DIP Episode 594 - 2025 USMLE Step 1 Free 120 Discussion Part 11a (Q101-105, super helpful for Step 2 and 3!)

Welcome, my name is Divine, this is episode 594 of the Divine Intervention Podcasts. And to this podcast we're going to be continuing the Step 1 3 120 series. I want to be done with this so that we can move on to some other topics I have in mind. So this is going to be Series 11 and again if you're studying for a step 2 step 3 you really should listen to this series as well. Alright, Question 101. A 25 year old woman gravity the one power one comes to the office because of a two week history of poppitations and heating tolerance. She delivered her child three months ago following an uncomplicated pregnancy and delivery. She is breastfeeding. She has no history of serious illness and takes no medications. She is 5 foot 4 inches tall and weighs 120 pounds. A BMR is 21. The temperature is fine. She is staggy cardiac, she is the kipnic. A blood pressure is okay. Examination shows moist palms and bilateral lead lag. No exo-thalmosis noted. The thyroid gland is enlarged and non tender. No murmurs are heard on cardiac examination. Deep tendon reflexes are 3 plus. Serum studies show an undetectable TSH concentration. Serum studies show a high blood pressure. Which of the following is the most likely mechanism of this patient symptoms? So we see a person delivered a baby three months ago. And now she is having signs and symptoms of hyperthyroidism. The TSH is undetectable and the T4 and T3 appear to be elevated. This person has signs of hyperthyroidism.

We have seen this happen again a few months or a few weeks postpartum. This is going to be pretty classic for postpartum thyroiditis. Postpartum thyroiditis. Okay, so let's see what answers. Because again we see recent delivery of our fetus. And within the first 12 months of delivering the fetus you have hyperthyroid symptoms. That's postpartum thyroiditis. So let's see if she has an activation of mutations of TSH receptors. No, that's not the mechanism behind this thing. In fact let's maybe discuss postpartum thyroiditis real quick. So the way this works is when a woman is pregnant she is actually immunosuppressed. Which makes sense? Because the fetus is you don't want to reject the immune system to reject the fetus and then you have a miscarriage. So there is a certain level of immune tolerance that happens during pregnancy. Now after the fetus is born it's almost like the immune system is like alright let's get back to normal. So that rebound in immune function can lead to the generation of autoantibodies against your thyroid gland. And when those autoantibodies begin to attack your thyroid. The thing that's going to happen is that your thyroid is going to explode. You're going to release a lot of thyroid hormones. So you're going to have this hyperthyroid phase just because of inflammation in the thyroid gland. And then over time you will go to a hypothyroid phase to hypothyroid phase. When you've kind of burnt out that thyroid you released all that preformed hormone.

You then go to a hypothyroid phase. And they usually are around 12 months or so after delivery. You then go back to a thyroid phase. So again it's antibodies that do a lot of this damage. And again those antibodies, maybe some of the antibodies you'll find in Hashimotoza thyroiditis. But again the sentinel event is that reduction in immune tolerance that happens after the baby is delivered. So option A says activation of mutations of the TSE receptors. That's wrong. That's not what's happening there. You don't have a TSE receptor mutation. You have antibodies that attack the thyroid. Option B says increase serum thyroid globulin concentration. That's true. This presence thyroid globulin should be high. Because remember whenever thyroid hormone is released from the thyroid gland you're going to release thyroid globulin at the same time. Remember thyroid globulin is like the CPAP type of thyroid gland. So this presence thyroid globulin will be high. But that's not the mechanism behind the presence symptoms. That's not the mechanism. Again remember the fact that a statement is true does not necessarily make it the right answer to an MBME question. All right. And then option C says is skimic injury to the hypothalamus. Is skimic injury to the hypothalamus is wrong. I think here they are kind of thinking you know seeing if you'll confuse this with something like what is this thing called? She hands syndrome. She hands syndrome is more like a skimic injury to the pituitary glands.

That usually happens in the setting of you know because if you think about your anterior pituitary kind of triples in size during pregnancy. I mean all those hormones don't drop from the sky. They do come from somewhere. Right. So because it triples in size it becomes very susceptible to ischemia. So if anything happens let's say you have a lot of blood loss during the process of delivery like liver and delivery. You can get an ischemic infarction of your anterior pituitary and that will cause pituitary sorry that will cause she hands syndrome that will cause she hands syndrome. I'm trying to make sure I don't confuse this with pituitary epilepsy where you basically have hemorrhage into your pituitary gland. All right. So option C is wrong option D says lymphocytic infiltration of the thyroid. I'm going to pick that answer why because if you really think about it where do antibodies come from they come from B cells they come from B lymphocytes right. So it kind of tells you that B cells will kind of infiltrate the thyroid. And remember by the way that same kind of lymphocytic infiltration of the thyroid will be found in Hashimoto's thyroiditis. Remember in Hashimoto's you're going to have these anti-thyro peroxides or anti-thyro globulin antibodies right. So again those antibodies come from B cells right. So the answer to this is D but this person has postpartum thyroiditis. Option E says presence of TSE receptor auto-antibodies that's Graves disease.

Remember Graves disease you have these thyroid stimulating immune globulins and don't get me wrong. Graves disease is the most common cause very high use is the most common cause of hyperthyroidism in the US. But again that's why you can not just go based off of an algorithm on you exam. That's not a smart play. On you exam you want to analyze things and look at things from the perspective of understanding and context right. Understanding and context. This person is postpartum that's the context. It makes more sense to be postpartum thyroiditis instead of Graves disease. Instead of Graves disease. So the answer here is going to be option D. Remember in Graves disease the auto-antibodies they stimulate the TSE receptor right. It's just one of these auto-antibodies where they actually do stimulation instead of destruction of a receptor. Now question 102 says if a 53 year old woman comes to the office because of a six year history of stiffness and pain of her hands. She has difficulty botting her clothes because of the symptoms. She takes no medications. Physical examination shows the findings in the photograph. An abnormality of which of the following is most likely to confirm the diagnosis in this patient right. So this is pretty straightforward. And by the way the postpartum thyroiditis I talked about in the first question. If you're having really significant symptoms like it seems like this person is you should give a bit of blocker.

Bit of blocker is really helpful because they inhibit that peripheral 5-prime diodeine disease that converts T4 to T3. So you have less T3 production. And also by giving a bit of blocker you're blocking bitter receptors because remember one of the actions of thyroid hormone is to cause you to insert more bitter one receptors on the surfaces of your myocardial cells that can cause tachycardia and all these things. So you can really dumb down many of those hyperadrenergic symptoms by giving a bitter blocker. All right so this is what person in question 102 what do we think this person has? Well it sure looks like this person has rheumatoid arthritis right. Diffness, pain in the hands, right. And we see the picture again although the picture really doesn't matter but this is rheumatoid arthritis right. So let's see which one will confirm the diagnosis option. He says anti-cytrolinated. You know sometimes an example they call this anti-cyclic citrolinated peptide anti-CCP right. That's the correct answer right. Anti-CCP antibodies you're pretty specific for rheumatoid arthritis right. They're pretty specific for rheumatoid arthritis right. So option A is the right answer. So let's look at the other answers and what they look it with. Option B says anti-metal congeal antibody assay that's going to be primary biliric colon itis right. That's usually going to be like a middle age woman that has like direct type of bilirinemia right.

Remember typically the raises from inflammation against the intra hepatic bowel ducts right. So you have inflammation against your intra hepatic bowel ducts and then you're getting trouble. You get in trouble right. They're going to have direct type of bilirinemia. We don't see that presentation here. I'm HLEQ2 that's going to be CLEAC disease. Remember DQ2 and DQ8 they're pretty strongly as we know CLEAC disease right. That's more of a Fat malabsorption right. They're going to have a lot of deficiencies of fat solo vitamins iron deficiency anemia because they have in issues absorbing stuff in their in their small intestine. Option D says precursor of the erythroid cell line that's wrong. E says precursor of the thrombopoidic cell line that's also wrong as well. That just doesn't really collocate with what is being discussed here. This person has CLEAR rheumatoid arthritis. And remember when a person has rheumatoid arthritis how do we treat it on the exam. How do we treat Array on the exam. I hope you're saying ooh divine. Array is going to be Trito methotrexit right. Array rheumatoid arthritis is going to be treated with methotrexit right. It's going to be Trito methotrexit right. It's a D-Mart. Remember methotrexit is a dihydrofolioreductase inhibitor. It's a dihydrofolioreductase inhibitor. Alright, so let's go to question 103. A 73 year old woman comes to the ED because of a 6 hour history of CVF-DMN.

She has chronic aphib and on the went placement of a prosthetic mitral valve. Four years ago her pulse is 120 per minute and irregularly irregular and blood pressure is 80 over 60 millimeters of mercury. Atheriography shows an embolus in the SMA lodged just beyond the p-10th mitral colic artery. A laparotomy is done. During this procedure which of the full insegment of the abdominal viscera is most likely to appear normal. This is a classic anatomy question. So let's kind of work this out. This person seems to have an embolus in the superior mesenteric artery just beyond the p-10th mitral colic artery. So what does the SMA do? What does exactly does it supply? So the superior mesenteric artery supplies, you know, it has a bunch of branches actually. It has like for example the inferior pancreatic adornal artery, you know, which anastomosis with superior pancreatic adornal artery, which supplies like the head of the pancreas. And then the superior mesenteric artery also gives rise to your genital arteries. Actually supplies some parts of the adornum, like the distal parts of the adornum. And then it gives rise to your genital artery, so it supplies the genum. It gives rise to your ilial arteries, it supplies the ilium. And it also gives rise to your iliocolic artery. Your iliocolic artery is the artery that supplies against some parts of the ilium. And actually your appendicitial artery comes off of the iliocolic artery.

Now some other branches of the superior mesenteric artery, we have the right colic artery that supplies your ascending colon, which makes sense, right? Your ascending colon is on the right side of your abdomen. And then it also gives rise to the middle colic artery. The middle colic artery supplies the proximal to thirds of the transverse colon. So here is a very nice principle of life to keep in mind with your arterial supplies. In general, when you have like an embolism, right, which this person has, and I'm going to explain why. Typically, if you're lower on the totem pole, you're going to suffer the most. If you're higher on the totem pole, you're going to suffer the least. It's just going to think of it this way, right? On a team, on a medical team in the hospital, you have like an attending, you have like the residents below the attending, you have like the first years, you have the medical student. Who is the person that is most likely going to get chewed out? Probably the medical student, right? Or kind of picked on it's probably going to be the medical student because you're just lower on the totem pole. Kind of the same thing happens with blood supply, right? Kind of the same thing happens with blood supply. The more the first people to receive blood, they're going to do well, right? Is only if you have like an actual occlusion, let's say you occlude the entire supermercent recovery. Then of course, every part of every branch is going to be messed up.

But the thing is the more distal parts, they are lower on the totem pole. So they're going to be more likely to suffer, right? So the one that's most likely going to be normal here is going to be the one that's operating the totem pole. You know, and I said that again, your supermercent recovery supplies some part of your distal, doggard num, supplies your jujunum, supplies your ilium. So those are probably a little earlier before we start going towards the colon and all those things, right? So if we look at option A, ascending colon, again, that's the right colic artery. That's a more distal branch of the SMA. Option B says distal ilium. Even as long as we see some jujunum answers, we should probably pick those over ilium because the jujunum is just higher on the totem pole, right? So we can probably get rid of option B and option D. And then between option C and E, option C says distal ilium, option E says proximal jujunum. I'm going to vote for proximal jujunum because the occlusion is actually far, far, far away from that, right? It says, ooh, just beyond the patent middle colic artery, right? So again, you've given off your jujunum arteries, you've given off your ilial arteries, right? At this point, right? So it just makes sense that the jujunum makes sense and the proximal jujunum makes sense because again, remember, the entire jujunum is supplied by the superior mesenteric artery, okay? The entire jujunum is supplied by the superior mesenteric artery, okay?

So again, please make sure that you know, make sure that you know the blood supply of the GI tract. Make sure you know the blood supply of the GI tract. Make sure you know the blood supply of the GI tract, right? Make sure you know the blood supply of the GI tract. Make sure you know the blood supply of the GI tract. All right. It's a very commonly tested thing, right? You know, cilia-cardory, superior mesenteric artery, inferior mesenteric artery. And this person has something called acute mesenteric ischemia, right? This person has something called acute mesenteric ischemia. That's something called acute mesenteric ischemia, okay? Acute mesenteric ischemia. So what causes acute mesenteric ischemia? Typically, it's going to happen when you have issues with your heart, right? Especially if you have like a history of aphib, like this person has. You may be like, do you know how do you know the person has a aphib? Well, it's told in the question, but if they didn't say it, we say that this person has an irregularly irregular rhythm, right? It kind of tells us all we need to know. This person's got aphib. So when you have aphib, or you've had a recent MI, your heart is not contracting as well as it should. And because your heart is not contracting as well as it should, you're going to form embolite. And those embolite can leave and peel off and go on or include something. They can go on or include a cerebral vessel and cause a stroke.

They can go on or include a limb vessel and cause acute limb ischemia. Or they can go off and include a mesenteric vessel and cause a mesenteric ischemia. This time on the USML, if they are going after a mesenteric vessel, they're going to go after the superior mesenteric artery. Although you can obviously go after the celiac or your inferior mesenteric artery as well. So please make sure you know the blood supply of your GI tract. It's pretty high you also know that stuff for, for example, right? Remember, the things proximal to the distal dwindle are supplied largely by the celiac artery, right? And then the things, you know, from the distal third of the transverse colon going towards the, you know, the sigmoid colon, the rectum, especially the upper rectum, those are supplied by the inferior mesenteric artery, right? So like the left collic artery, for example, is a branch of the inferior mesenteric artery. The, you know, again, basically from the distal third of the transverse colon all the way down to the upper rectum, that's IMA territory. All right. I don't want to go off on too many tangents here because there's so much stuff I can talk about with this podcast, but we're kind of short on time. All right. Let's keep going. So question 104 says a two year old boy is brought to the physician because of failure to thrive. He also has had loose fatty, false melons, stools and a cough during the past two weeks.

He's at the 30th percentile for height and 10th percentile for weight. Physical examination shows no other abnormalities. Lab study shows the artery and a sweat chloride concentration of 80 millimolar. A chest x-ray shows hyperinflation. Sputum culture grows. He morphiles in Fuenze and staff aureus. Secretion of which of the following substances is most likely to be decreased in this patient. Right. This question reflects something that the USMEL is love to do a lot these a lot of these days. They'll see which of the following is most likely to be decreased, which of the following is most likely to be increased. Whenever you see these kinds of questions, these are analysis questions. They want you to actually do some kind of analysis. Again, the questions the USMEL is right these days that depend on you being able to just blindly memorize plug and chug. Those things are becoming more and more extinct from the exams if you may. Right. So what does this shout have? This shout probably has cystic fibrosis, right? Which makes sense. Remember, cystic fibrosis can cause like a pancreatic insufficiency. And if you have a pancreatic insufficiency, you're going to have issues making things like lipids. So you're going to have fat malabsorption. So it makes sense that it has these loose fatty, false male installs, right? And also your respiratory secretions will be thick. So you have issues clearing respiratory pathogens. So it makes sense that they have these all these infections.

Right. You remember, especially if you're under each 20, the most common cause of pneumonia is stuff. Whereas if you're over 20, it's going to be more so the monos. And again, chronic lung infection. So it makes sense that they'll have this hyperinflation, right? And remember, what's the pathophase? It's a normal memory. It's an autosomal recessive disease, chromosome seven in the CFTR gene. So if you have a mutation and the most common mutation, remember is the delta F508 mutation, right? So if you have this mutation in the CFTR gene, the CFTR transporter is not going to work, right? And the CFTR transporter, remember, is an ABC transporter, right? It's an ATP binding key set. Probably you won't see that on step two, step three, but that's certainly something to contest on step one. And essentially, this transporter, what it does is that it secrets a bunch of stuff. It secrets chloride into the lumen of things, secrets bicarb into the lumen of things and secrets thiosyanate ions, right? So chloride, bicarb and thiosyanate is secrets those things into the lumen of things and sodium passively follows, right? Because those are a bunch of anions. So sodium passively follows and obviously because you have all this osmotic charge, water is going to follow. So that's going to make the lumen of stuff or your secretions, you know, watery, which is helpful, right? Because if it's watery, then it can flow well and all those stains and, you know, the works.

So if that transporter doesn't work, well, you're not going to be secreting out chloride, you're going to be seeking out bicarb, you're not going to be secreting out thiosyanate, right? And obviously, since those things are not being secreted, sodium will not follow, water will not follow, right? So your secretions are going to be very thick, right? There are many problems they can have, like absence of the vast difference because it doesn't develop well in utero, they can be infertile, right? Both males and females, they can have recoring respiratory infections, they can have a, they can have a, a fat malabsorption, right? And they'll have increased sweat chloride because this CFTR transporter, its job is actually to reabsorb chloride from sweat, one of the things it does is to reabsorb chloride from sweat. But if you're not reabsorbing chloride from sweat, then you're going to have a lot of chloride in your sweat. So you're going to have increased sweat chloride. All right. And again, we've talked about the pancreatic insufficiency angle with this. All right. So many of them are going to develop diabetes because the pancreas will get messed up over time, right? Although that diabetes, again, it's because of pancreatic insufficiency, it's going to be more, I guess, an endocrine pancreatic insufficiency.

Although if I'm being honest with you, most times on the USMLE exams, when the test cystic fibrosis, they tend to test it more from the context of exocrine pancreatic insufficiency. Right. Remember, endocrine insufficiency is when you cannot make insulin. Exocrine insufficiency is where you cannot make your pancreatic enzymes like lipase and things like that. All right. So it says which of the flu is most likely to be decreased. Sorry. Like, again, I know I try to cover 10 questions per podcast, but I don't think that that's going to happen with this one because these questions are kind of challenging. And I think it behooves me to slow down and try to explain these things. So you can kind of get these things down and truly understand them. So I have this airy feeling that we're not going to get to 110. So it's going to be a part B to all of this. All right. So option A says by by carb. So decreased. That makes sense, right? If the CFTR transporter doesn't work. Remember, I said there are three things you cannot secret. Chloride, by carb and thioscianate. Many people know about the chloride part, but many people don't realize that the CFTR transporter also kind of brings out by carb and thioscianate, but you should know that. All right. Option A kind of makes sense. So let's kind of keep that for now. Option B says gastric acid. And let's decrease of gastric acid. That's going to be found more in p is more like a stomach issue, right?

Let's say your pride cells are not working for whatever reason. You make gastric acid. You know, for example, if you make auto antibodies against your pride cells, as we've seen, pernicious anemia, remember, you make auto antibodies against pride cells on intrinsic factor. So that may make sense, but that's not really what's going on here. Option C says glucagon, right? So glucagon remember comes from the alpha cells, right? The alpha cells that we find on the periphery of the pancreatic eyelids. So don't get me wrong. You have that in a person that has cystic fibrosis. You can because they also have endocrine pancreatic dysfunction. So let's keep that. Option D says insulin. Insulin comes from the beta cells in the pancreatic eyelids. Again, when you have cystic fibrosis, because your secretions are too thick, you may auto digest and destroy your pancreas. Right? So that can certainly cause issues. Option D is also a sign of endocrine pancreatic insufficiency. So, I mean, you insulin should be decreased. Ah, so, okay, let's look at option E. Option E says intrinsic factor. No, that's not what's going on here, right? That's pernicious anemia of discourse that already. So, I love this question because it puts us in a very good conundrum that our friends at the NBM is love to toss people into on the exam, right? So, there are three potential factors that we can use in the NBM. So, there are three potential correct answers here. Option A is bicarb.

We know that bicarb will be decreased, right? Like, literally, if the CFTR transport is not working, you're not going to be secreting bicarb, you're not going to be secreting a chloride, and you're not going to be secreting thiosynid ions. Right? And the option C and D, right, will also make sense that they're probably decreased. Right? So, which one should we pick in this case? Again, let's go over a few test-taking considerations that may help you with a question like this. Number one is, I said that the classic way that cystic fibrosis is tested in terms of pancreatic insufficiency on the USML Es, we love to test it more from the context of exocrine pancreatic insufficiency instead of endocrine pancreatic insufficiency. So, because it's tested more from the context of exocrine, option C and D are just a lot less classic, a lot less classic, right? And typically, for people to develop endocrine pancreatic insufficiency, don't quote me on this in a cystic fibrosis. I think it's something that happens a lot later in life, not at each two. All right. So, let's kind of keep that in mind. Now, second consideration is that, man, options C and D are both signs of endocrine pancreatic insufficiency. Yes, option D is probably more classic between those two, right? Like, how many times do they test decreased local gun production? That's ridiculous, right? Most times, they test more of decreased insulin production, right?

But again, they are both signs of endocrine pancreatic insufficiency. It just seems like there's not much greatness. There's not much here in this question that helps those T's won, apart from the other, right? So, just less likely to want to kind of want to pick that. And then option, because those two answers are not very distinguishable if you may, right? And then option A says by carb, right? It's just a very direct answer. I think I've said this quite a lot in this website. I mean, in this series on the step one free 120, that the USM is they love direct answers, right? They love direct answers. They love direct answers, right? Because if your CFTR transporter doesn't work, you will for sure not make bike carb, right? You will for sure not secret bike carb from that CFTR transporter, right? So, it's just a more direct answer. So, I'm just more likely to pick that answer. So, we're going to go ahead and pick that one. All right. So, the answer is A. Again, I love these questions because I like being realistic, right? I don't want to come and just kind of blow smoking your face and say, oh, it's option A and not give you much reasoning, right? The thing is, again, I would really hope that you're seen from all I'm doing here, that doing well on the USM.L exams is not all about knowledge base. You also have to be a good test sticker. You also absolutely need to be a good test sticker. That's just the truth.

And again, if you want to become a better test sticker, you should consider the test-taking class I offer. It's a 2.5 hour class. It's for step one to step three. I actually have one taking place tomorrow. I'm interested. Shoot me an email. And I can give you some more information. All right. Now, question 105 says, 70 and it's over zoomed, by the way. A 73 year old man is brought to the ED by his family one hour after he walked into the left side of a doorframe, when living his bedroom and then tripped over a chair that was on his left side. Visual field testing shows left lower quadrant anopia. When tactile stimuli are presented on both the left and right sides simultaneously, the patient correctly identifies only the ones on the right. Okay. For the examination shows no model or language deficits. Okay. Proception is intact. This patient most likely has a brain lesion in which of the following lobes. Right. So remember your lobes of the brain. Right. There's frontal, there's parietal, there's temporal, there's occipital. Right. And again, this question is pretty straightforward. If you just know certain rules, right. The thing I love about neurology is most times if you have an understanding of what's going on. You're going to memorize a ton. Right. Now, let me teach you a very simple rule with this visual field cuts. One thing I've noticed that really, really helps. Really, really helps is what I like to call the rule of opposites, the rule of opposites.

Whatever visual field deficit they give you, just keep taking opposites of everything they give you. You're going to be in good shape. Right. Like for example, see left lower quadrant anopia. What's the opposite of left? It's right. Okay. Now what's the opposite of lower? It's upper. Okay. So upper or superior. Right. Quadrant anopia. So this is probably a problem going to be more like on the right superior side of the brain. Which makes sense. Right. Right. Super. Right. Superior. So you can probably get rid of all the left answers. You can probably get rid of a through C just like that. So you're kind of left with D E and F. Right. D E and F. D E and F. D E and F. All right. D E and F. And again, right superior. Well, between all these lobes, which one is more superior? Between the frontal, parietal and temporal. Well, the frontal and parietal are certainly more superior than the temporal. So we can probably get rid of option F. Remember, the temporal lobe is more inferior, closer to ears. Right. In the in the cerebral cortex. So we're going to be stuck between options D and E. Options D and E. And the thing is whenever you have these quadrantanopias, you almost always want to think about issues with the parietal lobe. Right. Remember, your optic radiations and all those things, they largely run through the parietal and the temporal lobes, the parietal and the temporal lobes. But if you have a temporal lobe issue, you have an upper quadrantanopia.

If you're taking that rule of opposites, if you have a parietal lobe issue, you're going to have more of an inferior or a lower quadrantanopia. Right. So the right answer here is probably going to be option E. It's going to be option E, right. Parietal lobe. Now, let's talk about a few more things here that I think may be potentially helpful. Right. You may say, okay, divine. Can you explain some of these other deficits this person has? So this person doesn't have a language deficit, which is very helpful. It tells you that this problem is probably not on the left side of the cortex. Because remember, your broken areas and your winnikis areas, those are going to be on the left side in most people. Right. Like your left, the left side of the brain. Right. We don't see, we don't see any language issues. So this is probably not a left problem. Right. And again, this is not a left parietal lobe issue because the person doesn't have signs and symptoms of a Gersman syndrome. Right. They don't have like acalcolia. Right. So inability to do math or a graphia. Right. Yeah. Inability to write and all those things. They don't have any of those things. Right. And perception is intact. Remember, perception kind of resides with your drosal columns. That's some of a spinal cord issue. Right.

Although if you also damage the medial brainstem or you damage your thalamus, that can cause perperceptive issues because those fibers, those drosal column fibers as they ascend, they go through the medial brainstem and they ultimately go to the thalamus. All right. So I think I've explained pretty, pretty conclusively why that's the case. Right. And again, if a person has issues on the right side of the brain, which this person does, it would make sense that they have issues. You'll see like body issues on the left side. Right. Like the person is like, ooh, this person walked into the left side of a doorframe. Right. A trip to a chair that was on his left side tells you that again, the issue is probably on the right side of the brain. Right. And the classic thing they love to do on the exams is this person keeps bumping into cars on the left side. Right. They keep having all these accidents. All right. More than 30 minutes. Let's see if we can maybe do one more. Let's see if we can maybe do one more. Because man, the other questions here, they're kind of, they're kind of intense. All right. So I think let's stop at one oh, you know what? Let's maybe stop at one oh five. I feel like I've kind of hit you guys with a lot of big stuff. Let's maybe do one oh six to one ten in part B. So that's going to be probably the next podcast actually. Right. So please, like the stuff I explained today, I'm just trying to be realistic with you.

The stuff is pretty high you to know for your exams. And these like thinking processes I walked you through in coming to the answers, especially like question 104. These are just very good frameworks to keep at the back of your mind as you're prepared for your exams. Right. Many of these tools and tips and tricks have been discussing throughout the series. They're very helpful testing strategies for the exams. And again, if you like the way I teach, again, I offer a test taking class. I have one taking place tomorrow. And then all the classes I have for step one to step three of our bio stats class. And I have a five hour social science and ethics class taking place this week actually. Those classes, they're not just like me throwing factoids at you. No, no, no, no, no, no. A lot of it exists. Planation and understanding. Again, many people are taking these classes from them to be helpful. And then for step two, step three, specifically, I have a last minute review this coming Friday, I have a 20 hour review next week. And then I have an epic 50 hour class taking place in the first two weeks of June. I've actually made separate podcasts where I discuss these classes. And then I also for one I want you to learn for all the USML and complex exams. And then I also help with ER As applications, mock interviews, personal statements and things of that nature. And then I have this podcast on Apple Google on Spotify. I have a You Tube channel.

You can check out that's where I post the videos I make. Divine intervention, USML podcast and videos. That's where I actually have my my shelf review videos. And then I have another website called Divine Interventional Life Lessons.com. Many of you know that I'm a Christian, proud to be a Christian. And every week I post like two or three podcasts where from a biblical perspective, address a life lesson. So check out Divine Interventional Life Lessons.com. There's an Apple Podcast associated with that called the Divine Interventional Life Lessons podcast. So thank you for listening to me today. I will see you in the next podcast again. Come prepared for the next one because again I'm going to be having a pretty in-depth discussion on a bunch of stuff with the next podcast as well. So thank you for listening to me. I'll see you in episode 595. I believe. God bless you and bye for now. Thank you.

Reduction in immune tolerance after delivery leads to autoantibodies attacking the thyroid gland.

Anti-cyclic citrullinated peptide (Anti-CCP) antibodies.

The proximal small bowel, such as the jejunum.

Failure to secrete chloride and bicarbonate into lumens, leading to thick secretions.

The right upper quadrant/Parietal Lobe.

Methotrexate (a dihydrofolioreductase inhibitor).

Autoantibodies attacking the thyroid gland, resulting from a rebound in immune function after pregnancy.

Anti-CCP (Anti-cyclic citrullinated peptide) antibodies.

The "totem pole" principle; proximal structures are supplied first and are most likely to be spared.

Chloride ($\text{Cl}^-$), Bicarbonate ($\text{HCO}_3^-$), and Thiosulfate ($\text{S}_2\text{O}_3^{2-}$).

The Parietal Lobe.

Superior Mesenteric Artery (SMA).

Autoantibodies attacking the thyroid gland, resulting from a rebound in immune function after pregnancy.

Anti-CCP (Anti-cyclic citrullinated peptide) antibodies.

The "totem pole" principle; proximal structures are supplied first and are most likely to be spared.

Chloride ($\text{Cl}^-$), Bicarbonate ($\text{HCO}_3^-$), and Thiosulfate ($\text{S}_2\text{O}_3^{2-}$).

The Parietal Lobe.

Superior Mesenteric Artery (SMA).