DIP Episode 597 - 2025 USMLE Step 1 Free 120 Discussion Part 12 (Q111-119, final part, super helpful for Step 2 and 3!)

Alright, welcome to episode 597 of the Divine Intervention Podcast. Into this podcast we're gonna be finishing the free 120 series for step one. Let's start with question 111. It says, 34 year old woman with my senior gravies comes to the ED because of a 2 D history of increasing weakness, shortness, or breath and abdominal cramping. Cream medications are prednisone and pirido stigma. If you look at her vital, she's pretty cardiac. Her respirations are high and shallow. So she's breathing at 25 per minute and her respirations are shallow. Her voice is soft and hyper-neasle and she coughs weekly when swallowing water. Breath and heart sounds are normal, pulmonary testing shows inability to generate a normal negative, respiratory force to reinforce the inspiration. The abdomen is soft and non tender with increased bowel sounds. Mosul strength is 1 out of 5 diffusely with severe continius and diffuse vasoculations. Deep tendon reflexes are sluggish but symmetric. Which of the following is the most likely cause of this patient's weakness? So we see this person has a history of my senior gravies and she's been treated properly. You know, she's on steroids and she's on pirido stigma. Remember, in my senior gravies you make auto antibodies against the nicotinic acetylcholine receptor. So, that's why she's taking pirido stigma. It's an acetylcholine esterase inhibitor. They'll bump up your levels of acetylcholine so that you can outcompete those nasty antibodies.

So the thing is inadvertently in certain circumstances, if you take too much pirido stigma, you have too much acetylcholine and you have a cholinergic toxidrum. So I know some of you may wonder, how do you know she has a cholinergic toxidrum? Let's work it out. She's pretty cardiac. Right? Acetylcholine slows conduction down the EV node. Acetylcholine can also cause bronchospasm. Right? So you see that she coughs weekly when she's trying to swallow water. And then, you know, rest and digest. It really makes your digestive tract go. So if you notice this person is having a lot of abdominal sounds. The person has hyperactive bowel sounds. And then you also see all this muscular problems. Again, remember acetylcholine acts on nicotinic receptors to cause you to have muscle contractions. But if you have too much, you can have abnormal muscle contractions. Right? So I'm going to vote for option E here. This person literally has a cholinergic toxidrum. Right? So if you look at the other answers, aspiration pneumonia, no, she doesn't have a fever. Don't they have like any evidence of like consolidation or whatever somewhere? So that's wrong. A guiomba re syndrome. Remember, it's going to be a symmetric sending paralysis after some kind of infection or vaccine. We don't really see that pattern here. Right? It doesn't explain many of the other things we see in this question. Option C says insufficient dose of prednisone.

No, it seems like a symptom of being controlled prednisone does not explain the predicaria and all these issues that she's got. And then option D says motor neuron disease. That's going to be something like ALS. You can't get ALS in two days. That's just know how life works. Sorry. All right. So question 12 says a 35 year old woman comes to the office because she has had three first trimester spontaneous abortions during the past three years. Physical examination shows no abnormalities. Lab studies show no endocrine abnormalities. Chromosomal ad analysis shows a paracentric inversion of the long arm of chromosome one. Each of the full invest describes this patient's risk for early spontaneous abortions and a live born child with a new ploy. So again, let's try to work this out. So I think the question we need to ask ourselves is what is a paracentric inversion? What's a paracentric inversion? So a paracentric inversion. So if you think about it, right? You know, most chromosomes are joined at least your chromosomes generally are joined by centromeres. And just think of those centromeres as like glue that hold the two sides of a chromosome together. You know, a chromosome is like one long rod and then there's one side to the rod, one end to the other end. Right? So sometimes those rods, you know, I just maybe let me give an analogy. So let's say you have a long rod and you break it somewhere in the middle, right?

You have two little rods that if you glue back together, you have your one long rod back. Some chromosomes are like that where it's like, oh, each arm of the rod is the same side, same size, sorry. But sometimes when you have those breaks, you know, it's almost like you have a chromosome that has like a very short arm, very long arm. Well, they are joined by a centromere. Now the thing is a parasentric inversion is when one of the arms, like, you know, like one side of one of the arms, this is something where I think looking up a picture online we're very helpful. But one of the arms, some of the genes within it, the flip within, they basically flip, right? So let's say like the long arm as it's been described here has genes that are labeled like A, B, C, D. Within that one arm, you have a flip. You have a flip. That's an inversion. It flips. So instead of A, B, C, D, it becomes like after the flip. So it flips and they research itself back into the chromosome. You have something like DCBA, right? So it's almost like things are reading in reverse. That's a parasentric inversion when it involves only one arm. So you don't affect the other arm. You don't affect the centromere. That's a parasentric inversion. That's a parasentric inversion, okay? That's a parasentric inversion. That's a parasentric inversion.

But if it involves, if you have an inversion where it's like things get flipped and it's like some things are flipped from one arm and some things are flipped from the other arm, that's a very centric inversion. Again, I really encourage you to look up a photo. It's going to make this make way more sense to you, right? So these are parasentric inversion. So the thing is in a parasentric inversion, you're still retaining the same genetic material. It's just flipped within that one chromosome. So obviously like having an issue like that is maybe not the most ideal situation of life. Because that's going to increase your risk of spontaneous abortions. Sometimes when you're doing crossover events during cell division, you're doing crossover events because things have been flipped, you may have the wrong crossover happening. So sometimes you may not have the right crossover, we may end up having like one chromosome longer than the other whatever. All those things can lead to the person having early spontaneous abortions. That's not something we don't have to guess very much. She has already had like three in this question, right? So probably makes sense that our risk is still high. So we can probably get rid of CND, we can probably get rid of CND. Now we're left with options in B. The thing is when we have these inversions, when we have these inversions, it's not like we're taking extra genetic material from another chromosome and tacking it on top of this chromosome, right?

So because remember, for example, an unemployed will be something like Trisomy 21, where it's like wow, especially when you have like some of these rubber Sony and translocations, like wow, one chromosome has like two, you know, you already know this extra excess genetic material that then makes you have an issue where if you bring another chromosome, you're having like three copies of chromosome 21, no, it's not like you're taking like this whole other chromosome and then just slap it on top of this. That's not what's happening here. So your risk for unemployed is low, right? But again, your risk for these early spontaneous abortions is high just because of all these issues that's happening. So the answer here is going to be option B. Again, I will encourage you if you look up a photo of this, this is going to make way more sense to you. All right, now let's do question one, 13. And he says that 25 year old man comes to the office because of a four hour history of readability, restlessness, tremor and populations. He is a new user of amphetamines. He's tacky, coridic, tecapnic, blood pressure is high. Physical exam shows no abnormalities, the most likely cause of this patient symptoms. It's in pathomy, my medics activity, arising from which of the following again, let's work this out. Right? So this person is on amphetamines. Well, how do amphetamines work? Amphetamines they do two things.

They make you release more caracolamines at the synapse and they prevent reoptic, right? They kind of work like cocaine in a sense, although cocaine largely prevents reoptic. But amphetamines, they increase release, they prevent reoptic and all those caracolamines they can stimulate adrenergic receptors so you can get tacky cardia like the beta one receptors on the heart, they can stimulate alpha one receptors on your blood vessels so you can get visual constriction and high blood pressure. So if we want to pick the right answer here, option A says decrease the intracellular metabolism of biogenic amines. So decrease metabolism, that's wrong, right? That's not how amphetamines work. Option B says decrease monamine oxidize activity. You're not taking some kind of MEOI like you know, isocarboxazine or trinocipramine or rastagelin cellulogen, that's not what's going on here. Amc says decrease preseptic receptor activation, that's not how it works. This says decrease in increase intracellular metabolism of biogenic amines. If you're increasing their metabolism, then there's less of them. You shouldn't be having these hyperagenergic symptoms. It says increase preseptic receptor activation. No. F is the right answer, right? This is release of biogenic amines. Biogenic amines is just another fancy term for a caracolamine. Alright, question 114 says a 14 year old boy is brought to the office by his mother because of a one week history of seizures and difficulty walking.

Fiskelig examination shows decreased sensation over the hands and feet and generalize weakness. He walks with an ataxic gate. Amosso biopsy specimen shows quarsely granular fibers that stain red with gomori trichrom that gives you all you need to know. You see mosos that stain red, ragged red fibers. This patient most likely has a genetic defect that most likely affects the synthesis of which of the following. So this person, you see ragged red muscle fibers, that's all you need to know. This is pretty classic for mitochondrial disorder. Let me ask you this, what does the mitochondria do? You don't have to overthink this question. The mitochondria is like the powerhouse of the cell. That's where the TCA cycle happens. That's where the electron transport chain happens. That's where the electron transport chain happens. So it's like a powerhouse of a cell. That's where you have ATP being produced. That's where you literally have ATP being produced. That's where you have what ATP being produced. So if you mitochondria don't work, you'll be able to make ATP. So the right answer here has to be option A. If you want the specific disorder, this person probably has a nerve. They have like these in cephalopathy. They have this ragged red fibers. They have seizures. Seasures are pretty classic in nerve. Stroke-like episodes are more seen in meelas. You see they have this person has seizures, has it, taxi, I think of a nerve, NERF. That's one of these mitochondrial disorders.

So honestly, the right answer here is option A. The mitochondria is the powerhouse of the cell. Now question 115 says a 72-year-old man is brought to the office because of a six-month history of increasing fatigue and a one-month history of numbness of his feet. Physical exam shows marked power. Proception and sensation to vibration are decreased in the lower extremities. Lab studies show. So we see this person has a macrositic anemia and the retic count is very low. And the B12 level is very low. So this is a pretty classic B12 deficiency question. And then he says histopathyology of gastric mucosal biopsy specimen shows it's trophic gastritis with extensive lymphocyte infiltration. Serelogic studies will most likely show to antibodies to which of the following-level cell types in the photomicrograph of non-mucosa or to one of its secretory products. So this person has B12 deficiency. They probably have preneciacinemia. And remember when you have preneciacinemia, it's an autoimmune disease. You're pretty much making antibodies against intrinsic factor or the cells that produce intrinsic factor. Those are parietal cells. So for this image though, you do need to know what these things are. So let's talk about what all these labelings are. Right? So option A, those are gastric mucosal cells. They are not the ones that make intrinsic factor. Option E, those are certainly your parietal cells. They're the ones that make intrinsic factor. So E has to be the right answer. Right?

Option B, you notice it's clearly pointing to a blood vessel. You know, making autoantibodies against blood vessels in preneciacinemia. C, those cells that kind of have that tubular look, they're your chief cells. They make Pepsi no gin. Remember, Pepsi no gin helps us with some protein digestion in the stomach, right? You know, making autoantibodies against those in preneciacinemia. And then E, that smoke muscle. Remember, for your GI tract to have that contractile function, it's going to have smoke muscle, right? You know, making antibodies against smoke muscle. So that's wrong. Right? So the answer here is going to be E. All right. So, this is the answer. It says, a 66 year old woman comes to the office for a full-up exam. One month after being diagnosed with paroxysmal E5. A proper pharmacotherapy was initiated at that time, and no more sinus rhythm was restored. A post is 76 per minute. And blood pressure is 132 over 86. Physical exams shows no abnormalities. The ECG is shown, represent before, and after administration of the anti-rhythmic drug. Right? So afterwards is the dash line. Which of the following drugs was most likely administered? Right? So if you notice, the QT interval looks like it's prolonged. And it looks like repolarization is prolonged. Right? There are two ways you can get the sensor very easily. We can see that, oh, repolarization looks like it's prolonged. And what are the things? What channel handles repolarization is potassium channels? Right?

So it probably makes sense that some kind of potassium channel blocker is the culprit here. And what's the only potassium channel blocker answer we have here? That's a mutor. So the answer is going to be option A. Right? Remember the jocsin inhibits the sodium potassium ATP spump. We really use it for A-fib. We can. We're really use it for A-fib. Mixillatin is a Class 1 B anti-rhythmic. That's a sodium channel blocker. So if anything is going to mess up your rate of depolarization, right? It's going to mess up your QRS complex. That's not what we see here. And we don't classically use it for A-fib. Option D says phenitoin. Phenitoin does not, is not being used to treat A-fib. My variable male is a Class 1-tyrhythmic. It's a non-dihydroperiodine calcium channel blocker. We don't use it for A-fib. Actually, we do use it for A-fib. But the thing is, actually, I take that back. We do use it for A-fib. But it doesn't have any effect on potassium channels, right? So it's not necessarily going to slow down repolarization. And honestly, like this question, you can make your life easy by just knowing the management of A-fib. So A-fib typically, we're going to give either, you know, we're going to do rate control or rhythm control. So rate control, we can use beta blockers or non-dihydroperiodine calcium channel blockers. We don't see a beta blocker answer here. But there are a milled deltias, they are non-dihydroperiodine calcium channel blockers. They can work.

But the thing is, those drugs do not prolong the Q-t interval. Okay, so that means rate control is not what we're doing here. Rhythm control is another strategy for managing A-fib. We do that with amuteroan. Amuteroan can prolong the Q-t interval. In addition to causing things like pulmonary fibrosis, liver problems, thyroid problems. Right? So the right answer here has to be option A. Right? If you just know the management of A-fib, the drugs we use and what we see on the EKG, then it's going to click in your brain. Now, one 17 says, a four-year-old boy develops fever three weeks after being admitted to the hospital for induction chemo. For treatment of ALL, chemotherapy medications are L-asparginase, dexamethasone, doxarubicin and vinchristin. He has a fever, he's stachycardic, he's the kipnic, he has palar, alopecia and osrysions over the gums. A central vinchristin with entreside in the redoper chest is present but has no serundinary theme. A blood-cultural growths grow negative roads after 36 hours. Which of the following on the line mechanisms is the most likely cause of this patient's susceptibility to infection? Right? So this person is on chemo and then surprise, surprise, he has a fever. Right? So this is, when you see a person that has chemo and has a fever, what do you think this is? It's going to be a neutropinic fever. Right? Your neutrophils are really susceptible to chemotherapy agents. So this person has neutropinia. The answer is going to be E.

You know, option A doesn't make any sense. That's a C5 to C90 effect. That's going to raise your risk of recurring eye-ceral infections. Hypogamaglobulinemia is something you're going to see in like CVID or in pertunsy gamma-globulinemia or hyperagym syndrome. That's wrong. C says, in pertilin post-site function, no. In pertilin post-site function, I'm going to see it in something like SCED or D-George syndrome. And then option D says, inhibition of TNF alpha function, right? That's what happens when you take a TNF inhibitor. That's not what's going on here. So the answer is E. This is neutropinic fever. You should probably start expressing on an anti-sudo-mono antibiotic. And then question 111 says, a six-year-old boy with ALL is brought to the office for a full op exam. He's receiving high dose methyl-traxat therapy. A drug is added to the patient's medication regimen to decrease the toxicity of this therapy to normal cells. The beneficial effect of this new drug on normal cells is most likely achieved by bypassing the cellular requirement for which of the following enzymes. So this person is getting methyl-traxate. How does methyl-traxate work? Methyl-traxate inhibits dihydrofolyl reductis, right? But because it inhibits dihydrofolyl reductis, like an S-phase actin agent, right? Sometimes you can get bone marrow suppression from it. And you can fix that problem. I believe I've said this in this series by giving local warning. Local warning is a full-inic acid analog.

It pretty much helps you bypass that dihydrofolyl reductis step. And that's helpful, right? So again, it's going to bypass the step that's inhibited by methyl-traxate. So the answer is going to be option A. Remember option B, methanine synthase converts homocysteine to methanine, right? That doesn't really have much to do with this process describing this question. Paravidic arboxylase, again, that's not a target of methyl-traxate. The timing prior phosphate is just the supercharged, the superactive form of timing. And then thymidyl-traxate synthase is the enzyme that's inhibited by five-floor-year cell, right? Remember, thymidyl-traxate synthase converts deoxy-ready monofosphate to deoxy-thymidine monofosphate. All right. Last question, 1.19. A screening test for breast cancer is administered to a thousand women with biopsy proven breast cancer and a thousand women without breast cancer. The test results are positive for 250 of the subjects with breast cancer. So that means the test is positive in 250 of the 1000 women that have breast cancer, so the sensitivity is 25%. And then it's the test results are positive in 100 of the subjects without breast cancer. So obviously those are false positives, right? So out of the 1000 women that don't have breast cancer is positive in 100 of them. So there's like, there's like, okay, so test results are, let's finish the question first.

So positive in 250 of the people that have breast cancer and 100 of the people without breast cancer, right? The screening test is now to be used on a population of 100,000 women with a non-prevalence rate of breast cancer of 80 per 100,000. Now which of the following is the expected number of false positives, right? So which of the following is the expected number of what? Of false positives, expected number of false positives, right? So remember false positives are people that test positive, but they don't have cancer, right? The test positive body don't have cancer, the test positive body don't have cancer. So if you notice, if this test has a, if breast cancer has a prevalence of 80 per 100,000 in this population, that means if you take every 100,000 people, if you take every 100,000 people in this population, 80 of them have, 80 of them have a breast cancer, right? 80 of them have a breast cancer. So that means like 99,920 don't have a breast cancer, right? 99,920 don't have a breast cancer. So we see that this test, we see that this test has a specificity of 90%, you may wonder define how do you get 90%. Well, if you notice, a thousand women that don't have a breast cancer, a hundred of them test positive. So that means like, wow, a hundred out of the 1000, 10% of the people that don't have breast cancer testing positive. So it's almost like it has a 10% false positive rate. So that means he has a 90% specificity.

So if the false positive rate is 10%, if the false positive rate is 10%, that means that wow, if in this population, since the prevalence is 80 per 100,000 for breast cancer, if you have 80 people that have a breast cancer out of 100,000, then you have 99,920 that don't have a breast cancer. Well, since this test has a 10% false positive rate, that means 10% of the 99,920 will test positive. 10% of the 99,920. So what's 10% of 99,920 is like 9992, right? So the answer is going to be option D. This is going to be option D. All right. So thank you for listening to me in this podcast. Again, this series is finally done because there's a lot of other topics I want to discuss, but I really wanted to finish what I started, finish the series before we start those new topics. So again, I do offer one or one tutoring for all the USML and complex exams. I have review courses for step one or the way to step three literally next week. I have a 25 hour step one class from the fifth to the ninth of May. It's going to be held over the next year. Again, many people have taken these classes and found them to be helpful. So it's a class for step one level one. And people taking step two level two, step three level three, they have four basic science foundations. And by the way, those exams, step two, step three, level two, level three are now infusing a lot of basic sciences. So again, I think you'd find the class we're hopefully it's over zoom. So 25 hour review.

And then I also have again, a bunch of other classes for step one to step three. I have a podcast I made where I discuss those classes. And then I have this podcast on Apple Google and Spotify. So just check those out. And then I have a You Tube channel, Divine Intervention, US Mly podcast and videos where I post the videos that I make. And then I also offer help with ER As applications, personal statements and all these application related stuff, mock interviews. And then I have another website called Divine Intervention Lifelessens.com. Divine Intervention Lifelessens.com. Basically like every week I post like two or three podcasts where from a biblical perspective I address a life lesson. There's actually an Apple podcast associated with that called the Divine Intervention Life Lessons podcast. I'm pretty sure there's almost like 330 episodes on there these days. So thank you for listening to me. I'll see you in the next episode. Have a wonderful day. God bless you and bye for now. Thank you.

It causes a cholinergic toxidrome due to excessive acetylcholine accumulation.

Paracentric inversion.

Ragged red fibers (RR Fs).

Parietal cells (which produce intrinsic factor).

Dihydrofolyl reductase.

Class III agents (e.g., Amiodarone).

Bradycardia, bronchospasm/bronchorrhea, and hypersecretions (SLUDGE syndrome components).

Increased risk of spontaneous abortions due to unbalanced crossover events during meiosis.

A mitochondrial disorder (defect in oxidative phosphorylation/ATP synthesis).

Intrinsic factor or parietal cells.

Dihydrofolyl reductase.

Amiodarone (Class III).

Bradycardia, bronchospasm/bronchorrhea, and hypersecretions (SLUDGE syndrome components).

Increased risk of spontaneous abortions due to unbalanced crossover events during meiosis.

A mitochondrial disorder (defect in oxidative phosphorylation/ATP synthesis).

Intrinsic factor or parietal cells.

Dihydrofolyl reductase.

Amiodarone (Class III).