DIP Episode 612 - USMLE Step 2/3 Rapid Review Series 125

All right, welcome. My name is Divine. This is episode 612 of the Divine Intervention Podcasts. In today's podcast, I'm going to be going over, I'm going to be continuing the Rapid Review Series. First step 2, see can, step 3. This is going to be series of 125. Again, I know I started a series on medical image and God will you, we're going to continue that. So let's jump right into it. So what if they give you a question about a patient? And you're told that this patient, you know, presents, you know, he has not seen a physician in the last three years, but that is coming in today because his abdomen has been swallowed for the last two months, and the swelling has gotten progressively worse. And you're also told that, you know, abdominal examination discloses a fluid wave and all these things. And then the ask your risk factor question, they say, which of the following is the most important risk factor for this patient's presentation? Well, I would really hope that you're going to pick the answer that talks about alcohol consumption, alcohol consumption. Right. So this person has probably developed cirrhosis and that cirrhosis has led, I mean, has led to poor, high pretension, which is creating the abdominal complaint that the patient has. Right. Remember alcohol causes a lot of problems, right. Literally causes a lot of problems.

Like literally after smoking alcoholism is the second most, you know, common preventable risk factor for death and just the bad quality of life in the US. So by quality of life, I mean something more like morbidity, right. So alcohol is like number two. What do you think is number one? Number one is going to be smoking, right. Number one is going to be smoking. Right. There are so many ways they can test alcoholism on your exams, right. Alcoholism on your exams. Right. Like for example, they can test it in the context of fetal alcohol syndrome, right. Alcohol is the most common tear hydrogen. Oh, really? Yes, it is. Alcohol is literally the most common tear hydrogen, right. And it can cause you to have cirrhosis, right. All that cirrhosis can damage the liver that can lead to hepatoceloocrosinoma, right. That can lead to things like hepatic insect fallopathy can lead to things like poor hypertension with the risk of adjuvary season, all these problems, right. Alcohol can cause many, many, many issues, right. Many issues, many, many issues, right. But remember, smoking is the number one preventable cause of morbidity and mortality in the US, right. And again, what are the associations with smoking? Smoking is the biggest risk factor for so many problems, right. Is the biggest risk factor for our cardioid infarction? Is the biggest risk factor for so many cancers, renacel carcinoma, pancreatic cancer, bladder cancer, lung cancer, right. COPD, right.

Smoking is the biggest risk factor, peripheral arterio disease, smoking is the biggest risk factor, renal autostenosis, smoking is the biggest risk factor, right. Smoking is the biggest risk factor for so many things you could see tested on your exams. Is the biggest risk factor for many things you could see tested on your exams, right. And one lab that I think I want to emphasize that you want to make sure you know with alcoholism is that alcohol is going to raise your GGT. Alcohol is going to raise your GGT. Remember, there are two causes of increased GGT on the US Emily's. Number one is going to be obstructive liver disease. But number two is alcoholism. So why does alcohol elevate a person's GGT? Well, the thing is GGT, also known as gamma glutamol transfer is an enzyme we see a lot in the mitochondria. And the thing is alcohols are mitochondrial poisons alcohols are literally mitochondrial poisons because they are mitochondrial poisons. They can cause you to get in a lot of trouble, right. They can cause you to you know the attack that mitochondria that mitochondria has to kind of let go of many things. And as a let's go of many things. One of the things that let's go of is GGT, gamma glutamol transfer. So your GGT levels are going to rise up. That's actually pretty high yield to know for your for your exams, right. And remember also another lab they love to test on the US Emily's with alcoholism. If it is an alcoholic, their AST is going to be greater than their ALT.

I'm going to say that again. If a person is an alcoholic, their AST is going to be greater than their ALT. Now, I know many resources and many people memorize, oh, AST to ALT greater than two to one greater than two to one. Again, the US Emily's they're not stupid. They realize that many people have memorized is that, oh, the AST to ALT is greater than two to one in alcoholism. Let me tell you something. Let me stop you right there. I can almost promise you that most of the questions you see on your exams are not going to have that pristine, amazing wonderful ratio. The ratio is going to be thrown out the window on your exam. So just be careful about that. But in general, the key thing to know is that your AST will be greater than your ALT, right. Your AST will be greater than your ALT. That's pretty high yield to know for your test. And then what if they give you a question about a patient and they tell you that this patient presents, you know, with, you know, it's a young female and you're told that she's reproductive age, but that she has no taste that she has, you know, that, you know, they show you like a picture of her face. And you see a lot of acne, acne, acne on her face. And you're told that, oh, this lady has just started, she started having a mentee's like six months ago, right. And, you know, they tell you that she comes to the office that she's really conscious of all these visual visions that she has.

And then they ask you for the most appropriate next best step in management. Can I tell you something should pick on your exams. You should probably pick the answer that talks about giving an OCP. There are some very unusual situations on your test where giving OC Ps is not a bad idea for certain disorders, especially for acne, right. I know many of you know the classic acne therapies, you know, things like topical salicylic acid, topical benzoid peroxide. But if you obviously have like severe, not a lociistic acne, you're going to use an isotret knowing. But I think one thing I really want to emphasize is that if a person is reproductive age and the question gives you the context, the story that this person's hormones or their mentees maybe associated with them having a lot of acne. Then the smart plan on the US Emily exams actually, if there are no contraindications is to give the person oral contraceptive pills literally give this person OC Ps give this person OC Ps. OC Ps are very, very helpful treatments, right. For acne, especially reproductive age females. That's a very high yield scenario to know for you exams. But now let's discuss some variations of this same thing so that is something that registers in your brain for your test. Are there some other disorders because you know, I know all of you know that OC Ps are to prevent pregnancy. But are there some other disorders that we use OC Ps to treat on the US Emily exams?

Well, the answer to that is going to be a big fat yes. So like for example, if a person has PCOS remember PCOS has three criteria, right. Policisticov is an ultrasound, signs of hyperanrogenism. And he also notices that the person has irregular mentees basically an ovulation. If you meet one of those three criteria, you have PCOS. OC Ps are the primary treatment for PCOS although people that have PCOS obviously they want to get pregnant then they're not going to be using OC Ps. But OC Ps are used as the primary treatment of PCOS, right. And then what if they give you a question again, I'm going to give like a few short vignettes here and then introduce the concept, right. So if a person has like they have a lot of infertility, they have very painful periods whenever the pulpit really hurts. Obviously, right, this is going to be a person that has endometriosis. Endometriosis is also managed with OC Ps. Remember, endometriosis occurs when you have endometrial glands and stroma outside the endometrium, right. Endometrial glands and stroma outside the endometrium. The primary treatment there is going to be OC Ps. It's going to be OC Ps. So please keep that at the back of your mind as you prepare for your exam. There are even some situations of adnomiosis that are going to be treated with OC Ps. So literally adnomiosis situations that are treated with OC Ps. So please make sure you know these things code for your exams. Make sure you know these things code for your exams.

Although you want to be careful about OC Ps, right. Because if a person has like a history of severe hypertension, you should not put them on an OCP, especially an estrogen containing OCP. In fact, the biggest risk factor, very high yield, the biggest risk factor for hypertension and reproductive age females is the use of OC Ps. It's the use of OC Ps. And obviously, if you also have a history of venous thrombone and bollic disease, getting an OC Ps a terrible idea. Why? Because remember, OC Ps, especially like, again, those that contain estrogen, estrogen increases the synthesis of clotting factors. Estrogen does work literally, increases the synthesis of clotting factors. Because estrogen increases the synthesis of clotting factors, it's going to make you hyperquaglable. It's going to make you hyperquaglable. If you become hyperquaglable, or you're going to get in trouble with venous thrombone and bollic disease. So if you have a history of venous thrombone and bollic disease, estrogen is, an estrogen containing contraceptive is not a good idea. It's literally not a good idea. Okay. It is literally not a good idea. All right. Now, what if they give you a question about a woman, right. She told that this woman received an epidural, right. She's in labor. She's at 38 weeks, she's station, she's in labor. And you're told that this is her first pregnancy. And you know, that she has been in labor now for the past like 30 plus hours.

She has, she received an epidural, right, which as we know is a risk factor for people having very prolonged labor. Right. And then you're told that this lady, they give you some labs. They tell you that morning labs are obtained. And we notice that this person's sodium is 128. So not a crazy severe hyponychromia, but a hyponychromia nevertheless. Well, I know some of you are like, if I never the less, I've never heard of that before. I read the Bible pretty frequently. So never the less is a pretty common thing you see in the Bible. But anyway, let's continue. But basically, they give you these labs. And you notice that this person has hyponychromia. And then our friends at the NBME ask you, oh, which of the following is the most likely theology of this patient's electrolyte abnormality? Well, I would really hope that you pick the answer that talks about drug toxicity or you talk about the answer that talks about oxytocin, right? Oxytocin. Many people do not realize this, but this is actually pretty high you to know for your exams, right? But oxytocin, oxytocin works kind of like ADHD in a sense. oxytocin works kind of like ADHD in a sense. It actually causes you to reabsorb a lot of water from your kidneys. So if you get a prolonged oxytocin infusion, you're going to get an ADHD-like effect. And you're going to reabsorb a lot of water from your kidneys, and that can dilute your serum and cause hyponychromia.

So if you see a person that has gotten an oxytocin infusion, and you notice that their sodium is low, it's typically not going to be a very severe hyponychromia. Then you want to think about oxytocin toxicity, right? That oxytocin causes hyponitremia. And you kind of want to be careful about that, because if the person already has a low sodium at baseline, and they start giving them tons and tons and tons of oxytocin, right, that can cause the person to get in some serious hyponitremia troubles. And I think one thing I want to emphasize here is that why did this woman have such a prolonged liver? Well, the reason it was prolonged is because this woman got an epidural, right? There are many risk factors for prolonged liver, right? Like if it's your first liver, for example, tends to be longer than others, another risk factor is if a person gets an epidural. Epidural tends to slow down liver. In fact, you may notice that in the stages of liver, there are sometimes where we add an hour, right? You know, the USMT is kind of required to memorize how long this face should take, how long this face should take, right? You pretty much add an hour for some of those times if you got an epidural, because epidurals are literally an aesthetic. They slow down liver, they slow down liver, right? So please, that's pretty high yield to know for your exams. Don't forget the association between oxytocin and hyponitremia.

Okay, please do not forget the association between oxytocin and hyponitremia. It's a pathophased question that many people get wrong on their tests. All right, now what if they give you a question? And by the way, you know, let's not forget that there are other things that can cause hyponitremia on the USMT, right? Like for example, if a person has a small cell lung cancer and SIEDH, that EDH can cause you to soak up a lot of free water from your urine, that can cause you to have hyponitremia, right? And then don't forget, if you're taking certain drugs like carbamazepine, carbamazepine is an anti-pileptic drug that can also cause SIEDH, right? That SIEDH can cause hyponitremia. Don't forget SSR Is. In fact, SSR Is are the most common drug cause of hyponitremia, very high yield. SSR Is are the most common drug cause of hyponitremia, very, very high yield. SSR Is, I'm going to say this again because it bears repetition. SSR Is are the most common drug cause of hyponitremia, the most common drug cause of hyponitremia from SIDH, right? They're the most common, let me put it this way. SSR Is are the most common drug cause of SIDH, right? And that SIDH can obviously lead to hyponitremia, can obviously lead to hyponitremia. All right. Now, what if they give you a question about a patient? And you're told that this patient came into the hospital.

For the last, you know, as being the hospital for the last two days, you know, presented initially was having a lot of shortness or breath and that the person has a history of an MI like 12 months ago, but has failed to follow up with their physician. And then now, you know, the person was in the hospital and this person was placed on phyrosomide and things of that nature, right, for a CCHF exacerbation, basically. And then now the person, you're told that this person has, you know, for the last 10 hours, the person has been having very significant shortness or breath, right? Worseening shortness or breath. And then you're told that when this person's lungs are escorted, you don't hear any pulmonary crackles. Well, this person's very short of breath, right? And, you know, this person, the person's heart rate is like 110 beats per minute, right? And you're told that, you know, it was previously normal, you know, the night before or something like that. And then they ask you, which of the following is the most appropriate next best step in management? I would really, really hope. I would really, really hope that you're picking the answer that talks about to get a CT chest angiogram with contrast. Whoa, divine. Where did you get that from? CT chest angiogram with IV contrast? Where did you get that from? This person has a PE. This person has a pulmonary embolus, right?

See, don't be surprised if our friends at the NBA needs give you a PE question in a person that has had a CHF exacerbation. You'd be like, wait, what? Why does this person have a PE from a CHF exacerbation? No, it's not the CHF exacerbation that caused the PE. But the thing is, by having a CHF exacerbation, how many people move around and walk around and take vitri laps in the hospital? Not many people as far as I know. Not many people as far as I know. Right? So this person is in a very big mess with venous stasis, right? Venous stasis. Because they've been bedbound, they've been in the hospital being treated for a CHF exacerbation. Right? So that stasis has made them hyper-quaglable. Right? The thing is, many people do not understand why will blood stasis cause you to be hyper-quaglable? Well, here's the thing. Blood has a certain rate of flow. I'm going to say that again. Your blood has a certain rate of flow. But if your blood begins to flow slow, if your blood begins to flow slow, then there is more opportunity for your clotting factors to interact. And if your clotting factors are interacting more and more, they can form an embolus. And that embolus can flick off and go somewhere and cause you to have a PE. For example, right? So don't forget, blood stasis increases the interaction time between clotting factors. And when there is more interaction between your clotting factors, that is going to raise your risk of forming an embolus. Right?

And then that embolus is going to go and deposit somewhere. It can deposit in a lower extremity vein, causing a DVT. It can deposit in your pulmonary vessels that can cause a PE and things like that. Right? So that's something you want to keep at the back of your mind for your exams. It's something you want to keep at the back of your mind for your exams. Right? And there are many things that can cause a person to have venous blood stasis. Right? So like for example, again, if a person is bedbound in the hospital for any prolonged period of time, or a person takes a long plane ride, although that long plane ride or long car ride, everybody has memorized that. So that's like not something our friends at the MVM is usually going to throw on exams anymore. Right? But other things, right? Like surgery, if you're getting surgery, right? A person that's getting surgery is going to be very mobilized for a long period of time. Right? And honestly, let me tell you something. If you have CHF, even just in and of itself, whether you have a CHF exacerbation or not, that is going to cause blood stasis because your heart has pump failure. Your heart literally has pump failure. If you have a pump failure, then you're not sending blood forward because you're not sending blood forward. That blood is actually kind of static, backing up, right? That's why they have all this demand stuff.

That static blood, that blood that is not moving, can make you have blood stasis, and that can get you in a lot of trouble. Right? Or you see a person that has polycythemia for any reason. If a person has polycythemia for any reason, renocel carcinoma making evil, hemantoblastoma making evil. Right? Polycythemia vera, COPD, right? That chronic hypoxia causing evil production causing polycythemia. Right? A person having OSA or obesity hypogen, ventilation syndrome causing you to make a lot of evil causing polycythemia. All those things with polycythemia, they're going to increase your blood viscosity. When your blood is very viscous, your blood does not flow as fast. It doesn't. And if your blood does not flow fast, then your clotting factors are going to have more interaction time. That's going to make you hyperquaglable. You're going to get in a lot of trouble. Right? So please, when things are not moving as they shoot in the body, it causes a lot of problems. Right? Like for example, if you have a stone obstructing your compound duct, right? And that's all that's happening. Well, that's collidocholothiasis. Right? But that collidocholothiasis is ascending colonjides in the making because that bar that is now static causes all these things that should not interact to start interacting. Like you can start having infections. And then you go the way to ascending colonjides. Right? So keep that phenomenon of stasis in your mind for your exams. Right?

So again, don't forget stasis. Anything that causes your blood to flow slow. Anything that causes your blood to flow slow can make you hyperquaglable. That's literally part of vehicle's triad. What are the other parts of vehicle's triad? Well, I want you to think of, you know, there's hyperquaglability, right? That one I feel like it's kind of a catch all turn. Remember, vehicle's triad is a she S H E, right? The S stands for stasis. I've kind of talked about that. The H stands for hyperquaglability. I'll kind of talk about that now. And then the East stands for endothelial dysfunction. Right? There are many things that make you hyperquaglable. This is cause the second part of the trial. Right? The main things that make you hyperquaglable. Like for example, I've talked about how if a person has is taking OC Ps, especially those that contain estrogen, estrogen increases the synthesis of clotting factors. That's going to make you hyperquaglable. Right? If a person is on tamoxifen, for example, or a loxifen, tamoxifen or a loxifen, those are serms. Those are selective estrogen receptor modulators. Remember, tamoxifen is an estrogen antagonist in the breast, but it's an agonist in the bone and in the uterus. Right? Those things are estrogen-like compounds because they are estrogen-like compounds that can absolutely cause you to become hyperquaglable. Right? Or we look at a person that has PCOS. PCOS actually makes you hyperquaglable. Well, why does that happen?

Well, the thing is PCOS, right? Those people are trying to get the same reaction. They don't have the same reaction. So, a lot of the time, they are stuck in the follicular phase of the menstrual cycle. I'm going to say that again, a lot of the time they are stuck in the follicular phase of the menstrual cycle. If you're stuck in the follicular phase of the menstrual cycle, then you have to get the same reaction. Right? So, you have an ovulation. They don't ovulate. So, a lot of the time, they are stuck in the follicular phase of the menstrual cycle. I'm going to say that again, a lot of the time they are stuck in the follicular phase of the menstrual cycle. If you're stuck in the follicular phase of the menstrual cycle, the thing that's going to happen to you is that you're going to be in that phase where you're making lots of estrogen, lots of estrogen, lots of estrogen. So, you're going to have hyperestrogenism. That hyperestrogenism is going to make you hyper-quaglable. Right? It's going to make you hyper-quaglable. Right? Or even obesity. Obesity also makes people hyper-quaglable because one, it decreases your mobility. But two, a person that is obese is going to be hyper-estrogenic. Well, what's the mechanism there? The mechanism there is that a person that is obese has a lot of adipose tissue. And adipose sites express a lot of aromatase. And what is the job of aromatase? Aromatase increases the conversion of androgens to estrogens.

It increases the conversion of what of androgens to estrogens. So, if you make a lot of estrogen, that's going to make you hyper-quaglable. Right? It's going to make you hyper-quaglable. Right? And then, what are some other things that can make you hyper-quaglable on your exams? Well, if they give you a question about a person where so many family members keep having recurring DV Ts, recurring P Es, you want to think about factor 5, lighting. Remember, it's an Orozomo dominant disorder where factor 5 is resistant to degradation by protein C and protein S. That can cause you to become hyper-quaglable. Right? How about a person that has a history of chronic proteinuria, like an euphrodic and euphrodic syndrome? Why would those people be hyper-quaglable? Well, those people are going to be hyper-quaglable because it's not just argument they are losing in their urine. They also lose antithrombin 3. Antithrombin 3 is a very powerful anticoaglant protein. How was it an anticoaglant? Well, it inhibits factor 2 and factor 10. It inhibits what factor 2 and factor 10. It inhibits factor 2 and factor 10. Right? So, if you've lost an inhibitor of factor 2 and factor 10 in your urine, then you're going to become hyper-quaglable. You're going to get in a lot of trouble. Right? And then anything that causes chronic inflammation, right? Especially like things like, for example, like a common divine thing, PNH, paroxysmal, noxional hemoglobinuria. That can cause you to become hyper-quaglable.

That can literally cause you to become hyper-quaglable. Okay? That can literally cause you to become hyper-quaglable. Right? Whenever you have so much inflammation, what causes the inflammation in PNH? Well, you have complement over activation. Right? So, let me tell you something. Our friends at the MVN is instead of putting PNH as the answer to a PNH question, right? Paroxysmal, noxional hemoglobinuria. They can put an answer choice that says complement over activation. Right? The thing is the USML is these days. They supply a lot of answer choices that are not the actual disease, but the mechanism, the pathophysiology behind that disease. That's something I want to keep at the back of your mind for, for example. Right? So, that's like a test taking principle right there. Right? So this person, right? If you have PNH, right? You have a PG mutation, right? So you don't have CD55 and CD59 on the surfaces of your red cells. So your red cells are not being protected from complement medicated damage, right? That membrane attack complex. Right? So that chronic inflammation can cause you to become hyperquaglub. Right? Those things can cause you to become hyperquaglub. Right? Remember pregnancy can also make you hyperquaglub. Right? Again, for many reasons, number one, impregnancy. Right? Again, you're making a lot of clotting factors because of all that estrogen that is around. Right? Also, impregnancy, you have bloodstasis going on. Right?

Because remember that gravid uterus, that gravid uterus is literally compressing your inferior veneceva. Right? It's compressing your inferior veneceva. That's why when pregnant women lay on their backs, they're told, hey, don't lay on your back. You can kind of feel hypotensive because you're literally compressing your IVC. If you compress your IVC, you're not going to get much of any venus return from your lower extremities to the heart. That's going to cure your cardiac output. Right? That's going to be a problem. Right? So that can cause bloodstasis and that can cause problems. Right? So, and also people that are pregnant, they are not very mobile. I don't see many pregnant women running my mouth on. Right? So that can certainly, again, cause you to be hyperquaglub. Right? Remember, if you have antifusually-pick syndrome, right? You know, with like lupus anticoagulanda can cause you to be hyperquaglub. Well, right? And also, if you think about, like for example, if a person has, you know, endothelial dysfunction. Right? So let's say for example, a person has like a line, please, like a central line or some kind of peripheral line, please literally when you're placing a line, right? You're literally puncturing your literally naked blood vessel wall. Right? So you're exposing subendothelial collagen. That's endothelial dysfunction. That's going to make you hyperquaglub. Right? That's going to make you hyperquaglub.

So a person has surgery, like vascular surgery, vascular surgeries are one of the highest risk surgeries for hyperquaglubility. Right? And also, remember, malignancies cancer can make a person hyperquaglub. Because cancers, many times, they release factors that can cause you to trigger the coagulation cascade. Right? They can cause you to trigger the coagulation, coagulation cascade. And that can certainly make you hyperquaglub. Right? Please, I'm really, really hoping that all these variations have shown you make you a hyperquagulability expert for you. This is actually probably one of my higher yield, a rapid review, although my all my rapid reviews years are pretty high. But this one is especially high yield. I feel like I've shown so many different variations of many different things. So let's go ahead and stop here. If you're interested in any of my classes, I have a bunch of very helpful classes in the month of July. On the first of July, I have an MBME test against strategies class for step one, all the way to step three. And then on towards the end of July, actually from the seventh to the 11th of July, I have a 20 hour step two step through review. There's many people that have taken these classes and don't extremely well on the exams. I've literally had people getting the 270s, even in the low 280s from taking my class. Actually, I have lots and lots and lots of 250s, lots and lots and lots of 260s. Right? Many people have taken my class.

I'm not seeing every single person. But many people have gotten results of that good from taking my class. And these are like recent people. This is not people from like five years ago. Right? And then I also have a bio stats class for some of my students.

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Smoking.

Elevated GGT (due to mitochondrial poisoning) and AST > ALT.

SSR Is (Selective Serotonin Reuptake Inhibitors).

Acne vulgaris, PCOS, and Endometriosis/Adenomyosis.

Stasis (Venous stasis).

Antithrombin III.

Alcohol acts as a mitochondrial poison, causing damage and leakage of enzymes like GGT.

AST > ALT.

Oral Contraceptive Pills (OC Ps).

Estrogen.

Hyponatremia; Oxytocin causes water reabsorption (ADH-like effect).

PCOS, Obesity, or use of OC Ps/Estrogen therapy.

The USMLE may ask for the underlying mechanism (complement overactivation) rather than just naming the disease.

Alcohol acts as a mitochondrial poison, causing damage and leakage of enzymes like GGT.

AST > ALT.

Oral Contraceptive Pills (OC Ps).

Estrogen.

Hyponatremia; Oxytocin causes water reabsorption (ADH-like effect).

PCOS, Obesity, or use of OC Ps/Estrogen therapy.

The USMLE may ask for the underlying mechanism (complement overactivation) rather than just naming the disease.