DIP Episode 596 - 2025 USMLE Step 1 Free 120 Discussion Part 11b (Q106-110, super helpful for Step 2 and 3!)

All right, welcome. This is episode 596 of the Divine Intervention Podcast. Into this podcast we're going to be continuing the step one free 120 series. This is going to be series 11b. Again, God willing series 12 will be the last. So here we're going to deal with, again, I want to do them in five or ten. So I'm going to do one or six to one ten here and then I'll go to willing in probably in the next episode where it's just going to finish up. Other remaining questions. All right, so question 106. I think the last podcast was kind of long because 101 to 105 just had a lot of pretty high health things to discuss. So question 106 says a 10 year old boy is brought to the physician because of a three week history of nosebleeds and easy bros ability. He's older brother has had similar episodes. He's at the 30th percentile for height and weight. Physical examination shows nasal and gingival bleeding and several echinocytes over the trunk and operand lower extremities in various stages of healing. Lab studies show a platelet count of 300,000 which is normal. Platelet adhesion testing shows a no more response to risk to sit in but aggregation does not occur in response to thrombic. Platelet morphology is normal. Per thrombing time and activated patch of thromboplastin time are within the reference ranges. A defect in which of the following is the most likely cause of the findings in this patient. This is a very simple question if you understand primary hemostasis.

Remember primary hemostasis has a bunch of steps, right? So the very first step is the adhesion step where GP1 B binds to the Williams factor. And then after that you have the activation step where after GP1 B binds to the Williams factor the platelet secretes ADP. And then that ADP binds to the ADP receptor which sometimes on exams is called the P2 Y12 receptor. And that triggers the third step, right? So when ADP binds to ADP receptor it's almost like an auto-crain secretion in a sense. Then you're going to express GP2 B3 A. And then GP2 B3 A from one platelet will bind to GP2 B3 from another platelet. And they're going to be joined together by Fibreno Gen. That's going to be the aggregation step. So the step number one is adhesion, step number two is activation, and step number three is aggregation. So one thing that's pretty high yield to know for you exams is the Ristocetin test. The Ristocetin test is sometimes it's called the Ristocetin cofactor assay. It is an excellent way to test for the integrity of the adhesion step of primary hemostasis. It's an excellent way to test the integrity of the adhesion step of primary hemostasis. So the thing is if you notice they say platelet adhesion testing shows a no more response to Ristocetin. So that pretty much rolls out of a vulnerable disease. Because remember for a vulnerable disease is a platelet adhesion problem. It's a deficiency of a vulnerable factor. You know, it's not a sumo dominant. It's a vulnerable factor deficiency.

And then the other one, Bernard Sulear disease, that's a GP1 B deficiency. That one is a Rizomore recessive. If you notice here, this person has normal platelet adhesion tested. So the response to Ristocetin is where it's normal. So this cannot be a vulnerable disease or Bernard Sulear disease. Remember, a vulnerable disease will also cause your PTT to rise because a vulnerable factor protects factor eight. But in Bernard Sulear, your PT and PT will be fine because it has no GP1 B has nothing to do with cloning factors. So we're told that aggregation does not respond, does not occur in response to thrombin. So this has to be a platelet aggregation defect. And remember, aggregation is GP2 B3 A. So this person probably has glansman thrombostinia. Glansman thrombostinia. Remember, glansman disease is a normal recessive disease where you have a deficiency of GP2 B3 A. It's a qualitative. It's not a quantitative platelet defect. If you notice, the platelet count here is normal. It's just the platelets do not work very well. Because they have the large GP2 B3 A. So it's a GP2 B3 A deficiency. So the answer has to be C. The answer has to be option C. Right? Answer has to be option C. You know, option A, factor seven proconverting. That's wrong. Factor seven defect. You're going to see when you have like liver disease, right? Your liver is a very important producer of Factor seven. I mean, when people have liver failure, you know, who are like really worried about their Factor seven levels.

So that can cause them to have a lot of bleeding. I remember factor seven is part of the, it's part of secondary hemostasis. So you're going to see abnormalities at least with the, with a PT, right? But here we're told that the PT and PT are completely normal. So that's wrong. Right? Option B says fibrenogen. Again, fibrenogen is what joins one GP2 B3 A to another GP2 B3 A. But again, typically on the USML is the love to test glansman thrombostinia. So we're going to go with that. And then granular storage pool that's wrong, right? And then when we learn factor that's wrong, I explained why that's the case. And please again, don't forget that when a person has glansman thrombostinia because it's a primary plate lead disorder, your bleeding time is going to be elevated. But again, GP2 B3 A has nothing to do with clotting factors. So your PT and PT will be fine. Bernard Solier disease, right? Is a GP1 B deficiency? It's a primary plate lead disorder. So your bleeding time will be up. But your PT and PT should be fine because GP1 B does nothing with clotting factors. And then for when we learn disease, it's a primary plate lead disorder. So your bleeding time is going to be elevated. But your PT will be elevated because again, when we learn factor increases the half life of factor 18 circulation. So even when we learn factor is not around because you have a deficiency of it, you will not be able to increase the half life of factor 18 circulation. So you're going to have high PT, right?

Your PT should be unaffected. So you may wonder, man, divine, how do I differentiate from we'll brand disease, which is an adhesion defect from Bernard Solier disease, which is also an adhesion defect? Well, the thing is both of those disorders will have increased bleeding time. But when we brand disease will have an increased PT and Bernard Solier will have a normal PT. And then remember that those are both adhesion problems. So you're going to have abnormalities with a Ristocetin Cofactorase. So the Ristocetin Cofactorase is abnormal both in Bernard Solier disease and in the Wulibrand disease. So please don't be surprised if they give you a question about a person that has because they know that many people know about Wulibrand disease is like, you know, a person that is having gum bleeds and all these stains, PT is high, bleeding time is up. And then they see which of the following additional lab studies will be abnormal in this patient. Pick the answer choice that says Ristocetin Cofactorase. That's actually a very nice way they can test that material on the exams. All right. So for sure, 107. And again, if you're taking step one, right? Like the first day of my step one class, I really try to hit just a lot of critical reasoning with step one questions. Again, that 25 hour step one class will be, will serve you really well. It's going to be taking place the first week of May. If you're interested, just shoot me an email. I can give you some more information. All right.

Now, question 107 says a previously healthy 45 year old woman who works as a park ranger comes to the physician because of a one week history of shortness or breath even at rest. She has lived in the mountains at 10,000 feet at both C level for two years. The physician's office is located at C level. Her pulse is 85 per minute. Respirations are 18 per minute and blood pressure is 125 over 90 millimeters of mercury. Physical examination while sitting upright shows JVD and two plus PDL adema. During the past two years, which of the following has most likely decreased in this patient. All right. So option A says height of P. So this person has been living on very high altitude, right? Let's work this out. Even on very high altitude, we know that your oxygen content in the atmosphere is lower at high altitude. Not because your FIO2 is low. Your FIO2 is still the same at C level or at higher elevations. The only thing is that your atmospheric pressure has decreased. So because your atmospheric pressure has decreased, your oxygen, you know, 21% of air. You're taking 21% of a lower atmospheric pressure. So overall, that's going to decrease the oxygen content. It's like the difference between taking 21% of like 760 versus 21% of 700, just something to keep in mind. So this person will probably have some degree of highpoxia. So we're going to talk about some of the changes that can happen with some of these answers here.

So option A says height of P waves in lead one of the patient's ECG. So that that's not going to be the case. And honestly, options in B are a very extensive discussion that I will very likely make in a future podcast. Again, I don't know when that future podcast will be, but I'll very likely make a future podcast. But this person, if you think about it, just maybe to give you like a really small brief preamble. This person probably has, you know, from living on high elevations, right, that highpoxia from the decreased oxygen content in the year. That is going to decrease the person's PBG A or two, right? So that's the avialer oxygen tension. So obviously, because that is low, the appeal in real to that's the arterial oxygen tension will be low as well. Right? That highpoxia is going to cause pulmonary viso constriction. When your pulmonary vessels constrict, it's going to become harder for blood to be ejected from the right side of the heart. If that happens, your right ventricle will get big and biffy, you develop pulmonary hypertension. So the right side of your heart is going to enlarge. So you're going to have like right atrial right ventricular hypertrophy and stuff like that. Your right atrium is going to enlarge. And typically, if you're right atrium enlarges, you're going to see kind of topi waves in leads to three avf, right? Those are your coronary artery leads. And also in leads V1 and V2, right? In leads V1 and V2.

And also the height of the R waves in leads V1 will go up. Right? So honestly, A and B are wrong. I know I'm just giving like a very brief explanation. Honestly, like it's just a much more extended discussion that is not now is not a good time, right? I just want to go through this series. Now is not a good time. Because honestly, like to really understand the keyages in that depth requires a very extensive discussion. And I just don't think this podcast is the appropriate forum for that. Again, that's a topic for a future podcast. So just believe me for now, A and B are wrong, right? But in general, if you have right atrial enlargement, right? The p waves in two, three avf will be increased in leads V1 and V2 will be increased. And the R waves also in leads V1 will be increased, right? So those are wrong. Option C says hematocrit. Hematocrit should actually be increased in this person, right? Because if you think about it, that hypoxia causes pulmonary viso-construction, right? And also, because you have, so I guess let me answer option D, right? Because it's pulmonary viso-construction, right? So because you're getting viso-construction of your pulmonary vessels, your pulmonary vascular resistance should go up, right? Because those vessels are constricted, right? Well, think about it when you have hypoxia, what happens to your ipo? Your ipo is going to rise because you want to increase the number of red cells.

So when you increase that number of red cells, that's going to raise your hematocrit. So your hematocrit is not going to be decreasing. And then option E says, right, ventricular dastolic compliance. Well, think about it. When you develop pulmonary hypertension, right? When you develop pulmonary hypertension, that's going to cause chronic pressure overload on the right ventricle. So the right ventricle is going to get very big and beefy, right? It's going to get very big and beefy. It's going to get very big and beefy. So because it's getting big and beefy, you're going to have, you know, you're adding sacrameres in parallel. It's going to become harder and harder for the right ventricle to expand, because it's just going to get very big and beefy. It's not as compliant as before. You know, I almost think of it as being like very similar to what you have in restrictive lung disease, like pulmonary fibrosis, where it's like, man, you've deposited so much stuff in the walls of your, you know, of your life that you don't expand very well. Here, the thing you've deposited a ton of is muscle, right? So it's like, oh, you're some, your, your right ventricle is so muscular, you cannot expand very well. It's kind of stiff, right? So it's not as compliant. So your right ventricular dastolic compliance will certainly go down. So option E is definitely the right answer. And then option F says, right ventricular wall thickness. That has to be wrong, right?

Because again, I just explained why your right ventricle should get big and beefy, right? So your right ventricle wall thickness should actually increase. So option F is rock. So the right answer here is going to be option E. All right. Now question one or eight says, five year old girl is brought to the office by her mother, because of a six hour history of bloody diarrhea. She's interactive and in no acute distress. Her blood pressure is 90 over 55. Domino examination shows normal active bowel sounds. Stool cultures are obtained and the patient's mother is advised to give the girl plenty of fluids. Five days later, the patient develops decrease urine output and is brought back to the office. Her blood pressure is now 135 over 88. Physical examination shows power. Now let's look at a lab studies, right? So she has anemia, right? Her hemoglobin is low, her monoclin is low. She has thrombocytopenia and she has what appears to be like acute kidney injury, right? Her creatinine is elevated. So which of the following infectious agents is the most likely cause of these findings, right? So we see a child that has had bloody diarrhea. And then we also notice that this person is now having anemia. This person is having thrombocytopenia. This person is having acute kidney injury, right? This is a pretty classic presentation of hemolytic uremic syndrome, HUS. Hemolytic uremic syndrome. And remember, there are two classic causes of HUS on the exam, right? There's going to be E.

coli, O157 H7. And then there's going to be shegella. Although E. coli, O157 H7 is way more common cause of HUS than shegella, right? So the right answer here has to be right. Remember, option A, Campylobacteria, Junai causes bloody diarrhea, but he generally does not cause HUS. Rhodovirus is the most common cause of gut infectious gastroenteritis in kids, but the diarrhea is usually watery, not bloody. So that's wrong. Now, Samonella also causes bloody diarrhea, but again, Samonella typically does not cause HUS on the exams. And then option E says you're senior, you're senior, right? You're senior pestis. I believe is what causes the bubonic plague. Remember, there's your senior enterocallerica, which can cause pseudo appendicitis. It can also cause bloody diarrhea, right? But that's your senior enterocallerica, not your senior pestis. I believe your senior pestis is what causes the bubonic plague. So that's wrong, right? That's wrong. This is not the bubonic plague. I can tell you that, right? So again, remember, what are the components of HUS? You're going to see fever, you're going to see anemia. And the anemia is usually going to be a micro-anguopathic hemolytic anemia. So you're going to see schistocytes on a blood smear, right? Sometimes they will have indirect hyperbular banymia because of all that he molasses, right? So you have thrombus at opinion, you have renophilia. And typically the treatment is just supportive.

You actually do not want to give anti-biotics when a person has HUS. Because here's the thing, if you give anti-biotics, if you give anti-biotics, that's going to cause a huge rocker's for the person. Because it's the toxin that's causing the disorder. So if you give anti-biotics, you kill more bog. If you kill more bog, you release more toxin. If you release more toxin, you'll cause more damage to the kidneys and stuff like that. So don't give anti-biotics. It's not every infection that should get anti-biotics. Just kind of a pro tip there. So the answer for this question, I think is option B, right? Equally, one, five, seven, H7 is the most common cause of, most common infectious cause of HUS. All right. Now question 109 says, we have a 78-year-old woman is brought to the intensive care unit because of diverticulitis, complicated by equalized sepsis. Treatment with c-pro-floxacine is started. Three days later, a serum creatinine concentration has increased from 0.7 on admission to 1.3. Your analysis shows multi-brown casts. The most likely cause of the findings in this patient is the scheme of which of the following structures. Right. So let's work this out. This person has probably has acutubula necrosis. We can see multi-brown casts. We can see this rapid rise in creatinine. So this is ATN. Although, let me say something here you want to be careful about.

Sometimes on the US Emily exams, instead of seeing the term acutubula necrosis, you may actually see the term acutubula injury. So just be careful about that. Let me use the term acutubula injury. And the thing is acutubula necrosis can have many different causes. Right. It can be caused, you know, sometimes they even call it like direct toxic, you know, like a toxic ATN. Usually that's going to be from a drug that's like nephrotoxic. So like they go my身 or like an amino glycoside or things like cisplatin, right. Remember, platenome agents are pretty nephrotoxic or even lube diuretics, right. It can be nephrotoxic, especially like ethycrinic acid. And then remember, a myoglobin. So like in the setting of ruptomyeluses or hemoglobin, like in the setting of some kind of like acute hemolytic transfusion reaction, those things can all cause ATN, right. But then there is a schematic ATN which usually arises from like a hypoperfusive state, right. So see, for example, a presence at an MI and they're not profusing the kidneys. Or a presence just had some kind of issue that's making them not profuse the kidneys well. That can cause a schematic ATN, right. But basically the sum to the level of this is your kidneys get messed up. So they won't be able to do the area of absorptive functions very well. So the phena, the fractional expression of sodium will be high. It will usually be more than 3% on your exams. So the key thing is who gets affected the most?

Well, the thing is if your kidneys are being torched by a nephrotoxic agent or you have hypoprofusion of your kidneys, the people that use of the most energy are going to be the people that are going to be the most heavily affected. So what parts of your kidneys use the most energy? Well, number one is your proximal tubule. Number one is your proximal tubule. That's why option D is the right answer here. But another part of your kidney that uses a ton of energy is the thick loop of heli, the thick loop of heli, right. The thick loop of heli, that's actually pretty high yield to know for your exams, right. The thick loop of heli, the thick loop of heli, right. The thick ascending lamp of the loop of heli, right. In the medulla, those are the ones that use the most energy, right. I mean, wonder, define why does the proximal tubule use so much energy? Well, that should make sense. I mean, think about it. It absorbs like most of the stuff that is filtered into your into your urine, right. So just something to keep in mind. So the answer is going to be option D. Honestly, none of the other answers make any sense here, right. Remember, the glomerulus is what is damaged in a person that has like nephritic syndrome. The interstitium is what is damaged in acute interstitial nephritis, right. Which usually has that trino fever, fever rash, right. An increase in your synophils in the blood plus or minus the urine, right.

And typically that's going to be after antibiotic exposure or like NZ exposure. Renovane, right. Remember, you can have renoven thrombosis when you have a nephritic syndrome, especially membranose nephropathy because remember in nephritic syndrome, one of the things you lose in your urine is, come on, divine thing. You lose antithromic in three, right. Nephritic syndrome can cause an acquired antithromic in three deficiency. An antithromic in three is an anti-conglant protein, right. Because it inhibits factor two and factor ten. So if you lose those, if you don't need a bit factor two and factor ten, they're going to have a longer half-life. They're going to make you hyperquaglable, right. So you're going to get in trouble. So actually, there's a very nice question. So that's why renoven thrombosis is a pretty common phenomenon in nephritic syndrome, especially with membranose nephropathy. Membranose nephropathy is probably, it's not, in fact, I'm not going to say probably here, it's almost certainly the most common kind of nephritic syndrome that's associated with renoven thrombosis. And one, so please make sure you know that, right. Make sure you know that. Again, that's why this 101 to 110, I kind of split it in two. It's just a lot of high-yield stuff you can discuss here. All right, let's do the last one. 110. A 19-year-old man who is a college freshman comes to the office because of a 40-history of tender, swollen glands.

He also has a 60-history of fever, malaise, and decreased appetite. His temperature is 101.7 degrees Fahrenheit, so he's got a fever. Physical examination shows swelling of the parodid glands. Which of the following infectious agents is the most likely cause of these findings, right. So this is pretty straightforward. We see a person in the Haspireitis, right. This bog also causes or chitis, right. Causes testicular inflammation. And this bog can also cause a kutbank retitis, by the way. This is pretty classic mumps, right. So the answer is D. Remember that or chitis can cause infertility. Just be careful about that. Right. And remember, mumps is an important cause of a kutbank retitis on the USML Es. Right. This is not EBV. EBV they're going to have like so thrilled they can have like hepato spleenomegaly. That's no what's going on here. Hebbi, right. In this case, they would have probably given us abnormal LF Ts. They're giving us these hebb serologies. Or you may have seen something about like a needle stick injury or sexual transmission or you know blood transfusion or something like that. We don't see that here. Remember measles. Measles is going to present with cough, choriza. That's runny nose and conjunctivitis. We don't see that here. And then mumps option D is the right answer. And then rubel option E is wrong. Rubela, you're going to have this rash that starts at the top of you like around your head or whatever and comes downwards.

And many times you have posterior oricula lymphatic anapathy. Again, we don't see that here, right. So option E is wrong. So the answer is option D. This is the mumps virus. All right. So let's go ahead and stop here. Again, if you're interested in any of my other classes like my test taking class, my bio stats class, my social science class, you know, my social science quality improvement healthcare systems, hospital medicine class. Those classes are first step one or the way to step three. You know, you should get an email through the website. And then if you're studying for a step two or step three, I have a last minute review taking place today. It's a three hour class. And then a 20 hour class taking place next month. I mean, sorry, actually next week, next week. And then I have this epic 50 hour class taking place in the first two weeks of June. Those are all for step two, step three. For step one, or for people studying for step two, step three, poor foundations, you know, let's see, you filled step one or let's say you really struggled. I forgot in most of your basic sciences, which these days are very important for step two, step three. You want to consider the 25 hour review I have in the first week of May. And then I have this podcast on Apple Google and Spotify. I have a You Tube channel where I post the videos that I make, the videos and podcasts I make. You know, it's called the Divine Intervention, US Family Podcasts and Videos.

And then I also help with ER As applications, personal statements, more interviews and things of that nature. And then I also for one or one tutoring for all the US Family and Complex exams, by the way. And then I have another website called Divine Intervention Lifelessens.com. Divine Intervention Lifelessens.com. Many of you know I'm a Christian. So every week I post about one or two or actually usually two or three podcasts. I really post that one just yesterday. I have more than 300 episodes on there. Every week from a biblical perspective, I address a life lesson. Actually, many people listen to these podcasts and they find them to be very, very helpful. So Divine Intervention Lifelessens.com. There's actually an Apple podcast associated with that called the Divine Intervention Life Lessons podcast. So thank you for listening to me today. God willing, we'll go to series 12. And I think we should be done with this step one free 120 series. And by the way, if any new free 120 comes out, just let me know, please, just just let me know. I like this process of kind of talking through the questions and answers. I feel like it's very helpful for a lot of people. So it's something I love to do. Right. So I mean, not always be checking the US Family websites if you see. Right. So just if a new free 120 comes out, just tell me and I will try to make a series on it like I've done for the step three free 137 for the step two free 120. I'm now doing for the step one free 120. All right.

So thank you for listening to me today. I will see you in episode five, 97. I think. So God bless you. Have a wonderful day and bye for now. Thank you.

The Ristocetin cofactor assay (or Ristocetin test).

Glanzmann thrombasthenia.

Anemia (microangiopathic hemolytic), Thrombocytopenia, and Acute Kidney Injury (AKI).

Right ventricular diastolic compliance.

E. coli O157:H7.

Because the disorder is caused by bacterial toxins; killing the bacteria may release more toxin, worsening kidney damage.

Decreased response to Ristocetin due to impaired platelet adhesion.

Both VWD and Bernard-Soulier syndrome, as they are platelet defects that do not involve clotting factors.

Mumps virus infection (Mumps).

The proximal tubule.

Microangiopathic hemolytic anemia (MAHA), characterized by schistocytes on blood smear.

Bernard-Soulier syndrome.

Decreased response to Ristocetin due to impaired platelet adhesion.

Both VWD and Bernard-Soulier syndrome, as they are platelet defects that do not involve clotting factors.

Mumps virus infection (Mumps).

The proximal tubule.

Microangiopathic hemolytic anemia (MAHA), characterized by schistocytes on blood smear.

Bernard-Soulier syndrome.