DIP Episode 381 - Some HY Pharmacology Vignettes for Step 2CK/3

Okay, welcome. My name is Divine. This is episode 381 of the Divine Intervention podcast. And into these podcasts I'm going to be visiting a topic that I'm going to be calling higher from Acology Vignettes for the USML Step 2 CK slash Step 3 exams. Okay, higher from Acology Vignettes for the USML Step 2 CK Step 3 exams. Okay, now before I go into my discussion, if you're taking your USML Step 2 CK or Step 3, or complex level 2 or 3 exams within the next one month, I do have courses that will be very helpful to you. I have an MBA Me Testicking Strategy course. It's going to be taking place on the 22nd of April from 5 to 7 30 PM Pacific Standard Time. So that's each to 10 30 Eastern Standard Time. PM in the evening. And then the 20 hour course and really the Testicking Strategy course I guess I would say is being taken by tons of people, right? We discussed like very methodical approaches to avoiding MBA Me traps, getting useful information from questions, dealing with situations where you are able to narrow down your answers to two answer choices and you're wondering which one to pick. We talk about how to answer ethics questions. We talk about how to cross out answers that make no sense or answers that make that sound good but actually wrong. And then I also have a 20 hour step 2 CK step 3 course. That's going to be taking place on the 23rd and 30th of April. So half 10 hours each day is going to be from 8 a.m. to 6 p.m. Pacific Standard Time. So that's going to be from 11 a.m.

to 9 p.m. Eastern Standard Time. Again, all these courses are going to be via Zoom in this course. So going to be reviewing internal medicine, PEEDS, surgery, OBGYN, neuropsych, biostatistics, ethics, communications, healthcare systems, professionalism, and also multi-systems, processes and disorders. So if you're interested in any of these courses, just shoot me an email through the website and I'll be happy to give you more information. You may notice that the test against strategy courses on a Friday evening and then the 20 hour course is divided between two Saturdays and trying to do that so that I can be more accommodating of people's schedules. Okay, so let's go right into the vignette. So what if they give you a question about a patient and they tell you that this patient is brought to the emergency room because her friend found her vomiting and you know she has like significant red-o-pocodrant pain and the difference is that the last time she saw her doing well was yesterday. But that today you know she has been, she found her in our apartment, she was passed out, she was vomiting, she looked very sick. And then they give you some labs and you notice that the ESDLT is like crazy crazy crazy crazy high. So what are you thinking about in these circumstances? Well, I really hope you're saying hum, divine. It sounds like this person has a sedominofin toxicity. Right? So remember I said a menophen is very good at messing up a person's lever, right?

It's a common thing that's used by many people when they want to commit suicide. Right? So the key thing you want to keep in mind with a sedominofin is that a sedominofin is not an NSAID. That's like the very first thing I want to establish. Many people mess up a sedominofin on exams. But a sedominofin is not an NSAID. Okay? It works like an NSAID, but it is not an NSAID. Right? So the thing he does is it inhibits, you know, it inhibits the synthesis of prostaglandins. What is mostly a centrally acting agent? It works in the hypothalamus. Okay? It works in the hypothalamus. That's very high. It works in the hypothalamus. Right? So it decreases that sensation of pain. It's a very good anti-piratic, very good analgesic. Right? But it doesn't work like regular NSAID. Right? It doesn't work like regular NSAID. But remember, you can explode your liver because if you take a ton of it, you'll make this metabolite known as any PQI. Right? Any PQI or napkin. Some more calling napkin. Any PQI. Right? So any PQI is a very powerful oxidizing agent. So it can cause neck curses of your hepatocytes. It can cause liver damage. Right? It can cause liver damage. Now, one of the ways you can rescue is by using an acetyl cysteine. Right? Remember an acetyl cysteine will basically help you resurrect your glutathione. Right? Because remember, glutathione, that glutathione system helps you deal with oxidative damage. Right? Helps you deal with oxidative damage in the body.

So by regenerating that glutathione system, right? And acetyl cysteine is helpful in that in that regard. So again, acetylmenophen, you know, again, can be used for suicide purposes. That's a common use on exams. Right? And it can cause hepatic neck curses. Right? Like the central lopula hepatic neck curses. Again, very high yield to know those things for purposes of exams. Now remember, there are so many of the things you can also use acetylmenophen for an exam. Right? So you can give you a question about a child that, you know, had like a February viral illness, right? And then had seizures, right? That's like a, and the seizures are for less than 15 minutes. That's very important. Less than 15 minutes. Right? That's a February seizure. February seizures. Going to go ahead and give acetylmenophen. Right? And then in terms of pharmacotherapy for the management of osteoarthritis, acetylmenophen is still first line. Again, I don't even see some resources say NSA, NSA, NSA, that's true. Right? But an in-be-me exam, which is what the spot cast is for. I'm not, none of this is for clinical anything. So in-be-me exam purposes, right? You see that acetylmenophen is still the first line medication in terms of pharmacotherapy. Many times when people have osteoarthritis, you're gonna try stuff, you know, like exercise. You're gonna try to strengthen like their, their, their, their thymus also so that you can hold up the anneagron as well and things like that to ultimately help them.

Okay? So acetylmenophen, that's kind of like a big thing on a keeping mind, right? Basically when, when you see a question that involves giving like pain control, but you're like, huh, I don't feel comfortable using an inset. Acetylmenophen is probably a good idea in those circumstances. Okay. Now, what if they give you a question about a patient? They tell you that the patient was recently started on some kind of anti-hypertensive. And then you notice that after the patient was started on that anti-hypertensive, like two, three weeks later, the acryptin is risen up astronomically. And they say the abyssalin was like 1.1 and I was like three, right? And then you also notice that that creatinine has, it has like double or something like that. When you see something like that, I mean, the buenas like, like basically your buenas gonna be a lot, right? So when you see something like that, what should you think about? Well, I would really hope you're thinking about EC inhibitor toxicity, right? EC inhibitor toxicity. So what's the deal with EC inhibitors? Why is this person's creatinine rising with this ACE inhibitor? Well, there are many good reasons for it. But probably like the big one is that we know that ACE inhibitors, they are very powerful dilators of the efferent material, right? So just look at it. Again, remember, we have the kidney system. We have the afrin material leads into the glomerular capillaries, which leads into the efferent material, right?

That's an arterial portal system. It's a system of capillaries that are fed by an arterial and drained by an arterial, right? Remember, that's kind of weird compared to the rest of the body, right? Most of the body have a capillary system that's fed by an arterial drained by a venial, right? But here, you have a portal system. Portal systems arise where you have a blood capillaries of capillaries that are fed and drained by the same kind of vessel, right? Usually use those when you're in a very relation, right? So like in the liver, we have like the venous portal system, right? Where we have veins, we have the portal vein draining into the sinusoidal capillaries that line the hepatocytes. And then those ultimately drain into the hepatic vein, right? That's a venous portal system. Remember, we also have a portal system in the brain with the hypothalamus and stuff. That's a venous portal system, right? But the kidneys, we have an arterial portal system, right? The glomerular capillaries are fed by an arterial. That's the afrin material and they are drained by an arterial. That's the efferent material. Again, you'll find portal systems where you want to do like very heavy regulation of stuff, right? So if you think about it, right? East inhibitors, they are dilators of the efferent material. Okay. So why does that matter?

Well, if you dilate the efferent material, you can already begin to see that you're going to be reducing the hydrostatic pressures that exist within your glomerular capillaries. If you reduce those hydrostatic pressures, then you're not favoring filtration, because you need hydrostatic pressures within your glomerular capillaries, right? To filter stuff out of those glomerular capillaries into women's space, right? So that you can ultimately become urine or whatever. So if you're lowering those hydrostatic pressures, you're killing the creatinine, right? Now, that's not a big deal in most people, right? But if, for example, you happen to have bilateral red and all other stenosis to start, right? So you already have red and all other stenosis. Remember, you're in all other stenosis. You're not going to be profusing your kidneys well at all, right? So your afrin material is not getting enough blood. So your glomerular capillaries are not getting enough blood either, right? So the thing that's going to be happening in these people is that you're going to have, they already have something that is killing, right? Because by not sending enough blood to your afrin materials, right? You're ultimately reducing the hydrostatic pressures in the glomerular capillaries. When you add like a double problem in the sense of dilating the efferent materials by way of taking an is inhibitor, one angiotensin-2 receptor blocker, then you're basically giving a double hit.

You're giving two things that will kill the person's GFR, right? That's going to raise the creatinine, raise the BUN, right? And the person can go into fluorid-renofilium, right? So remember, this is one of the reasons why is inhibitors, another good idea at all, in people that have bilateral red and all other stenosis, right? Not a good idea. And they remember that is inhibitors, right? They have the ability to cause like dry cough, right? That's many times a limiting side effect for some people. And then people are like, you know what, we're going to go ahead and take an angiotensin-2 receptor blocker instead, right? Because again, why do is inhibitors cause this dry cough? Well, remember, it's all in the bradykining, right? It's all in the bradykining because remember, angiotensin-converting enzyme has the ability to break down bradykining, okay? Bradykining causes a dima, it, you know, stimulates your, like stimulates coffee and things like that, right? So if you inhibit ACE, well, bradykining is going to build up, you're going to run into a lot of trouble with dry coughs. In those circumstances, you're going to use an angiotensin-2 receptor blocker, right? Now, remember that ACE inhibitors, right? So I guess we're talking about this bradykining and ACE inhibitors. Might as well talk about a disease where they can tell you about like a family, really, just really bad reactions to like ACE inhibitors.

And many times these people are going to have like swelling of their face, your lips, they're going to have abdominal pain, just because of intestinal dima, right? Like mucosa la dima and things like that. When you see this, I would really hope you're saying, hmm, divine. This person has hereditary angiodema. Remember hereditary angiodema arises from a C1 esterase inhibitor deficiency, right? A C1 esterase inhibitor deficiency, right? It's actually a lot of it's more dominant in heritins. So the thing that happens in those people is they literally have a deficiency of an enzyme called C1 esterase inhibitor. Notice I did not see C1 esterase. I said C1 esterase inhibitor. When you have a deficiency of C1 esterase inhibitor, right? You're going to have a big buildup of, you're not going to be able to bradykining. But that's not a big deal because guess what? And you're tensing, converting, enzyme can also help, right? So for those people, as long as they don't take acin inhibitors, they're fine. But when they then decide to take acin inhibitors, those acin inhibitors are going to bump up their levels of bradykining, right? And that's going to cause significant problems, right? And they're going to get in trouble, right? So that's hereditary angiodema. Those people should not take acin inhibitors. Now remember, acin inhibitors on in-beam exams are also just pretty good for hypertension, right?

Especially when you have hypertension and some kidney problem that kind of tags alongside, right? So say for example, if you're seeing a hypertension and like an end-stitular disease, you know, acin inhibitors will be good, right? Or hypertension and they have like diabetic nephropathy, right? Acin inhibitors will be good in those populations, right? Because again, by diluting that efferin arterial, right? You're essentially reducing the hydrostatic pressures in those glomerular capillaries. That essentially gives the kidney arrest, right? So the thing is, these drugs are renal protective in a sense, right? Because they prevent hyper-filtration injury. The way I just kind of think about it, right? So let's assume you're in Libreon James, right? All Libreon James is, in my opinion, the best basketball player in the world, the best person that has ever played basketball, at least you're on a professional level. Search for Chicago Bulls or people, but anyhow. So when you, if Libreon is playing like heavy minutes, let's say like the 72 game NBA season, he's playing like 40 minutes every night, right? That's going to wear him out. But Libreon is going to be a lot more spry when he's only playing like, let's say he's playing like 20 minutes a night, right? Then he'll be much better prepared for the postseason, considering we're himself out all through the season. Kind of the same thing as your kidneys, right?

Ace inhibitors, because they lower the hydrostatic pressures in your glomerular capillaries. Your glomerular capillaries don't have to work as hard, right? It's almost like you're kind of saving them for the glomerular postseason if such a thing exists, right? So basically those kidneys are chilling, right? So it's renal protective. Yes, they're going to still be getting damaged because you have diabetes or whatever is going on, but it's going to be at a much slower rate, okay? So this is why Ace inhibitors, they are very good in people that have hypertension and some comorbidity, right? Like diabetes, some kidney related comorbidity, right? So like if a person has diabetes and they're hypertensive, Ace inhibitors will be a first-line agent in those people, right? Because again, they're renal protective, right? They're renal protective. Now remember, if a person has hypertension and they're African-Americans and so they have hypertension, the African-Americans, and they have like no kidney thing going on. They just have like just straight up essential hypertension, but the kidneys are completely fine. I would encourage you to not pick Ace inhibitors or ARBS as a first-line anti-hypertensive in those people, right? Again, the only time you should give an African-American or an Indian exam, an Ace inhibitor or an ARB is if they have something that torches your kidneys, right?

Or if they have a situation like, again, just if they have a situation that demands that they take an Ace inhibitor, then you can give them that Ace inhibitor. But if they just have guardian variety, hypertension and really know the comorbidities that weren't taking an Ace inhibitor, then those people shouldn't be given Ace inhibitors. That's actually very high you to know for, for exams, right? Now remember, Ace inhibitors, they also one of these drugs, right? That again help with diabetic nephropathy, right? Because again, remembering diabetic nephropathy, you have those chemo-stale, well-seen nodules in the kidneys, right? Pretty damaging to the kidneys. In fact, diabetes is probably like one of the most common causes, it's very high you to know. It is one of the most common causes of institutional disease in the US, right? Hypertension is also another pretty common one, right? So if you gave Ace inhibitors or ARBS to those people, right, you're going to protect those people's kidneys. Now also do not forget that Ace inhibitors, they are one of the drugs that improves survival in heart failure, right? There are many drugs that improve survival in heart failure, right? Like your beta blockers, like my toporal law, carvedi law, be super law, right? Your, your, your, outdo store and antagonist, right? So drugs like Spurano-Lactone and I play a known also improve survival, right? You like so somebody that nitrate hydrolyzing combo, right?

That's bi-deal, also improve survival, right? Or when you do inserting people, especially people that have like a YQRS, right? Cardiac risk synchronization therapy has the ability to improve a survival, right? And then remember, drugs like Intrestore, right? You know, these drugs that are like Ace, they're called like Arnie's, right? Like it's like a combination of like an ARB, like Valsartan and then they're realizing inhibitors like Sacubitrile, right? Valsartan's or Cubitrile, if you combine those drugs together, they actually do improve survival in people that have that have a heart failure, right? So Ace inhibitors are one of those drugs that have the ability to improve survival in heart failure, right? And then please, please, please, don't forget, they give you a question about a person that whenever they step out in the cold, if your hands get, you know, I don't know, like blue, your hands get like blue, you know, they kind of get some, not again, they're in their extremities in their digits, right? And they tell you that this person has like a long history of GERD, right? That requires like DLEPPI therapy, right? And then they tell you that this person's blood pressure is like 290 over 200, like some crazy high blood pressure, right? And really, we'll wonder those circumstances, you're thinking of like a sclerodermarino crisis, right? Remember, I just described some of the, some of the antecedents of the crest syndrome, right?

Where they have like calcylosis, they have renotes phenomenon, right? They have us over geodesmotility, right? And they have, uh, tendentutations, right? So those people remember, they can get a renal crisis, they can get a sclerodermarino crisis, uh, sclerodermarino crisis, the drug of choices and Ace inhibitors, Ace inhibitors are extremely useful in those, in those people. It lowers the blood pressures, right? And it actually improves morbidity in the cellular of a sclerodermarino crisis, right? So again, that's something higher to kind of keep keep on the back of your mind there, right? And then remember, it's an easy inhibitor, something you want to give to a person that has like, I don't know, like, uh, that's like pregnant, well, I hope you're saying no, right? Because again, they can give you a question about a woman that got pregnant, uh, you know, she has a huge rough hypertension, she'll be taking her prescriptions, doesn't see the doctor regularly. And then they tell you that she's pregnant and she has oligohydramials. Well, what happened? Well, it's that Ace inhibitor, that Arab that's, you know, ultimately causing problems, right? Um, remember, probably key thing to know here is that Ace inhibitors and Arabs, they are tear-out agents, you don't give them to pregnant women, because they can cause renal damage in the fetus. If you cause renal damage in the fetus, then the fetus is not going to be making urine at all.

If the fetus is not making urine, then the source of amniotic fluid has pretty much dried up, right? The source of amniotic fluid has pretty much at that point dried up, dried up, right? Because remember, babies urine eats, that's what constitutes amniotic fluid, and then they swallow it, and then the urine eats, and that forms amniotic fluid, and then they swallow it. So if you're preventing the baby from urinating because the akines don't work, because you give mom an Ace inhibitor and Arab, or mom took it in advertently, right? That can cause renal damage in the fetus, right? That can cause renal damage in the fetus. That's something you certainly want to know for the purposes of your exams. And then, what did they give you a question about 70, no, like 35-year-old female, you know, the tale that she's hearing voices, and things like that, right? So they tell you that you started on her peridol, but then she starts having like pog-willing, starts having, you know, like a poverty of speech, she's not speaking very well, she has pog-willing, she has all these problems, right? When you see things like that, or she's very rigid, you want to think of a person that has a drug-induced Parkinsonism, right? The drug-induced Parkinsonism in this case is from the halloweparidol, right? The halloweparidol is causing a drug-induced Parkinsonism, a drug-induced Parkinsonism, a drug-induced Parkinsonism, an anticycotic. So in those circumstances, when people have Parkinsonism, right?

The thing you typically want to do is you want to give them a most chronic antagonist, right? So you can give them something like Benstropin, right? Or you can give them Trihexifenedyl, Benstropin is spelled B-N-Z-T-R-O-P-I-N-E, and then Trihexifenedyl is T-R-I-H-E-X-Y-P-H-E-N-I-D-Y-L, Trihexifenedyl. That's a, those are both, you know, cholinergic receptor blockers, right, that are helpful in that. But if you don't see those as an answer, what answer can you pick? You can pick a dopamine agonist, right? For treatment of Parkinsonism, right? Remember Parkinsonism is one of those extra pyramidal features of side effects of taking an anticycotic, right? So you're going to see people take drugs like bromo-cryptin or carburegulin, right? Bromo-cryptin or carburegulin, right? So these drugs, they're actually pretty helpful, right? Because again, they can actually help with this, you know, Parkinsonism from the anticycotic, but they actually also help with like just real straight-up Parkinsonism, right? Real straight-up Parkinsonism. People that have real straight-up Parkinsonism can take, especially early in the course, they can take a dopamine agonist like bromo-cryptin or carburegulin. Now don't forget that bromo-cryptin or carburegulin are also pretty useful drugs in the management of prolectinomins, right? When a person has a prolectinoma, in general, you want to put those people on a dopamine agonist, right?

Let me say this right now, it is extremely rare for surgery to ever be the right answer as therapy for prolectinoma or nambium exams. When nambium exams, when a person has a prolectinoma, right? The thing you're going to do, right? The thing you're going to do in those circumstances is, you know, obviously you see the prolectin levels are very high and then you're going to get an mRNA of the brain with contrast, you're going to see the tumor, right? Remember those tumors can compress the optic chaiosimmon cause a bite temporal homo-anopsia, right? Sorry, a bite temporal hemianopsia, right? A bite temporal hemianopsia, right? So that's one thing that they can cause, right? But these prolectinomins, again, you treat them with dopamine agonist because anodinin for dopamine is prolectin inhibiting factor. So you give a dopamine, when you give a dopamine agonist like bromo-cryptin or carburego lean that can certainly help with downregulating, prolactin production. It actually fixes the problem for most people. I remember people that have prolectinomins, these people is going to be really hard for them to get pregnant, right? Or you know, the men will have like low libido on all those things. Well, what's the reason behind that? Well, the reason behind that is prolectin, it has a very powerful inhibiting effect on GNRH, right? So it lowers your GNRH. So by lowering your GNRH, it's going to lower your FSHLH and it's going to lower your ability, right?

To make things like estrogen, right? So because you're going to drop in the low, your FSHLH is low, your estrogen is low, this is going to be an example of a hypo-gonadotropic hypo-gonadism, okay? Hypo-gonadotropic hypo-gonadism. So I think I'm going to stop here. Again, I'll have more podcasts like this where I just go over some from a college covenants for a step 2 CK step 3 and then we'll kind of go from there. So as I draw the end of every podcast, I do offer one or one two-year-old for many exams. Step one, step 2 CK, step 3, pre-clean climatical exams, 30-ish-off exams. I took her for the internal medicine, body exams and injury and exams and then if you want to help with your ERAS applications, I've worked with tons of people on the ERAS applications, I've worked with lots of people that have matched, that are residents all over the country, in very competitive specialties, very competitive hospitals. So if you're interested in any of those things, I feel free to reach out to me. I've worked with people from pretty much, I'll see most people like 95% of the disciplines that are out there and then I also offer review courses. Again, I offer like my 75-hour step 2 CK step 3 school, also obviously for complex level 2 and 3. That's going to be in the first weeks of the month of May, is capped at 40 people. I made a specific podcast on that.

It's a 75-hour school, but it's a very in-depth, very comprehensive, extremely high-level review for step 2 CK step 3 or complex level 2 and 3. And then I also have my monthly review courses, I have again the test taking course on the 22nd of April and the 20-hour course between the on the 23rd and the 30th of April. So if you're interested in any of those things, just shoot me an email through the website and I'll be happy to give you some more information. And then I also have these podcasts on Apple podcasts, some Google podcasts on Spotify, at least the most recent 150. If you want everything from Episode 1, all the way to the present time, just check out the website, Divine Intervention Portcasts within s.com. And then I also have a You Tube channel called Divine Intervention, USMLE, Podcasts and Videos. So again, if you go on that website, I mean, if you go on that You Tube channel, you can find the videos that I make. And then finally, I have a new website called Divine Intervention Lifelesses.com. Divine Intervention Lifelesses.com. In on that website, I post like Bible-based teaching in the form of podcasts, right? You know me, I love audio-visual learning. So in the form of podcasts, most of them are like 10, 15 minutes long, they're like devotionals, you can listen to, you know, use this Bible-based teaching to give some solutions to certain problems that humanity is faced. So I even have the podcasts as well on Apple podcasts.

If you go on Apple podcasts, you see, referred to as the Divine Intervention Lifelesses Podcasts. So thank you for listening to today's podcast. I wish all the best. I'll see you in the next episode. God bless you and thank you.

Acetaminophen (APAP).

NAPQI (N-acetyl-p-benzoquinone imine).

N-acetylcysteine.

The efferent arteriole.

They increase bradykinin levels, which is the underlying cause of the severe swelling/angioedema.

Hyperfiltration injury (by lowering glomerular hydrostatic pressure).

NAPQI formation, which depletes glutathione stores.

N-acetylcysteine (NAC).

AKI due to efferent arteriole dilation reducing glomerular hydrostatic pressure.

Accumulation of bradykinin.

Cholinergic antagonists (e.g., Benztropine) or Dopamine agonists (e.g., Bromocriptine).

Risk of fetal renal damage leading to oligohydramnios.

NAPQI formation, which depletes glutathione stores.

N-acetylcysteine (NAC).

AKI due to efferent arteriole dilation reducing glomerular hydrostatic pressure.

Accumulation of bradykinin.

Cholinergic antagonists (e.g., Benztropine) or Dopamine agonists (e.g., Bromocriptine).

Risk of fetal renal damage leading to oligohydramnios.