice that, oh, wow, the next morning their cortisol is actually elevated, it failed to suppress. That tells you that the person likely has hypercordisolism. But again, the thing is when you're working on hypercordisolism, you need to figure out what exactly is causing the hypercordisolism, right? So the thing is after you've documented by one of these three techniques that, oh, okay, it's personally a hypercordisolism. The next thing you then do on an in-bim exam is to measure the levels of ACT-E. You measure the levels of ACT-E.

Because again, there are some cases of hypercordisolism, where ECT-E is high, and there are some cases of hypercordisolism, where the ECT-E is low, right? So again, all these things are just helping you to pretty much walk down a logical diagnostic trip. So you check the ECT-E. If the ECT-E is low, that means there must be something that is suppressing it. So this person likely has the acordisol excess because they just have a ton of cortisol, right? Maybe from some kind of adenoma that's making a ton of cortisol. That adenoma making a ton of cortisol will cause their ACT-E to be suppressed, right? So if you check the ECT-E levels and you're like, wow, the person's cortisol, the person's ACT-E is low. Then your next step on an in-bim exam, in that circumstance is to get abdominal imaging, can get like an abdominal CT, like an adrenal CT on an adrenal MRI to find the adenoma. But if the ACT-E is high, well, it can be because, oh, the normal source of ACT-E, the anterior pituitary gland, right? Has some adenoma that is presiding on a ton of ACT-E. That's scushing disease. Or it could also be a person has some other location in the body, like the lungs, in a person having a small cell lung cancer. That's producing that ACT-E. So how do you tease those two apart? You tease those two apart by doing the high dose dexamethasone suppression test, right? Normal tissue will suppress the acordisol, right? In response to high dose dexamethasone.

So when you give high dose dexamethasone, that is going to suppress the ac T-E that is produced in an anterior pituitary gland adenoma that's making a ton of cortisol, again, pushing a ton of ac T-E, sorry, aka cushing disease, right? So, if you notice, oh, wow, okay, we give this person high dose dexamethasone. And then the next morning, the acordisol has suppressed. Then that tells you that you're dealing with cushing disease. And in that case, obviously, you're going to get an MRI, not a CT scan, an MRI of the brain, right? Remember when you're dealing with brain pathologies, MR Is, other than bleeding for the most part, MR Is are just better in general, right? So to find that pituitary adenoma, you get an MRI of the brain, right? But if you notice that the next morning, the cortisol did not suppress, and you're worried about a topic ac T-E's production. In that case, you're going to get like some kind of lung imaging, either like a chest X-ray or a chest CT scan, right? To find the small cell lung cancer that is producing the topic ac T-E, right? So again, that's how you work up hyper cortisolism, right? And again, how do you treat hyper cortisolism? For the most part, you can give something that inhibits steroids synthesis. You can give like keto-conazole, stuff like that, and the person will be fine. Or you know, you just try to treat the underlying cause if you could, right? So that's adrenal excess, right? That's cortisol excess, right? This is not an adrenal podcast.

This is a cortisol podcast, but invariably, I'll have to see quite a bit about the adrenal glands. Now, so adrenal insufficiency, right? So again, cortisol deficiency is something that can happen for many reasons, right? In the United States, the most common cause of adrenalin insufficiency, right, is it's going to be adescent disease, right? Adescent disease is what we call a primary adrenaline-sufficiency, right? Primary adrenaline-sufficiency, right? So sometimes you may see it on an ambient exam because they like you to use many means for the same thing. You may see them refer to it as an autoimmune adrenalitis, right? An autoimmune adrenalitis. It's an adysse, it's inflammation of the adrenal glands because of an autoimmune destruction, right? And many times when people have adescent disease, the thing that is actually being destroyed in the adrenal glands is 21-21 hydroxylis, right? Like literally, they make autoantibodies against 21- hydroxylis. As you know, 21-hydroxylis is necessary for the production of cortisol and outdoor sterile, right? Cortisol and outdoor sterile. That's why many times when we're treating adrenalins-sufficiency, the only thing we're replacing is glucocorticoids and mineralocorticoids. We give them steroids to replace the glucocorticoids and we give them fluidocorticoids to replace the mineralocorticoids, aka outdoor sterile, right? So again, many people that have adescent disease, they make autoantibodies against 21-hydroxylis.

And one construct you should keep at the back of your mind on NV Me exams in people that have adescent disease is that those people tend to have some other pass medical history in the NV Me question of another autoimmune disease, right? This is something you'll find in about 90% of NV Me questions that deal with autoimmune disease. They will place a pass medical history of some other kind of autoimmune disease, like having like Hashimoto's or the person having, you know, Videeligo or Prinyshosa Nemia or something of that sort, right? In fact, one thing I will say is there are these group of autoimmune diseases that tend to kind of stick together, right? If you see a person having like adescent disease or you see a person and they have it maybe like an association with like some thyroid problem because remember, you can have autoimmune thyroid disease that causes thyroid hypo function, aka Hashimoto's, or you can have autoimmune thyroid disease that causes thyroid hyper function. In this case, grapes disease, right? You see that in association with type 1 diabetes, right? So it's a triad. I call it the DTA triad, D for type 1 diabetes, T for thyroid autoimmune problem, A for adescent disease. If you see that together, that's autoimmune polyglondular syndrome type 2, right? That's autoimmune polyglondular syndrome type 2. Remember, those things that associate with air, AIRE, air gene mutations, right?

Air is like a transcription factor that essentially helps you present endocrine gland antigens in the thymus in utero, right? If you have a mutation in that, you're not going to present those endocrine gland antigens so that your immune system trains itself to like not kill these things, right? So if that training is not there, it means it's going to be like, oh, this looks boring and begin to destroy endocrine glands. That's the pathophysiology right there, right? So the thing is again, just like we said for the hyper cortisol, we broke it down by primary, secondary and tertiary, right? Primary adrenal insufficiency again, the most common cause in the U.S. is adescent disease. Worldwide is going to be TB, right? TB is a common cause of primary adrenal insufficiency, although the other things that can cause primary adrenal insufficiency, right? Like if a person has like my seramine ingestedness, right? It can guanim basically destroy the person's adrenal glands, right? And he can get like waterhouse, phrygric, sen syndrome, right? That'll be a cause of primary adrenal insufficiency, right? But again, as I've said, adescent disease, this is fluently high, you know, for purposes of the U.S. Emily exams. Usually it's caused by autoantibodies against 21 hydroxylis, right? Another cause of primary adrenal insufficiency, again, is instead of making autoantibodies against 21 hydroxylis, you just have a literal deficiency of 21 hydroxylis.

Remember, 21 hydroxylis deficiency is the most common cause, very high, only is the most common cause of congenital adrenal hyperplasia, right? So it'll be a new born, that is born with that construct of adescent, right? So it'll be a new born, or whatever, although it can also happen in teenagers, right? It can develop antibodies later in life against 21 hydroxylis, right? And that'll cause a certain like literal phenotype of congenital adrenal hyperplasia. But you notice that, oh, these people, they will have hyponitremia. Do you remember, whenever your cortisol is low, your itch will be high. I've talked about that earlier, right? So they will have hyponitremia, they will have hypercalemia, they will have metabolic acid doses. Usually it's going to be a normal and my own gap metabolic acid doses, right? And then you will have skin hyperpigmentation. Again, if you have primary adrenal insufficiency and you're not making cortisol, there's no negative feedback at the anterior pituitary gland. So you're going to make a ton of cordy, a ton of ECT-E, and that ton of ECT-E that's going to be made, it's going to be made with a ton of MSH. So you stimulate your melanocytes and have skin hyperpigmentation, right? So 21 hydroxylis deficiency, you're going to not be able to make cortisol or out of the stool, right? So that's again another cause of primary adrenal insufficiency, or an NV Me exams, right?

Secondary adrenal insufficiency, you can get it in many ways by having a problem with the pituitary, so you're going to the pituitary, right? At this point, right? So it's going to be a pituitary problem, right? So if you have some kind of pituitary adenoma, right? Let's see like, even craniofiring geoma that basically like causes like destruction overgrows in the pituitary gland, that's going to prevent your corticotrophs from making ACT, right? So you're not going to be stimulating cortisol production, so you're going to have cortisol deficiency, right? Tessionary adrenal insufficiency, that's a problem with the hypothalamus, they're super rare, right? But if a person has like a hypothalamic tumor, right? Or a person has used exogenous stairs for a long time, that's going to cause atrophy, right? Remember negative feedback, if you use stairs for a long time, that's going to cause atrophy, right? Of the corticotropin released in the hormone producing cells in the hypothalamus, or the corticotrophs in your anterior, anterior, anterior, anterior gland, right? So all these things, right, can all cause adrenal insufficiency and again, I've talked about why people that have adrenal insufficiency will have hyponitremia, they'll have hyperkalemia, right? You have metabolic acidosis, remember? Basically people that have cortisol deficiency, right?

Again, especially like, let's see from other things disease where they also don't make an out of theosterone, they'll have a type 4 RT, remember, that's the low out of theosterone RTA, that will cause a normal anion, gap metabolic acidosis, that's like the hyper-kilemic renotibular acidosis, right? And then those people will have, again, orthostatic hypertension because they've lost muscular tone, again, remember, I said that the cortisol has a permissive effect on the sympathetic nervous system, and then usually these people also have elucinophilia, because again, as I've said, in many podcasts in the past, steroids cause elucinophilipoptosis, right? So whenever you have a steroid efficiency, you're gonna have less, you're gonna have an increased half-life of your elucinophilip. So the person will have an elucinophilia, that's why adolescents disease is part of the differential diagnosis of elucinophilia on mbim exams. Again, many, many, many, many, many, fans can cause adrenal insufficiency, right? So if a person has like adrenalinucodistrophy, right? Adrenalinucodistrophy will be a child that is losing motor milestones and then they'll tell you usually on mbim exams that, when you look in the brain of the child, you can see like diffuse demilination or like diffuse white matter disease. If you see that, think about something called adrenalinucodistrophy, it's actually acquired on mbim exams in an ex-linked recessive fashion, right?

So it's gonna be in a boy on a test, not a girl, a boy on a test, right? So it may be like, why does that cause adrenaline insufficiency? Well, remember, and adrenalinucodistrophy, you have problems with the peroxysone, right? So you're gonna have problems with the beta-oxidation of very long-chain fatty acids. If you have issues with the beta-oxidation of very long-chain fatty acids, right? Remember, fatty acids, we need them to make myelin, that's why they have that demilination. But remember, many of the adrenal cortex hormones are steroid hormones and the abacursteroid, the abac bone is cortisol and cortisol is made, I mean, sorry, is cholesterol and cholesterol is ultimately made from fat. So if you have problems with beta-oxidizing, very long-chain fatty acids, you can already begin to imagine that those people have problems in the adrenal glands, right? So those people, they tend to have like lipid problems, they tend to have adrenal gland problems, right? So they also tend to have, so they can have adrenaline insufficiency, they also again tend to have problems with myelin, right? Again, most of those people die pretty early in life, unfortunately, right? And again, there are many, many other things that can cause adrenaline insufficiency again. If you withdraw steroids, because again, if you've been taking steroids for a long time, right?

You're taking steroids for a long time, that's going to suppress your HPA axis and that suppression is almost like a genetic suppression, right? You're literally going to suppress, because remember, cortisol is a steroid hormone, so it works at a genetic level, right? So the thing that's going to happen is you're literally going to suppress, you're going to cause atrophy of the corticotrophs in the anterior pituitary gland and you're going to cause atrophy of the CRH, producing neurons in your hypothalamus, right? So if you have those problems, you can really begin to see that, this is potentially going to be a huge, going to be a huge issue for this person, because if the person is then subjected to stress, right? Like, in fact, they call this like critical illness associated with adrenal insufficiency, they usually set the stop as a person that is in shock and you're giving the person fluids and you're giving the person and they're not responding to those pressures, right? Those are those people that end up needing like a stressed dose of steroids, right? So the thing that's happening in that case is you're subjecting these people to stress, but the structures that are capable, because many times when you're stressed, your body can increase its cortisol production up to like six four, right? But if you have atrophy of those things, those things can not just suddenly hypertrophy. No, for something to hypertrophy is a process that takes days, that takes weeks, right?

So if you're not able to respond in that way, then the person can go into an adrenal crisis, right? So they can even give you this question, the person that literally is already taking steroids, right? But the thing is, if you are taking steroids, then your HP access is suppressed. So when they get into like a critical illness, or they are thrown into the ICU, and they are in trauma, they are in an accident, or they undergo surgery, right? They can't be for the production of steroids, because all their HP access is atrophied, right? So in those cases, you need to give those people a stress dose of steroids to cover over for those atrophied HP access organs, right? So that's something that's very high up to now. Or one of the things your friends at the MIMI can do on an example, generally in sufficiency, they can give you a question about a person that has a bit of lipoproteinemia, right? Remember, people that have a bit of lipoproteinemia, they cannot construct those lipoproteins very well. If they can construct them well, guess what? Then you're not going to be able to reabsorb lipids and triglycerides from your GI tract, right? Again, if you have a lipid or triglyceride deficiency, they're not going to be able to make many of these terrible hormones, like cortisol, for example, that can cause adrenal insufficiency, right? So how do we diagnose adrenalin insufficiency on MIMI exams?

We will typically do it is we will do some kind of stimulation test, where we do a stimulation test, right? Remember, as a general rule in endocrinology, when you have a deficiency of something, you want to accompany that with a stimulation test, but when you have an excess of something, you want to accompany that with a suppression test, right? So you do a co-symposium stimulation test, co-symposium tropin is basically like an ACTH analog. If you give that, and you notice that, a person's cortisol fails to rise with co-symposium stimulation, that is diagnostic of a person having like a primary adrenal insufficiency, right? So again, just very high yield to know that, and remember, when you have primary adrenal insufficiency, because you're hypotensive, right? You're reading an adeptance, and our doctrine system will be revved into high gear. So your reading is going to be high, right? Your angel tension, one, your angel tension, two, is also going to be high. But guess what? Your adeptance is going to be low, because again, if you've made autoantibodies against 21 hydroxylase, you are literally incapable of producing an adeptance, so your adeptance is going to be low, right? But if a person has a problem that is causing the adrenal insufficiency outside the adrenal gland, like a secondary or tertiary adrenal insufficiency, right?

The substance of the adrenal cortex is still there, just not being stimulated, and remember, ACTH is not the thing responsible for out-dostroin production, right? But, so in those cases, because those people will still be hypotensive, right? They are really not-dostroin system will be revved into high gear, and you'll be able to stimulate the production of out-dostroin, although usually that production is not great, usually ends up still being low. But again, for NV Me purposes, just imagine that in a present that has secondary or tertiary adrenal insufficiency, the adeptance will actually end up being high, right? For NV Me purposes, in the real world, that's not really the case, right? But again, that's not really the whole point of my conversation, and again, for present-absorbing adrenal insufficiency, you're just going to go ahead and give them steroids, right? Like Dexamethasone, and you're going to give them Fluidric Cortison, right? Remember, Fluidric Cortison is a synthetic mineral Corticoid, or again, you can also just give hydrochlorizone. Usually hydrochlorizone is the right thing to give in terms of, like, oh, a pressing means a stress loss of steroids on NV Me exams. Give hydrochlorizone. Hydrochlorizone has both mineralocorticoid and glucocorticoid activity. So I'm going to go ahead and pause here, again, as I do at the end of every podcast. I will say this for those of you that are studying for step 2, see case step 3. I have a course that's coming up next week.

There are still some spots available. So if you want to sign up, just shoot me an email. It's a 20-hour step 2, see case step 3 course. It's from Wednesday to Saturday next week, from 11 a.m. to 4 p.m. Pacific Standard Time. And then there's a test-taking NV Me strategy course on Tuesday from 2 to 4 30 p.m. Pacific Standard Time. So if you're interested, just shoot me an email through the website in the contact button, and I will give you some more information on cost. It's going to be over Zoom. And then I'll throw one on one to learn for all the USML exams, step 1, step 2, see case step 3, pre-clinical medical exams, 30-ish-off exams. And then please subscribe to the podcast. It's an Apple podcast. It's on Google podcast. It's on Spotify. And then the website divineinterventionpodcast.com. If you subscribe to that, you'll get an email notification whenever I make a new podcast. And then I also have a You Tube channel, right? Divine Intervention, USML, podcast, and videos. If you go to the You Tube channel, you'll see all the videos that I have made. So thank you for listening to this podcast. And if you need help with ERAS, my do-offer ERAS consulting, again, just shoot me an email, kind of in a hurry. That's why I'm kind of blabbing through these pretty quickly. So thank you for listening. I'll see in the next podcast. This is a Florida Hire podcast. It's going to help you get many questions right on your test. So have a wonderful rest of your day. God bless you. Thank you.

The glucose level on a non-fasting blood sugar (NBM) exam will be low in adrenal insufficiency, but high in DKA or HHS.

Inhibition of $3\beta$-hydroxysteroid dehydrogenase type 2 ($\text{HSD}2$).

Addison's disease, Type 1 Diabetes (D), and Thyroid autoimmune problem (T/A).

Hyperkalemia and hyponatremia.

Exogenous steroid use (taking too many steroids).

The ACTH level will be high (or inappropriately normal) because the pituitary is trying to stimulate the failing gland.

Obesity/weight gain, skin hyperpigmentation, and hypochylemia/metabolic alkalosis.

Proopiomelanocortin ($\text{POMC}$), which releases ACTH (and MSH).

Addison's disease; autoantibodies against 21-hydroxylase.

Hyponatremia, hyperkalemia, metabolic acidosis (normal anion gap), and skin hyperpigmentation.

High-dose dexamethasone suppression test; pituitary tumors suppress cortisol, while adrenal adenomas often do not.

Deficiency $\rightarrow$ Stimulation Test; Excess $\rightarrow$ Suppression Test.

Obesity/weight gain, skin hyperpigmentation, and hypochylemia/metabolic alkalosis.

Proopiomelanocortin ($\text{POMC}$), which releases ACTH (and MSH).

Addison's disease; autoantibodies against 21-hydroxylase.

Hyponatremia, hyperkalemia, metabolic acidosis (normal anion gap), and skin hyperpigmentation.

High-dose dexamethasone suppression test; pituitary tumors suppress cortisol, while adrenal adenomas often do not.

Deficiency $\rightarrow$ Stimulation Test; Excess $\rightarrow$ Suppression Test.