DIP Episode 593 - 2025 USMLE Step 1 Free 120 Discussion Part 10 (Q91-100, super helpful for Step 2 and 3!)

Alright, welcome. My name is Divine. This is episode 593 of the Divine Intervention Podcast. Today's podcast will be contained in the series on the Step 1 3 120. It's gonna be series 10. We're gonna be doing questions 91 to 100. Alright, let's get on with question 91. A 4-year-old girl with type 1 diabetes is brought to the ED by her father. Because of a 4-hour history of 4 episodes of restlessness, sweating and confusion that occurred during the night. Yesterday, he allowed her to eat cupcakes and cut in candy at a county fair. At her bedtime, that evening, he increased her dose of sub-Q. In midi, acting and long acting in solid. Her symptoms began six hours later than results spontaneously. After being informed this morning of this nighttime episode, the mother insisted the father bring the patient to the hospital. On arrival, the patient is alert, her vital signs are within normal limits. Examination shows normalities. Her finger stick blood glucose is 72. Your analysis is negative for glucose and ketones. Which of the following is the most likely explanation for this patient's nighttime symptoms? Right, so again, let's work this out. This person, the dad kind of bumped off her dose of insulin. And surprise, surprise, the person is sweating blah, blah, blah, blah, blah. Alright, and confused. Many people don't think about this, but hypoglycemia can actually be pretty deadly. Hyperoglycemia will kill you, but it's kind of a slow process.

Well, hypoglycemia can certainly end you pretty quickly. And we see a glucose is low. So this person has hypoglycemia. So you can pretty much get rid of options A through C. We see that all these symptoms were preceded by that just really bumping on dose of insulin. That was not maybe not the wisest thing to do. So it has to be a hypoglycemia answer, again, because the dad just gave too much insulin. So the answer is going to be option D. Again, this person literally does not do hyperoglycemia. And then option E says, hypoglycemia caused by excessive renal glucose loss. Well, do we see glucose in her urine? No. Hypoglycemia caused by increased glucose-gone secretion. That'll be something that you would have when you're in a state of low insulin. Because remember, insulin is made by the beta cells that are in the center of the pancreatic eyelids. As insulin is living those pancreatic beta cells, it kind of stops glucose-gone production. Insulin is actually a very good inhibitor of glucose-gone production. That's why when people develop an insulin deficiency, glucose-gone and all these counter-evolutory hormones rise, and then they go into decay or HHS. But again, this person actually got insulin. So their glucose-gone should actually be low. And glucose-gone actually raises your blood glucose. It doesn't lower it. So that's wrong. That doesn't make any sense. And this is not a nightmare sleep terror. That's where they go last. So let's go to question 92.

75-year-old woman comes to the physician because of a three-year history of pain in her wrist and hands. She says that the pain has become more severe during the past three months. She has difficulty botting her coat because of the pain. Physical examination shows the findings in the photograph, which of the following additional hand findings is most likely in the patient. So we see a person that's 75. We look at her hands, and even if you don't see a picture of the hand, even if you don't know the hand picture is showing. An old person would join problems. They probably have osteoarthritis. They probably have osteoarthritis. Again, one thing that just kills people on the USMLS is just something simple and basic. They just try to make it harder than it needs to be. The USMLS is trying to trip you up. Just read your question, pick the simple answer. This is osteoarthritis. So now it's just about knowing what you find on imaging and a person that has osteoarthritis. So what would we find in a person who has osteoarthritis? Well, remember, what are the classic, let's kind of walk through this. I think this is actually a useful thing to do. So what are the classic findings in osteoarthritis? Well, osteoarthritis, you're going to see asymmetric joint space narrowing. You're going to see osteophytes. You're going to see the joint space narrowing because of the thinning of the articulocardialage. You're going to see sub-control sclerosis. You're going to see sub-control cysts.

And make sure you can identify those findings on imaging. Those are actually things that the USMLS loves to test. Then contrast our rheumatoid arthritis where you're going to see symmetric joint space narrowing. You're going to see a panace. It's just like reactive synovium because of all the inflammation and things like that. So let's look at the answer. The answer is called a cool thinning. That's wrong. We tend to see that mode osteoporosis. Osteoporosis. The generative changes of the cartilage. Yeah, I'm going to pick that. A joint space narrowing. That's what causes it because of the degeneration of the articulocardialage. So, B is the right answer. Inflammation. Osteoporosis is more of a non-inflammatory arthritis. So C is wrong. That's more RA. Option D. Neutral flicking. Filtration of the synovium. That's more RA. Option E. Thickening of the synovium with panace. That's more RA. All right. Again, it's pretty straight for a question. All right. So, question 93 says, a 66 year old man who was recently diagnosed with Parkinson disease comes to the... So please, knowing the joint findings of... Like things you find on imaging or whatever, in these joint disorders is kind of high yield. All right. 66 year old man who was recently diagnosed with Parkinson's disease comes to the physician for a full-up exam. Carbidopa-livodopa therapy was initiated at the time of diagnosis. The patient tells the physician that he still has episodes during which he freezes.

He has a clumsy gate and there's rigidity of his upper extremities and hands. And a joint therapy designed to inhibit which of the following enzymes is most likely indicated in this patient. Right. So, this person looks like Carbidopa-livodopa is not controlling symptoms. So, we need to find some other drug that can kind of target his Parkinson's symptoms. Right. So, option A says aromatic Elaminocidicurboxylase. That doesn't really make any sense. There's no Parkinson's drug that targets that enzyme. There's no Parkinson's drug that targets that enzyme. And then option B says dopamine beta hydroxylase. No. That's not going to be... That's not going to be the right answer. So, dopamine beta hydroxylase converts a dopamine to a neuropinephyrate. Right. That's... That... No. Right. That there's no Parkinson's drug that works on that. Option C says monaminocidase B. That's the right answer. Right. There are Parkinson's drugs like cellulina or acetylene. They work by inhibiting MAOB. MAOB is an enzyme that breaks down dopamine. So, if you shut it down, you'll stop breaking down dopamine. Your dopamine levels will rise. So, C is the right answer. Option D says phenol ethenolamine and methyl transferase. That's an enzyme that converts a neuropinephyrate to a penephyrate. Remember, the big difference between a penephyrate and a neuropinephyrate is that a penephyrate has a methyl group. Right.

So, you take a methyl donor, like esadenosilmethyonine-sam, and it kind of plumps a methyl group on a neuropinephyrate. So, you can make a penephyrate. Right. Again, that has nothing to do with dopamine metabolism. That option E says tyrosin hydroxylase. Tyrosin hydroxylase converts tyrosine to L-duper. Right. Again, there's no Parkinson's drug that works like that. So, the right answer has to be option C. Monaminocidase B. All right. A two-week old male newborn is brought to the office for a well-challenged exam. He was delivered following an uncomplicated spontaneous vaginal delivered for the one-week gestation. The mother has no history of serocelness and did not receive prenatal care. Her only medication is a prenatal vitamin. She has consumed a large amounts of vodka. Oh no. Ninety for ten years. Which of the following examination findings is most likely to be present in this patient? So, this one is considered a ton of alcohol. So, they are pretty much asking about fetal alcohol syndrome. Remember, fetal alcohol syndrome, you're going to see the smooth philtrum. Man, they love to test that, right? The smooth philtrum. The thin vermilion bother. They will have these as short-pop fiber features. They will have the epicanthal folds. They can have a lot of cardiac defects like VS Ds, for example. There's a bunch of stuff that they can have. And remember, alcohol is actually the most commonter hydrogen. They can literally test that as an epidemiologic question on your exam.

Literally, the most commonter hydrogen is alcohol. All right. So, let's basically pick out the right answer. I'm hypospidia, that's wrong, right? That's where your urethra, instead of coming out straight through the penis, comes inferiorly through the penis. Remember, people that have those, that problem, either hypospidia or epispidia, you don't do a circumcision for them, because you're going to use the foreskin to fix those urethro defects. Option B says limb hypoplasia. Well, that's, that's fochomilia, right? That's thali doma, that's no fetal alcohol syndrome. Option C says neck, webbing. Remember the webbing of the neck? Uh, those are cystic hygromas. We tend to find it in turner syndrome. Remember, that's an example of a congenital lymphedema. Very high, you'll know the stuff, for example. It's a congenital lymphedema. That's turner syndrome. That's not what's going on here. Option D says shop pop, people are features. That's the right answer. Option E says, but sticity. Hmm, sticity. We tend to find that with like a neurological defect or something like that, you know, like cerebral palsy or something, along those lines. That's not what's going on here. So we're going to skip that. All right, so the answer is D. Okay, now, the next one is a HPI question, right? So it's a 16 year old male, Hispanic coming to the clinic. It's puberty hasn't started. Doesn't have pubic and facial hair.

And again, I think I've said this, in a podcast in this series, your pubic and acillary hair is an indication of what your testosterone is doing, right? And then your breast size and the indication of what your estrogen is doing. That's a very high-yield thing to know. It helps with many of these disorders. Okay, so small penis, absentech, it's testicle is small too. Okay, doesn't take meds, doesn't have allergies, doesn't use drugs or anything like that. And honestly, his vital signs, let's see, his BMI is a 94% towel. Wheat is 97% towel, high than 90% towel. So this person is kind of tall. His tall kind of seems obese, I guess. Okay, let's look at his physical exam. Long extremities, no facial or acillary hair, bilateral organic homosteia. So see a tall guy with got a homosteia, that's you're gonna tell you something, right? Small testicles, poor development, sexual maturity reading. To remember, SMR is the same tenor stage and basically I've talked about that earlier in this series. So, and then we look at his labs. And his testosterone is pretty low, right? And his FSHLH, again, I'm not gonna look up those lab values, but those values look kind of high to me, but you can look those up in your own time. TSH looks completely fine. So, he says, which of the following is the most likely on the line cause of this patient's condition? Again, remember on the USML, he's just stick with the classics. Stick with the classics and you won't get in trouble on your exams.

We see a guy that's pretty tall, right? And this guy has got a homosteia and he asks a micro penis, small testicles. It's pretty classic for client filters syndrome, right? It's pretty classic for client filters. Pretty classic for client filters. That's what's going on here. All right, so now let's look at the answers. So, option A says constitutional delay in puberty. Now, constitutional delay in puberty, the child is actually gonna be short, right? And many times when you take x-rays of the left wrist, you'll notice that the bone age is less than the chronological age. The chronological age is your real age, right? And many times you'll notice that those kids, they have a history of parents having like delayed growth. You know, the parents did not grow very well as like, you know, very young kids. And then later in puberty, they just skyrocketed in terms of how quickly they grew. But those kids, all their vitals, everything will be completely normal. It's not as early as you're gonna commas you anything like that, right? And the child will be short, not tall. This person is in the 90th percent. He's six, he's a six footer. No, that's not what's good. So he doesn't have a concert delay in puberty. Okay, ocean b says hypoplesial hypotheramic genariche neurons, right? So that's gonna be common syndrome, right? So, you know, your genariche producing neurons do not work. So basically your genariche is low, FSH LH is low. So your gonads will not be stimulated.

So you're gonna have low sex hormones. So you could be that, right? Because this guy's testosterone seems like it's low. But this FSH and LH look pretty robust. Again, I don't remember the exact values, but it look pretty robust. And also in common syndrome, you should have an ausmia. We don't see any an ausmia giving on physical exam in this person. So that's wrong. Option C says in activity mutation of the FSH receptor. So if you have an activity mutation of the FSH receptor, all right, fine. You won't make FSH. And that will cause your gonads to not, you know, make testosterone because your gonads also not make estrogen, right? So if you're not making estrogen or testosterone, then yeah, that explains the low testosterone values. But the thing is that would not explain this person being tall, that would not explain this person having gynecomastia, right? Because if your gonadotropins are low, then your estrogen is probably gonna be low. And you probably will not have gynecomastia. So again, that doesn't completely feel with the data we have here. So that's wrong. Option C says mutation in the 21 hydroxylase gene. Remember, that's the most common cause of congenital adrenovipraplasia. I'm just gonna have like salt wasting, right? So you're gonna have like signs and symptoms about nocturn deficiency. So they have like hypo-neutrymia, hyperkalemia, metabolic acid doses.

And in addition to that, they will also have skin hyperpigmentation because they're not making corduz also. There's no negative feedback. So their ACT is high. So the ACT is high. They're melanocytes. They will let you know hormone who will also be higher. Remember, MSH and ACT are made from the same ancestral monocleopom scene, right? And also those people will have, they will have like a bigotry and stuff like that, right? That, that, well for a guy, for a guy I guess, because this is male, they may not have a bigotry. Because actually in 21 hydroxylase deficiency, you make a lot of DHS, right? So that actually, that young guy, a guy with 21 hydroxylase deficiency will have pre-cushious puberty. Okay, let me clarify this. This is actually extremely high utonoferexamps. So the effects 21 hydroxylase deficiency in a lady, because she's being exposed to a lot of DHS and stuff. She may have like, and bigotry and atelier, right? But a guy that has 21 hydroxylase deficiency, because they're making a lot of DHS, they will actually be like super guys, right? So because they're making all this exogenous, like not, it's endogenous androgen, right? But it's coming from the adrenals. DHS is a weak androgen. That will actually cause the guy to have signs and symptoms of pre-cushious puberty. So you have, you will have like pretty robust puberty can accelerate here. So actually that does not matter what we have here. So that's wrong.

So you see we've conclusively got in rid of A through D. So E is obviously right, right? So option E non-disjunction of ex chromosome during myosis. That's the right answer. That's something you're gonna see with fragile X, sorry, client-felture syndrome, right? 47 XXY. So they acquire an additional X chromosome, because during myosis, during anaphyse, two of the homologous ex chromosomes fail to separate. So it's like one gamut gets both, right? So that's how you get in trouble, because if you get a Y chromosome from that, and then you have a gamut from mama, whatever, the has two excromosomes, then you're gonna get in trouble, right? So that's how you get for the 7 XXY. So the answer is E. Remember non-disjunction is when homologous chromosomes fail to separate during anaphyse of meosis. All right, so question 96, of 57 year old man with chronic low back pain comes to the office for routine health maintenance exam. Last week to the office was two years ago. Today's doing about the same, except that it is gained 22 pounds. Actually, it's the weight gain to inability to exercise because of his back pain. He's now considering applying for disability benefits. It was evaluated by a back pain specialist three months ago, God an MRI. The understand was especially so sane. Well, some who don't do good jobs as doctors. Medical history also is remarkable for hyperlipidemia, allergies, opioid use disorder, hasn't used opioids since he stopped taking oxycodone five years ago.

He takes a tovers starting like Lufena, kind of lorata deen, develops skin flourishing when taking Niasaimbo, has no drug allergies, he has smoked a lot, two packs for 25 years, previously drunk two years daily, but hasn't consumed any alcohol or used any nutritional drugs for the past five years. Okay, so he's kind of turning his life around. His BMI is 33, so he's kind of obese. Vital signs are within normal limits, blood pressure is one, 20 over 70. Okay, well, standing patient leans forward slightly. Okay, range of motion on a lumber extension and flexion is decreased. The remainder of the exam shows no abnormalities, results of fasting serum studies are shown. I look at all these labs, honestly, these labs look pretty good to me. Well, sterocoolestero is kind of high. So, excuse me, I think I may be getting over something, but he's sterocoolestero is kind of high. But all that and that, I think it looks pretty good to me. MRI of the lumber spine is shown, which are full in factors in this patient's history, most strongly contributed to the MRI findings. So, again, I know some people are like, oh no, I gotta get my radiology residency done to read this question. No, I've said this too many times. Again, most of the time on the USML is the image doesn't matter. Right? Just read the question carefully. Think of what is simple and classic and you're good to go. This guy, basically like he has this stoop forward, because he has back pain.

Well, you see people that have back pain and they're like stooping forward to feel better. That's a pretty classic presentation of like a lumber spinal stenosis, right? They get better when they push a shopping cart, when they stoop forward. When they bend forward, that's lumber spinal stenosis. Again, many times you're gonna get it because of like osteoporosis, right? That osteoporosis is gonna cause like stenosis of the spinal canal, right? So we just need to find an answer here that relates with osteoporosis, right? So, oxygen is says alcohol. Alcoholism does not necessarily cause osteoporosis. Secret smoking certainly has a big as your osteoporosis, right? So we're gonna keep option B, you know, dichlorofenacuse, that's an end set. That's really cause osteoporosis. Lorette, then that's anti-histamine. Doesn't cause osteoporosis, right? That's more for like nasal allergies, opioid use. No, and this guy's in use the opioid in a long time. And the alcohol also, don't get me wrong. Can alcohol cause osteoporosis? It can actually. But the thing is this guy does not have a recent alcohol exposure. It could drink in a long time ago, right? We should kind of give this guy kudos for doing the right thing, right? Secret smoking is the right answer. So the answer is B. What are some other risk factors for osteoporosis? If you have low weight, but it's not present in this guy.

If you're taking a ton of steroid, you know, for some systemic disease, or you have like cushing, that can raise your risk of osteoporosis, right? Or if you're taking, if you have like hyperthyroidism, or you have like primary hyperthyroidism, right? Hyperthyroidism is gonna increase the metabolic activity of osteoclastic and kind of, you know, true of pure bone. Or if you have primary hyperthyroidism, that high pTH is kind of true in up your bone, right? So, but he doesn't have any of those risk factors. So the answer is gonna be option B. Actually, cigarette smoking, they love to test it on the USMT is a lot as a risk factor for osteoporosis, right? That osteoporosis is what has led to this guy's Lombard Spinosis and Ossus again. I don't care about what the MRI says. Although you can, if you know what you're looking for, the MRI clearly shows Lombard Spinosis, but again, you don't really need that for your exams. All right, question 97 says, a 15 year old boy is brought to the office by his parents to discuss results of a biopsy done three days ago from rapidly and large in neck mass. He first noted the mass one month ago. Two weeks ago, he was evaluated for an episode of prolonged epistaxis. I was found to have a right ear effusion, which was treated with amoxicin and clavolanic acid. He has no other histrocyrosion as antics and medications.

Highly is at the 10th percentile, with is at the fifth-ehrth percentile, BMI is at the 75th percentile, vital signs are within normal limits, right? Okay, physical examination shows a right ear effusion on a four centimeter firm mass in the right posterior triangle of the neck. Results of a biopsy specimen show squilloseypithelium with indistinct cell margins and large dtpcone nuclei and absencharate information. Which of the following infectious agents is the most likely on the line cause of this patient's current condition, right? So this is a young kid. And we see that he seems to have like a cluster of like, no problems, right? So like, he had bleeding in the nose, had an ear infection, and he has this neck mass, right? And we're told that this neck mass has, you know, indistinct, squilloseypithelium, indistinct cell margins, and large dtpcone nuclei, absencharate information, right? So again, I kind of know what I'm looking for here, but this will be, I think for most students, it would be an example of a question where they're like, what? I don't know what they're talking about. And you should be able to answer these questions, right? So let's kind of walk through this, right? Let's do the process of elimination, right? So let, I wanna try to put myself in the shoes of the average test taker, put yourself in your shoes, and then let's kind of walk through this question in a good way, right? So option D says, HHV8, right? We know that HHV is a zero-caposis recover.

Caposis recover, tend to find in immunocompromised people, and they put a half HIV, right? Or like post transplant patients, and you know, they'll present as a lot of skin lesions. We don't see that in this question, so that's probably wrong, right? And then option C says, HIV. Well, the thing is HIV, you know, will present, can cause like an acute ritual viral syndrome, you know, they'll have like diarrhea, they'll have like diffusal lymphatic anopathy, and all those stains, and it's gonna be the present as like sexually active and whatnot. We don't really see evidence to that here, so we're gonna go ahead and cross that off, right? Option B says, HIV, V. Well, what are the things you know as you know, HIV, V? We know that HIV can cause oral hair, you look oblique here. HIV can cause mono nucleosis, HIV, V can cause a Burkitz lymphoma, or the Burkitz lymphoma, it's a lymphoma, right? So, main times, it can present as a neck mass, though. It can present as a neck mass. So, this person has a neck mass. But the thing is, right, remember in Burkitz lymphoma, you're gonna have that 814 translocation, you're gonna see a lot of lymphocytes, because it's a lymphoma. The biopsy, not sure any lymphocytes here, right? So, I don't know if we should pick that answer, but EBV. Also EBV, right, let's not forget, it also causes like post-transplant lymphoperli free-liptive disease, and also it also causes Nezopharyngeal carcinoma, Nezopharyngeal carcinoma, right?

Look at the name, Nezopharyngeal, Nezonose, firing, pharynx, Gial carcinoma, right? So, you can cause issues with the nose, you can cause like a lesion in the nose, it can cause a lesion in the pharynx, right? We tend to find it in people that are from like East Africa, people from Asia, right? In fact, let me tell you this. If you see any thing about the nose or the throat, in a person from Southern China on your exams, that's Nezopharyngeal carcinoma, right? So, B actually seems pretty good for this one. So, let's keep it. But let's look at A, CMV, right? So, remember CMV causes are ignitus in HIV, in people that are immunocompromised, it can also cause colitis, right? I'm gonna see those A's, A, nuclei, A's, nuclei, right? We don't see that here, right? We don't see that here. So, that's wrong. So, honestly, just by the process of elimination, option B makes a ton of sense as the right answer. So, I'd go ahead and pick option B. This person, again, if you don't know what this is, this is Nezopharyngeal carcinoma. You know, many people are used to it being tested as a nose mask, but it can also present as a pharyngeal issue, right? Again, that's, it's called Nezopharyngeal carcinoma for a reason. I just wanna kind of throw that out there. Nezopharyngeal carcinoma, I said it all in EBV, right? And the thing is, even if it's a zero in EBV, you're gonna notice a lot of squamous epithelium, right?

You're gonna notice a lot of squamous epithelium, but it's not a squamous cell carcinoma. It's not a squamous cell carcinoma. That's a very important thing to keep in mind. And one of the ways we know it's not a squamous cell carcinoma from this question is that carotene is not formed. Remember, you typically are gonna find carotene positivity in squamous cell carcinomas in pretty much every region of the, at least in most regions of the body, right? So this is not a squamous cell cancer. It's a Nezopharyngeal carcinoma, strong as your EBV. EBV is like the causing like more than 90% of cases or something like that, right? So that's something pretty high to know. Many times, again, it's gonna present with like a mass in the nose or a corn nose bleed. Sometimes they can have like, you know, like recurring ear infections and things of that nature. That's probably why this child kind of had this ear, fusion or whatever, all right? Because again, sometimes these things can cause obstructive symptoms. All right, let's go to question number 98. 48-year-old woman with type 2 diabetes comes to the physician for a full-up exam. Cream medications are made for me and ones daily in soul. She travels frequently and works long hours. She says that her meals are usually fast food. She leads a sedentary lifestyle. She often forgets to measure a blood glucose concentration. Alastair 1 C was 8.4%.

Which of the following is the most upper reduction by the physician to help the patient improve for a diabetic control? So this person, right, like, a diabetic is no longer a control. But everyone sees pretty high, right? This person is on a slippery slope to disaster, right? A slippery slope to disaster. And, you know, she does eat healthy food, right? Of course, that's going to push up your A1 C, right? Now, for patients like these, you don't want to demean them, right? You want to be gentle with them. And you want to, again, use this technique known as motivational interviewing, right? But if you're not interviewing, you're not the one speaking. You're basically listening to the patient. And you're trying to get them to see things out loud. When you get people to see things out loud, it's actually a very good way to kind of bring them on board with things, right? And many times you just want to ask them like, hey, you know, what are your goals for your health? You know, basically just keep them talking, keep them talking, right? Keep them talking, right? The thing is, if you get them to name things, to talk through things themselves, it's really, really helpful. So let's look at the answers here. Option A says, create an exercise regimen for the patient. You've not talked to her about this diet or whatever, it's just like, hey, I'm just going to make a workout in regimen. And again, remember, for these ethics questions, you want to talk with the patient, right?

Option B says, explode barriers to diet adherence. That's a great one, right? Because you're pretty much like saying, hey, okay, like what? What are some things in your life that maybe make it hard for you to adhere to a good diet, you know? And then you can get them to stand naming strategies of their own to maybe keep a healthy diet. I'm going to keep option B. Remember, for ethics questions, you got to rule out every answer. Option C says, increase the patient's insulin dosage. That's not a good thing to do. That's bad medical practice. Some physicians will do that. But that's bad medical practice. You're not addressing the underlying problem, right? You're literally not addressing the underlying problem. So that's wrong. Option B says, it's kind of the same thing as option C, right? You're like, I'm just going to give you drugs, but you don't fix the problem that the person has, right? That's one of the biggest problems with, sorry, I don't mean to get on a sub box today, but that's one of the biggest problems with healthcare today. We just want to give people drugs for stuff. And we don't want to like, although it's not every, it's not sometimes the physician's problem is the pressure from administration where press gaming scores and got a crank through patients and all that craziness. But again, yeah, option D is kind of like option C. Option E says, measure the patient's blood glucose concentration. No, her, her AOC is 8.4%. We know it's going to be bad, right?

Option F says, other measurement of the patient's micro opiumin. Do you see that none of these answers are like other than B, are like, hey, let's talk about this diet of a thing. Let's talk about this C dietary lifestyle of a thing. Option G says, refer the patient to a nutritionist. Again, you can do that if that's what a patient names, but talk the patient, talk about these lifestyle things first. Many of the diseases we have in this country, are really all over the world, but in this country, especially from metabolic issues, talk this patient through those things. Then just kind of do a crash course with a patient unlike, oh five minute visit, no, that's not very good, right? Okay, so that's what we're going to do. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. So, we're going to do a lot of research. Let's see. Right? So, this person is going to an MI. You want to increase your blood pressure. You don't want to juggle her pulse. So, let's just work through this. Right? I love pharmacology. It's like amazing. All right.

So, option A says dopamine. That's not a good idea. Remember, dopamine at medium doses is a beta one agonist. Right? Because the beta one agonist is going to increase your heart rate. That doesn't achieve what we're trying to do here. Right? Option B says epinephrine. Epinephrine has some adrenergic activity. Right? It can stimulate beta one receptors as well. That can costachycardia. Not a good idea. Isoprotary knowledge is a beta one and a beta two agonist. Right? So, it can stimulate beta one receptors. It can stimulate beta two receptors. That can cause problems. Right? That will certainly increase the person's pulse. Don't do that. Option D says no epinephrine. No epinephrine is like a very powerful alpha one and beta one agonist. Right? You give it. It's going to stimulate beta one receptors like crazy. Your pulse is going to rise. Fetal effrin is the right answer. Right? Clearly, it's an alpha one agonist. So, it's a very potent visual constructor. By visual constricting, it's going to increase your systemic vascular resistance. It's going to raise your blood pressure. Well, because your blood pressure rises, your virus receptors are going to be like, Oh, no. My blood pressure is too high. Right? And if that happens, that's going to cause you to have a reflex pretty cardio. Right? So, your pulse will actually not increase. Your pulse will actually decrease when you take phenol effort. Right? Remember, it's an alpha one agonist.

Another drug that's in that class is a fedric. Right? They usually test this in a person that's very hypotensive. Like, sometimes after like getting like an aesthetic. You know, and the geologists use this a lot. You know, you get an aesthetic, it tanks your pressures, and then you're like, Oh, shoot. I got a raised this person's blood pressure. You can do that by giving an alpha one agonist like phenol effort or refedric. All right. So, the answer is E, right? None of the other answers make any sense. All right. So, question 100. Last question here. So, a two-month-old girl is a minute to the hospital because of severe pneumonia. She has a history of mucus, creatinus, kind of ISS and chronic diarrhea. Her pulse is 160 per minute and herestations are 40 per minute. Cracles are heard over both long fields. Her nucleocycone is 5,400. Okay. So, that's normal. It is 6% segmented, neutrophils, 6% lymphocytes. Huh. That's pretty low. 8% monocytes. We know a lot of testing of a specimen obtained via bronchoscopy, especially for PCP. All right. The most serious is your vets. Fluocyte tometry shows normal concentrations of NK cells, but no T-obili-info sites in the peripheral blood. Oh, okay. So, she's got skid. There's also a PCR test of the email-globalin-vdg-arrogens from a bone marrow specimen shown absence of characteristic re-arrangements. This is skid. The most likely cause of these findings is an alteration of which of the following.

So, I don't know if you're like, okay, define this is skid and maybe like, define how do you know this is skid? Or, first, you don't have B and T lymphocytes. So, you have skid. That's one. Two. Even if they didn't give that, right? This is one of the most generous questions in this set we're doing today. Right? Look at this girl. She's having issues so early in life. She has lived for only like two months. That's like a pattern. That's a pattern. Right? She has lived only for two months. Right? And she's already having all these problems. Right? That tells you that this is probably like some kind of combined immune deficiency. Right? Usually when it's a pure B cell problem, you're going to have issues starting around like five, six months of life. Because you have that IgG from mom that kind of tidies you over. But when you have like T cell problems especially, it's going to start manifesting very early. Another classic pattern we see here is that this person has like the macissus-druvitz infection, a lot of candidiasis. You're struggling with a lot of viruses and fungi. That tells us that, you got a T cell problem going on. Right? So, this same vineyard could have been written for a person that has like the George syndrome or a person that has like, um, so yeah, I'll say the George syndrome is probably a big one. And the George syndrome and skid. The George syndrome, your third and fourth foreign geopolities do not form.

And if that happens, you won't have a thymus, you won't have a T cell. You won't have T cells. And you won't have a thyroid gland. Right? So you won't make PTH. Um, but this person will be people that have that they'll have like hypocalcemia and seizures and whatnot. Right? So, I know many of you are like, ooh, divine, okay, this is skid. Great. So, I'm looking for the answer that talks about a denocentiaminis deficiency. And you're like, hmm, I don't see that as one of the answer choices. Okay. Remember, a denocentiaminis deficiency causes a lot of excessive skid. Okay, you're like, okay, well, the other one I've learned, um, interlooking to receptor deficiency, right? The gamma chain. That's another cause of skid. That's a cause of exlinked recessive skid. Uh, because remembering to look into is necessary for B and T lymphocyte proliferation. So, if the receptor doesn't work, your B and T cells will not proliferate. You're going to get in trouble. But you're like, hmm, divine. I don't see that as an answer here. Right? Again, you're going to get questions exactly like these on the exams where the stuff you know is not going to check out. Right? Again, do the process of elimination. Right? Um, there is no reason if you get this question wrong and you've like kind of studied, even if you don't know what's going on, you should still be able to answer this pretty convincingly. Right? Option E says Britain's tires in kinese. That's, that's a exlinked thing gamma global inemia.

Right? And by the way, exlinked gamma global inemia. Hmm. She is exlinked recessive. This is a girl. She can have Britons on the exams. Just that simple. I'm telling you this. Let me teach you one nice memory. Haka use one tool I use with a immunodeficiency diseases. I know the ones that are exlinked recessive. So if I see a girl having an immunodeficiency disease, all the exlinked recessive ones are just kind of scribbled out of my concentration. Like, for example, uh, Britain's a gamma global inemia is exlinked recessive. So A is wrong. Um, CGD chronographed Lomonus disease is exlinked recessive. So D is wrong. Right? CD40 ligand. That's, uh, what do they call this then? What do they call this thing? Come on divine think hyper-IGM syndrome. That's exlinked recessive too. So B is wrong. Mivalonate kinase. Have you ever heard of any immunodeficiency? Don't get me wrong. There may be one. But just from all your studying, is this something you've ever heard about? Probably not. So that's wrong. Right? The only thing I know about Mivalonate is that I know it's in the cholesterol synthesis pathway. No, that's not what they're testing here. Right? So that's wrong. The answer has to be E. There is no reason why you should get this question wrong. Right? An option A like Bruton styrosine kinase is a B cell problem. Right? You're going to see issues with B cells there. And whenever you have B cell problems, what's the pattern?

The pattern is going to be a lot of bacterial infections. This basically is struggling a lot of viruses and fungi. Right? Chronic diarrhea. That's not the pattern for a B cell issue. That's not the pattern for a T cell issue. For T cell issue. And Brutons is a pure B cell issue. Right? They can have very low levels of immunoglobulins. Of all immunoglobulins. Right? CD40 ligand, that's hyper IgM syndrome. Remember, it's a class switching problem. We're, because remember, the first antibody that makes to any infection is IgM. Right? But from that IgM, you're going to make IgG, IgN, IgE. To do that, you got a class switch. But you need CD40 ligand, interacting with CD40, to have that class switching happen from IgM to all the other immunoglobulins. Well, if CD40 ligand doesn't work, then you won't be able to class switch. Right? So this will have very high levels of IgM and low levels of every other antibody. Right? But again, because it's an antibody problem, a humoral immunity problem, you're going to struggle mainly with bacterial infections. We don't see that pattern here, so that's wrong. Again, my valinear kinase, we're going to ditch that answer. Option D says, any DPH oxidase deficiency. Again, that's going to be chronic granulomadus disease. Chronic granulomadus disease. Those who are going to have like recurrent infections with catalyst positive organisms. Most times on the exams, they're going to have a lot of skin infections with stuff for you.

So a lot of stuff, or else abscesses. We don't see that here. Right? We don't see that here. We don't see that here. Right? People that have any DPH oxidase deficiency, the anutrophils really struggle. Right? And again, honestly, like again, that's the thing. That's why sometimes it's just good to be a multi-modal in your thinking and understanding and your knowledge. Because there are many different ways you can arrive at answers. Right? Like for example, for me, you know, this question some people would kind of like start thinking long and hard through everything. But just by the mode of inheritance and the fact that this is a girl, you could easily get through get rid of A, B and D. See again, just ditch it. Right? Again, if something you've never seen anything in any resource, it's probably wrong. Although that's not always true. There are some things you've never found in any resource that are things you're actually supposed to know. There are things you're supposed to know. All right. So option E says rag 1 and rag 2. Right? So I'm sure some of you are like, you've never heard of rag 1 or rag 2 before. And that's okay. Okay? That's okay. You've not heard of rag 1 and rag 2. Right? So those things they help us with a VDG recombination. VDG recombination is necessary for B and T lymphocyte development. Right? So if that doesn't happen, your B and T cells are not going to develop. You're going to have low levels of B and T cells. Right? So that's what's going on here.

But again, you did not have to have that knowledge to get this question right. That's what I'm trying to convince you. You did not have to have that knowledge to get this question right. Right? Again, having a good knowledge base is very helpful on the USM list. But that's not the end or B. All right? You're going to meet some questions on the exam that you're not sure of, where you've never seen the information before. But it doesn't mean you shouldn't be able to get those questions right. Okay. So I'm going to go ahead and stop here. If you're interested, you may notice I emphasize a lot of test-taking tips today. If you want to get good at testing, I have a test-taking strategy class coming up next week. Next week, Tuesday, actually, I'll over Zoom. It's for Step 1 to Step 3. Many people have taken this class. Found used to be extremely helpful. And then also, Step 1 to Step 3, I have a bio-starts class next Wednesday. It's a four-hour class. And social sciences, quality improvement, health care systems, hospital medicine class. On Thursday, it's a five-hour class week. Go over almost 300 scenarios. Many people again. Step 1 to Step 3, tick those classes. Find used to be helpful. And then, if you're for Step 1, in the first week of May, over Zoom as well, I have a 25-hour Step 1 review. If you notice today, I mean, with many of my podcasts, I emphasize like the MBMI patterns. I go over a lot of these MBMI patterns.

And again, if you like the way I teach, where I make integrations, I help you understand pathophage, you're going to love that class. I've had many people tick that class, and they've comfortably passed Step 1. And also, people with poor basic science foundations studying for Step 2, Step 3, that's a class you probably find to be really, really helpful. And then, for Step 2 and Step 3 specifically, I have a last minute review, taking place next week Friday. And then, the week after next week, I have a 20-hour Step 2, Step 3 review. And then, I have this epic class, taking place in the first two weeks of June. It's going to be held only once this year. And all these classes is me that teaches all of them, right? You're going to be getting divine teaching all these classes. And again, many people of taking these classes found them to be helpful. Actually, I have a separate podcast where I talk about these classes. To explain to you how they are different from my podcasts. But again, it is well worth it, wow. The one-man-mejority of poor that do my classes, they do very, very, very well on their exams, right? And again, I talk about a lot of test-taking tips. And again, I just really emphasize things from an NV Me perspective. And sometimes I do all go over things that you may not find in any resource, but it actually ends up being pretty high-youther, no, for your exams. All right. And I also have this podcast on Apple Google and Spotify.

And you can also check out the You Tube channel that I have. Divine intervention, USMD, podcasts, and videos. That's where I post the videos that I make. And then I also help with ERAS applications, mock-interviews, personal, statements, and things of that nature. And then I have another website called Divine Intervention Lifelessens.com. Pretty much every week, I post like two to three podcasts from a Biblical perspective address a life lesson. Divine Intervention Lifelessens.com. There's actually an Apple podcast as you know with that call the Divine Intervention Life Lessons podcast. So thank you for listening to me today. The one life lesson I want to leave you with today is this. Be conscientious, right? Be conscientious. You know, do everything with all your heart. The thing is, you know, these days, people are just comfortable with doing like the bare minimum. And you're just like, hey, I'm just going to do the bare minimum. I'm going to move on. That's not a good way to live, right? You know, it's always good to treat people the way you would want to be treated. You know, especially some people in healthcare, you can get so irritated that you stop like kind of caring about patients. You're just like, uh-huh. You just see the patient five minutes you dart into their room's dart out.

That's not a good thing to do because if you were in the hospital and you were in the patient's shoes, got for a bit, you would want somebody to give you a little more love and care and affection. Right? So be that kind of physician because many times people kind of lose sight of those things. And it's not a very good thing to do. It's really not. Right? Because it hurts patient care and it hurts patients. Right? Those people are invulnerable situations and you're kind of treating them like trash. It's not a very nice thing to do. I'll tell you that. So again, just be nicer. You know, take that little extra time. The thing is there are ways you can take a little extra time with your patients, do right by them and still be efficient. Right? Um, it's just many times balls down to having the right priorities. Because you see some people they're like, oh, I don't have time to see my patients as much as I want to. But you have time to do a lot of things at work that add no value to the work that they do. But different discussion, different conversations. So thank you for listening to me today. I'll see you in a episode 500 and I think 94. Well, God bless you. Have a wonderful day and bye for now. Thanks.

OA shows asymmetric joint space narrowing, osteophytes, and subchondral sclerosis. RA shows symmetric joint space narrowing and synovial pannus formation.

Monoamine oxidase B (MAO-B), which breaks down dopamine. Inhibition increases synaptic dopamine levels.

Smooth philtrum, thin vermilion border of the lips, and short popliteal fossa.

It is a pure $\alpha_1$ agonist; it causes potent vasoconstriction, increasing SVR, which in turn triggers reflex bradycardia.

Defects in RAG1 or RAG2 genes (Recombination Activating Genes), necessary for V(D)J recombination during lymphocyte development.

21-hydroxylase deficiency.

Klinefelter syndrome.

Primary hyperthyroidism increases metabolic activity leading to increased osteoclastic resorption (bone loss).

Hypocalcemia and potentially seizures.

Preventing the breakdown of dopamine within the synaptic cleft, thereby increasing available dopamine levels.

21-hydroxylase deficiency.

Klinefelter syndrome.

Primary hyperthyroidism increases metabolic activity leading to increased osteoclastic resorption (bone loss).

Hypocalcemia and potentially seizures.

Preventing the breakdown of dopamine within the synaptic cleft, thereby increasing available dopamine levels.