DIP Episode 584 - 2025 USMLE Step 1 Free 120 Discussion Part 4 (Q31-40, super helpful for Step 2 and 3!)

All right, welcome everybody. My name is divine. This is episode 584 of the divine intervention podcasts. In today's podcast, we're going to be continuing the series on the USM at step one free one, 20. This is going to be part four. Again, you're studying for step two, step three, very useful podcasts to listen to a lot of very good knowledge and learning here. And many of these questions, they're kind of like examples of like the shorter step two, CK step three questions you see on your exams. All right. So let's pick up with question 31, three year old boy is brought to the office because of a 2-day history of origin of his left eye. He says his left, his eye hurts. He has no history of major medical illness or recent trauma into the area and receives no medications vital signs are within normal limits. Physical examination shows exopthalmus of the left eye. MRI of the brain shows a two centimeter mass involving the ocular muscles of the left eye. Okay. The ocular muscles of the left eye, a biopsy specimen of the mass shows malignant cells, some of which have striations, which of the following is the most likely diagnosis. Right. So let's try to work this out. So we see this person has exopthalmus, you know, you know, many of us probably know it's a zero gravestis, but again, it's highly unlikely that a three year old will have gravestis and this question stem says nothing about like a neck mass. Right. So it's probably not gravestis.

And another thing to also point out here is that this we're told that this person has a mass involving the muscles. So this is probably a muscle based mass, a muscle based mass, a muscle based mass, a muscle based mass. And another thing that also kind of guides us in that direction is that, you know, the cells are malignant and they have striations. Remember, muscle tends to be strided or obviously they strided muscle and they smoke muscle. Remember, your strided muscle are going to be skeletal muscle or cardiac muscle. Those are your strided muscles. So we need to find a muscle based mass answer here, right? A muscle based tumor. So option A says neuroblastoma that's going to be wrong. Remember many times on the exams that will lead up present as a as an abdominal mass, right, that crosses the midline that is calcified. Although sometimes you can shop in the media, it's not. But because it's a neurogenic tumor, it's going to show in the post-traumatic, it's not. A few chromosidoma is going to be wrong because that's going to present with like episodic headache hypertension. You know, those are pressure like symptoms. That's wrong. Option C says retinoblastoma. Retinoblastoma is not a muscle based tumor. And many times when retinoblastoma presents on the USMLC is going to present in a child instead of having a red reflex, they will have a white reflex. Remember that arises from an RB mutation and that increases the child's risk of osteosarcoma in the future.

A rapdoma is sarcoma, right? It's probably going to be the right answer here. Mayo, that's muscle, right? It makes sense. Rapdoma is sarcoma. It's one of these small blue cell tumors kind of like medallodlastoma or ewing sarcoma or small cell lung cancer, right? It's a muscle tumor so it makes sense that it's going to have striations. Remember, rapdoma is sarcoma's, or let me say a close cause in a rapdoma yoma, a cardiac rapdoma yoma, you may find it in people that have a tuberous sclerosis, right? But rapdoma is sarcoma is a really bad kind of tumor. You know, many times it's going to be in soft tissue. Actually, the most common location is in your genital urinary system. But occasionally you may find it in the eye. In fact, in about 10% of people, about 10% of rapdoma yoma are sarcomas pop up in the eye, right? And then option E says thyroid cancer. That's not what's going on here, right? We don't see anything about a neck mass or anything of that nature here. All right. Now, let's go to question 32. He says, an 18-year-old woman with sickle cell disease is brought to the ED by her parents because of a two-hour history of severe abdominal pain in nausea. Her parents say that she had a cheeseburger, milk, shake, and chocolate bar for a launch. Sounds like a nice meal. Okay, so a temperature is 98.6. Physical examination shows tenderness over the right upper quadrant of the abdomen, radiating to the right shoulder.

Autostanography of the right upper quadrant of the abdomen shows gallstones, which are the following is the most likely on the line cause of this patient's current condition, right? Again, everything you need is going to be in the Q stem, right? So, why would a person with sickle cell disease develop gallstones? Remember, there are many kinds of gallstones. You can have cholesterol gallstones. You can have bilirubin gallstones. When I'm going to hope that you're saying that, ooh, divine, this person probably has bilirubin gallstones. Probably has bilirubin gallstones, right? Because the person has sickle cell disease. It causes himalosis. When you humanize a lot of red blood cells, you're going to make a lot of uncongiagated bilirubin. That uncongiagated bilirubin can get you in some very deep trouble. So, this person is making too much uncongiagated bilirubin. So, they have too much bilirubin in their bowel, right? So, that's why they're having problems, right? So, option E obviously has to be the right answer. Let's look at the other answers here. Decrease the hepatic secretion of less a thin, that's kind of a bogus answer there, right? Option B says decrease your absorption of bowel salts. Again, it's kind of a bogus answer there. Option C is actually kind of a nice one. High ratio of cholesterol to bylacids in bile. That's actually something you can see with cholesterol ghost stones, right? You're making a ton of cholesterol.

Many times we're going to find it in the classic obese person, right? Or a person that has had a lot of rapid weight loss because one of the ways your body gets rid of fat is that cholesterol. So, that's why this person has, you know, may have that problem. But again, this person is not obese, at least we're not giving that information. So, the fact that she is an unhealthy male doesn't mean that she's obese. We don't have any BMI or anything like that. So, we're going to skip that. And then option D says, infestation of parasites, secretion beta, glucoronides, right? That's ridiculous. Right? No, that's not what's going to be causing ghost stones, right? So, the answer here is going to be option E, because just because of the himolises that this person has. All right. Now, question 33 says, in a sample of 100 individuals, the mean leukocyte count is 7,500 per millimeter cubed, with a standard deviation of 1,000. If the leukocyte counts in this population, follow a normal or Gaussian distribution, approximately 50% of individuals will have which of the following total leukocyte counts. Right? This is an easy question. Again, like many bio-stats questions, you don't actually need the formulas these days on the USM list for the most part in my experience. Right? So, remember, a normal distribution, what are the key things to know? Remember, in the middle is going to be the mean. For a normal distribution, in the middle, you have your mean.

And then remember, within one standard deviation of the mean, you have 60% of the population. Within two standard deviations, you have 95% of the population. Within three standard deviations, you have 99% of the population. Right? So, if the mean is the middle, that means everybody below that, half will be below that, half will be above that. So, what's the mean? The mean is 7,500 per millimeter cubed. So, that means, oh, 50% of the individuals will have which of the following total leukocyte counts. Well, it's going to be under 7,500. So, half of the people, because the mean is in the middle, it's the mean is like in the middle. Right? It's in the middle. Right? It's in the middle. It's in the middle. Right? So, half of the population, be below, half will be above. Right? So, half of them will have leukocyte counts less than 7,500, half will have leukocyte counts more than 7,500. It's a bio-stats question, but no math needed. All right. Let's go to question 34. Previously, healthy 52-year-old woman comes to the physician because of a two-month history of fatigue, constipation, and frequent urination. Her temperature is 98.8, pulse is 80 per minute, respirations are 14 per minute, and blood pressure is 140 over 90. The few crackles are heard bilaterally. Her serum calcium concentration is 11.1, and serum per-authorized hormone concentration is decreased.

The chest excretion is bilateral hyaluril in fattenopathy, and interstitial infiltrates, which of the following is the most likely cause of this patient's hypercalcemia. Right? This is pretty straight forward. Right? So, we see a person, right? Bilateral hyaluril at an apathy, has hypercalcemia, pTG is reduced, has all these pulmonary problems. This sounds an awful lot like sarcoidosis, like sarcoidosis. Those are sarcoidosis. Remember, sarcoidosis, there's a bunch of findings, right? And they will have increased LDH, increased ACE levels, right? But remember, one high-yield thing to know about sarcoidosis is that they're going to have hypercalcemia. Why? Because remember, sarcoidosis is a granuloma of us disease, and these granulomas have a lot of epitheliod macrophages. Well, what in the world does an epitheliod macrophage do in sarcoidosis? Well, those macrophages make a ton of one alpha hydroxylase. One alpha hydroxylase is an enzyme that converts calcium diol to calcium trial. So, these people make a ton of calcium trial. Chalcitriol, remember, another name for it is 125, 125 dihydroxyl vitamin D. That's the active one of vitamin D, and that's going to cause you to reabsorb calcium from your gut. If that happens, you're going to have hypercalcemia, right? And because you have high calcium, that's going to suppress your pTH production. That's going to suppress your endogenous pTH production.

So, remember, in people that have sarcoidosis, they're going to have hyper vitaminosis D because of the excess expression of one alpha hydroxylase by the epitheliod macrophages. So, those people are going to get in trouble with hypercalcemia, all right? So, the answer has to be option A. Answer has to be option A. You know, option B says local res option of bone by metastasis, right? This is for patients like bone met. But we don't see anything about bone met in this question, right? Remember, cancers like breast cancer, prostate cancer, and all those things, they love to go to the bone. Option C says parathired hormone-related peptide secretion, that's wrong, right? That's going to be with squamous cell lung cancer. This person does not have any lung mass. So, that's wrong, right? Option D says secretion of parathired hormone. Well, that'll be primary hyperparthyroidism. Say, for example, if you have like a parathired adenoma, again, we don't see anything about a parathired adenoma here. And in that case, your pTH levels will be high. That doesn't make sense for the values we're giving here. And then option E says secretion of thyroid stimulating hormone, that's wrong. Don't get me wrong, actually, hyperthyroidism. Many people don't know this. But hyperthyroidism is actually a cause of hypercalcemia because you're pretty much stimulating. You're born, making your bone go hard. So, you can get reserved.

You can increase the metabolic activity of your osteoclast, resorb your bone and cause hypercalcemia. But again, that's not exactly what's going on here. That's not exactly what's going on here because this person doesn't have all the signs and symptoms of hyperthyroidism or anything like that, right? This person doesn't have signs and symptoms of hyperthyroidism because you may think that, oh, if you're making a ton of TSH, then obviously you make a lot of T3, T4 and that can cause problems. But, no, that's not what's going on here. I wouldn't see any evidence to that regarding this question. All right, we're going to go to question 35. A 55-year-old woman comes to the clinic because of a two-month history of increasingly severe vaginal pain and each and during sexual intercourse. She avoids intercourse with her husband because of the symptoms. She has been in a monogamous relationship with her husband for the past 25 years. She has type 2 diabetes melodies, her vital signs are within normal limits. Physical examination shows a dimadolce and erythematos, vaginal mucus are with white discharge. A photomicrograph of vaginal smears shown, which of the photo means the most likely causal infectious agent, right? This question is pretty easy, right? And this is a picture. You should make sure you're able to identify on your exams. Make sure you're able to identify the stuff on your exams. Super, super high yield to know this stuff for your exams.

Extremely high yield to know this stuff for your exams, right? So we can see a lot of pseudo-high fee, right? We can see a lot of pseudo-high fee. This is candidiases. And honestly, even if they did not give this histological image, this should be pretty obvious. This person has diabetes. Diabetes raises your risk of vaginal candidiases. Why? Because if you're diabetic, you kind of have like a sugary body, right? And a sugary body is very attractive for candidi. Right? People that are diabetics actually have a pretty high risk of candidile infections. That's actually a very high yield association to know for your exams. And also people that have recently used antibiotics, they actually also have a high risk of candidile infections because by using antibiotics, you're going to alter your skin flora. And that can raise the risk of candidile overgrowing. And that can get you in some big trouble. So the answer is A, right? You know, many times when people have candidiases, they have this cottage cheese, you know, white-ish discharge, an option B is wrong, chlamydia trocomitis. A chance is that you won't have chlamydia going over two months straight up, right? That doesn't make any sense, right? That doesn't make any sense. And it's not going to present with pseudo-high fee. Actually, remember, candidata does not gram stain because it's an intracellular, I mean, sorry, chlamydia does not gram stain because it's an intracellular organism.

Hicces is going to present with vesicular lesions that attend here. And they're going to have painfully inguinal lymphatic, we don't see that here. HBV, right? It's going to present with these warlike lesions, we don't see that, that's wrong. And then tricomoniasis, many times it hurts a lot, right? And you're going to see like this frothy green discharge, vaginal pH is going to be over 4.5. And on a KOH prep, you're going to see these are motile proteins, right? This tricomona. So we don't see that in this image, so that's wrong. Right? So the answer is going to be A. And remember, candidiasis, you're going to treat it with an oral lesion, right? Give the person an oral lesion, and the person should be in good shape. Right? Question 36, a 24-year old woman is brought to the physician one month after she was involved in a motor vehicle collision that left her weak and unable to walk. Physical examination shows weakness of both hands and atrophy of the intrinsic hand muscles bilaterally. There is weakness and increased muscle tone of the lower extremities on passive range of motion. Okay, deep tendon reflexes are normal at the biceps and triceps bilaterally. And I increased at the knees and ankles. Babinsky sign is present bilaterally. Sensation to pin prick is absent at and below the level of the clavicles. The lesion in this patient is most likely located in which at which of the following spinal cord levels, right?

You know, for those of you, because I know many of you listen to this podcast at taking step one, but for those of you listening to step two, this is a classic cervical my lopathy question, right? Remember, my lopathy is a spinal cord problem, right? So what exactly do I mean by the word my lopathy? My lopathy is a spinal cord issue, right? And one of the slam dunkues to know you'd learn the spinal cord issue. I've said this many times in this podcast, is you're going to have low moron neuron lesions and upper levels of the body and upper moron neuron lesions at lower levels of the body. I'm going to say that again, low moron neuron lesions at upper levels of the body and upper moron neuron lesions at lower levels of the body, right? So if you notice, this person has like hyperreflexia babinsky, right? Those upper moron neurons signs at lower levels of the body, but you see a lot of lower moron neuron signs at so you see upper moron neuron signs at lower levels of the body. We're seeing a lot of lower moron neuron signs at upper levels of the body. So again, I'm going to say it again, low moron neuron signs at upper levels of the body, upper moron neuron signs at lower levels of the body, right? We see this person having like muscle weakness, right? And this person has like atrophy of muscles, muscle atrophy, that's those are low moron neuron symptoms. We see those at upper levels of the body. This is very classic for cervical myelopathy, right?

So the question then is, or how do you know what level? Right? Well, if you notice the intrinsic muscles of the hands are messed up. So that tells you that, ooh, honor nerve is screwed up. Remember honor nerve is C8 T1, right? C8 T1. So option C has to be the right answer. These are one of those things where you don't know it or you don't know it. Remember C5, the person is going to have like respiratory problems, right? Because remember C345 keeps the diaphragm alive. That's your phrenic nerve. C7 is going to be something like like your like your like your like your forearm and things like that and like your triceps reflex, those are intact, right? So that doesn't really make sense because the triceps is completely intact in this person. So that's wrong. T1 is definitely the right answer. T3, T3 is a lower level. The person is more of a thoracic vertebra problem, but you see that this person has like upper extremity problems. Your upper extremities go from like C5 all the way to T1, right? This person is in the upper extremity. So this has to be a T1 or higher problem. So T3 is wrong and you know T5 is also wrong. Remember T5 is your nipple line, right? If a person loses sensation at the nipple line, that tells you they have a T5 lesion, right? Okay, so that's it for that one. So the right answer here is going to be option option C. All right, let's go to question 37. So 45 year old man is brought to the ED 30 minutes after the sodium onset of crushing chest pain.

His father, maternal aunt and paternal uncleal died of MI's under the age of 50. Physical examination shows tendinus and thomas on the hands and thickened Achilles tendons. Certainly, it studies show total cholesterol concentration of 410. Oh, that's pretty high. HDL of 30 and triglycerides of 140. The diagnosis of MI is made, right? 45 year old. It's kind of odd, right? The patient most likely has a deficiency of which of the following, right? So let's think about this, right? So you see many people dying of MI's early in life, right? This is easily a familial hypercholesterolemia, right? And again, what's the pathophys behind this usually? It's going to be from an LDL receptor mutation. Remember, the LDL receptor is really important because what does it do? It clears LDL from your circulation to lower your serm LDL so you don't get MI's, right? So if the LDL receptor is mutated, that can get you in some hot order. Remember, that's actually kind of related to how statins work, right? Many people do not understand this, but actually the way statins work is that they make your hepatocytes express more LDL receptors on their surfaces, right? So remember, your statins are HMG-coiriductase inhibitors. When you inhibit HMG-coiriductase, when you inhibit HMG-coiriductase, the intracellular concentration of cholesterol within your hepatocytes is going to go down. If that goes down, guess what's going to happen? Your hepatocytes are going to be like, we don't have cholesterol.

This is so bad. So what are they going to do? They're going to express more LDL receptors on their surfaces so you can clear more LDL from the circulation. That's actually how statins work in reducing the presence of their MLDL. So again, familiar hypercholestrolymia, if your LDL receptor is not working, can clear a deal from the circulation. So that's wrong, right? It will be 48, right? Remember, we're going to see this in a person that these people, they will have a better lipoproteinemia kind of deal, right? Because if you lack it will be 48, then all these epolipoproteins, because you have a micro-sumotransfer protein mutation, then you cannot assemble epolipoproteins. You cannot assemble things like chylo-microns and whatnot and get them from the GI tract into your bloodstream. So these people actually have pretty low levels of many of these lipids. That doesn't fit with what we have in this question stem. So that's wrong, actually. So that's wrong. I'm able to see that's that's wrong, right? Again, it's one of these transfer proteins for epo- this your epo-b system. Deficiency of HMG-coeeriductase activity, again, that's not what's going on here. Remember steroids, I mean, if a person actually has a deficiency of HMG-coeeriductase activity, they will actually make less LDL, right? They'll make less LDL in their hepatocytes. They'll actually make their hepatocytes express more LDL receptors and bring down the LDL, right? So option, option C makes no sense, right?

And option E says a lipoprotein lipase activity that's wrong. Remember, lipoprotein lipase breaks down, breaks down lipids. That's not exactly what's going on here. And he breaks down lipids, but that's not what's going on here. You see multiple family members getting their eyes. That's going to be a family hypercholestrolemia LDL receptor problem. Alright, let's go to question 38. So a previously healthy 19-year-old man is brought to the ED 30 minutes after he collapsed while playing softball. He had severe sharp upper back pain prior to the game. He's 6'5 inches tall. That tells you all you need to know, right? His temperature is 98.6, his tacky cardic is the caponic blood pressure is super low. Physical exam shows pala and no JVD. Breath sounds are clear. The crudid pulses are weak. A great father, six, lead to a stolic memory is heard at the left of your external border, right? That sounds like the moment of aortic regurg. Which of the following is the most likely cause of the patient's cardiac findings? So tall person, bacheus pain, right? This person probably has morphins, bacheus pain, this is aortic dissection. Remember, poor that have morphins, they can have aortic aneurysms. Those things can pop the order and they can get in some hot water. They can get in some hot water. So this person has aortic dissection or they may have like a ruptural aneurysm. We know this person has some kind of aortic problem, right? So the right answer has to be E, right?

I remember whenever you have like dissection or whatever, that dissection can create a false looming and that can actually prevent forward flow of blood within the order. So blood that cannot flow forward in the order will begin to back up towards the left ventricle. So many times you actually have the murmur of aortic regurgitation. That's why this person has this father, six, lead to a stolic memory of the Lord, left, external water. So the answer has to be E, right? Option A says etrocepto defect. That's wrong, right? You're going to see a white fixed split of the S2 heart sound. We don't see that. Option B says mitro stenosis. That's going to be a stolic murmur, right? Herde best at the apex. We don't see that here, right? Option C says papillary muscle rupture. That's going to present with the murmur of mitro regurgitation, right? So that's going to be a whole, like a whole stolic murmur at the apex. We usually see that as a complication of an MI within a few days of the MI. That's not what's going on here. A perforated tricospid valve. Remember, if that happens, that may cause a tricospid regurgitation. That's going to present as a stolic murmur, probably as a whole stolic murmur at the left-lower external border. Because remember, that's where the tricospid valve is. Again, that doesn't feel what we have here, right? So that's wrong. That's wrong, right? Because it's a stolic murmur at the left-lower external border, not a stolic murmur. So that's wrong.

Question 39 says, the 27-year-old one is brought to the 80 because of a two-week history of double vision. Okay. Neurologically examination shows that the left eye does not adduct, 80 duct, past the midline on horizontal gaze when the patient looks to the right. Horizontal gaze noise stug must in the 27-year-old woman that tells you something, right? Left-ward horizontal gaze is normal. The patient's ocular movement deficit is most likely caused by damage to which of the following structures. Come on. What do you think this is? Whenever you see a woman in her 20s or 30s with eye problems, it's probably a woman that has MS, multiple sclerosis, right? Remember, in MS, you can have two hypothologies. You can have painful, sudden, unseid vision loss, right? Or an after-improbably-defect. That's optically right, this. But another thing you can also see is inter-nuclear ophthalmoplesia. Remember, whenever you want to do horizontal conjugate gaze, right? So let's say you want to look towards the right, for example. If you want to keep your head straight and fuller moving object towards the right, your right eye has to AB, AB, abadduct. That's cranial six, right? That's your lateral rectus muscle. And then, for your left eye to follow that movement, your left eye has to add duct. Okay? So you're having this conjugate movement, right? One eye is abducting, that's the right eye. One eye is adducting, that's the left eye. If you're trying to fuller an object right, right? Right?

If you notice that, wow, the adducting eye is having a problem. It means that the thing that coordinates that horizontal movement, right? There's like a coordinator of one eye abducting and one eye adducting. That's going to be the MLF. And it's usually going to be the MLF on the same side as the adducting eye. The MLF on the same side as the adducting eye. So if you're having an adduction, my stag muscle horizontal conjugate gaze, then that tells you that, ooh, the controller is not working, right? So since the person is having issues with adduction, right? Of the left eye, it means the left MLF is messed up, right? So the answer has to be option B, the answer has to be option B. Okay? The answer has to be option B. I may ask yourself divine, but isn't adduction controlled by media rectus? You know, what if this is an actual cranial three deficit? One way you can tease that apart is by just checking the presence accommodation. People that have MLF problems, they'll have normal accommodation because the MLF has nothing to do with accommodation, right? So let's look at the other answers. Option A says left abducing nerve. That's wrong, right? If you have an issue with your left cranial six, you're not going to be able to ab doct your left eye. This person has issues with adduction of the left eye. Option B says left MLF, right? We've already said that that's the right answer. Option C says left nucleus of the abducing nerve. Again, that's wrong, right?

We're going to have eye abduction problems. We don't see that here, right? That do sense nerve again. It's going to be a right eye abducing problems. We don't see that here, right? MLF. If you have a right MLF issue, then you will see the effects of that lesion when you're trying to follow a leftward moving object because we're trying to follow a leftward moving object. Then your left eye, your left cranial six has to help with your left eye ab docting and then your right eye has to adduct. So if you see an adduction, my stagmas in the right eye on horizontal conjugate gaze trying to follow a leftward moving object, then option E will be right. But that's not what's going on in this question. And then option F says right nucleus of the abducing nerve again. That's wrong, right? That's wrong. And also if you damage the nucleus of the abducing nerve, it's in the ponds, right? And the abducing nerve is in the medial ponds. It's in the medial ponds. So the person is going to have, if you're damaging the actual nucleus, you're going to have other issues, right? You're going to have issues like, for example, Dorsal column issues because the Dorsal column runs in the medial brain stem, you're going to have other issues like cortical spinal tract issues because the cortical spinal tract also runs in the medial brain stem. We don't see any of those problems. So that tells us that this is probably not a brain stem issue.

That actually, the fact that we lack cortical spinal tract problems in this question and the fact that we lack Dorsal column medium lemnescus problems in this question tells us that this is not a brain stem issue. This is not a medial point in issue by any stretch. So we can cross that off, right? That's actually a pretty, pretty good one there. All right, question 40. A 45-year-old woman is recovering from ARDS secondary to Ghoston pancreatitis, a joint of the aviolar wall is shown, which of the following labeled cells will most likely proliferate and reestablish the injured epithelial layer in the speech. Again, before we start dealing with these questions, work it out for us, right? So remember, whenever you injure the lungs, there are many kinds of cells in the lungs, right? So, you know, your lungs has type 1, the most sides. Those are the things that participate in gas exchange. And then we have the type 2 numo sites. What's their job? Remember, the type 2 numo sites, the mix are factants, right? And if you have lung injury, they can regenerate, they can differentiate and form a type 1 numo sites, right? So that's something that's pretty high yield to know for your exams. So we need to pick out the cell, right? Again, the thing is whenever I see pictures like this on the exam, I always ask myself, what do I know? Right? Many times if you orient yourself, that's the name of the game with anything with imaging.

So this is, I guess, a pro tip for anyone going into radiology, a pathology, just always orient yourself first. Ask yourself, what do I know? And then kind of work your way outward from there, right? Red blood cells, I feel like most people can deal in it or red blood cells pretty easily on an exam, right? They look like coins, right? They have this kind of weird shape. So we can see this from this diagram that B, because we're looking for the type 2 numo sites here, right? But obviously, B are the red cells. We know that B does are the red cells, right? So at least that gives us some degree of orientation. We can think and build from there. So what will be the thing around the red cell? We'll remember red cells flow within blood vessels, right? They flow within blood vessels. So that means we're probably dealing with the endothelium of the of the capillaries, right? In the endothelium of the capillaries, because that's pretty close to the red cells. So option A has to be the endothelium of the capillaries. Well, let's look at C. C seems to be like on the other side, right? So remember, your type 1 numo sites are very, very close to your your pulmonary capillaries, right? Again, so you can have that gas exchange. So C is probably a type 1 numo site. C is probably a type 1 numo site. And then we see D. D is probably the type 2 numo site. You see how big it is, where you see how big it is. And it seems to have all these like granules within it.

Those things are surfactant, actually. Those things actually surfactant. So D has to be the right answer. You can see option E. We have these cells with all these projections. That's very, very, very, very classic for a macrophage. Remember, sometimes they actually called dust cells. Those are the things that clear away junk from your lung, the clear away junk from your lung. Remember, one of the things that those things make in doing their inflammatory business are proteases, right? If you're a big time smoker, there's always going to be a lot of junk in your lung. All those proteases that are made by the macrophages to help you deal with stuff. Those proteases can begin to drop your lung pyrexoma, and you can begin to get emphysema. Remember, if you look at things from another perspective, if you have alpha and antitripsin deficiency, you're not able to make antiprolesis like alpha and antitripsin. So you can deal with the proteases that come from those macrophages, right? Those are viola macrophages. So the answer here has to be option D. All right. So this is the end of part four. Let's stop here. Again, if you like the way I teach, you're going to love my classes. I have classes for step one or the way to step three. Today, actually, I have a last minute review for step two, step three is over Zoom. It's this evening. The next week I have a 20-hour step two through review.

And then in the first week of May, I actually have a 25-hour step one review if you're interested in that. And I have other classes like a Biosdats class, a test-taking class, social sciences, QI ethics class. Again, if you're interested in those classes, just shoot me an email. Many people who have taken these classes and don't extremely well on their exam, shoot me an email, I can give you some more information. And these are even people that have taken the exams as recently as like this month and last month, right? So these classes are very well put together, really helps a lot of people. And then also, if you want to want to learn for all the USML and complex exams, and then I have this podcast on Apple, Google and Spotify. So check those out, you know, also have a You Tube channel, Divine Intervention, USML, Podcasts and videos. That's where I post the videos that I make. And then I also help people with ERAS applications, mock interviews, personal statements, and things of that nature. And then, finally, I have another website called Divine Intervention Lifelessens.com. Many of you that listen to this podcast, you know, I'm a Christian. So I have another website called Divine Intervention Lifelessens.com. And every week, my post like two to three podcasts were from a biblical perspective address a life lesson. There's actually an Apple podcast associated with that called the Divine Intervention Life Lessons podcast. So thank you for listening to me today.

Again, if you're interested in any of my classes, just shoot me an email. I can give you some more information. And also our specific podcasts have made where I discuss these classes. So thank you for joining me today. I wish you the best on your exams. I'll see you in episode 585. God bless you. Bye for now. Thank you.

Bilirubin (pigment) stones, due to increased unconjugated bilirubin from hemolysis.

1-$\alpha$-hydroxylase, leading to excessive calcitriol production and gut calcium absorption.

Pseudohyphae (or thick white discharge).

C8-T1.

Aortic regurgitation (AR) murmur, as blood backs up into the left ventricle.

They differentiate and regenerate into Type I pneumocytes to reestablish the gas exchange surface.

Bilirubin (pigment) stones, due to chronic hemolysis increasing unconjugated bilirubin load.

Epithelioid macrophages within granulomas overexpressing 1-$\alpha$-hydroxylase, leading to excessive calcitriol production.

C8-T1 (Cervical Myelopathy).

Aortic regurgitation (AR) murmur.

Type II pneumocyte.

Candidiasis (Candida species).

Bilirubin (pigment) stones, due to chronic hemolysis increasing unconjugated bilirubin load.

Epithelioid macrophages within granulomas overexpressing 1-$\alpha$-hydroxylase, leading to excessive calcitriol production.

C8-T1 (Cervical Myelopathy).

Aortic regurgitation (AR) murmur.

Type II pneumocyte.

Candidiasis (Candida species).