DIP Episode 581 - 2025 USMLE Step 1 Free 120 Discussion Part 2 (Q11-20, super helpful for Step 2 and 3!)

Welcome everybody, my name is Divine, this is episode 581 of the Divine Intervention Podcast. In today's podcast we're going to be continuing the series on the free 121st Step 1. This is going to be part 2. We're going to do questions 11 or 20. God will it. Let's begin. Question 11 says, a 60 year old man comes to the office because of weakness, tingling of his hands and feet, irritability and forgetfulness for four months. Physical examination shows power, weakness and spasticity. Deep tendon reflexes are increased. Sensation to vibration is absent in the lower extremities. Laps studies show megaloblastic anemia, serum antiparital, cell antibodies and increased serum concentrations of methanol, malonic acid and total homocysteine. The synthesis of which of the following amino acids is most likely impaired in this patient. So again like you see for many of these USMLA questions, it's usually smart to try to work out what's going on. First, before you start jumping into the answers. So we can see clearly that this person appears to have B12 deficiency. And there's many reasons why we can see that. Number one, the person's methanol malonic acid is increased. Remember, B12 catalyzes two reactions in the body. Number one is conversion of methanol malonocoae to succino-coae. That's how you make convert-ochine fatty acids to ultimately convert them to glucose. That's like a TCA cycle intermediate that uses the enzyme methanol malonocoae mutates. It uses B12 as a cofactor.

So if B12 is not working, a methanol malonic acid levels will rise. And then if you want to go from homocysteine to methionine, there is an enzyme known as methionine synthase that also uses B12 as a cofactor. Although, fully it also plays a role in that reaction. So you can already begin to see that, hey, if you have B12 deficiency or fully deficiency, that reaction will not work well. So that's why the homocysteine levels are elevated. So don't forget, we have a B12 deficiency. The homocysteine and your methion, your homocysteine levels and your methanol malonoc acid levels will be elevated. But when you have a fully deficiency, it's only your homocysteine levels that will be elevated. And we can also see that this presents a lot of neurologic deficits, right? Because the thing is, when you're having issues with breaking down methionine and whatnot, that can actually begin to mess up the, that can make myelin less stable. And if myelin is less stable, you're going to have issues with nerve conduction and all those problems, right? So see, this person has like hyperreflexia, per seasol, these neuro deficits. Because remember, when you have B12 deficiency, you can also have this thing called a subacute combined degeneration of the spinal cord, right? So, you know, like the drosol columns are not going to work. And we see that this person's, this person has like some drosol column issues, right? Like, sensation to vibration is not working, right?

So something to keep in mind here, right? So the answer that makes sense here is definitely going to be option C, methionine. It's going to be methionine. The only other thing I'm going to comment on here is, remember, phenylalanine is converted to tyrosine by the enzyme, phelanalanine hydroxylase. That's the enzyme that's messed up in a person that has BKU, right? Although it's you, if you also have a problem with the cofactor tetrahydrobiopterine, there's an enzyme that actually makes THB, THB reductase, tetrahydrobiopterine reductase. If you have that mutation as well, you can make the cofactor for phelalanine hydroxylase. You also have BKU. All right, let's go to question 12. So 65 year old woman comes to the office for a full-up exam. Only after she won the WENTO operative resection of the right colon and chemotherapy for stage three colon cancer. All right, she reports fatigue. So physical examination shows abnormalities, a staging CT of the chest, an abdomen shows five new two to three centimeter masses in the liver and both lungs. The patient's cancer most likely spread to the lungs via which of the following structures. Right? So the thing is our friends at the MV is they love to test atrial and venous drainage. Just in instrumental ways, right? They are not going to say which of the following drains XYZ? No, they'll integrate it with some kind of concept. Right? So remember, right?

And one thing I found that's always helpful with these vessels is knowing the arterial drainage. Once you know the arterial drainage, many times you'll know the venous drainage. And many times the lymphatic drainage also kind of follows the same pattern. Right? So like, for example, we know that the Celiac artery is the primary blood supply to the foregut. Right? And then we know that the superior mesenteric artery supplies, um, um, uh, you know, most parts of the, um, most parts, you know, some parts of your small intestine, but it also does like your right, your, your ascending, uh, colon, right? That's done through the right, correct, colic artery. And then your transverse colon, at least the proximal two thirds, that's done through the middle colic artery. And then the inferior mesenteric artery kind of picks up the slack from there and does the, you know, final third of the transverse colon, right? And it also does your descending colon, your descending colon does your left colic artery. Uh, I remember your appendix is also supplied by your SMA, your superior mesenteric artery, right? So this person, let's look at the cancer she had. She had a right-sided colon cancer, right? So that means all the arterial supply was the IMA. So the venous drainage has to be the, I mean, sorry, the arterial supply was the SMA, the superior mesenteric artery. So the venous drainage has to be the SMV, the superior mesenteric vein, right?

The superior mesenteric vein, um, is ultimately, uh, gonna join up, give rise to the portal vein, right? So like your splinic vein and your superior mesenteric vein, they come together to form the portal vein and then the portal vein, you know, obviously will drain to your hepatic sinusoid and then, uh, after that you form the hepatic vein, right? So that's a portal system right there, right? We have a system of capillaries, right? So remember your sinusoid, senior liver, are capillary networks. They are fed by a, because usually a system of capillaries are fed by arterials and drained by venules. But here you have a system of capillaries that are fed by venules and drained by venules. So fed by the, like, portal vein or whatever and drained by the hepatic vein, that's a portal system. I'll talk about that in a little question today. And then, you know, it becomes the IVC and then from the IVC, obviously you can go to the right side of the heart, the positive in the lungs, cause problems, right? So I think I'm going to go with the option, let's see, option, where's the IVC answer? Option B, right? Option A doesn't make any sense, right? Because the inferior metering vein drains the, the proximal, the distal third of your transverse colon and your descending colon and, you know, like sigmoid and rectum and stuff. So that will be wrong. Option B, IVC is the right answer, I would say. Left colleague vein, left colleague vein drains the descending colon.

So that's going to be wrong. So colleague artery supplies the proximal two thirds of the transverse colon. That's wrong, right? We're talking about venous drainage here because the cancer is spreading, right? The cancer is spreading. So we're taking from the cancer and depositing elsewhere. It has to be a venous network that's doing that. Pomerary vein that's wrong, right? Pomerary vein sends blood to the left side of the, of the heart, right? To the left side of the heart. But this person has like long issues. So that's wrong. Superior metering artery that's wrong, right? That's the blood supply to like your, I've talked about it already. SVC, remember SVC largely drains your brain, your neck structures and things like that. All right. And that's not where the cancer is coming from. All right. Now, I'm going to go to question 13. 26 year old man comes to the office because of a one week history of increased urinary frequency accompanied by excessive thirst. He says he has been urinating hourly. Physical examination shows no abnormalities. Serum chemistry studies are within the reference ranges. Urinary malality is 50, millilose malaus per kilogram of water. After the administration of ADHD that's a visopressin, he's urinary malalities within the reference range. The most likely cause of this patient symptoms is dysfunction of which of the following structures, right? So this person, we see this person has a very low urinary malarity.

Again, don't, don't overthink this and say, oh, his serum chemistry studies are within the reference ranges. You know, he doesn't have a hyper neatramia. So I'm not going to pick diabetes in sepetus, but this guy clearly has diabetes in sepetus. I'll say clearly, he has central diabetes in sepetus, right? Central diabetes in sepetus. Basically, this is a problem where you have like an ADHD deficiency. You don't make an ADHD. So you get in trouble, right? Because remember, ADHD helps us to suck up free water from our urine. Helps us to basically concentrate our urine in the sense, right? So this person has a very low urinary malarity. Many times people have hyper neatramia, but sometimes they can have normal serum values, right? So just be kind of careful about that, right? The fact that a little something is not really fitting your schema doesn't mean that the whole something is wrong, right? Just be careful about that. So this person has central Di because we gave ADHD and he kind of fixed this problem. So this is going to be central diabetes in sepetus. Okay. So he says most likely cause of the patient symptoms is this function of which of the full instructions, right? So, actually he says anterior pituitary. That's going to be wrong, right? ADHD is made from the posterior pituitary gland. So that's wrong. B, B, B, C, no, right? This is an ADHD deficiency problem. You are talking his work. If you had enough ADHD, it would respond right. So B, B, C, is wrong.

When an error is wrong, hypophysioportal system is wrong, right? Remember the hypophysioportal system is like this. Again, that's another portal system. That's a venous portal system. Basically you have your, your, you have a system of venials from your posterior pituitary. They drain stuff into the capillaries and then from those capillaries that constitute the hypophysioportal system, you drain stuff into some venials that also feed your, your anterior pituitary, right? So that portal system transmits like your growth hormone, releasing hormone, when you're dropping a release in hormone, thiratropium release in hormone, corticotropium release in hormone, right? So that's your portal system. The thing is many times you use portal systems when you want to do a lot of regulation of stuff, right? So they're kind of special in that regard. And I guess we've kind of talked about two venous portal systems. But are there arterial portal systems in the body? Yes, they are. There's actually one, you know, there's probably only one actually. So there's the one in the kidneys, right? Where your afranatural feeds your glomerular capillaries and then your glomerular capillaries drain into your effranatural, right? So that's an arterial portal system. That's going to be wrong. I don't think that that's necessarily correct. Although of a through d we've looked at so far, these, the one that at least kind of relates a little bit, illubit, and that's wrong, right?

F-superoptic nucleus, I think I'm going to go with that. Because remember, the superoptic nucleus produces ADHD, right? The superoptic nucleus produces ADHD. So if your superoptic nucleus is not working well, then of course, you're going to probably run into some degree of trouble. Right. So we're going to go to a question 14. So a 52 year old woman comes to the office because of a six month history of intermithenedetics. Sometimes the pain improves when the patient lies down in a quiet room. Her temperature is 99.5, pulse is 86, her dispersions are 16, and blood pressure is 154 over 100. The lungs are clear. cardiac examination shows the PMI displaced to the left and ocational skipped bits. There are no murmurs or robs. There's no S3. Rest in echocardiography shows left axis deviation with our waves greater than 30 millimeters in leads V5 through V6, which of the following processes best explains the development of the live ventricular abnormalities in this patient, right? So this person, what are some key facts of this case, right? So we see that this person's PMI is displaced, right? We have a displaced PMI EKG showing left axis deviation. These are all signs of live ventricular hypertrophy. And what may have caused this in this woman is actually pretty straightforward, right? So she's got hypertension. Many people do not think of this, but hypertension causes an increase in afterload, right? Let's look at our systolic blood pressure.

Our systolic blood pressure is literally 154 millimeters of mercury, literally 154. So if you think about it, the live ventricle, if the live ventricle wants to get blood out of the heart, it needs to generate systolic pressures that are higher than 154 at least, because remember, flow happens from high pressures to low pressures. So because the live ventricle has to generate such high pressures chronically, that's something we call chronic pressure overload. And chronic pressure overload will cause the live ventricle to overcome that problem. It's going to try to lay down sacrameres in parallel, right? Lay down sacrameres in parallel. And when you lay down sacrameres in parallel, that's going to basically reduce the cavity size of the live ventricle, right? Because you're going to have like a little thickening of the live ventricle wall, right? We call that concentric hypertrophy, concentric hypertrophy. Remember, it's a hypertrophy, it's a hypertrophy, it's a hypertrophy, right? And many times that's going to be a pseudo-d an S4 heart sound, right? And again, because you're getting very thick live ventricle walls, you're decreasing the cavity size of the live ventricle. So that's going to cause that systolic dysfunction, because there's so much muscle in the way, there's not enough space to fill, right? So let's look at the answer to the option E says excessive alcoholism glycogen. No, that's wrong.

Option B says fibrosis of intraventricular conduction pathways, that's wrong. That'd probably be more like heart block. Option C says increase synthesis of contractile filaments. Okay, those are your sacrameres, that's probably right. Let's keep option C for now. Option D says misfolding an aggregation of cytoskeloidoproteins, that's wrong, right? Protein is folding, that's not the problem here. One high ophthalmology to know for you exams that involves protein misfolding is alpha-1 antitrepsin deficiency. The mutation many times causes a misfolding of alpha-1 antitrepsin. And then that causes those hepatocytes from the group of toses, but that's a different discussion. The option E says myocide hyperplasia, as a result of induction of embryonic genes, that's totally wrong. Not hyperplasia, it's hypertrophy that happens in the heart, not hyperplasia. Definitely going to go to option C here, good to go to option C. This person has a concentric hypertrophy from lean-down sacrameres in parallel. Many times that's going to be a zero on an S4 heart sound, by the way. All right, question 15 says, a 53-year old man comes to the physician because of a dry scaley rash on his body for the past year. A 15 kilogram, that's 33 pound weight loss during the past year. He is 5, 4, 10 inches tall and weighs 120 pounds. BMI 17, he still has a large volume float. Which of the following nutrient deficiencies is most likely? Right, so let's see, what do we see from this question?

So his person has a rash on the skin. Okay, that doesn't give much information, so let's keep looking. But this person has been having large volume stools, a lot of floating stools. Whenever you see floating stools, you always think of Fatman absorption. That's like a signature on the USM list for Fatman absorption. Again, I encourage you to learn things in context. That's one thing I love about the classes I teach. I try to teach things in context. When you see things contextually, even if you may not know the deep, deep, deep sciences behind it, at least you kind of know what you're talking about. But that's something many people kind of lose sight of. But this person has Fatman absorption. So, okay, so let's ask ourselves, is there a link between Fatman absorption and like skin rash? Well, yeah, because remember, when you have Fatman absorption, you're also going to have issues with your fat soluble vitamins. So like that means A, D, E, and K. Because that means A deals with a lot of specialized epithelium. Like for example, like your skin, your eyes, things like that. So you can have like night blindness and all those things. A vitamin D, remember, is like your bones, bones, bones, bones. Vitamin E, remember, if you have vitamin E problems, that can cause like eight cantholusitis. Vitamin K, it's going to be a lot of bleeding problems. Because remember, vitamin K, boxy reductase, which helps you gamma-capoxyl ether and activate factors 279 and 10 and protein CNS.

It depends on vitamin K, right? So, we're going to pick some answer here that relates to vitamins A, D, E, or K. My looks like option B is going to be well-oppa-ali. So I think we're going to go to option B for this one. Option A is wrong, magnesium. Magd efficiency, we tend to find that in people that are alcoholics, right? Remember, hypomagnesemic and cause a prolongation of QT interval. And then vitamin B, 12 deficiency is wrong, right? That's going to be terminal helium problems, like a Crohn's disease patient. And they'll have like neuro deficits and stuff like we've kind of talked about already. But I mean C, they're going to have like a lot of issues with like bleeding, you know, a lot of collagen synthesis problems. They can have like issues with your teeth and gums, right? That's not what's going on here. And the option E zinc, right? We have a zinc deficiency. You have those dermatitis. Again, but the thing is that doesn't explain this large volume floating stool, right? So it kind of explains the rash, but doesn't explain the stooling, right? So I'm not going to pick that. So I'm going to go with option B for this one. I'm going to go with option B for this one. All right. Now, question 16 says, a serum LDL cholesterol concentrations are measured in blood samples collected from 25 healthy volunteers. The data follows a normal distribution. The mean and standard deviation for this group are 130 mixed predestinator and 25 mixed predestinator respectively.

The standard error of the mean is five with a 95% confidence level. The true mean for this population from the true mean for the population, the true mean. Okay. So let me read that carefully. With a 95% confidence level, the true mean for the population from which this sample was drawn falls within which of the following ranges in mixed predestinator. Okay. So we're pretty much trying to calculate the 95% confidence interval. Well, how confidence intervals calculated? Pretty straightforward. You take your mean plus or minus your Z multiplied by the standard error of the mean, right? And your Z numbers are things you're supposed to know. So your mean plus or minus your Z multiplied by a standard error of the mean. So the mean is 130. We have that. The Z, well, it's 95% confidence interval. You got to know your Z's for your exam. For a 95% confidence interval, it's roughly two. You know, it's like 1.96, 1.90, but just use two on your exams. Make your math easy. For 99% confidence interval, remember, your Z is 2.6, right? So we have the standard error of the mean, right? So the Z is two here since we're doing 95%. So two times the standard error of the mean, that's five. So two times five is 10. So we take 130, which is the mean plus or minus 10. So that's minus 10. That's 120 plus 10. That's 140. So the standard, the confidence interval should be 120 to 140. There's no point in going through the other answers. No other answer makes sense except option B. All right.

Those are one of those things that you don't know. All right. Let's go to question 17. 39 year old man comes to the physician because of a six month history of progressive shortness of breath. He has had a cough productive of white spirit for two years. He spoke to one pack of cigarettes daily for 16 years, but quick 10 years ago, he's a mild respiratory distress with perslips and a biochest. He's using the accessory morsels of respiration. Breath sounds are distant and crackles are present in the lower lung fields bilaterally. Pognary function tests show decreased F512 VC ratio, increase residual volumes and decrease diffusion capacity, and extra of the chest shows hyperinflation, hyper-translucency of the lower lobes of both lungs, which of the following is the most likely diagnosis. So this is like a classic question. This guy is 39. It's pretty young and he seems to have signs and symptoms of obstructive lung disease. What do you think this guy has? I hope you're saying divine. This sounds an awful lot like alpha-1 antitripsin deficiency. And if you said that, that will be absolutely correct. This guy does in fact have alpha-1 antitripsin deficiency. I remember it's a protein-14 problem. Because alpha-1 antitripsin is an anti-produce. Because especially if you're a smoker, it makes a lot of pretty easy in your lungs. And those pretty easy is kind of chop your lung perenchema. So one thing that helps you deal with those pretty easy is our anti-produce.

And alpha-1 antitripsin is an anti-produce. But if you have a protein-14 problem, because you have alpha-1 antitripsin deficiency, then you cannot deal with those pretty easy. And then those pretty easy are going to chop your lungs. So you're basically reducing your surface area available for diffusion. So because your surface area is going down, that's why your DLC goes down. And also, because this is an obstructive lung disease, it makes sense that your volumes are high. And remember many times in obstructive lung disease, your FVV1 is going to plummet. Your FVC is going to plummet. It's just that your FVV1 plummet's faster than your FVC1, than your FVC. So overall the ratio goes that it's going to be less than 0.7 on your exams. So this person looks like they have infezima. Looks like they have infezima from alpha-1 antitripsin deficiency. And again, remember, again, like I said, in alpha-1 antitripsin deficiency, the problem is with misfolded alpha-1 antitripsin. Alpha-1 antitripsin is made in the liver. If it's misfolded, it's going to hang out in the liver. It's not going to be exported. And those misfolded proteins, when they are accumulated within hepatocytes, you know, these same positive with PES, periodic acid shift. It's going to cause those hepatocytes cells to die, right? So that's why these people also going to liver failure. But again, those things you're not exporting to the lungs are going to cause you to have problems.

That's why they have the panaceinar infezima. Right? And many times these people, if they don't smoke, they will actually do relatively fine. But if they smoke, it's almost like you have an antiproduce deficiency. And then you do something that raises your level of produces. AKA smoking. So you're going to get in trouble, right? So I'm going to go to option E for this one. I'm going to go to option E for this one. Asma is wrong, right? Asma, the symptoms tend to be more intermittent. Bronky exercises. Those people tend to have like tons of cough. Productive cough, like gobs and gobs and gobs of cough. And many times when you do an x-ray, you're going to notice that they have like dilated airways. That's not what's going on here. So that's wrong. Chronic pulmonary fibrosis. Remember, if you have pulmonary fibrosis, it's going to present with a restrictive pattern of long disease. Your FVV1 to FVC is going to be normal or increased. Right? Remember, in restrictive disease, your FVV1 drops, your FVC drops. But your FVC drops faster than your FVV1. So overall, the risk is going to be normal or increased. Right? And usually when you have restrictive disease, you're going to have like lower-long volumes. So that doesn't fit with the data we have here. So that's wrong. Cystic fibrosis, that's wrong. Right? It's wrong. This president doesn't have the, you don't see like chronic lung infections and all those things. That's wrong. So option E is going to be the right answer.

All right, let's go to question 18. Investigators conduct a study that evaluates the effect of finasteride on the incidence of prostate cancer in 500 patients. The investigators recruit an additional 1,000 patients for the study. I wish I prefer only effects will this have on the research study. Right? So again, work things out before it's that jumping into the answers. Right? So they said it with 500, they added a thousand. So literally what changed the day make? Again, let's just use wisdom here. Watching the day make. They added a thousand patients. They literally increased the sample size. We increased the sample size. What do you think you're doing? You're literally increasing the power of a study. And literally what does power mean? Power literally means your ability to detect a significant difference that is there. Basically, the question your answer of power is, hey, is there a significant difference? If yes, am I going to find it? Am I going to find it? And the thing is the more rocks you turn over, the higher your chance of just finding something. It's like, for example, let's say you want to find a person named Divine. Divine, I don't know how common of an name it is. Many people call me Devon or Devin or whatever. But my name is actually Divine, DIVI any. Like you know, in Divine Intervention Podcast. So there's not many people named Divine. Let's put it that way. Actually, my phone name is Divine Favor. Right? There's not many people called Divine Favor. Right?

But so if you just look at 10 people, you're probably not going to find the person named Divine Favor or, of course, 10 people. But if you're someone like 1500 people, you have a better chance of finding that's significant difference. So finding a person called Divine Favor, you probably find them. Right? So basically, you turn over more rocks, you're going to increase the power of a study. Right? And again, if a significant difference is there and you're increasing your ability to detect it, you're actually lowering your chance of a type 2 error. Because what's a type 2 error? Remember a type 2 error is when you see there are no significant differences. When there actually are significant differences, there's a significant difference there, but you're saying that there is not. Right? And that's like a power error. So again, by increasing power, you're lowering your risk of a type 2 error. Right? Remember, the type 1 error is where you say that there is a significant difference when there is not. Right? You're saying that, oh, there are significant differences, but no, there's actually nothing there. Right? That's an alpha error. That's an alpha error. That's something more related to the p-value. Right? So options m be a wrong. Option c release more to the alpha p-value. That's wrong. Option d is going to be the right answer. Option e says impossible to predict. That's a bogus answer. So we're going to skip that. All right. Let's go to question number 19. Okay.

So an 82 year old woman has a seven month history of increasing in digestion, upper abdominal bleeding, and early satiety. That's not good. Photo micrographs of the, photo micrographs of the, of her gastric wall are shown. A is a hematoccelin and eocene stain. So H&E, B is a musin stain, and then C is an immunostean for cytokaritin. Which of the following is most likely to have decreased expression in these cells. Right? So, um, again, and one thing I'm going to say is this. Right? Many people kind of stress about images, right? Uh, and don't get me wrong. Am I saying you should never know images and stuff for you exam? No, no, no, no, I'm not going to say that. You should definitely know images for your exams. But the thing is, they are not as germane to you being able to answer your questions correctly as many people make them out to be. Right? So just kind of be careful about that. Kind of be careful about that. Um, be careful about that. Right? Many times if you just read your question carefully, uh, you're going to be in good shape. Right? So, for example, this person, right? She's person is pretty old. Right? Early satiety, upper abdominal bloating, increasing in digestion. Right? And they're telling you that they're showing you gastric something. Right? This is probably cancer. Right? Why would they give something like this to an 82-year-old a woman? This is probably cancer. It's probably gastric cancer. Right? And even this early satiety abdominal bloating. Right?

You know, you, you, they're also symptoms you may see with ovarian cancer. Remember, sometimes gastric cancer is love to spread to, to the ovaries. Uh, sometimes we call those a crook and burk tumors. Many times you're going to see those as signate ring cells on histology. Right? So think about it. Um, so let's just look at these answers. I think many times, uh, just reading the question you're going to be, you're going to be set. But yeah, if you actually look at this, uh, but let's look at the answers first. So option A says cathepsin D. Uh, cathepsin D is, I'm pretty sure that's like a lysosumol enzyme. Right? So remember, a lysosum basically fagglesisotose something into a cell. And then the lysosum has these like nuclear stuff that uses to kind of like a lysed bacteria and kill bacteria and whatnot. So that's a lysosumol thing. I don't know how that's going to factor into gastric cancer. So I'm going to cross that off. Option B says epithelial catherines. Uh, catherines, that kind of makes sense. Uh, this does definitely a cancer related answer. Because remember, catherines are cell adhesion molecules. Right? So, um, if I think the word catherine, catherine, cell adherines, cell adhesion, right? So if your catherines are not working, your cells are going to kind of break apart. And they're going to start going to places that they should not go, um, you know, like spreading, invading, and all those bad things. So let's keep that answer. That's probably correct. Right?

Option C says heprin binding fibroblast growth factors. Um, I don't think I'm going to pick this one because fibroblast growth factors literally stimulate fibroblast to lead on collagen. Um, I don't know why collagen will be such a big opiti thing we're worried about here in a person that has a gastric cancer. Uh, so that's wrong. I'm going to cross that off. Option D says integrins. Remember, integrins are for transmigration. Right? They're the things that are kind of messed up in a person that has local side adhesion deficiency, you know, the lead separation of the umbilical cord and all that fun stuff. Uh, that's not what's going on here. So that's wrong. Option E says type four collagen is type four collagen is. Uh, what do you think a collagen is? Well, collagen is something that breaks down collagen. Um, and by the way, one thing I guess I shouldn't emphasize here, uh, friends at the NBM is they're like using alternate names for things, right? So type four collagen, another name for collagen ises are matrix metalloprotein ises, MM Ps, MM Ps. Just something you want to keep in mind. You may not see that term collagen is. You may see the term matrix metalloprotein is, right? Uh, matrix metalloprotein is, um, I don't think that's what's going on here. Adherence just make the most sense because if you look at these H&E stains, again, I'm not a pathologist, but these cells look pretty spread apart, right?

Like think about your, or all they're like, uh, H&E's of like abdominal mucosa. Those cells should be closely adhered to each other, right? They're all broken apart. Tells you that things have kind of got in here, wire with cellula adhesion. So I think I'm going to go to option B for this one. All right, this is our final question question 20. So, uh, 54 year old woman comes to the physician because she would like to lose weight. Um, she has been on numerous diets in the past with limited success. Uh, both appearance have type two diabetes, Melitus. She's five foot three inches tall, weighs 152 pounds, a gay mice 27 kilograms per meter squared. Her blood pressure is 140 over 90. Uh, fasting serum glucose concentration is 102. Uh, compared with a woman of the same age, whose weight is normal, which of the full-in serum of normalities is most likely in the patient, right? So this person is overweight. I remember overweight is a BMI above 25 to, I think, 30 or less, right? So this person is overweight, right? So, you know, probably have some insulin resistance or whatever going on. Let's look at the answers first. So option A says, so basically compared to a person of the same age with a normal weight, right? So option A says, uh, a degree of cholesterol, called excretion. Hmm. Less excretion of cholesterol. I mean, hey, maybe your cholesterol is high. But we don't have cholesterol numbers in this question, right? So, I don't know if I'm going to pick that answer.

Option B says decrease estrone, nah, I'm not buying that, right? This person is overweight, so she has more adipose tissue. Remember, your adiposeites express aromatis that converts hundreds of astrogens. This person, if anything, will have more estrone. That's wrong. Uh, decrease leptin. Decreased leptin. Um, no, I don't think that that's what's happening here. Remember, leptin is your satiety hormone, right? People that are overweight, they may have like dysregulation of their satiety, right? So they tend to feel hungry. They don't have like good satiety signals, right? So I will say that this person does in probably doesn't have good satiety signals compared to a normal person, right? So, uh, a normal person should have like good leptin concentrations. This person should have probably, uh, uh, this person I don't think has good satiety signals. Um, yeah, so I'm not going to pick that answer. Option D says increased fasting insulin concentration. Um, so this person probably has insulin resistance, right? Basically, like as your BMI rises, you're going to have more insulin resistance. So I'm going to go with option D for this one. Um, yeah, because remember, people that have diabetes, especially type two diabetes. I remember type two diabetes tends to be, uh, very, uh, concordant genetically. It tends to run in families, right? So it's an insulin resistance problem. It's not an insulin deficiency problem actually. You make insulin, your body just doesn't respond to it.

So people that actually have type two diabetes, believe it or not, their insulin is actually higher than the general population, right? So probably going to go to option D for this one, actually. Option E says increased growth hormone, right? This person doesn't seem to have like acromegaly or gigantic them. So that's wrong. Option F says increase, uh, TSA, right? Now, right? This person is not hypothyroid. So I'm not going to go with that answer. And then I'm going to go to option D for this one, right? Option D for this one. So please, uh, let me just talk about grilling and leptin real quick, right? So remember, grilling makes you hungry. Grilling makes you hungry. Leptin tells you that you're, you're full, right? Grilling makes you hungry. Leptin tells you you're full. So if you're a person that is overeating, right? You probably have increased levels of grilling and decreased levels of leptin. So I know some of you may say, oh, divine. Decreased leptin makes sense as an answer in this question. But the thing is, so option C, don't get me wrong, is actually a pretty decent answer. But honestly, option C is just not as good as option D. The thing is you're running to, again, I'm just trying to be flat out honest with you. You're going to run into some of these conundrums or conundra, if they're, I think conundra is a real word on your exams, right? Where there are two answers that appear good, right? Because the thing is think about it.

How many times do you hear about leptin as being discussed in, you know, in an insulin resistance or whatever question? There's just so much in this question talking about like diabetes, and this person is kind of hypertensive, she's overweight. If option D was not available as an answer, then I'll probably go with option C. But option D, just better, just has more hooks with this question that we're seeing. So I'm going to go with option D. I'm going to go with option D. I hope I'm not mixing up great in an leptin, but I'm pretty sure that's correct. Grilling is, you know, is the hungry hormone, leptin is the full hormone, right? So if you have decreased leptin, you won't necessarily feel full. Believe it or not, there are actually some of drugs that have been made, or have been made that kind of modulator presence are leptin signaling. But that's more of a research discussion, not necessary for the USMLE, so I'm not going to talk about that. All right, so I'm going to stop here. Again, if you like the way I teach, I think you'd be interested in the classes I offer. If you're taking step one, I have a 25-hour step one class taking place in the first week of May. Many people have taken those classes, found them to be extremely helpful. And also I have some step one, two step three related classes, starting next week. They're going from Tuesday to Thursday. It's like a test taking class, biostat class, social science, ethics, QI, hospital medicine class.

Those are first step one or the way to step three. And then on Friday, I have a last minute review. And the week after that, I have a 20-hour step two step three review. Those are more first step two step three. Then I have this big class in June, first weeks in June. The 50-hour step two step three class. Again, very, very great class. I've made podcasts where I describe what you get from these classes and how they are different from my podcasts. So just listen to those. If you want some more information, just shoot me an email and I can give you some more information. And then I also offer one or one tutoring for all the USM Lian Cummlex exams. And I help with your application, mock interviews, personal statements, and all that fun stuff. And then I have this podcast on Apple Google Spotify. And I also have a You Tube channel, Divine Intervention, USM Lian podcast and videos where I post the videos that I make. And then finally, I also have another website called Divine Intervention Lifelessens.com. Divine Intervention Lifelessens.com. Many of you know I'm a Christian and I'm proud to say it. But that website, I post like two or three podcasts every week, where from a biblical perspective, I address a life lesson. There's actually a ton of food that I listen to those podcasts. I have more than 300 podcasts on there. I mean, you will find it to be helpful. There's actually an Apple podcast associated with that. I'll call the Divine Intervention Life Lessons Podcast.

So thank you for listening to me today. I'll just leave you with a quick life lesson. And that's about the value of wisdom. The value of wisdom. And I hope you're kind of seeing some of that play out with some of these podcasts, right? The thing is, I'm not saying you shouldn't learn as much as you can learn. You should learn. You should definitely learn, right? You're in medical school for a reason. You're a physician for a reason. You got to learn so you can take good care of your patients. But the thing is wisdom really matters. You know, wisdom really matters. You know, wisdom really matters. Because when you have wisdom, you learn the right way. And when you have wisdom, you can take that information. You've learned and applied in instrumental ways. You can integrate information. Because that's one thing. Believe it or not, a lack of wisdom can actually kind of hamper you in life. You may notice that you don't do it as well on exams as you can. Because you just lack wisdom. Literally, you just lack wisdom. Right? Because if you have wisdom, it will help you approach questions a certain way. It will help you think through scenarios a certain way. It will help you work with potentially limited information, but still kind of whistle your way to the right answer. Wisdom, right? You know, you may call it in a testing perspective, like being a good test teacher. Right? A good test teacher, you know, is not just knowledge they have. Right?

Because they're such a thing as knowledge. And then there's understanding. And then there's wisdom. Right? Knowledge, you have the factual knowledge. Right? On key or with a success or whatever. Right? You accumulate knowledge. Understanding means all you truly understand. Right? And then wisdom is, hey, that information you've understood and you've acquired, you've accumulated. Can you apply it in an instrumental way for benefit? Right? Many people that are preparing for the USML is they have a lot of knowledge. Right? They memorized first aid, they've much else on monkey deck or whatever. But they don't actually have good understanding. They really don't have good understanding. Right? The thing you don't, many people don't realize is that understanding is actually a testing strategy. Literally, it's powerful. Because the more you understand, the less information you will need in a question to answer it correctly. Right? You see many people they see divine. How are you able to answer so many questions? And you know, because the thing is, if I'm being honest with you, I mean, not necessarily know as much as some of you. I do know a lot, thankfully. But I mean, not necessarily know as much as some of you. But because the understanding is there, which, you know, pathophase, having that actual understanding, it actually helps you make your way through questions. Right? Like, for example, that gastric answer question is just basic understanding.

And I hope you're kind of getting that sense from this podcast now. Wait, man, all this information I thought I needed to answer this question correctly. Gee, I did not really need all that stuff. Right? Because you see people, they think that they have to memorize five million things to do it on the USME Ls. No, it may actually know a smaller subset of knowledge and do better than a person that has a larger subset of knowledge. Why? Because you have understanding. You know, first principles. Right? Well, many people kind of ignore that these days and then they kind of wonder why they're getting in trouble. Right? And then wisdom just, hey, applied knowledge. Hey, this not thin, I've understood. And again, wisdom is a test, taking principle. Right? Because if you're wise, then you can apply what you have learned. Right? Like, for example, in making integrations with these podcasts, that's kind of like an example of wisdom at play. Right? It's like, hey, with another name for collagenases, matrix methaloprotinis, or hey, this is the link between homo-system and this. And this is the link between this and that. Right? Even the NBM is to write these questions, requires wisdom. Right? A person that writes good questions has wisdom. Right? So just being able to apply that knowledge, because honestly, like, and I kind of talked about this in the, you know, fairly recent podcast, but you see many people, they're just learning to pass a test. That should not really be your goal.

Don't get me wrong in the rigor and the pressures of medical school and residency. Sometimes that's all you're just kind of focused on. But honestly, like, at some point, you got to ask yourself that, wait, what am I learning this information? Because you're going to actually be like, you know, like caring for patients in the future. So it's probably useful to learn this information well so that you can use it for patients in the, in the future. Right? You may think that, oh, learning biochem and learning all these things is kind of useless, but it's, it's really not. You'll be amazed at where you would use that knowledge and save a person's life. You'll be amazed, right? I remember, like, for example, there was a patient I had a couple years ago, actually, just for, you know, hip-hop reasons. I'm not going to see much about this. But this person had like some kind of lipid metabolism and disorder, right? And I was kind of working in, you know, on their circumstands, where the person had to be intubated, right? And we know that if a person is intubated, you're going to be pleased on some kind of sedative, right? So they're going to put it on something like fentanyl or purple fall or whatever, right? And just having that biochemistry knowledge kind of taught me that, oh, wait, this person, you have a problem with lipid metabolism. It's maybe not the best idea to put you on purple fall, right? Because purple fall, if you've seen purple fall, it's like packaged with lipid.

So it's like, hey, let's maybe use something different instead of purple fall, right? So you may think that, ooh, that biochem knowledge is kind of useless until you then encounter a patient. It may be a small thing, but it may be the difference between life and death for a patient or good patient care and bad patient care or medical error and no medical error, right? Another good example, like, I've seen a lot in ICU. ICU is kind of a good minefield for people that have good knowledge bases. You do really, really well in ICU, right? I don't know, I'm seeing these things, but I really hope that this is ministering to somebody. But like, for example, like, it's not every, you'll think that if a person has hypoxia, you get oxygen, right? No, it's not like, it's actually not every case of hypoxia that is fixed with oxygen. There are some cases of hypoxia where if you give the person oxygen, you'll actually be worse in their condition, right? And again, I'm going to, this is something I think I may have talked about in ICU series or whatever. But it's just something to keep in mind. You may wonder like, man, that doesn't make any sense. But it will make sense if you actually have, if you actually have understanding and wisdom, and you'd not just accumulate knowledge, because that's one problem we see a lot in healthcare these days. You see people making all these errors with impatient care. I'm not saying people cannot make mistakes. I make mistakes.

I'm a fallible person, right? I'm a flawed person. I also make mistakes, right? But the thing is, you can minimize the errors you make by just learning the material well in the first place, right? There's many healthcare professionals and I'm not going to mention any names, but there are many healthcare professionals that just depend on, oh, I just have experience. I've seen this a few times, right? They don't have that solid knowledge base. And unfortunately, some physicians and medical students were pumping out into residences these days. That's kind of where they are. They're just kind of studying to pass a test to get those scores. And that's it, right? The thing is, that's a very short term mindset, because long term, you're screening yourself over and you're screening your patients over. So just really encourage you. Don't just focus on accumulating knowledge. Focus on understanding and focus on accumulating wisdom, right? There's this Bible verse that says, wisdom is the principle thing. Many people think that knowledge is the most important thing. It's really not. Your knowledge base is not what is most important. It's your ability to use that knowledge. Your ability to have understood that knowledge and then use it in then four ways. Applied knowledge. That's wisdom, right? To kind of make a useful change. All right, so thank you for listening to me today. I'll see you in episode five, five hundred and eighty two, I think. Well, God bless you. Bye for now.

Thank you for listening to me.

Conversion of methylmalonyl-CoA to succinyl-CoA (TCA cycle intermediate) and conversion of homocysteine to methionine.

Vitamin B12 deficiency. Elevated homocysteine alone suggests folate or B6 deficiency; elevated MMA/MMA + Homocysteine suggests B12 deficiency.

Superior Mesenteric Vein (SMV). The SMA supplies the right colon, and the SMV collects this drainage into the portal system.

Central DI is due to a deficiency of ADH production/release (posterior pituitary issue); Nephrogenic DI is due to kidney resistance to ADH action.

Concentric hypertrophy. The ventricle thickens its walls in parallel to overcome high afterload, reducing the cavity size and potentially causing an S4 heart sound.

Fat-soluble vitamins (A, D, E, K). These vitamins require dietary fat for absorption.

It acts as a cofactor for methionine synthase and methylmalonyl-CoA mutase.

Elevated Methylmalonic Acid (MMA) levels are characteristic of B12 deficiency; elevated homocysteine is seen in both B12 and folate deficiencies.

The Superior Mesenteric Vein (SMV) and Splenic Vein combine to form the Portal Vein.

Nephrogenic Diabetes Insipidus (the kidneys are resistant to ADH).

Chronic pressure overload (e.g., severe hypertension), forcing the ventricle to generate higher pressures and lay down sarcomeres in parallel.

Vitamin K deficiency. These factors require Vitamin K-dependent carboxylation for activation.

Obstructive lung disease (e.g., emphysema or chronic bronchitis).

It acts as a cofactor for methionine synthase and methylmalonyl-CoA mutase.

Elevated Methylmalonic Acid (MMA) levels are characteristic of B12 deficiency; elevated homocysteine is seen in both B12 and folate deficiencies.

The Superior Mesenteric Vein (SMV) and Splenic Vein combine to form the Portal Vein.

Nephrogenic Diabetes Insipidus (the kidneys are resistant to ADH).

Chronic pressure overload (e.g., severe hypertension), forcing the ventricle to generate higher pressures and lay down sarcomeres in parallel.

Vitamin K deficiency. These factors require Vitamin K-dependent carboxylation for activation.

Obstructive lung disease (e.g., emphysema or chronic bronchitis).