DIP Episode 536 - USMLE Step 2/3 Rapid Review Series 115 (with included worksheet)

Welcome to episode 536 of the Divine Intervention Podcast. Into this podcast we're going to be continuing the Rapid Review series for the US Emily Step-to-Sea-Kenn Step 3 exams. This is going to be series 115. One thing I'll encourage you to do is there is a worksheet that is attached to this podcast. So if you can, I will strongly encourage you to print out the worksheet and annotate as we go through this podcast. If you want to take it as a quiz at the end of this podcast that is absolutely fine. Or if you want to preview before you listen to this podcast that is absolutely fine. If you're like, I want to get the best learning from this, my recommendation is preview. Just for a quick spin like a minute before you listen to the podcast. And then listen to the podcast and then take it as a quiz at the end. An alternative is preview for like a minute or two before you listen to the podcast. And then annotate as you go through the podcast. And then just this worksheet go through it down the line. Alright. So what if they give you a question about an old guy and your tool that this man is having to crank up the TV whenever he's watching an NBA game, was watching golf, was watching a basketball game. And they'll tell you that his grandkids are always complaining that the TV set too loud. Well, what should you be thinking about there? I hope you're saying, oh wait, divine. This is a pretty classic case of press by QSIS. This person has press by QSIS sometimes on the exams.

They make collate and age related here in loss. So what's the big deal press by QSIS? Well, the key thing to know here is that it's a kind of sensor in your hearing loss. Again, remember the USML is these days have said this so many times on the spot cast they dealing derivatives, they dealing what derivatives. So basically they take what you're not expressing in other terms. So sometimes instead of putting press by QSIS as an answer or putting age related here in loss as an answer, they can literally put sensor in your hearing loss as an answer. Press by QSIS is a kind of sensor in your hearing loss. So what usually causes this? Well, for the most part, the structures in your inner ear degenerate. So like your cochlea is just not working great in case they ask about pathophase. Your cochlea is degenerating, your organ of cordy, that's like the sensory organ for hearing in your inner ears. So those are workers great to losing like stereocilia. That's why you may wonder like, well, why is it that people that have upwards and from the off hearing problems? Well, the thing is the type 4 collagen that they're lacking. Remember, it's a COL 4 E5 gene mutation. The type 4 collagen they're lacking is part of your inner ear structure. So the stereocilia is lost and these people again, when they have press by QSIS, it's high frequency hearing loss that they have and usually is going to be by lateral. And here's the thing, press by QSIS is the most common cause of hearing loss.

Again, remember our friends at the MBM is care a lot about these most common causes these days. And you may wonder like, divine, is this something that gets better unfortunately, not really? Because the thing is, most mammals, they can regenerate the cochlear sensory cells, the organ of cordies and whatnot, or at least sensory structures in their inner ears. But human beings cannot. Human beings cannot. And since I guess we're talking about hearing loss, remember our friends at the MBM is they can slap on some other hearing loss vignettes on your exams, right? So, especially with drugs, I don't know why people just ignore this, but it's one of these things is pretty high to know for your exams. So for example, they can give you a question about a person that is being treated for some kind of pseudomonal infection. And obviously you notice that they develop hearing loss. You want to think about an amino glycoside like gentamysin. Remember the amino glycoside certainly cause hearing loss. I mean, you can also think of the amino glycosides with people that have cystic fibrosis. I remember both of us, CF, we tend to give them inheld tuberomasin as the treatment for pseudomonas. Remember, people that have CF, over the age of 20, the most common cause of pneumonia in those walks is pseudomonas aeroginosa. Tuberomaicin is an amino glycoside. It covers, it covers pseudomonas pretty well.

So they can pretty much create any kind of amino glycoside vignette with gentamysin, tuberomaicin, neomysin. Neomysin, I believe sometimes is used as bowel prep in certain procedures. So neomysin, amicasein, just keep those in mind. Or they can give you a question about a person that is being treated for some kind of malignancy, you know, like testicular cancer for example, and they develop hearing loss. You want to think about this platinum agents, they have very, very big auto toxicity. And then they can give you a question about a person being treated for CHF. Remember your lube diuretic, especially if a chronic acid loves to cause drug-induced auto toxicity, drug-induced hearing loss. Or they can give you a question about a person that recently had an MI, and this person has been on chronic pharmacotherapy since. And then the person develops hearing loss, especially when you're taking big doses. Or they can give you a question about a person that has like dress-ler syndrome or like a post-MI Peric raditis. They want to think about aspirin. Remember aspirin, especially in high doses, the salicylates they can cause hearing loss. Again, you can see all the integrations they can make with this stuff. I know maybe hearing loss is not high-yield for the exam, I promise you it's really high-yield. Or you get a question about a person that came into the hospital for CDF treatment. And this person then develops hearing loss afterwards. You want to think about vancomycin.

Remember, vanc came cause hearing loss. Vanc is auto toxic. Vanc is auto toxic. And again, they have many vanc-wing aids they can write. We use vanc to literally cover MRSA, use a cover CDF. So they can give you like an IV drug user kind of situation. Because IV drug users that develop endocratitis, they're probably going to be on vancomycin for some reason. So just kind of keep that in the back of your mind. Now, what if they give you a question about a person that is like super angry, has a lot of trouble sleeping. You know, as we have in this constant feeling of hunger, performpoli and a quiz on an exam. And that this person quit smoking like a week ago. What should you be thinking about? Well, I hope you're seeing way divine. This sounds a lot like nicotine we draw. This person is we're drawing from nicotine. This person is we're drawing from nicotine. And the thing is one unusual question you may see on your exam is they can ask you like which of the following are bringing your transmitters? Is responsible for this person's chlorine symptoms or was responsible for the person's dependence on the substance? The answer is going to be dopamine. The answer is going to be dopamine. That's why nicotine is kind of hard to quit because you see people, they may drink a nicotine drink, especially if you do it regularly. There's going to be a small amount of dopamine that is released in your brain. That's like the reward center. So just kind of keep that in the back of your mind.

I mean, most of these things that are addictive, social media, screwing on your phone, blah, blah, blah, blah, blah. It's just like some kind of dopamine reward. That's how the addiction is developed. And that's how we draw also kind of happens because it's almost like you just feel like you're in such a horrible, horrible, horrible downstead. You can seem to get out of it. So what are we going to do for these people? Well, typically when a person has nicotine withdrawal, we generally try to start off first line with nicotine withdrawal therapy. I mean, nicotine replacement, not withdrawal. Whoops, nicotine replacement therapy like what? You want to think of something like a nicotine patch or a nicotine gum or just many different nicotine things you can try. And if that is alone, it's not controlling the person's symptoms. They can add on pharmacotherapy. Don't stop the nicotine replacement therapy, but add on pharmacotherapy. So what do you add on as pharmacotherapy? Well, you can add on something like bupropium. That's an NDRI. Remember, it's a neurobenefriend dopamine. We're taking inhibitor. You can add that on. But again, remember, don't give bupropium to people that have a history of seizure disorders because they lowers the seizure threshold. Don't give it to people that have eating disorders because they can have all these electrolyte problems like hyponitramia, hypokillemia, what not. That can cause them to have seizures. So don't give it to those people.

Again, many people are used to these bupropium contraindications being tested just in people that are, who are taking bupropium for depression, right? Because many people love bupropium for depression because it doesn't have sexual side effects. And it doesn't cause weight gain. Actually, it causes weight loss. So people like it. But again, our friends at the MDM is, it's not like the inventive topics to test. You know, every now and then, they slot in a bunch of new topics. But what they usually do these days is that they just take what you know and test it in a fashion that is not very... common for many people, right? Like testing bupropium contraindications in a person that is studying treatment for nicotine we draw. It's not something you think about all the time. It's a classic thing they love to do an example, right? Remember, another drug you can use if you don't want to use bupropium is you can use variniclin, many of us know it as chantics, I believe. This is a partial agonist, that the nicotinic receptor is a partial agonist, that the nicotinic receptor. Although the thing is we try to be careful about variniclin. If a person has like a history of like zero psychiatric disorders, that can be problematic in those populations. Now, what if they give you a question about a person that has been sleep deprived because they've been studying for some exam? And they don't be getting enough sleep.

And then they have this severe pain on the side of the head, like on the right side of the head, so on one side of the head. And they tell you that man, this headache is throbbing, is pulsating. What should you be thinking about? Well, I hope you're saying, oh, divine, this is a migraine. This is a migraine, right? This is a migraine. This is a migraine. Don't overthink it. This is a clean cut case of a migraine, clean cut case of a migraine. So what are you going to do for this person? Well, for migraine, remember, you can use a serotonin receptor agonist like a triptan, like so much triptan, for example. Or you can use an n-set. So here's the thing. If you don't see a triptan as an answer for migraine, so you examine consider using an n-set. I gave you a note of friends that the NBA needs can give you a migraine question. And the acute treatment is literally an n-set. Just something I want to keep in mind. Well, remember, there are certain contraindications to a triptan, right? So, see, for example, you have a histro of MI, or you have a histro of like viso spasim. So let's say, for example, you have a histro of like virions, angina, which we used to call prismetal angina back in the day. So much triptan may not be the smartest idea in the world, right? So I'm just going to keep that in mind. Believe it or not, n-sets can also be used for acute migraine management on the USMLE exams.

But one thing our friends at the NBA needs love to test is when you see people having migraines multiple times a month, then those people need to be on some kind of prophylaxis. So what kind of prophylaxis are they supposed to be on on your exams? Well, the thing is you can use many different things. You can use a bit of blocker. You can use a tricyclic antidepressant. You can use... You can use topiramate. You can use calcium-shadowed blockers. You can even use a tricyclic. I believe I've mentioned that already. So here's the thing. Many of you may wonder, Ben, which one do I pick? Well, in general, if they don't give you the person having any comorbid disorder, just pick the answer choice that is the least toxic. I will say probably of all these drugs, I don't know, maybe like a bit of blocker, calcium-shadowed blocker is probably the least toxic. But the thing is many times on the USML Es, they will give you these migraines prophylaxis questions and they will give you like a comorbid disorder, where it's like, wow, you can kill two birds with one stone by picking those drugs. So, say for example, the person has migraines and they have peripheral neuropathy or they have migraines and they have depression. I try to say that you can't tell you the person is not a bad idea, because it's going to manage the neuropathy, it's going to manage the depression, it's going to manage the person's migraines. Okay, how about bit of blockers? Bit of blockers are really good ideas.

Say for example, the person has a history of something that can be true to bit of blockers. I can probably make a podcast on bit of blockers in the future, actually. But there are so many things you true to bit of blockers. Like say for example, the person is hyperthyroid and they have migraines. Bit of blockers are pretty good, because bit of blockers will help the hyperagenergic symptoms of the migraines, but not just that, they are also going to help with the person's own. I mean, the hyperagenergic symptoms of their hyperthyroidism will also help with the migraine symptoms. Bit of blockers, if a person has like angina and they have migraines, their blockers make a lot of sense. So just kind of keep that in mind. Calcium channel blockers, again, we can use them for angina, we can use them for variant angina, we can use them for hypertension. So just kind of keep that in the back of your mind. Although, you know, most times if we're dealing with a headache disorder, and we're trying to give a person a calcium channel blocker, we're thinking more along the lines of the non-dihydropyredine calcium channel blockers, like Vera Pameil, for example. And Vera Pameil is no use to money-shyee pretension. So I take that back, actually. Vera Pameil is something we can use for angina, for sure, not for hypertension. For hypertension, you're going to use more of the dihydropyredine calcium channel blockers, like aloe de pine, feloe de pine, and things of that nature.

To pyramid for seizure disorders, right? But it's also again pretty good for migraine, perphylaxis, right? And again, a quick thing I want to say is, what's the most common cause of headaches? That can just, you can get like these straight-up epidemiology questions on your exams. And then the most common of the big three headaches right between tension, cluster, and migraines. What is the most common? It's going to be tension. Remember, tension headaches tend to be bilateral. And then the one that is the second most common is migraines. I remember migraines tend to be worsened by loud sounds, light, photophobia, photophobia, stuff like that, they may be nauseous, they may be vomiting. And then remember, cluster headaches are the least common of the big three. The least common of the big three. Remember, those who tend to have like, is a unilateral headache, red eye. You know, these tend to have eye findings on the same side. Now, there are some distractors though that are afraid you probably want to keep at the back of your mind for your exams, if you're dealing with headaches, especially migraines. There are some distractors that you may think that, one, reading a migraine question, but they're testing something completely different. So, say for example, they can give you a question about a person that has like, this severe sodium onset headache or one side worsened by loud sounds and light. But this person doesn't have any history of migraines.

And they give you like a crazy high blood pressure in the chest. And they use them when you see stuff like that. I would really hope you're saying, ooh, divinings. This person probably has a sub-rocknoyed hemorrhage. You should get a non-contrast head seat in that case. Remember, sub-rocknoyed hemorrhage can cause like this thunder clapper headache. Another costly distractor that they can give you is a person that has again, pain very bad on one side of the head. But worsened by loud sounds, lights, yada yada yada, you're like, ooh, this is migraine. But you see this person having like this mastianastee fever, this crazy local cytosis, this sepsis-like picture. That person has meningitis. That person has meningitis, right? Probably back to meningitis. And then what if they give you a question about a person that is over 50? And if you're having these very severe one-sided headaches and things like that, if you see that you want to think about a brain cancer, a person probably has a brain tumor of some sort. You need to get some kind of brain imaging in that person. All right, so let's kind of work through some rapid fire thingies. I just wanted to kind of hit those topics with this rapid review. But let's run through some rapid fire things and then we'll kind of wrap this podcast up. So what if they give you a question about an obese guy that has a very loud P2 heart sound?

Remember, whenever you have a here a loud P2, first he has pulmonary hypertension, what's going on in this person's life? This person has obstructive sleep apnea. Although this person could also have obesity, hypogenitilation syndrome. So how do you differentiate between those two disorders? Well, just check their P-A-C-O-2, the P-L-L-D-A-C-O-2 during the day. So if you have daytime hypercapnea, that person has obesity, hypogenitilation syndrome. The management is pretty much the same. You're going to get a sleep study, you're going to get a polysomnogram. And then the person is going to be placed on CPAP. Okay, especially his personal pulmonary hypertension. If honestly, if they're pretty obese, you need to do something about that obesity. Okay, what if you get a question about an old guy, you know, that has like rising creatinine and he sleeps poorly at night because he always seems to get up a lot, he's going to be one P, one P, one P. This person has BP, he's been an hypersetic hyperplasia. So remember for this person, when you go ahead and check the oppose-void or is it all volume, it's going to be pretty high because they're not able to empty their blood, well, and off at all. And some other things you may see on your exam says, you know, this person, you probably want to put them on an alpha-1 blocker to open up the bladder next to the compete. But long-term, you can consider things like finasteride or detasteride.

Those are five-over-inductive inhibitors that decrease the production of DHT that can shrink the prostate and relieve the ABPH symptoms. Okay, now what if you see serious fatigue, sore throat, in a young female, what should you be thinking about? I would hope you're saying, oh, divine weight, this is infectious mononucleosis. This is literally infectious mononucleosis. And remember, for the half-infectious mononucleosis, you can do the monospot test. It's caused by EBV. And remember, people that have mononucleosis, if you give them a drug like ampecylline, they can have this full body rash. And a classic temptation on exams is to say, oh, because they have this full body rash, I can never give them ampecylline or amoxicine anymore. No, it is not an allergic reaction. Those people can literally get ampecylline and amoxicine in the future. Just one of those weird things, we now see this cost him any resources, please very, very high you to know for your exams. Okay, now what if they give you a question about like a young person, like a young male, the has sex with other men? And this person has chronic fatigue, weight loss, fever, myalches, you know, generaliselymphotonopathy. What is that? That's acute HIV syndrome. That is literally acute HIV syndrome. They love to test acute HIV syndrome on the exams. Obviously, for those people, you're going to test them for HIV. And then you're hopefully going to put them on highly active antiretroviral therapy. All right.

Now what if they give you a question about like very serious fatigue in a woman that has, you know, heavy menstrual bleeding and, you know, a bleeding time, so elevated and she has an elevated PTT. When you see something like this, I want you to think of iron deficiency anemia. I know you're going to be like, define this person's vulnerable and disease. Yeah, I know. Definitely vulnerable and disease. But the thing is our friends at the end being these, we don't even put vulnerable and disease as an answer. They may literally put iron deficiency anemia as an answer. So I know many of you can be scratching your heads like the vine really? Yeah, really. That, this iron deficiency anemia is causing fatigue. Anemia classically on the exams causes fatigue. So what's the link there? Well, first thing's first, this first thing has a Williams-Brand disease. That's an old zoom-out dominant disorder where you have a deficiency of a Williams-Brand factor. If you don't make a living from a Williams-Brand factor, then you're going to have a very, very bad time trying to do the first step of primary and most stasis. So those people's believing time is going to go up. But remember, Williams-Brand factor is like a protecting group. It's like a big brother. It's like a private security for factor eight. So when you lock the Williams-Brand factor, factor eight will have a shorter half-life. So your coagulation cascade will not work very great.

So your PTT, not your PTT, your PTT is going to be elevated. So these people tend to bleed, bleed, bleed, bleed a lot. If you bleed a lot, you're going to be losing a lot of blood. That can cause you to develop an iron deficiency anemia. That's going to make you become very fatigued. People that are anemic, they are classically quite fatigued. In fact, if you see serious fatigued on one that is pregnant, you should probably screen her for iron deficiency anemia. So, and you know, there are actually a couple of other things they can ask you with this iron deficiency anemia business. Like for example, what's going to be trove of the person's blood oxygen carrying capacity? It's going to be decreased, right? It's going to be decreased. I remember where you have anemia. You don't have an off-hymoglobin. If you don't have an off-hymoglobin, then you're not going to be carrying enough oxygen in your blood. Although what would be trove these people's SAO to the hemoglobin saturation on oxygen? It's going to be completely normal. That has nothing to do with anything. The hemoglobin saturation will be completely normal. What would be trove their PTT to AO2? That's also going to be completely normal as well, right? Because the fact that you have anemia does not mean that blood is on, like oxygen is unable to dissolve in your plasma. Just kind of keep those things in mind. What would be trove these people's heart rates? If you have chronic anemia, or we'll be trove your heart rate?

I hope you're seeing the findings going to be elevated, right? Because again, if your blood oxygen carrying capacity is diminished, your tissues are going to be hypoxic. Whenever there is tissue hypoxia, that's typically a company ban increase in cardiac output, because you want to produce those tissues better. Now, what if they give you a question about 35-year-old female that has been very fatigued for the last two months? She has deplopia, and she has blory vision, especially at night. I want to think about my estenia graphics, right? I remember I would have my estenia graphics. They have these anti-acidoculin receptor antibodies. And remember, for those people, not about idea to get a chest CT, just to screen them for thymomas. Thymomas have a very strong association with my estenia graphics. And remember, for these people, after they had diagnosed you've got to put them on pharmacotherapy, you want to put them on a drug like pyridosteeglina. Pyridosteeglina is an acerocholinesis inhibitor. That's going to inhibit acerocholinesis, you know, bump up your levels of acerocholine. So that you can now compete those nasty antibodies, those nasty autoantibodies that you've seen on the surfaces of the nicotinic acerocholine receptor. And remember, again, the nicotinic acerocholine receptor is an ion channel. Okay? It is not a GP or T-copyri receptor. It's one of these bizarre things that you may be like, oh, I only needed to worry about that on step one.

But then you get a step two C-key question, get a step three question, you're like, whoa, where did this come from? So whoa, I am telling you right now. Those nicotinic acerocholine receptors, they are ion channels. They actually some pretty high-yout ion channels I'll see you try to know for you exams. Number one is the nicotinic acerocholine receptor. It's an ion channel. And then number two is the GABA receptor. It's a chloride channel. That is rare benzoes and buried to its work. Remember, benzoes, the increase the frequency of opening of the GABA receptor. By beats of rates, increase the duration of opening of the GABA receptor. Don't forget those for your exams. The nicotinic acerocholine receptor transmits sodium ions. Something you want to keep at the back of your mind for exams. Okay. Now, what if you see chronic fatigue, bradycardia, in a female that is infertile? What are you thinking about? I hope you're thinking about a person that has hashylodos. Remember, if you hypothyroid, you're going to be very, very fatigued. You're going to be very, very fatigued. Very, very fatigued. And remember, they're going to be bradycardic because they're not putting beta-1 receptors on the surfaces of their cardiac cells. Remember, one of the jobs of T3 is to help you insert more beta-1 receptors on the surfaces of your cardiac cells. So, if you don't have enough beta-1 receptors being inserted, you're going to be able to respond to cardiac holomins like norepinephrine very well.

So, you're going to become a bradycardic. I wonder why are they infertile? Well, pretty simple. If you think about it, if you're hypothyroid, your T3 T4 is low, are you going to have negative feedback in the hypothylamus? No, you're not going to have that. So, your T-RH is going to skyrocket your thyroid tropine releasing hormone. Well, the thing about T-RH is that it's also very powerful stimulant for a prolactin production. So, you're going to have hyper-prolactinine. And prolactin is a very powerful inhibitor of genery. So, you're going to become an infertile. You're going to have a hypogonadotropic hypogonadism. What do I mean by that? Well, your gonadotropines are going to be low. Your genery is going to be low because prolactin is shutting it down. So, obviously, if your genery is low, your FSH will be low, your LH will be low, your estrogen, your testosterone is going to be low. So, you're going to have infertility because your HVGX is pretty much does not work. So, hypogonadotropic because your gonadotropines are low, hypogonadism because your actual gonad is not being stimulated. So, your gonad is not producing an alpha-sexy-sexy-romose. So, what if you see severe headache, brain bleed, a person that went to a pizza parlor, or a person that went to a winery, and this person has a depressed person that has, like, treatment resistant depression was recently studied on some kind of pharmacotherapy. But I hope you're thinking about MEOI toxicity.

Monamine oxidase inhibitor toxicity. I remember you're monamine oxidase inhibitors are going to be drugs like isocarboxazide or trinocyperamine. Trinocyperamine is spelled as T-R-A-N-Y-L-C-Y-P-R-O-M-I-N-E. And then isocarboxazide is spelled as ISO-C-A-R-B-O-X-A-Z-I-D. I believe that's the right spelling. So, remember, these things can cause a tyramine crisis. So, what's the pathophysic? Because many people just memorize it. Tyramine crisis, tyramine crisis, tyramine crisis. So, what's the pathophysic? Well, here's the thing. Normally, monamine oxidase in your GI tract breaks down tyramine. But if you're taking that monamine oxidase inhibitor, then you won't breathe down tyramine. You're going to reabsorb it in your GI tract. And tyramine is like a false, neuro-transparent, like, is like a false cadecolamine in a sense. Basically, what it does is that it displaces cadecolamine, like neurobeinephrine, from synaptic vesicles. So, if you're, it's almost like the carbon monoxide for your cadecolamine. Remember, carbon monoxide kind of hits up hemoglobin and then oxygen can bind. So, basically, what terming does is that it binds to synaptic vesicles, that contain cadecolamine, so it displaces them. So, those cadecolamine are just released into the synapse. They're going to get a mastinasty hypertensive crisis. Remember, we tend to get this from, like, cheeses, meats, wines, things of that nature.

Okay, so, I guess, as we wrap up today, I want to end up with people that have red skin. You know, people that have, like, skin flushing or skin that's just really red. This is, like, a very classic kind of USMLVNA. There are many things they go after with that. So, if they give you, like, an IV drug user that will study on pharmacotherapy, has red skin, think of vancomycin, right? Remember, vancomycin causes you to release more histamine. And histamine is a very prominent visual dilator, so that can cause you to have red skin. They give you a question about a person that has a narrow complex regular attack here with me. You're thinking about an SVT, a superventricular attack cardia. One of the ways you can rapidly abort an SVT is with adenosine. Adenosine is a very good, very amazing visual dilator that can cause you to have skin flushing. I mean, think about it. Why do you think your skin flushing is when you exercise? Why do you think that happens? Why do you exercise your muscles are working over time? So, you're breaking down ETP to ADP, ADP to AMB to adenosine. Adenosine is a very powerful visual dilator. And that's actually useful because if you dilute the vessels, the blood vessels that feed your muscle, you can get better proficient of that muscle, so you can keep working out. So, that's one of the reasons why your skin is flush. It's something you want to keep at the back of your mind for, for example.

And then remember, if they give you a question about a person that's trying to raise their HDL, and they're taking it like some supplement to get their lipid levels good, because think of my SM, because my SM doesn't only raise HDL. So, again, remember, it's the best at raising HDL, but it also lowers LDL, and it also lowers your triglycerides. But again, it's not as good at lowering LDL like your HMG query inductees inhibitors to their statins. And it's not as good as lowering your triglycerides like your P-PAR alpha, again, it's like your fibrates. So, things like Gen-Fibre-ZL, Fibrate, Glow Fibrate, things like that. But it can do those things. Think of niacin, think of niacin, niacin, niacin. And then they give you a question about a person, study on an anti-hypertensive, and they have peripheral adema, and their skin gets red and flushed, and what not. Think of calcium channel blockers. Calcium channel blockers, your dihydroperidine calcium channel blockers like amlodipine, felodipine, and things like that, they can cause flushion of the skin. Because remember, these things are very good at tearyolodilators. So, because the dilute your materials, there's going to be more blood flow through your body. That more blood flow is going to cause you to have a redden of your skin. You're going to have skin flushed. Although, remember, why do they cause that peripheral adema? Well, they cause it because by diluting materials, what are you doing to your systemic capillaries?

You're literally sending more blood to your systemic capillaries. As you send more blood to your systemic capillaries, you're going to increase the hydrostatic pressures within those systemic capillaries. That's going to cause fluid extroversition, you're going to get peripheral adema. Is there some way you could treat that? I've talked about this in previous podcasts before. You can give something that can dilute your systemic veniomes like ACE inhibitors. Because ACE inhibitors, when they dilute those veniomes, they're going to be pulling blood away from the capillaries. Because remember, your capillaries are fed by materials and they are drained by veniomes. If you dilute those veniomes, you're going to be draining those capillaries. You're going to bring down the hydrostatic pressures within those capillaries. That's going to reduce that fluid extroversition. You're going to have less peripheral adema. Now, what if they give you this reddening of the skin in a person that has, like, a retotis function or a person that has hypopituitarism, signs of hypopituitarism? Think of hereditary hemocromatosis. Because remember, in hereditary hemocromatosis, these people just have crazy, crazy, crazy amounts of iron reabsorption. All that excess iron reabsorption is going to cause problems. Because iron loves to generate free radicals. Those free radicals can cause damage in your pituitary.

So, in the half-signs of hypothyroidism, like bradycardia, and what in the half-signs of adrenaline and sufficiency, like they can have, you know, low blood pressure. Because remember, cortisol has a permissive effect on your sympathetic nervous system. So, you're going to have, so basically, those people are going to be very, not very visual active. Because they're in a cortisol-deficient state. Because, you know, they have hypopituitarism, so they're not making any city. So, they're not stimulating. They're adrenal cortex. So, they can have all these problems. They can have all these electrolyte anomalies. Because when you have a cortisol-deficiency, cortisol kind of works like an australian sense. So, when you have a cortisol-deficiency, you're probably going to have some kind of hyperchylenia. You're going to have some kind of hyponitremia. And remember, those people can also, you know, just have many, many different issues. But remember, they will not have skin hyperpigmentation because of the, because of their hypocortisolism. No, if these people actually have low levels of ACCH. So, please, let me take a step back. Because hair-dehydrohematosis causes your skin to be red. Because you have a ton of iron kind of running around in your body. Okay? That skin hyperpigmentation is not because of ACCH. If you have hypopitrytripsin from hair-dehydrohematosis, you're not going to have high ACCH.

Because again, many people think that, oh, when a person has low cortisol, their ACCH is going to skyrocket. And then they'll have skin hyperpigmentation. No, no. It depends on the cause of the hypocortisolism. If you have hypopitrytripsin, your pituitary gland is gone. If it's not working, you're not going to be making ACCH. If you're not making ACCH, you certainly are not making MSH, melanosystimulating hormone. Remember, those two things come from an ancestral malacolidinous pom-si. So remember, the cause of the hypocortisolism determines if you have skin hyperpigmentation or not. So say, for example, you have other sense disease, where your general glands have been torched by autoantibodies. Then, of course, you're not making cortisol. There's no negative feedback. But your anterior pituitary is still intact. So you're going to make a ton of ACCH. You're going to make a ton of melanosystimulating hormone as well. So you're going to have skin hyperpigmentation. But not so. Absolutely not so. When we're dealing with hypocortisolism because you have like a pituitary or some kind of hypothelanic disorder, just kind of keep that in the back of your mind. And again, you can have your reptile dysfunction. That's a very classy presentation of hereditary hemocromatosis. I remember it's an ultrasonic-issusive disease where you have a HIV mutation. And just reabsorb a ton of iron from your gut. And that just causes a lot of problems. That iron can also torch your pancreas.

So they can develop diabetes. They can cause, they can have many problems from those things. And then, final, we need to talk about, we see a person that has, again, ridding of the skin. And they have like hypertension. They have headaches. They have a lot of chronic or echereous, especially with showers. Think of police, I think, me a ver. Remember, that's a japtum mutation. They have a ton of hemoglobin. And so because they have a ton of hemoglobin, their blood is very viscous. If your blood is very viscous, remember, parcells, your total preferred resistance is going to go up. That's going to cause you to have a high blood pressure. And again, they'll have all these headaches because their blood is so thick, blood is belly-flowing in their brains. They can have his skin and all those things. Remember, those people can also get botcarous syndrome on the USM in the exam. That's like thrombosis of the hepatic vein. All right. I think I'm going to go ahead and stop here. There's a rapid review series. It's going to for long enough. But again, just real quick. I just want to know you want to go. But I'll encourage you to just listen to this real quick. So if you're interested in any of my USM-Ly courses for step one, I have like a 25-hour step one class in July. It takes place from the first of the fifth of July. And that class is also good for people that are taking step two or step three and they have poor basic science foundations. Or you failed your step one.

You should definitely take that class. But starting next week on Tuesday, I have a bunch of classes for step one of the way to step three. I have a test against strategies class. I have a on Tuesday, I have a bio stats class on Wednesday. I have a social sciences and ethics class on Thursday. I have a last minute review on Friday. The last minute review, though, is just for step two and step three. And these classes are all over Zoom. And then the week after that, I have a 20-hour step two, step three class. Obviously, also useful for people taking complex level two and three. And then starting from June 1st to June 14th, I have a 50-hour step two, step three class. That is a class that has a very limited attendance. I can't accept too many people into that class because I want to invest in everyone that attend. So there is definitely a hard cap on that. It's a 50-hour class. We go over like 500 multiple choice questions, make a lot of integrations, teach a lot of critical thinking. And that class is held once every year because it's such a huge time commitment. But again, I'm telling you, if you attend that class, there are many people that have attended it last year. They found it to be extremely helpful. So if you're interested, shoot me an email. And these classes are not lectures. There are all scenarios, exam style scenarios, NV Me style questions where you just become an expert at NV Me.

If you like the way explained things, explain pathophase, making integrations, you're going to love my classes. You're going to love, love my classes. I've meet separate podcasts where I talk about these classes. And if you want more information, you can shoot me an email. I can give you some more information. I also offer one on one tutoring. And I help with many of the things like the ERAS application, recommendation letters, personal statements, smoking interviews. And I tutor again, one on one for all the USML Es, all the complex exams, all the medical exams. And then I also have these podcasts on Apple, Google, and Spotify. So you can check that out if you want. And have a You Tube channel where I post videos that I make. And then finally, I have another website called divineinterventionlifelessons.com. Every week I post like one or two podcasts, usually two podcasts, where from a biblical perspective, I discuss a life lesson. So if you actually have an Apple podcast associated with that, it's called the divineinterventionlifelessons podcast. Again, the website is divineinterventionlifelessons.com. So just check that out. I think you'll find it to be extremely helpful. So I will see you in the next podcast. Again, I really hope that you enjoy this worksheet. And you use it to study and it helps you in the future. God bless you. I'll see you in the next podcast. Bye for now. Thank you.

Sensorineural hearing loss.

COL4 E5 gene mutation (Type IV collagen).

Aminoglycosides (Gentamicin), Platinum agents, and Salicylates (Aspirin).

Dopamine.

NSAI Ds or an N-set (e.g., Dihydroergotamine).

Calcium channel blockers (CC Bs) or potentially tricyclic antidepressants, as they treat multiple comorbidities.

Tension headaches.

Vancomycin (histamine release) or Adenosine (vasodilator).

It is a Norepinephrine-Dopamine Reuptake Inhibitor (NDRI).

Bupropion.

Fever, sore throat, fatigue, and generalized lymphadenopathy.

T3 is required for inserting beta-1 receptors on cardiac cells; deficiency leads to reduced sympathetic response.

Hypopituitarism (pituitary failure) does not cause hyperpigmentation because the pituitary is not producing MSH.

MAO Is (Monoamine Oxidase Inhibitors); they prevent the breakdown of dietary tyramine by gut flora, leading to massive release of catecholamines.

Nicotinic Acetylcholine Receptor (Na+ channel) and GABA receptor (Cl- channel).

It is a Norepinephrine-Dopamine Reuptake Inhibitor (NDRI).

Bupropion.

Fever, sore throat, fatigue, and generalized lymphadenopathy.

T3 is required for inserting beta-1 receptors on cardiac cells; deficiency leads to reduced sympathetic response.

Hypopituitarism (pituitary failure) does not cause hyperpigmentation because the pituitary is not producing MSH.

MAO Is (Monoamine Oxidase Inhibitors); they prevent the breakdown of dietary tyramine by gut flora, leading to massive release of catecholamines.

Nicotinic Acetylcholine Receptor (Na+ channel) and GABA receptor (Cl- channel).