DIP Episode 438 - USMLE Step 2/3 Rapid Review Series 91

All right, talk on my name is Divine. This is episode 438 of the Divine Intervention Podcast. In today's episode, I'm going to be continuing the rapid review series for the USMLE step two and step three exams. This is going to be series 91. Series 91. What if they give you a question about a 25-year-old male and they tell you that he presented, he was brought to the hospital by his wife because he had burned through their credit cards, spent a lot of money, and he had not been sleeping, and he had been just more talkative at home. And he tell you that he was given an anti-psychotic and another agent. Both that since all of this happened, he has been having polyurean polydipsia. And then you are asked, how could this have been prevented? Well, sounds a lot like this person has nephrogenic diabetes and symptoms from the use of lithium because this person, you know, they had many deep fast symptoms. Sounds a lot like bipolar disorder. When a person has bipolar disorder, they are acutely manic. When they come to the hospital, you're going to give them an anti-psychotic because it's going to work immediately and kind of calm them down. But you're also going to start a more stableizer. Lithium is a pretty good more stableizer. But remember that lithium can enter through the principal cell of the collecting duct to cause problems. And we enters, and the message of the signaling cascade of EDH is by the inek channel.

The inek channel, remember the principal cell of the collecting duct has two major channels. Has the inek channel that brings in sodium, and then he has the wrong key channel that brings out potassium. Our dose turn activates those processes. So our dose turn makes you bring sodium in through that inek channel, and you're in it potassium out through the wrong key channel. So lithium again, just going back to some college chemistry. Lithium is in group one of the periodic tables just like sodium. They literally have like one electron in the atom shells. So since that's the case, you know, they have very similar chemical properties. So they can, if sodium can go through that inek channel, you better believe that lithium can go through said inek channel as well. So it goes in message of the signaling cascade of the viso percent receptor. So you don't you don't respond to EDH. So how could you prevent that? Well, if you put a gate or if you put a security guard over the inek channel, the lithium will not get in unclosed problems. So what is the security guard? The security guard is going to be something like a millerite or triumtory. A millerite or triumtory. They're the potassium sparing diuretics, but they literally work maybe in inek channel blockers. Now what if they give you a question about a patient? They tell you that this patient has a history of e-fib and the patient was studied on pharmacotherapy a few weeks ago for chronic management of their symptoms.

And then you're told that this patient has, you have a lot of weakness, a lot of fatigue, and this patient, you know, is also gained like five pounds. And that this was, I mean like six weeks ago, in a replacement of pharmacotherapy. What should you be thinking about? I hope you're seeing old divine. This sounds a lot like a muterone. So remember, a muterone is kind of a high value drug to know for you exams. We use it for like a ton of stuff. Well, I exactly those a muterone work. I mean, the other one, the official thing it does is that it's a clast three, and I will explain why all these things that I said are true. It's a clast three anti-retinic. So it's a potassium channel blocker, block potassium channels. So because it's a potassium channel blocker, it's an anti-retinic, but it also has effects on many things. It can block sodium channels, can block beta adrenergic receptors. It can literally is like the ultimate anti-retinic. It blocks many different things. So this is a muterone toxicity. So what are some of the things you can get with a muterone toxicity? One, a muterone, notice it has iodine in it, amyodero, that iodine literally stands for iodine. So you can cause both hypo and hyperthyroidism. A muterone can cause both hypo and hyperthyroidism. That's something you want to keep in mind for for exams. This person has hypothyroidism from a muterone. Because remember, there's these wolf tricoph and your beast down effects.

I've discussed this in many other podcasts. So for the sick of time, since these are rapid reviews, I'm going to keep it in tune. But the wolf tricoph and the your beast down effects, those explain the hypo and hyperthyroid effects associated with amyodero. Remember, amyodero can also cause pulmonary fibrosis. It can cause pulmonary fibrosis. And maybe let me backtrack on the thyroid a bit. One easy way to remember the thyroid association is that literally what does your thyroid used to make thyroid hormone? Use this iodine. So it makes sense that amyodero can very easily collect in a person's thyroid gland and cause these problems. So just you want to kind of keep that in mind. And at least the hypothyroidism usually happens because you inhibit the organification step. You inhibit the organification step of thyroid hormone synthesis. So that's how amyodero can cause hypothyroidism. So that's why it presents gaining weight and all that stuff. And again, remember when you're a hypothyroid, you're going to have a few problems. Like you can have like a dimofilure extremities. You can have capotonal syndrome because all that when people are hypothyroid, you know, it begins to put them in a demeritous state. So you know, some of that a dimac can involve the capotonal they can get capotonal syndrome. And this will can gain weight because the metabolic rate kind of grants to a pulp. And they can even give you, you know, a person that your heart rate is less than 60.

Most times when the mbim is giving you a hypothyroidism question, the person is going to have a heart rate that's less than 60 because, you know, hypothyroidism really kills your metabolic rate. I mean, think about it, like the opposite of what you get with hyperthyroidism where thyroid hormone causes you to insert more beta-1 receptors on the surfaces of your cardiac myocytes. If you insert in more beta-1 receptors, this is going to raise your heart rate. So if you're hypothyroid, you have less beta-1 receptors in your cardiac myocytes. That's going to ignore your heart rate. So that's not going to be good, right? But hyperthyroidism raises your heart rate by putting more beta-1 receptors, hypothyroidism, it lowers your heart rate by, you know, basically you have less beta-1 receptors in your cardiac myocytes. So put that half amuterontoxicity, they can have hypothyroidism, they can have hyperthyroidism, they can have pulmonary fibrosis, amuterontoxicity fibrosis, it can cause like these weight pigmentation of the cornea, of the skin heaven. So those are all things you want to keep at the back of your mind with amuterontoxicity. But remember, amuteront, again, like I said, is a very high-value drug. You can use it in E-fib for rhythm control.

Although many times when people have E-fib these days, we're like, let's put this tri-read control instead, you know, with like a beta-blocker or a non-dihydroperiodine calcermin channel blocker, like very early beta-lodial tyrosine, because those drugs just have fewer side effects than amuter rune that over time is going to be completing the body and cause issues. So, but you know, rate control rhythm control, both of them are equally effective for E-fib. But you can also use amuteront for a person that has V-tac, and that person is hemodynamically stable, sorry. If you're pressing else V-tac, that's a white complex regular tacky rhythmia. V-tac, you can absolutely treat it with amuteront. You can absolutely treat V-tac with amuteront. That's actually pretty important to know for, for example, V-tac that is hemodynamically stable with amuteront. If you add V-tac, and you're hemodynamically unstable, that's where you do a synchronized cardioversion. Synchronized cardioversion, right? We call that direct-chorean-cardiversion or direct-chorean-comter-shock. Those all examples of synchronized cardioversion. And then if you had V-tac and you had no pulse, that's bad, right? Pressing is almost dead. In that case, you're not going to do anything crazy.

I mean, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, it, you're going to do an unsynchronized cardioversion. You're basically going to perform a different relation in those circumstances. Now, what if they give you a question about a patient? And they tell you that this patient was recently started on an anti-psychotic. And now this person is having trouble with movement. So they say, oh, they were pleased on this thing like a few days ago. And you know, they're having trouble with movement. The notice that they've been having like their hands shaking. And you know, they're just having a lot of movement issues and a lot of moto issues. If you see that, that's going to be Parkinsonism. Remember Parkinsonism is a pretty classically described side effect, pretty classically described side effect of the anti-psychotics, just because you're blocking the migra-striatal pathway. Well, when you block the migra-striatal pathway, again, you're going to have a stripper or middle symptom. So which one of them is Parkinsonism? So how do we treat that Parkinsonism? Well, we can treat that Parkinsonism with an anti-colonergic drug, something like Ben's tropine. The tropine is a most chronic antagonist that can be used in those Parkinsonian symptoms.

But if you don't see that as an answer on your exam, one thing you should definitely consider is dopamine agonist. So something like bromo-cryptin or carburegulin, that's something that'd be very helpful in that in that circumstance. I remember Ben's tropine, you don't just use it alone for Parkinsonism. You can also use it for acute dystonia. It's more like a second-line agent for acute dystonia. Typically, when a person has acute dystonia, you're going to go ahead and try Diphon hydramine first. It's an anti-histamine, but it has very powerful anti-colonergic activities. But if you don't see that as an answer, you really should consider Ben's tropine. Again, Ben's tropine is a most chronic antagonist that's really helpful in those circumstances. Now, what if they give you a question about a patient? And they tell you that this is like a 30-year-old female. She's in, she went into preterm labor, and at 31 weeks. And then you'll notice that she was given a drug to try to slow down the labor while she's loaded with appropriate pharmacotherapy for the baby to perform, fit along a tridian everything. But then they say that an hour or two hours after the person's pleased on this one, her therapy, the heart rate goes up a lot. What's the mechanism behind the elevated heart rate? What's the mechanism behind the elevated heart rate? I really hope you're saying, oh, divine. This person went into preterm labor. This person got a tocoletic. This person got a tocoletic.

And this tocoletic, the person probably got is my fadipin. I remember you can actually use endomethacin actually as a tocoletic. But when you start getting into the later parts of pregnancy, and you're getting to a little parts of pregnancy, so maybe for this question I should have used maybe like 30, she's at 32 weeks or something like that. So let's change the, I think I said 31 weeks, let's change that to 32 weeks. So the later part of pregnancy, you only use endomethacin. Endomethacin is a shift, is the shift tocoletic, but you only use it before 32 weeks. After 32 weeks, using endomethacin is not a great idea. Because endomethacin can cause a cause of a lot of problems. A shift of which is to close the doctor's arterial system. I mean, it's literally a cyclopsis, it's an inhibitor. That's going to be CRISPR's, the glandins, synthesis. That's going to close the doctors in uterine, and that would kill the baby, right? That's obviously not a good thing. When your doctor's arterial system to be open while you're still in the womb. So after 32 weeks, we usually use my fatty pin. My fatty pin is a dihydroperidine calcium channel blocker. So because it's a dihydroperidine calcium channel blocker, the thing it's going to do is that it's going to basically cause arterial dilation. It's going to dilute your arterial. So think about if you dilute your arterials, that's going to lower your blood pressure.

If you lower the blood pressure, your arterials are going to be like, wow, your blood pressure is low. So it will signal to the brain that, wait, my blood pressure is low. We need a sympathetic discharge. So that sympathetic discharge will be given back to the heart. And that's going to cause an increase in heart rate. You're going to get a reflex stachycardia. Reflex stachycardia is a very common side effect of really an immediate visual dilator like your dihydroperidine calcium channel blockers like my fatty pin for example, or like your alpha one blockers like Prasocene, Doxazocene and all those things. And then you can also find your hydrolyzein as well. So all these things can cause a reflex stachycardia. Now, I think this also kind of lense credence to why what a person has an eiotic dissection, one of the things we do is to give a beta blocker. The reason we love to give beta blockers is that in the eiotic dissection, think about it, the blood is literally ripping through the intima into the media. So one of the things you do when a person has eiotic dissection is to say, let me reduce the force with which blood is coming out of the heart. If I can bring down the force with which blood is coming out of the heart, then that blood is not going to rip through, literally, it's not going to rip through the intima as effectively. So you're kind of buying some time. So beta blockers are good because they'll literally slow down your heart rate, they'll reduce contractility.

So your heart will not be pumping with as much force because those are negative ionotropes. So if your heart is not pumping with as much force, the blood that's going to come out of it, I'd like to think of it as Wimpy blood. The blood is not going to be coming out with a ton of force. So since the blood is not coming out with a ton of force, it's not going to be ripping through that intima and getting into the media as much. And this precisely also explains why hydrolyzein is an awful idea when a person has an antibiotic dissection. Again, hydrolyzein is literally a viso-dialiter. It's an arterial viso-dialiter. When you dilute your vessels, you're going to lower your blood pressure, your bioreceptors are going to freak out. So you're like, okay, let me go ahead and give a sympathetic discharge to the heart. Well, that sympathetic discharge is going to primarily be beta-1 receptors. So as you hit those beta-1 receptors, your heart rate is going to go up. And also your force of contractivity is going to go up. That's not a good thing. Because the blood is going to be coming out of the heart from that reflex-dialiter, from that sympathetic discharge. It's going to be forceful blood. That blood is going to more likely rip through the intima and getting into the media.

Because the reason I would use any kind of big time viso-dialiter for this, we'd like to focus on hydrolyzing because it's one that pops up on exams and it simulates students consistently, consistently, make this mistake. You know, don't be one of those people. Because many times when people have aortic dissection, the blood pressure is going to be really high on your exam. Hydraulic zines, nobody want to be given to lower that blood pressure. I'm telling you, it's literally not one you want to be given to lower that blood pressure. It's not a good idea. I'll tell you that. It's not a good idea at all. Because again, it's going to bring out blood from the heart with more force. That more forceful blood is going to cause lots and lots and lots of issues for that person's heart. So just for the person's heart and the dissection. So just be careful, careful about that. Be careful about that. Be careful about that. That's just one thing I'm going to say. Be careful about that. And you know, I said earlier on that when a person has Parkinsonism as an anti-psychotic side effect, you know, because you've blocked the microsrattle pathway. I said that a second-line agent you can use is bromo cryptic carburetin carburegoli. Remember, bromo cryptic carburegoli, and those are dopamine agonists. They're used for things other than just Parkinsonism with anti-psychotics. You can use them for straight-up Parkinson's disease.

In fact, if you remember, when a person has Parkinson's disease, we try to not start them immediately on carbidopanlyphodopa. Because those are like the last line drops you can really use. So typically, you're going to start off with the other stuff like a monadine. You can start off with a dopamine agonist like bromo cryptic carburegoli. Because remember, Parkinson's, your substantiant migraines gone. So you don't really have much dopamine. So you're basically giving drugs that are actually dopamine, like carbidopanlyphodopa, or drugs that decrease the breakdown of dopamine, right? So like your MOP inhibitors like cellulogen or acetylene, or your comtein inhibitors. You've got a whole methyl transferase inhibitors like an tachypone and tucupone and tucupone and tucupone, the endympone. You give those drugs. Or alternatively, you can give drugs that increase the release of whatever little dopamine you're having in your brain like a monadine. Remember a monadine is a drug that was used for the flu back in the day. Well, there's like pretty much like 100% resistance, but hey, it's pretty good for treating a Parkinson's disease. So you know, you can start off with any of these things that you can use again, dopamine again is like bromocryptonal carburet cooling. Before you then go for the carbidopa, livo-dopanlyphodote end.

And with the livo-dopan, you know, does his own thing, but the carbidopa basically inhibits dopamine in the periphery, so that you don't convert that livo-dopan to dopamine in the periphery because in a half-part Parkinson's, the problem is low dopamine in your brain, not low dopamine in your periphery. So you want that dopamine to go to the brain. So you don't want that livo-dopan to be made straight up into dopamine by dopamine decarboxylase. So that's why you give carbidopa. I think of carbidopas like the beta-lactamines inhibitor that goes with livo-dopan. But in this case, you know, you're not attacking beta-lactamines, you're attacking dopamine decarboxylase. You shut it down. El-dopa, you basically increase its bioavailability to the central nervous system that way. And then the central dopamine decarboxylase, which is not acted on by carbidopa, can then convert that livo-dopan to dopamine and that can relieve solve your symptoms. So, Bremocryptin carburegoline again, the chemist for Parkinsonism, you can use them to treat straight-up Parkinson's disease. You can also use them for hyper-prolactinemia. In fact, to be honest, with you, people that have prolactinomas, the first line treatment, this very high of the first line treatment, or prolactinoma, is a dopamine agonist. Because remember, these dopamine agonists, dopamine literally inhibits the release of prolactin. Maybe as a sidebar question, what is the thing that increases the release of prolactin?

That's going to be TRH, thyrotropic releasing hormone. In fact, another thing for TRH, believe it or not, is prolactyrolase-infactor. That's why many times, when people are hypothyroid, they become infertile because if you're hypothyroid, your T30 T4 is low, there's no negative feedback. Your TRH is high, your TRH is high, you're allergic to release more prolactin because it's also called again, prolactyrolase-infactor. So, it will make sense then that, you know, you give a dopamine agonist, that's going to shut down prolactin production. When you shut down prolactin production, that's helpful. Most times, when a presence of prolactinoma surgery is not going to be the right answer on the exams, I'll say that again, many times when a presence of prolactinoma on your test, surgery is almost always not going to be the correct answer. Okay, so you can use dopamine agonists to treat prolactinomas, just something I want to throw there. Now, as I come to an end, I do offer one on one T30 T4, the USM in exams, step one, just step three, prickly and cool exams, third year, clerkship shelf exams. I have review courses for step one, I have one coming up next month. I have other review courses that are more for step one, just step three. Although the review course for step one is more for people that have like a very bad knowledge base. You know, some people, they think that well, they barely pass step one by the skin of their teeth, or they say they failed step one or whatever.

And they're like, ooh, okay, my knowledge base is just partially going to get better on step two, step three. It doesn't usually the way it works. You need to fix your foundation before you start progressing. So if you want to fix that foundation, I become very good at basic science again, from a clinical perspective, the step one review course is precisely what you need. You know, beneath step one resources, just give it information, but most times the USM is these days, even on step one, they're like super clinical. So if you want to learn the concepts from a clinical perspective, and not just a clinical perspective, like an exam based perspective, and you're learning test taking strategies along the way, and also along the way you're learning things on a very deep level, that's a class you want to attend. I think you're going to find it to be extremely helpful. And you know, so it's for step one, but it's also what people take in step two, step three, they have poor, poor, basic science backgrounds. Just basically if you if we're performing very poorly, you're dedicated period for step one, or you barely pass the phone by the skin of your teeth or you feel step one, if you're taking step two, step three, honestly, that's a class you should take. And then for step two, step three, I have a review course, it's a 20 hour course. We're just wrapping up the one for this month, but we're going to be having another one next month, God willing.

A 20 hour class covers a lot of very high-y old stuff for the exam, again in a clinical fashion. And again, you know me, I love to make integrations. You're not going to be getting lectures, you're going to be getting a lot of integrations. More than 90% of the courses straight up integrations. And you're going to be learning things again from an exam, exam perspective, exam perspective. And again, you see, I don't just like throwing facts at you. I'm going to actually explain what's going on, give you time to ask questions and things like that. And then you know, for step one, to step three, you know, I have some other courses that apply to all of them. I have my MBA me testing and strategies class. That's going to be coming up pretty soon. I'm actually going to make an announcement podcast on that shortly here. And then I have a bio statistics bootcamp. Again, if you struggle bio stats, most of the bio stats questions is these on exams. There are not questions where you're just plugging into a formula. Many of them are like reasoning questions. So if you want to again understand bio chemistry, I mean, bio stats from an applied perspective, applied bio statistics, right? Where you get a clinical scenario, you have to manipulate it, you get to an answer. You want to reason through those concepts. In the four hour bio stats bootcamp is exactly what you need. I have one coming up this Monday. And then I have social sciences and ethics class.

Because again, social sciences and ethics for step one, two, step three is now 10 to 20 percent of the exam. All this stuff about quality improvement, healthcare systems, communication, professionalism. Just all those weird things. Something that you really benefit a lot from by attending the class is a five hour class. That's actually going to be taking place this Sunday in the afternoon, afternoon late evening. So I mean, late afternoon. So if you are interested, there's still some spots for the Sunday class. The social sciences and ethics class is a five hour class. But again, I'm telling you, you're going to see with a clinical perspective, you have to learn certain very core cogent principles that are actually represented on the exam. I'll also be talking about a lot of ethics. So if you are interested in any of these classes, just shoot me an email and I'll be able to give you some more information. So thank you for listening to me today. Also, you know, help with your applications, more interviews, personal statements. I have these podcasts on the major podcasts up Apple Podcast Google Podcasts on Spotify. And then I have a You Tube channel, Divine Intervention, USM, many podcasts and videos. That's where I post the videos that I make. And I also post versions of this podcast on that platform as well. And then finally, I have a website called Divine Intervention Lifelesses.com. That's where I post the life lessons that I make.

You know, people say, oh, Divine, I love your life lessons. So I started a whole new website. There's actually an Apple podcast associated with it, Divine Intervention Life lessons podcast. Every week I post like two podcasts, about 10 minutes long ish typically 10 to 20 minutes long. And from a biblical perspective, I address a life lesson. So thank you for listening to me today. I hope to see in the next episode episode of episode four thirty nine. Have a wonderful weekend. God bless you. Bye for now. Thank you.

Lithium enters the principal cell of the collecting duct through the E NaC channel, interfering with sodium reabsorption and causing polyuria.

Amiloride or Triamterene (they block E NaC).

It can cause both hypo- and hyperthyroidism.

Bradycardia (Heart rate < 60 bpm) because the metabolic rate is slowed, leading to fewer beta-1 receptors in the myocardium.

They cause a drop in blood pressure, triggering reflex sympathetic discharge and massive tachycardia/increased contractility, which increases shear stress on the tear.

Dopamine agonists (e.g., Bromocriptine).

Potassium-sparing diuretics (Amiloride, Triamterene).

They mimic/replace dopamine activity. In prolactinomas, they inhibit the release of prolactin.

Methotrexate (MTX) and Amiodarone.

Hypothyroidism lowers heart rate by reducing beta-1 receptors; Hyperthyroidism raises heart rate by increasing beta-1 receptors.

Carbidopa inhibits peripheral dopamine decarboxylase, preventing the conversion of levodopa to dopamine outside the CNS, thus maximizing central dopamine availability.

Endomethacin should only be used before 32 weeks gestation because after this point, it can cause premature closure of the ductus arteriosus.

Potassium-sparing diuretics (Amiloride, Triamterene).

They mimic/replace dopamine activity. In prolactinomas, they inhibit the release of prolactin.

Methotrexate (MTX) and Amiodarone.

Hypothyroidism lowers heart rate by reducing beta-1 receptors; Hyperthyroidism raises heart rate by increasing beta-1 receptors.

Carbidopa inhibits peripheral dopamine decarboxylase, preventing the conversion of levodopa to dopamine outside the CNS, thus maximizing central dopamine availability.

Endomethacin should only be used before 32 weeks gestation because after this point, it can cause premature closure of the ductus arteriosus.