DIP Episode 539 - 50 HY Corticosteroid Facts To Know For Step 1-3 (+ PDF worksheet)

Welcome to episode 539 of the Divine Intervention Podcasts. In today's podcast, I'm going to be addressing a very, very high-yield topic for the USMLA exams. To be honest with you, this podcast applies to step 1, step 2, ck and step 3. And in today's podcast, I'm going to be addressing a topic I call 50 high-yield choricosteroid factoids to know for the USMLA's. 50 high-yield choricosteroid factoids to know for the USMLA's. So let's jump right into it. First things first, we know that the most important choricosteroid is cortisol. And cortisol is made in the adrenal cortex. So we know that the adrenal cortex has three layers, the zonal dumeralosa, where you make mineralocorticoids, the fasciculata, where you make glucocorticoids like cortisol, and the reticularis where you make six steroids, especially androgens like DHAS. That's factoid number one. Factoid number two, if a person has a state of cortisol excess, what kind of electrode abnormalities would you expect? Well, one thing people don't realize is that cortisol has some mild mineralocorticoid activity. So because it has mild mineralocorticoid activity, it can make you lose potassium in your kidneys, that can cause hypochylemia. And it can also make you lose hydrogen ions in your kidneys, and that can cause a person to have a metabolic alkenosis.

Alright, factoid number three, what if they give you a question about a person that has a history of Hashimoto's, and this person then has hypotension, skin hyperpigmentation, and hyperkalemia? Well, I really hope you're saying, wait, divine, sounds like this person has a heart of sin's disease. Remember, another one for heart of sin's disease is primary adrenaline and sufficiency. And it's an autoimmune disease. In fact, one thing I've found that's very useful in the USM disease, now when the USM disease is a testing one autoimmune disease, they will often give a pass medical history of another autoimmune disease. So for example, this person has a pass medical history of Hashimoto's, and then now they have hypotension and skin hyperpigmentation. That's adolescents. And let's explain why. Well, the thing is adolescents autoimmune style, you destroy your adrenal cortex, not your adrenal medulla, your adrenal cortex. So you pretty much develop a cortisol deficiency and an outdoor deficiency. So for these folks, that low cortisol they have, you're not going to have any negative feedback. So their ACTH is going to rise. And again, as you know, ACTH doesn't drop from the sky. It's made from a precursor malocodonus pomc, proupio melano-cortin. So proopu, opu. So it gives rise to bitter endorphin, melano, MSH, melano-sized stimuli, that's how you get the skin hyperpigmentation. And then cortin, ACTH. So the ACTH is going to be high.

And again, with that outdoor deficiency, obviously they're not going to be absorbing sodium from their kidneys. So they'll have hyponitremia. They cannot excrete potassium from their kidneys. They'll have hyperchilemia. And they cannot excrete hydrogen ions from their kidneys. So they're going to hold onto those hydrogen ions. They're going to get a metabolic acidosis. If you want to get super specific, it's going to be a normal anion gap metabolic acidosis. All right. Now, factor number four. What if they give you a question about a person that uses steroids chronically for whatever? And this person, then, you know, is a motor vehicle accident or requires a surgery. And the upload pressure is just persistently low. And you're giving them pressures, giving them IV noripinephrine, liver fed, and they're not getting better. I hope you're thinking of some kind of adrenal crisis. So remember, if a person uses steroids chronically, it's going to cause a suppression of their HPA access. And you suppress the HPA access. Again, it's not a big deal because you're getting an exogenous steroids. But over time, your adrenal cortex is going to atrophy. And again, it's not a big deal, as long as you're facing the same level of stress in life.

If you get to a situation in life where your stressors increase, then you're going to get in some very, very deep trouble because you're, say, for example, surgery or medical illness or trauma or whatever, you're not going to be able to operate your HPA access to make extra cortisol for that extra stress you're going through. And again, remember cortisol has a permissive effect on the sympathetic nervous system, especially like it's visoactive effects. So you're going to see these people get through into an adrenal crisis. So for those people, you want to give them a stress dose of steroids in that circumstance. Okay, factor number five, what if they give you a question about a person that has used the arbiterol in healer for a very, very long time? I mean, they've been using it more frequently. And you notice that, man, this person seems to be using it more and more. And it doesn't seem to be controlling their asthma symptoms. Well, I would hope you're saying divine. The next thing we should add to the pharmacotherapy is an inhaled cortical steroid. Many times, if the first wrong one, the latter for asthma management is a sabah, a short act in beta to agonist like arbiterol. But if that stops working, you need to go ahead and tackle an inhaled cortical steroid. All right, factor number six, they give you a question about a COPD patient.

Remember, most COPD patients in terms of management, we typically go with a short act in agent, like a short act in most grainy antagonist, like epratropium, or you can use a short act in beta to agonist like arbiterol. But after that, if their symptoms are not well controlled, typically you're going to give them a combination inhaler that involves a laba or a llama of some sort and an inhaled cortical steroid. So they're going to get a combination of something like tiotropium and an inhaled cortical steroid, like flutica zone or whatever. You're going to combine those two things. Or a lava along acting beta to agonist like sabiterol or flutica, plus an inhaled cortical steroid. So remember, you can use inhaled cortical steroids if you look at a point number of five and six to manage asthma and COPD chronically. All right, now what if they give you a question about a person that has a lot of itching and on the skin and they tell you that, oh, you see a lot of red patches on the skin, they may have some plaques or whatever. If you see this, I hope you're saying we divide this person probably has an exam. Remember, another name for exam on the USML is atopic dermatitis. Now, Xima, how do we treat it? Well, we're going to treat Xima typically on the exams is a combination of two things. You're going to use an emolient to keep moisture on the skin, but you're also going to use a topic of cortical steroid.

And it's actually kind of weird, but it's pretty high to know that Xima is associated with mutation in a genonus filagrine. One of these red factors, you think too low yield for the exams until the pops up and you're like, well, where did that come from? Well, now you've heard it. And also, it's important to know that there are certain diseases that have an association with Xima. So remember things like, we've got all Dritch. Remember, it's an immunodeficiency disease. They'll have low platelets. They'll have Xima and they'll have recurrent infections and it's excellent recessive. So it's only going to be found in boys on your test. And then don't forget Job Syndrome. That was the old name. The current name is Hyper-IGE Syndrome. When you have very high levels of IGE, you see them have a lot of like cold abscesses on their skin and their IGE levels are extremely high. That has a very strong association with Xima. All right. Now, remember, another, so that's factor number seven. Now, factor number eight, remember, when a person has an asthma exacerbation, you can absolutely give those people steroids. Most times when you're having an asthma exacerbation, you're going to get IV steroids. Typically, we're going to start off with a short acting brunque dileaders first, but in addition, you're going to get IV steroids, IV steroids. Okay. Now, how about factor number nine? How about a COPD exacerbation?

When a person has a COPD exacerbation, many times they're going to have increased put on production. They're going to be shot of breath. They're going to have a rising, the PACO to above baseline. Those people have a COPD exacerbation. COPD exacerbations, the primary management again, you can use short acting brunque dileaders, but those people are also going to get IV cortical steroids. In fact, it's actually pretty high to know that when you have a COPD exacerbation, typically, for the next few days, when you're discharged, you're going to be giving a few days worth of oral steroids, just again, to prevent recurrence of that COPD exacerbation. All right. Now, that's factor number nine, factor number 10. If they give you a question about a person that seems to have an issue with, you know, they're always pulling out stuff from their nose every morning. They just always feel their nose is always congested, congested, congested. Now, you're going to notice that these people they seem to have deviation of the nasal septum. I would really hope you're thinking of something known as chronic rhinocyanocides with nasal polyposes, chronic rhinocyanocides with nasal polyposes. The drug of choice for actually managing that disorder is an inhaled cortical steroid. Now, please do not forget something that is salient but extremely important. People that use NSAI Ds, they actually have a high risk of polyposes in the nose, because remember, NSAI Ds inhibit cycloxygenase.

If you inhibit cycloxygenase, you're going to have more flux. Because remember, Arachidonic acid can be converted to luchotrines by lipoxygenase or prestaglandins by cycloxygenase. So, if you take an inset and inhibit that cycloxygenase pathway, you're going to have more flux through the lipoxygenase pathway. And that's going to cause you to make a ton of luchotrines. And all those luchotrines you make is going to make it really hard. Right? You're going to be making a lot of polyps in your nose and whatnot. That aspirin induced asthma, which these days we call aspirin exacerbated respiratory disease, has a very, very solid association with nizopolyposes. And remember, you can also see nizopolyposes in people that have cystic fibrosis, just FYI. All right. Now, factoried number 11, what if they give you a question about a patient? And this person has asthma that's like super difficult to control. And you're told in the Q-stem that, man, this person's eocenophil count is pretty high. And you have these pulmonary interstitial infiltrates. Well, if you see this, I hope you're saying, wait, divine, this person has ABPA. This person has a allergic bronchopominary aspergillosis. Remember, the treatment of choice for allergic bronchopominary aspergillosis is going to be corticosteroid. You're going to give those people oral sterate. Now, do not forget that those people you're going to do a skin test, now you're going to see some positivity with aspergillus antigens. All right.

Factoid number 12, what if they give you a question about an African-American female that has like dry cough, you know, has bilateral hyalurate and apathy? That's pretty classic. That's sarcoidosis. Right. Remember, sarcoidosis, if they are asymptomatic, you're not supposed to treat them. But if they have symptoms, you should go ahead and give them steroids. Steris are the treatment of choice for sarcoidosis. And don't forget, people that have hypercalcemia from sarcoidosis, and they ask you, oh, how do you treat the hypercalcemia from sarcoidosis? I would really, really hope you're saying, oh, divine, I'm going to use the steroid as well. Monoid is a steroid as well. Because remember, if you control the problem, the inflammation, the problem will go away. Because think about it, sarcoidosis is a granulomata's disease. So because it's a granuloma, there's going to be lots of epitheliod macrophages. Those macrophages, they make a ton of one alpha hydroxylis. That's going to convert calcium to calcium trial. That calcium trial is going to cause you to, you know, that's activated in D. You're going to reabsorb a ton of calcium from your gut. You're going to have hypercalcemia. All right. Now, what if they give you a question about a patient? This person has HIV. And you know, for the past few days, the person has been very short of breath, very dysmnick. And you check their lab, their very high-boxic. And again, you get a chest x-ray.

And you see pulmonary interstitial infiltrates. And you notice that, wow, those people, they're just really, really struggling, really, really struggling. You know, they tell you that you get an induced pylom sample, and you see silver, stained positive organisms. And that's going to be numocystis-yurvetzi. And I remember numocystis-yurvetzi is the most common cause of interstitial pneumonia in HIV patients. So how do we manage it? We're going to manage it with a combination. Usually with just trimethyl brimsoffamethoxysol. But one thing you never want to forget is that sometimes you need to add corticosteroids. Especially if you appeal a little aoteu. Your arterial oxygen partial pressure is less than 70, just to improve outcomes in those people. All right, factor number 14. What if they give you a question about a person that has a skin disorder? You know, they're not doing really well. They have a fever. And they tell you that they have all these lesions on their skin that, if you just apply gentle pressure to those lesions, they pop easily. So that's necosci positive. I hope you're saying, oh, divine, yeah, that's pethicos vulgaris. Remember pethicos vulgaris? It's an autoimmune disease. You make autoantibodies against desmosomes. Typically, that can be managed with topical steroids. Although you can also manage it with retoximap. Oh, sorry, not topical steroids with oral steroids. You can give the person oral steroids or retoximap.

And then remember when we talked about, so this is factor number 15 I'm going into. So remember we talked about adescent disease? That's an autoimmune disease. Well, because the adrenal cortex has been damaged and you're not making cortisol or outdo steroid, you want to go ahead and manage those people by giving them something to replace cortisol, like a steroid and something to replace outdo steroid like a flujro cortisol. Remember, we typically don't have to replace the adrogents in people that have adescent disease. All right, factor number 16. Now, it's pretty high yield to know that steroids, especially IV steroids. We tend to use them for flares of things, for flares or exacerbations of certain diseases. We've talked about how you can use IV steroids for asthma exacerbations. We've talked about how you can use IV steroids for COPD exacerbations. Well, please don't forget that you can also use IV steroids for exacerbations of things like multiple sclerosis, things like lupus, things like inflammatory bowel disease. You can give IV steroids to manage those things. And then what if they give you a question about a newborn? So this factor number 17, a newborn that is superhypotensive, has the few skin hyperpigmentation, has hyponitremia, has metabolic acidosis. If you see something like this and has hyperchilemia, if you see something like this, I'll really hope you're thinking about the classical case of CAH, congenital adrenal hyperplasia.

Remember, CAH is the most common cause is a deficiency of 21 hydroxyl. So when you have a 21 hydroxyl is deficiency, you're going to make a ton of DH As. But you're not going to be making cortisol, you're not going to be making our dostor. So it's going to be like you have adescent disease. It's going to look like you have adescent disease. It's pretty high yield to know that those people are also going to be treated with steroids to replace the cortisol they're not making and fluid cortisol. If you notice the electrolyte and momelies are going to be eerily similar to people that have adescent disease. All right. Now what if they give you a question about a female? So it's factor number 18, a female that, you know, for the past couple of months, she's been very tired, feeling very fatigued, has a lot of right upper corduropin, you know, she's nauseous, has a rash on the skin. And you notice that their liver labs are elevated, their AS Ts, their L Ts are elevated. But their alkaline phosphatizes completely normal. The ability to remain is completely normal. And you notice that this female has primary menorrhia, she's in fertile. When you see something like this, what should you be thinking about? Well, I hope you're saying divine. This sounds an awful lot like autoimmune hepatitis. It's actually an autoimmune disease. And remember, it's going to be associated with antibodies against smooth muscles, so anti-smooth muscle antibodies.

Another association you mentioned you exams are those anti-liver kidney micro-summon antibodies. That's actually pretty high yield to know for your test. And remember, this will not be managed with corticosteroid. All right. Now, factor number 19, what if they give you a question about a person that has recently had some kind of viral infection or a person that has lupus? I you notice that their hematocritus is completely fine. Their white blood cell count is completely fine, but their platelet count is crazily decreased. If you see something like this, I'll hope you're saying, oh wait, if I, this person has it. This person has immune thrombocytopenia. Remember, it is an autoimmune disease. You pretty much make auto antibodies against GP2 B3 A. So that's going to cause the splinic macrophages when they see antibodies bound to your platelets to completely obliterate those platelets. That's why these people have thrombocytopenia. Remember, the first line treatment for it is corticosteroid. It's the first line treatment. Although if that doesn't work, you're going to slide to second line, which is IVIG. If that doesn't work, you're going to slide to third line, which is a splinectom. Take those splinic macrophages that are causing havoc out of the equation and problem is going to be solved. All right, now what if they give you a question, factor number 20, about a lady that has proximal shoulder pain and weakness and a ESR CRP is elevated. That's pretty easy, right?

This is going to be polymyalgia, rheumatic. Remember, the management of choice for polymyalgia, rheumatic is going to be corticosteroid therapy. And then factor number 21, they give you a question about a lead over 50 or close to 50. And this person has like eye pain, blurry vision on one side. And you notice that man, their temple is really hurting on that side. And again, high ESR, high CRP, think of giant cellaritis. It's a large vessel vasculitis. Giant cellaritis, which sometimes we call temporal arytis. Remember, the treatment of choice is going to be steroids. You're going to give steroids first, actually. Before you won't start worrying about a temporal artery biopsy, because that's actually an ophthalmologic emergency. You don't want this person to go ahead and go blind. All right, now factor number 22, they give you a question about a person that has proximal muscle weakness, you know, so trouble climbing stairs, trouble lifting objects with your arms. And they tell you that, oh, they have like redness around their eyes. They have these weird grutes around their knuckles and things like that, those are gotrons, papules. The stuff I described around the eyes, that's the raccoon eyes. And you see the proximal muscle weakness. And you notice that their CPK is pretty high. When you see this, I hope you're thinking of a myopathy like dermatomyocytis. Although remember the close causing is also polymyocytis.

These folks, again, the treatment of choice for them is typically going to be steroids. You're going to use steroids to manage those things. And then what if they give you a question about a child? So factor number 23, a child that has chronic joint pain. Chronic joint pain. But for the last two, three days, this child's eye has been hurting. And this child's ESRCRP is elevated. I would hope you're seeing, wow, divine. This person kind of sounds like being a child, they have GRE. Driven our rheumatoid arthritis. Remember GRE, especially if you're a ligua-ticular kind, rates like 1 to 4 joints that are affected, is associated with anterior uviitis. In fact, these people require anuslytlamp examinations of the eyes, just to make sure that they don't have anterior uviitis. So this person has anterior uviitis. Again, some homologic emergency. You don't want these kids going blind. So what are you going to do? Make sense. It behooves you to go ahead and give those people steroids. Topical steroids. You're going to give steroids in the eye. That's the treatment of choice actually for anterior uviitis. Okay. Now, what if they give you a question, factor number 24, about a patient that has MS, that over the last few hours, has had very severe eye pain. And they tell you that they have an offering-popillary defect. But if you see something like that, I hope you're saying, wait, wait, wait, wait, wait. Divine, this sounds an awful lot like optic neuritis.

Remember, optic neuritis can cause issues in people that have MS. It's inflammation of cranial nerve number two. And the management for that disorder is going to be sterile. You're going to give IV steroids. And you're going to diagnose it with an MRI. But again, it's an ophthalmological emergency. You have to make sure you treat it so the person doesn't go blind. Okay. And then, for factor number 25, in fact, I'm going to title this factor with the steroid and cyclophosphamitriol. The steroid and cyclophosphamitriol. What am I talking about this? There's a series of disorders on the USMELIS that are managed with the combination of steroids and cyclophosphamitriol. And this is actually a pretty high list to know. So what's this list? Well, the first one is going to be Wagner's. Wagner's. Wagner's. Granolomatosis with polyangitis. Remember, that has a C-enka association. The next one is going to be church trials, which these days we call EGPA. Eocenophilic granolomatosis with polyangitis. That's going to be managed with steroids and cyclophosphamitriol. And then remember, if you see a young male smoker that is puking blood and has blood in the urine, they have nephritic syndrome. And you have this rapidly climbing renal function. That's RPGN. Rapidly progressive glomerulon arthritis with good posture syndrome. We're also going to manage those folks with steroids and cyclophosphamitriol. And just a quick segue before we jump to point number 26.

If you're taking step two or step three, within any time soon, I will strongly encourage you to consider, no, the two classes I have, I have a class today called the last minute review. It's a three hour class. We go over in a very short time, a bunch of very high-yield things for step two and step three. It's going to take place over zoom between 7 and 10 pm Eastern time this evening. So if you're interested, just shoot me an email through the website. I can give you some more information. And then also next week, I have a 20 hour step two, see case step three course. I'm is going to be taking place from Monday to Thursday, from 5 to 10 pm EST every day. It's going to be over zoom. Again, it's 20 hours, but you're going to learn a lot. And if you know me, you know that I'm not a person to just throw factoids at you. No, what I'm going to do is, I'm going to show you how it's going to present in a question. I'm going to explain the path of physiology. I'm going to make integrations. And I'm going to remove a lot of fluff. I'm going to focus primarily on what you need to know for your exams. There's tons of people that are taking this class and they've done extremely well. I'm pretty sure of hot scores as high as the 280's from people that are taking these classes. I've gotten a lot of extremely positive feedback on it. So if you're taking your exams soon, remember step two, see case scores matter these days.

I would encourage you to reach out to me and I can give you some more information on the class. All right, let's go to question, factor number 26. So what if they give you a question about a person that has a history of SQL cell disease? Remember, if you have SQL cell, your splitting is not working. So you're going to struggle with encapsulated augmentings. And you're told that man, over the last two days, this person has been having severe headaches, high fevers, and the person has no core rigidity. And they do a lumber puncture and you notice that, wow, this person, you see grand positive coxine in chains. Well, if you see something like this, I hope you're saying, oh, wait, divine. This person has pneumococcal meningitis. Well, how do we deal with pneumococcal meningitis? Obviously, we're going to give IV antibiotics. We're going to give IV antibiotics. You're going to give something like Ceptriaxon, for example. But don't forget that when a person has bacteria meningitis, especially from strepnumal, it is super high you to know that those folks need to get steroids as well to improve their outcomes, to improve their outcomes. Okay, factor number 27. What if they give you a question about an old lady that is eaching a lot down there? Right, has very itchy vulvar and they tell you in the queue stem that, this thing kind of looks like crinkled paper. Looks very thin, very thin vulvar. Well, I hope you're saying, oh, divine. This sounds a lot like Lycan sclerosis.

Well, Lycan sclerosis, typically the way we're going to manage it is with a hypotency, topical steroid like clopetasol or halubetasol. A hypotency, topical steroid. You see, again, I promise you this podcast is super, super, super high yield. All right, now factor number 28. What if they give you a question about a person that has moon faces, a buffalo hump and all those things? And they ask you for the most likely cause. But what's the most common cause of Cushing Syndrome? It's actually pretty straightforward. The most common cause is exposure to exogenous cortical steroids, like a present-dicking steroid, chronicly for whatever disorder. Although, remember, the second most common cause is going to be Cushing's disease. Cushing's disease is when you have a pituitary adenoma that's making a ton of ACTH. Remember, that one's does not suppress with low-dose dexamethasol, but it's going to suppress with high-dose dexamethasol. All right, factor number 29. Remember, what if they give you a question about a person that is on chronic steroids, and then their A1 C has risen? It's going to be pretty straightforward. Remember, steroids, they pretty much antagonize the actions of insulin, so they can cause a person to become hyperglycemic. In fact, we try to be careful about giving cortical steroids to people that have diabetes, although sometimes you're kind of caught between a rock and a heart-please, and you've got to do what you've got to do. All right, now factor number 30.

What if they give you a question about a person that is on chronic steroids, and then they've got to be in two accidents within the last few months, because they're having trouble reading root signs at night? Well, that's cataract. Remember, steroids have a very strong association with Codin causing a cataract. That's something that's very high you to know for your exams. And then factor number 31, what if they give you a question about a person for the last two days? They've had crazy high fevers, and they tell you that man, in fact, they give you a picture of the extremities, looks like blue-black, and they tell you that man, the margins are rapidly expanding. That's pretty easy, right? That person has neck fascia. Necroticis infasciitis. Remember, necroticis infasciitis has a very strong association with cortical steroids. Remember, when a person has neck fascia, they're going to de-breed deletion, and you're going to give IV antibiotics. But the breedment, the breedment, the breedment is something you absolutely need to do. If not, their limb is going to disappear. All right, factor number 32. Now, one thing that's actually high, you know, is kind of related to something I've talked about already. But remember, we said that when a person has no more cystic pneumonia, and the PEO3 is under 70, you're going to give them TMPSMX, and in addition, you're going to give steroids. But remember, if you're chronically on steroids, you're going to be coming immunocompromised.

That immunocompromised from taking steroids chronically can actually increase your risk of PCP pneumonia. So that's actually something that's pretty high, you know, for exams. Our friends at the MBM is actually love to test this factoid a lot. You see a person that's on chronic steroids for something like Janssel at Ridesh, and then they develop like, you know, hypoxia, shortness or breath, they're puking, puking, puking a lot. They're coughing up a lot of stuff, you know, sputum-wise. And you see, you know, the sputum sample, you see silver, steam positive organisms. That person has literally developed pneumocystis, Jervetti. Remember, it's not only people that have HIV that can get a PCP pneumonia. And then factor number 33 with steroids is that remember, glucochorticoids, they can actually activate your osteoclast. So you can see people that have, that have been taking steroids for a long time, they actually have a pretty high risk of osteoporosis. In fact, sometimes if people have to be on steroids for a long period of time, we typically try to put them on these phosphonids as well as osteoporosis are for phylaxis. So you may see these people having like fractures with minimal trauma, just gonna keep that in mind that wait, steroids can actually activate osteoclast, they're gonna drop your bone, you're gonna have osteoporosis. Okay, factor number 34, factor number 34.

If they give you a question about a person that has like really severe bloodied area, and they tell you that they have a right-up or quadrant pain, you do imaging, see a liver abscess, and they tell you that you see a lot of protozoans in the person's stool. I'll hope you're thinking about intamibah histolyrica. The thing is intamibah histolyrica causes bloodied areas, one of these protozoans that causes bloodied area. Well, that's not all. When people are steroids, and they have a histolyrica infection, they tend to have really, really bad outcomes. These are one of those things that people don't pay attention to, but I promise you, it's actually pretty high yield to know for your exams. All right, now what if they give you a question about a person that has an asthma exacerbation or COPD exacerbation, so these factor number 35, and you notice that they've been treated, and by the next morning, they're actually all crazy. They're saying, oh, I'm hearing someone chasing me. I'm hearing someone speaking in my ear, blah, blah, blah, blah, blah, blah, blah, when you see something like that, that person has steroid induced psychosis. Remember, steroids can make a personal crazy. You can cause psychosis. How you gonna manage that? Well, you're gonna go ahead and give an anti-psychotic, although sometimes, so what if care is all you need, but you can give them an anti-psychotic. Okay, factor number 36. What are the skin changes we see with people that are taking steroids?

Remember, you can see things like moon faces, buffalo hump, you know, they can have atrophy of their muscles. Remember, steroids can cause lipodistrophy, lipodistrophy, and they can cause muscle atrophy, they can cause muscle weakness. Just something you want to keep in mind. Now, one thing I want to say real quick, is there a HIV drug class that also causes lipodistrophy? I wonder what it is. I'll hope you're saying, oh, divine, that sounds a lot like your proteins inhibitors, like your proteins inhibitors. That's a very high-yield factor to know for your test. Again, you'll notice I'm really trying to keep this podcast short because I want to make it like very short-sweet, but incredibly high-yield. All right, let's go to factor number 37. Now, what if they give you a question about a person that, you know, is has very severe asthma, their chronicly, you know, oral steroid. And then this person over the last few days, they've been having trouble walking upstairs, lifting heavy objects. And they tell you that the creatine-forceful kindness is like 50. It's not very abnormal, or it's like completely normal. Or if you see that, I hope you're saying, we're divine, this person has a steroid-induced, myopathy, a steroid-induced, myopathy. Okay, and then factor number 38. What if they give you a question about a person that is on, you know, chronic steroids. And the person has been getting a lot of accidents.

They tell you that they keep bumping into cars on their sides, you know, on the, like, city streets and whatnot. That's pretty easy, right? That's glaucoma. Remembering glaucoma, remember first things first, steroids have an association with glaucoma. But that's not all. Steroids, by causing that glaucoma, glaucoma is going to make you lose your peripheral vision. When you lose your peripheral vision, you're going to be having all these side swipes and things like that. You're going to be having an accident because your peripheral vision is just not great. All right, factor number 39. What if they give you a question about a person that, you know, got, you know, was treated for like an asthma or COPD exacerbation. And in this person is not having very significant abdominal pain. And the person is coughing a lot. Well, I would hope you're really thinking about peptic ulcer disease. Uh, steroids have an association with peptic ulcer disease. Steroids do actually a ton of stuff. They're going to make you make more gastric acid. That's going to raise your risk of ulcers. And they're going to decrease the production of first-agglendants. When you make less first-agglendants in your GI tract, you're going to get in a lot of trouble. I kid you not. I mean, think about it. Why do you think NS Aids cause peptic ulcer disease? Because the hippycycloxigenase. If you hippycycloxigenase, you're not going to be making prostagglendants. That's going to get you in some hot water, right?

And remember, you know, so how do steroids actually inhibit prostagglendant production? Well, think about it. The inhibiting enzyme-forceful lipase A2. Think about it. Fustal lipase A2 converts membrane-forceful lipids per-acadonic acid. Arachidonic acid is the feedstock that is acted upon by cycloxigenase for you to make prostagglendants. So if you inhibit phospholipase A2, you only make your arachidonic acid. If you don't make your arachidonic acid, you only make prostagglendants. Less prostagglendant production is going to make you to make a ton of gastric acid. And that can cause you to have peptic ulcer disease. All right. Now, factor number 40. What if they give you a question about a person that uses inhaled stares for like their asthma or COPD? And then this person has been having like dysphagia or like painful swallowing. That's what I know. Fagia, well, you want to think about candidiasis. Remember, people that are using inhaled stares especially, they have a pretty high risk on the USML use of developing oral resophageal candidiasis. Obviously for those people, you're going to give them oral results or an oral my starting. That's going to help their condition. All right. Factor number 41. What if a person starts having forceful contractions at less than 34 weeks? What are you going to do? Well, I hope you're saying, oh, divine. I'm going to go ahead and give them pathomethousone in two doses to promote fetal long maturity.

Remember, steroids promote fetal long maturity. If you're going to liberate less than 34 weeks, you've got to receive steroids to promote surfactant production to promote the maturity of the fetal locks. All right. Now, factor number 42. What if a person is started on corticosterotherapy? And you notice the next day, the white count is like 25,000 or some crazy high number. They will try to trick you on your exam and say, ooh, this person has a new infection because they immunocompromised from the steroids. No, no, no, no, no. Remember steroids cause demargination of neutrophils. Demargination of neutrophils. So they can really raise your white count. In fact, sometimes if you want to mess with your head on exams, they will just slap the term lookamoy reaction on it. Steroids literally cause that demargination. It's going to raise, raise, raise your white count a ton. So they can give you a question about a person that has COPD or asthma, had an exacerbation. God, I have these steroids. And then the next day, the white count is extremely high. It's because of that steroid induced demargination. And then factor number 43, remember, they actually some chemotherapy regimens that include steroids. The two high you'd want to know are CLL and Hodgkin's lymphoma. CLL and Hodgkin's lymphoma. Those people's chemotherapy regimens actually include corticosteroid therapy. Okay, factor number 44. What are some skin changes you may see in people that have taken steroids?

I've talked about the lipodistrophy and Buffalo home moon faces. Don't forget that steroids, the inhibitory of fibroblasts. So you're going to have easy bruising. You're going to have thinning of your skin. You're going to have skin atrophy. Just something you keep in mind. All right, factor number 45. What if they give you a question about a person that is on steroids, you know, chronically, for whatever? And then they have this pain in their right hip. You know, it really, really hurts. They have introuble ambulated on that hip. They're limping on that hip. That's going to be vasculine and crosses. Steroids have a very, very strong association with vasculine and crosses. Sometimes on the USM Ds, they actually call this osteonecrosis. All right, factor number 46. What if they give you a question about a person that has a history of breast cancer? And then they tell you that for the last two days, this person has become paralyzed in their lower extremities. And then they tell you that when you pop it, they're back. You know, they have like pinpoint tenderness along their back. That's pretty easy. And many times those who's out force will be extremely elevated. They may have hypercalculative malignantcy. Think of spinal cord compression from steroids. Remember, you're going to diagnose that with an MRI. But those people need steroids pronto to reduce that swelling around your spinal cord. All right, factor number 47. Basically, I'm going to call this the second line factor.

Remember, steroids are second line for a bunch of things. They are second line for gout. Remember, first line for gout is an n-set. They also second line for pericarditis. Remember, first line for pericarditis is going to be an n-set plus coaches in an n-set plus coaches in. All right. Now, factor number 48. What if they give you a question about like a child? You know, that has a lot of muscle weakness. And this child is hypertensive. This child has hypokillemia. Has metabolic alkylosis. And they tell you that, man, this child's chaudosu理 is very, very depressed. Almost undetectable. Their reigning is very, very depressed as well. But they tell you in the queue stem that they have an elevated free cortisol to cortisol ratio. When you see something like this, I want you to think of a disorder known as same. Same means the syndrome of apprenminoral corticoid excess. Syndrome of apprenminoral corticoid excess. It's actually a genetic disease. It's a autosomal recessive chromosome 16. And you have a mutation in a gene known as 11 beta hydroxy steroid dehydrogenase 2. 11 beta HSD2. 11 beta hydroxy steroid dehydrogenase 2. The thing is, what does this gene product do? Well, what it does is it converts cortisol to cortisol. Because your body understands that, man, cortisol has some mineralocorticoid properties.

So what your body tries to do is it tries to, express this enzyme so they can convert cortisol, which has mineralocorticoid properties to cortisol, which is inactive and does not have mineralocorticoid properties. But if you don't have this enzyme, when you're going to get in trouble, you're going to have a ton of cortisol. It's going to give you those mineralocorticoid-like properties. And you're going to have hypertension, hypokilymiametabolic alkalosis. And obviously that hypertension is going to turn down your reigning and your tensile-dosterone system. So your reigning is going to go low. Your outdosterone is going to go low. And again, that's why these people have a high level of free cortisol to cortisol. Because their cortisol is rising, but they're not able to make converted cortisol. Remember, licorice can also cause the same problem. Remember, licorice contains something called glycerinic acid. Glacierinic acid actually has the ability to inhibit this 11 beta HSD2. And in addition to that, it actually decreases the gene expression of 11 beta HSD2. That's going to be an acquired cause of that same, the syndrome of upper mineralocorticoid excess. And then let me ask you this. If a person has pushing syndrome, what do you expect their ocenofield count to look like? That's factor 49. Well, their ocenofield count is going to be low. Remember, your ocenofils, your ocenofils, the steroids cause epoptosis of your ocenofil.

So when people have cortisol excess, they're going to have a lowered ocenofield count. But think about it, if you have a steroid deficiency like adescent disease, you're going to have a high ocenofield count because you're no longer causing epoptosis of your ocenofil. So your ocenofils are going to have a much longer half-life. That's why ocenofilia is part of the differential diagnosis of adescent disease. And then factor number 50, they give you a question about a person that has a fib and their eyes are bulging. Obviously, that person probably has graves disease and they have propitosis. Remember, in graves disease, you have these thyroid stimulates in immune globulins and autoimmune disease. So those things pretty much stimulate the TSH receptor. So your entire thyroid gland is going to be stimulated. You're going to make a lot of T4 and T4. So your TSH is going to be suppressed. But those antibodies stimulate the TSH receptor. But remember, is they knew of the cell in the body that has TSH receptors? I wonder what? Maybe fibroblasts. So if those antibodies stimulate your fibroblasts, it's going to cause them to make things like glycosaminoglycans. And that's going to deposit in your eye and that's going to cause propitosis. So how can we fix this problem with steroids? Well, give steroids because steroids, what do they do in hippy fibroblasts?

If you're a hippy fibroblast, you're going to inhibit the production of those extracellular matrix things like glycosaminoglycans and you're going to fix that propitosis. So I'm going to go ahead and stop here. Again, I promise you this podcast, you're going to get multiple questions right on your exams from this one podcast. And just real quick, again, I also offer one on one tutoring for all the USMLA exams and all the complex exams. And I have these review courses. Again, I talked about the last mini review for step two, step three, taking place today. And the 20 hours step two, step three, cross taking place next week, between Monday and Thursday. Over Zoom. Again, there are not lectures. If you're expecting a lecture, you're in the wrong course. These courses focus primarily on questions. But again, you'll notice that with those questions, you learn so, so, so much. I've literally had people that between day one and before of the class, you know, they came in, they took a practice test before they won of the class. And then by the end of the class, they've improved by like 30 points already. So I'm not saying everyone will have that improvement, but I've heard that story more times than I can remember. And then I also help with errors, applications, recommendation letters, personal statements, and things like that. I've done this for many years. So if you're interested, just shoot me an email and I can give you some more information.

And then remember, I have these podcasts on Apple, on Google and on Spotify. So just check those out. But again, if you want the worksheets, so this podcast has a worksheet. If you want the worksheet, I'll encourage you to go to the website, divineinterventionpodcast.com, and you see a PDF below the podcast episode. You can download the worksheets like a quiz that if you listen to the podcast and really understand what's going on, you can actually fill out that worksheet. And then you have something that can just study to review the material very quickly again. And then finally, I have another website called, divineinterventionlifelessons.com. Every week I try to post one or two podcasts. I just uploaded one this morning about following your heart. I post one or two podcasts every week where usually less than 10 minutes, but I use the Bible to discuss a life lesson. Many people have actually listened to those and found it to be helpful. It's again, it's a website, divineinterventionlifelessons.com. It's actually an Apple podcast associated with it called the divineintervention life lessons podcast. And again, I also have my You Tube channel. Check that out. That's where I post many of the videos that I make. So thank you for listening to me today. I will see you in episode 540 of a wonderful day. God bless you and bye for now. Thank you.

Cortisol.

The zona glomerulosa.

Hypokalemia and metabolic alkalosis (due to mild mineralocorticoid activity).

The adrenal cortex (not the medulla).

High ACTH levels are released; ACTH shares a precursor with MSH (melanocyte-stimulating hormone), causing skin darkening.

Combination of emollients and topical corticosteroids.

Pemphigus Vulgaris.

Inhibition of COX shunts arachidonic acid metabolism toward leukotriene production via LOX.

Granulomatosis with polyangitis (Wegener's), EGPA, and RPGN.

Glaucoma/Cataracts/Osteoporosis are all associated with chronic steroid use.

21-hydroxylase deficiency.

Causes hypokalemia and metabolic alkalosis due to mineralocorticoid activity.

High (due to lack of negative feedback from cortisol).

Chronic steroid use combined with immunosuppression/hypoxia.

Pemphigus Vulgaris.

Hyponatremia, hyperkalemia, metabolic acidosis, and skin hyperpigmentation.

11-$\beta$ Hydroxysteroid Dehydrogenase 2 (11$\beta$HSD2).

Exogenous corticosteroid exposure.

Giant Cell Arteritis/Temporal Arteritis.

Job Syndrome (Hyper-IgE Syndrome) and Atopy.

21-hydroxylase deficiency.

Causes hypokalemia and metabolic alkalosis due to mineralocorticoid activity.

High (due to lack of negative feedback from cortisol).

Chronic steroid use combined with immunosuppression/hypoxia.

Pemphigus Vulgaris.

Hyponatremia, hyperkalemia, metabolic acidosis, and skin hyperpigmentation.

11-$\beta$ Hydroxysteroid Dehydrogenase 2 (11$\beta$HSD2).

Exogenous corticosteroid exposure.

Giant Cell Arteritis/Temporal Arteritis.

Job Syndrome (Hyper-IgE Syndrome) and Atopy.