DIP Episode 401 - USMLE Step 2/3 Rapid Review Series 78
Topic
Pediatric Cardiology (VSD, Murmurs); Gastrointestinal Pathology (Pyloric Stenosis); Acid-Base Physiology; Differential Diagnosis of Vomiting.
Key Takeaway
The diagnosis and management of pyloric stenosis require recognizing the classic triad of non-bilious projectile vomiting, an olive-like mass, and critically, addressing associated electrolyte abnormalities (metabolic alkalosis, hypochloremia, hypokalemia) before surgical correction via pyloromyotomy.
Episode Notes
Source / episode info
- Episode: 401
- Title: Divine Intervention Episode 401 – USMLE Step 2/3 Rapid Review Series 78
- Published: 2022-07-07
- Source: Episode page
One-liner
This episode provides a high-yield review of pediatric cardiology concepts including VSD physiology and cardiac murmurs (fixed vs. physiologic splits), alongside the detailed workup and management of pyloric stenosis, emphasizing associated metabolic derangements.
High-yield summary
- VSD Murmur Timing: A Ventricular Septal Defect (VSD) murmur may not be appreciated at birth but typically becomes louder over weeks to months of life due to increased pressure gradient between the left and right ventricles as pulmonary vascular resistance drops.
- Fixed Split S2: An Atrial Septal Defect (ASD) causes a fixed, wide split of the second heart sound (S2) because blood flow from the left atrium to the right atrium is constant regardless of respiratory cycle (inspiration/expiration).
- Right-Sided Murmur: A cardiac murmur that increases in intensity with inspiration suggests increased venous return and preload to the right side of the heart, consistent with a Y-pattern.
- Pyloric Stenosis Presentation: Classic signs include non-bilious, projectile vomiting and an palpable "olive-like mass" in the epigastrium. The diagnosis is best confirmed by ultrasound.
- Pyloric Stenosis Electrolytes: Vomiting gastric acid leads to a metabolic alkalosis and hypochloremia. Volume depletion activates RAAS, leading to potassium wasting (hypokalemia). Treatment must correct these electrolyte imbalances before surgery.
Learning objectives
- Describe the physiological changes in cardiac murmurs related to respiratory cycle and shunt location.
- Identify the classic signs, physical exam findings, and diagnostic imaging for pyloric stenosis.
- Explain the pathophysiology of metabolic alkalosis, hypochloremia, and hypokalemia resulting from gastric acid loss.
- Differentiate between fixed and physiologic splits of S2 heart sound.
- Outline the critical sequence of management for pyloric stenosis (electrolytes -> surgery).
Board exam buzzwords
| Condition | Key Finding | Association | Board Exam Tip |
| Ventricular Septal Defect (VSD) | Murmur louder over time; Loud P2 in Eisenmenger syndrome. | Left-to-right shunt initially; Right heart failure/PH later. | Remember that the murmur gets louder as the child ages and pulmonary resistance drops, increasing flow. |
| Atrial Septal Defect (ASD) | Fixed wide split of S2. | Constant left-to-right shunting from LA to RA. | The "fixed" nature means the split is present on both inspiration AND expiration. |
| Pyloric Stenosis | Non-bilious, projectile vomiting; Olive-like mass. | Obstruction proximal to the duodenum/bile ducts. | Always suspect pylorus if the vomit is non-bilious and forceful in a young infant. |
| Metabolic Alkalosis (due to loss of H Cl) | Hypochloremia + Hypokalemia. | Volume depletion -> RAAS activation -> K+ wasting. | The electrolyte abnormalities are often more critical than the obstruction itself; treat them first! |
Rapid review table
| Topic | Key Point | Context | Exam Relevance |
| VSD Murmurs | Smaller VS Ds tend to be louder. | Flow velocity is proportional to the size of the defect (like a narrow hose). | A loud murmur suggests high flow, which may indicate significant hemodynamic stress. |
| Fixed Split S2 | Occurs on both inspiration and expiration. | Atrial Septal Defect (ASD) allows constant shunting from LA -> RA. | This is the classic "fixed" split; differentiate it from physiologic splitting (which only happens on inspiration). |
| Pyloric Stenosis Diagnosis | Ultrasound is the preferred diagnostic modality. | Visualizing hypertrophy of the pyloric muscle and measuring channel length/muscle thickness. | Do not rely solely on history or physical exam findings for diagnosis; imaging is key. |
| Electrolyte Correction (PS) | Treat metabolic alkalosis, hypochloremia, and hypokalemia first. | Vomiting H Cl leads to loss of acid, causing the body to retain HCO3- and lose Cl-. | Failure to correct these imbalances can lead to cardiac instability or death, even if surgery is planned. |
Board-speak -> diagnosis
| Board-speak / Vignette phrase | Diagnosis / Concept | Why it fits |
| A murmur heard best at the left lower sternal border in a child with pulmonary edema/sweats when eating. | Ventricular Septal Defect (VSD) | The physical exam findings and context point to a large septal defect causing increased flow across the VSD. |
| Cardiac murmur that increases in intensity during inspiration. | Right-sided heart pathology / Increased preload | Inspiration decreases intrathoracic pressure, increasing venous return and thus right ventricular filling/flow (Y-pattern). |
| Wide, fixed split of S2 heard regardless of respiration. | Atrial Septal Defect (ASD) | The defect allows constant left-to-right shunting, maintaining a large flow through the pulmonic valve irrespective of respiratory cycle. |
| Non-bilious, projectile vomiting with an epigastric olive-like mass in a young infant. | Pyloric Stenosis | This is the classic triad for pylorus obstruction; non-bilious suggests obstruction proximal to the common bile duct/duodenum. |
| A child presenting with metabolic alkalosis, hypochloremia, and hypokalemia following severe vomiting. | Pyloric Stenosis complications | The loss of gastric acid (H Cl) causes the electrolyte derangements that must be treated first. |
Differential diagnosis / distinguishing features
Fixed Split S2 vs. Physiologic Split S2
| Key Features | Distinguishing Findings | Next Step |
| Fixed Split S2 | Occurs on both inspiration and expiration. Associated with ASD or Patent Ductus Arteriosus (PDA). | Confirm diagnosis via echo/cardiac cath; monitor for pulmonary hypertension progression. |
| Physiologic Split S2 | Occurs only during inspiration (Y-pattern). | Suggests increased venous return to the right side of the heart (e.g., tricuspid regurgitation, severe asthma exacerbation). |
Management pearls
- Pyloric Stenosis: Always prioritize aggressive IV fluid resuscitation and electrolyte replacement (H Cl/K Cl) before considering surgical correction (pyloromyotomy).
- VSD Murmur Interpretation: A murmur that increases in intensity with age suggests increasing flow across the defect, which is a key physiological finding.
- Fixed Split S2 Workup: If a fixed split of S2 is found, suspect an ASD or PDA; these defects require monitoring for pulmonary hypertension and potential intervention.
- GI Obstruction Management: For any suspected bowel obstruction (e.g., ileus), initial management involves NPO status, IV fluids, and NG decompression; imaging (CT/X-ray) guides further steps.
Don't miss
Integration & clinical reasoning
- Cardiology \leftrightarrow GI: Both VSD and Pyloric Stenosis require understanding of flow dynamics. In VSD, increased pressure gradient causes a louder murmur; in pylorus, obstruction changes the path of least resistance for vomiting.
- Acid-Base Physiology \leftrightarrow Nephrology: The body's attempt to compensate for metabolic alkalosis (by retaining bicarbonate) is limited by the lack of chloride ions needed for renal excretion mechanisms.
- Pediatrics \leftrightarrow Imaging: Ultrasound is the primary, non-invasive tool for diagnosing pyloric stenosis and evaluating cardiac defects like VSD.
OMM / COMLEX integration
- Acute Care Priority: In any patient presenting with severe vomiting and suspected obstruction (e.g., pylorus), standard emergency management takes priority: NPO, IV fluids, NG decompression, and electrolyte replacement are mandatory before considering definitive surgical intervention. OMT is adjunctive only after stabilization of the airway, breathing, and circulation.
- Electrolyte Management: Understanding the systemic impact of \text{H Cl} loss (metabolic alkalosis) reinforces the importance of fluid/electrolyte resuscitation in acute GI emergencies.
Concept connections / cross-references
- No explicit cross-references.
High-yield association table
| Condition | Association | Mechanism | Clinical Significance |
| Pyloric Stenosis | Non-bilious, projectile vomiting. | Obstruction proximal to the duodenum/bile ducts; acid loss ({H Cl}). | Requires immediate electrolyte correction (IV {Cl}^- and {K}^+) before surgery. |
| Atrial Septal Defect (ASD) | Fixed wide split of S2. | Constant left-to-right shunting from LA to RA, regardless of respiration. | The fixed nature is a key differentiating feature on the exam. |
| VSD | Eisenmenger Syndrome. | Chronic L -> R shunt -> Pulmonary Hypertension (PH) -> Right heart failure -> R -> L shunt. | Indicates severe, long-standing pulmonary vascular disease and requires careful monitoring of PA pressures. |
| Metabolic Alkalosis | Hypochloremia + Hypokalemia. | Loss of gastric acid ({H Cl}) combined with volume depletion/RAAS activation. | The combination is highly characteristic of pyloric stenosis or severe vomiting. |
Key terms glossary
| Term | Definition | Context | Example |
| Non-bilious Vomiting | Vomitus lacking bile pigment (green/yellow). | Suggests an obstruction proximal to the common bile duct, such as at the pylorus. | Pyloric stenosis is a classic cause; distal obstructions (e.g., small bowel) often yield bilious vomit. |
| Fixed Split S2 | A wide split of the second heart sound that persists during both inspiration and expiration. | Pathognomonic for defects like ASD or PDA, where shunting occurs constantly. | Differentiates from physiologic splitting (which only happens on inspiration). |
| Pyloromyotomy | Surgical incision into the pyloric muscle to relieve obstruction. | The definitive surgical treatment for pyloric stenosis. | Must be performed after adequate correction of metabolic derangements. |
| Metabolic Alkalosis | Elevated blood {HCO}_3^- due to loss of acid ({H Cl}). | Caused by severe vomiting or diuretic overuse; leads to hypochloremia and hypokalemia. | The body attempts to compensate by retaining bicarbonate, but the lack of chloride limits this process. |
Study optimization
| Topic | Study Approach | Priority | Resources |
| Cardiology Murmurs | Use flow dynamics (Boyle's Law, preload changes) to explain murmur intensity and timing. | High | Review cardiac anatomy/physiology; practice differentiating fixed vs. physiologic splits. |
| Pyloric Stenosis Workup | Focus on the sequence of pathophysiology: {H Cl} loss -> Alkalosis -> Hypochloremia -> Volume depletion -> Hypokalemia. | High | Use flowcharts to map electrolyte changes; memorize the triad (non-bilious, olive mass, ultrasound). |
| VSD/Shunts | Understand the progression of shunting: L -> R -> PH -> R -> L (Eisenmenger). | Medium | Visualize pressure gradients across cardiac defects. |
Question pattern recognition
- Clinical Clue: Non-bilious, projectile vomiting in an infant < 6 months old -> Pyloric Stenosis .
- Physical Exam Finding: Palpable "olive-like mass" in the epigastrium -> Pyloric Stenosis .
- Lab Pattern: Metabolic Alkalosis + Hypochloremia + Hypokalemia following vomiting -> Pyloric Stenosis (or similar severe GI loss of acid).
Test yourself
Common mistakes to avoid
Common traps
Original transcript with highlights
Original transcript with highlights
Okay, welcome everyone. My name is Divine. This is episode 401 of the Divine Intervention Podcasts. And in today's podcast, we're going to be continuing the Rapid Review Series for the US Emily Step 2 CK and Step 3 exams. And if you, so this is gonna be Series 78, and if you're taking Step 2 or Step 3 or Complex Level 2 or 3, I have a review course that's taking place starting next week one day. It's gonna be for five days. We won't have a session on Saturday, but it's gonna be for, I mean on Wednesday, sorry, but it's gonna be from Monday to Saturday, five to 9 p.m. Pacific time, 20 hours total, over internal medicine peds, surgery, OB-guine, site neuro, multi-system persists and disorders, ethics, biostatistics, healthcare systems, and things of that nature. Again, many people have attended these courses, they found it to be supremely helpful. That's course applies specifically to those taking Step 2 or 3 or Complex Level 2 or 3. And then I have an MBME Testic and Strategy course. It's gonna be taking place tomorrow between five to seven thirty p.m. Pacific Standard Time. All these courses are on Zoom. The Testic in course is specifically for people that are taking their shelf exams or Step 2 or Step 3. Again, there are many people that by applying these principles, they've seen increases in their Euro percentages, increases in their practice test scores, increases in their real exam scores. And then I also have a bio-statistics slash epidemiology bootcamp.
It's gonna be taking place on the 21st of July from four to 8 p.m. Pacific Standard Time. So if you're interested in any of these courses, all of them over Zoom, shoot me an email through the website. I'll give you some more information and you can register. So let's just jump right into it. So what if they give you a question about a child and they tell you that this child has a holosis stomach murmur that's heard best. They tell you that the child has like pulmonary dima, you know, sweats when they're trying to eat. And then they tell you that you hear a holosis stomach murmur at the left lower sternal border. If you see this, what this should be your next best step in diagnosis. I'll really hope you're gonna be getting some kind of echocardiogram. So what does this child have? Well, we know that first and foremost, this child has a VSD, okay? Remember, VSD is a ventricular septal defect. Now, why do we get an echocardiogram? An echocardiogram can help us evaluate the hemodynamic significance of the VSD so that you know if it's something you need to intervene with, which is probably gonna be the case in this child or not. Now, what are some key things our friends at the MBA Mies want you to know about VSD's? Well, one is that VSD's, they get louder. You may not appreciate them when you're born, but by the time you hit a few weeks of life, you're going to appreciate those VSD's. You're going to be able to hear them. Why is that the case?
Well, if you're remembering utero, the lungs essentially don't work. So, the inner utero is a state of relative hypoxia. After that child is born, right after you're born, you know, that relative hypoxia still persists. Right? And we know that hypoxia causes a pulmonary viso-construction. So the pressures on the right side of the heart, they are pretty high in utero, but they also high at birth, although over time, over days, over weeks, they decreases. Right? But just after a child is born, let's say like the first few hours or thereabouts, the right side of the heart pressures are still a little bit elevated. So guess what's going to happen? Since the right side of the heart has elevated pressures, I mean, we obviously know that the left side of the heart, the pressures are going to start going up after birth. The spread between those pressures in the left side of the heart and the right side of the heart, that spread is not too great. So because the spread is not great, there's not much flow. And because there's not much flow, there won't be much flow across the VSD. So you may not hear it much. But after a few days, after a few weeks of life, when the child has lived for a measurable period of time, you'll notice that okay, wow, things then kind of begin to look more like adult physiology. So the left side of heart pressures, they get to like standard pressures, the right side of the heart pressures decrease to standard pressures.
So the thing that will happen is the spread between those pressures now gets bigger. As the spread between those pressures gets bigger, then there's going to be more flow across that VSD from the left to the right ventricle. And if there is more flow, you're going to hear that remember more, okay? So in general, you may not appreciate a VSD at birth, but you will hear it as the child lives a longer life. That's a very high-ealth thing to know. The thing is our friends at the MBM Es, one area where they love to pounce on your knowledge of physiology, especially on because they know that you know, step one, there's a lot of physiology, I need a lot of pathophysiology, well, step two, step three, one area they love to pounce on with physiology is cardio, especially with pediatric questions. So it's something you kind of want to make sure you understand. I mean, another physiological related thing I guess with VSD is also just remembering the people that have VS Ds, the smaller the size, the louder the murmur. Again, you may be like, well, divine, why won't a large VSD cause a louder murmur? Well, let me explain. Let's say you're using a guardian hose. If you have a guardian hose, you're just letting the water flow out like normal. You're going to get a pretty, pretty soft sound, but if you put your finger on top of that guardian hose and I'll put some part of the opening of the guardian hose, the water is going to come out with more force, more velocity, right?
And with more sound, it's going to be louder. So smaller VS Ds tend to be louder. So actually, the VSD that's loud probably has fewer consequences than a VSD that is not loud. That's something I want to keep at the back of your mind on exams. And remember, though, a VSD, if you have a larger no VSD, most, you know, if you live with it longer enough, and you don't do anything about it, the thing that may happen is that the right side of the heart is not built to handle those really high pressures after you've been born. But if you keep seeing all those high pressures, high pressures, high pressures, high pressures, the thing that will ultimately happen is that you can develop pulmonary hypertension. And then when the person develops bona fide pulmonary hypertension, the right side of the heart pressures become very great. And then what was previously a left to right is a cell notic shunt. Then becomes a right to left, a cell notic shunt, because the right heart ventricular pressures can grow so large that be overwhelmed with the left ventricular pressures. So blood will now start flowing from the right ventricle to the left ventricle. And if that happens, that's a phenomenon known as IZ-mengar syndrome. That's a phenomenon known as IZ-mengar syndrome. And the thing is many times when people have IZ-mengar syndrome, right, you'll tell you that in the key system that, oh wow, these people have a loud P2 heart sound.
So you're going to notice that the pulmonary heart sound is very loud. So that's something those are like key things. You want to keep at the back of your mind with VS Ds, for example. Now, the next topic I want to address, what if they give you a question about a patient, and they tell you that this patient has a cardiac murmur. And this murmur increases in intensity with inspiration. What should you really think about just in general? The key thing I want you to think about in general is that this person has a right-sided heart murmur. If you think about the Y, then it will make perfect sense. Because again, when you inspire, you're literally pushing your diaphragm down. If you push the diaphragm down, your intracuracic volume goes up. Now, according to Boyle's Law, that you probably learned from General Chemistry in college, as your intracuracic volume goes up. Franchial thoracic pressure is going to calm down. So you're creating a low pressure system within the thoracic cavity. And that would almost be like transmitted equally to the heart. You're going to have like low pressure system as well within the heart. So since you're creating a low pressure system within the heart, any part of the body that has higher pressures will want to send blood towards the heart, which is essentially what you're trying to do. So, venus return goes up. Preload goes up when you take a deep breath to the right side of the heart.
So since the right side of the heart has to process more blood, there's going to be more blood flowing through the tricospid valve. There's going to be more blood flowing through the pomonic valve. So if you have issues with any of those valves, since there is more flow, you're going to get a louder sound. Since there is more flow, you're going to get a louder sound. That's something that's pretty high to know for the purposes of exams. That's something that's pretty high to know for the purposes of exams. And I guess another thing that may be also be helpful for people listening to this podcast is many people hear this term or divine. What is these? They say that it's associated with a wide fixed split of the S2 heart sound. Why is that? Well, let me explain. If you think about it, right? I just said that when you inspire, when you're taking a deep breath, more blood flows through the right side of the heart. And if more blood is flowing through the right side of the heart, the right side of the heart is just processing more blood. And like I said, more blood will flow through the tricospid valve first, which is also called the right atroventricular valve. And then that more blood will flow through the pomonic valve. Since more blood is flowing through the pomonic valve relative to the euric valve itself, then those valves will not close at the same time.
And really, if you want to extend this a little bit further, when you put more blood, when you're having more blood flowing through the right side of the heart, there is more blood in the right ventricle. That more blood in the right ventricle, essentially in a sense, bulge itself, like makes the right ventricle bulge a bit through the interventricular septum into the left ventricle. So the left ventricle does not feel with as much blood as it can. So since it cannot feel as much blood as it can, it doesn't have to when it's contracting for the in order to receive the blood. There's not much blood relative, you know, if you compare with the pomonic valve that flows through the euric valve, because normally your pomonic valve euric valves they should close at roughly the same time. But if the right side of your heart is dealing with more blood and the left side of your heart is dealing with less blood, then with less blood flowing through the left side, more blood flowing through the right side, the euric valve is going to close before the pomonic valve. That's a physiologic split of the S2 heart sound. The split is basically the one valve closes before the other. But again, as I've explained, that split is something that should only happen on inspiration. And we've covered this in detail already that the reason that it happens on inspiration is more blood gets on the right side of the heart. Now, think about it.
If you have an ASD and etroceptor defect, then whether you're having an inspiration, an expiration, it doesn't matter. Blood is always going to be flowing from the left atrium to the right atrium. If blood flows from the left atrium to the right atrium, then there's always going to be more blood flowing from right atrium to right ventricle through the pomonic valve. Regardless of if you're inspiring or you're expiring. So since there is more blood always flowing through the pomonic valve, the thing that's going to happen is that the pomonic valve will pretty much always close later than the euric valve. So that split is not something you will observe just on inspiration. It's something you'll observe, you'll observe both on inspiration and expiration. That's what's called a fixed split of the S2 heart sound. That's a very path on the morning feature, often ASD on MBA Me exams. Now, what if they give you a question about a child and they tell you that, oh, this child is five weeks old and his mom says that he has been vomiting significantly for the last two days. He has been vomiting significantly and she said that the vomit is colorless, right? And she says that it's a large volume vomit. What should you be thinking about? I really hope you're saying, oh, divine, this sounds an awful lot like pyloric stenosis, right? This sounds an awful lot like pylosterosis. It's not going to be greenage vomit, it's going to be non-bilius. So why is it non-bilius?
Remember in pyloric stenosis, the primary problem is there is a lot of hypertrophy of the muscle that you find around the pyloric sphincter. Remember the pyloric sphincter is like the gate man. It's like the gateway of food from the stomach to the doggone. But if whatever is in your hypertrophy of that muscle, then it's going to be really hard for things to go from the stomach to the doggone. But those things have to go somewhere. They can just keep chilling in the stomach. So since the lower pathway from the stomach to the doggone is not available, then the upper pathway is the path of list resistance. Things will pretty much always take the path, not always, but for the most part, we'll take the path of list resistance. So it's going to come out through the mouth. So those kids are going to vomit. So what are some key features of pyloric stenosis? Again, they're going to have non-bilius vomiting. Remember, whenever you have any obstructive problem with the GI tract that is proximal to the pyloric sphincter, your vomiting will be non-bilius. But if you have anything that's distal to that sphincter, get to the doggone, gendron, helium, colon, stuff like that, you can have bilia vomiting in those circumstances. So the vomit is going to be non-bilius. It's going to be described as projectile. And sometimes on physical exam, you may see like an olive-like mass in the epigastrium. An olive-like mass in the epigastrium.
Besides seeing an olive-like mass in the epigastrium, you may also find like this pulsatility. This pulsatility, longer presence stomach again, around the epigastric area. But again, how likely is it that our friends at the MBM Es will present that data to you very, very unlikely, right? Very unlikely. If they did that, you know, maybe exam too easy. So they may do it, but again, it's not something I would be expecting if I review on tests. So how do we make the diagnosis of pyloric stenosis? Many times on MBM Es, the right thing to do is to get an ultrasound. An ultrasound is a very good, reasonable study to eating the diagnosis of pyloric stenosis. And if you don't see an ultrasound as a diagnostic test, is there something you should also consider? Well, one other thing you can consider, but again, it's not preferred, is an upper GI series. An upper GI series is also a decent diagnostic test in people or in children that present with pyloric stenosis. But again, it's almost almost 100% that you would not see that as a diagnostic test on your exams. So if you see pyloric stenosis on your exams, I want you to pick an ultrasound as an answer. I want you to pick an ultrasound as an answer. So how do we treat pyloric stenosis? The way we treat pyloric stenosis on MBM Es is we treat it, we treat it by first treating the electrolyte abnormalities that the child has. So I guess the big question is, what are these electrolyte abnormalities? I'm going to talk about them.
But remember, treat the electrolyte problems first before you take that child to surgery. Surgery is the second step. The surgery, I believe it's called a Ramsted Pyloromyotomy. On exams, just remember pyloromyotomy. That's the key critical thing you want to remember. But do not forget, is the electrolyte anomalies that can kill the child, not necessarily the pyloric stenosis. So you always address the bad stuff first. You fix the electrolyte anomalies first before you then take the child to surgery. So what are these electrolyte anomalies? Well, if you think about it, again, this is a very good construct, a very good platform for the MBM Es to test a lot of physiology. Think about it. The content of your stomach is acid, hydrochloric acid. So you're going to be vomiting a lot of acid. If you're vomiting a lot of acid, you're going to be basic. You're literally going to have a metabolic alkylosis. You're going to have a metabolic alkylosis because you're puking acid. And also, since you're puking out so much chloride in terms of chloride ions, you're going to be hypochloremic. So in your bloodstream, the person is going to have low chloride. So they're going to have low chloride and they're going to have a metabolic alkylosis. So their bicarb is going to be high. And these people also will have hypochylemia. Because if you think about it, these people have low volume. We have low volume because they're losing volume through this vomit.
So when you have low volume, what happens to the activity of the reigning and utensil in our doctrine system? It goes up. And our doctrine, one of its jobs is to make you dump potassium in your urine. So if your dose urine levels are high, which it will be in these people, they're going to be dumping a lot of potassium in your urine. So you're going to have hypochylemia. And there are many other things that potentially the hypochylemia in these children. For example, think about it. You'll notice that these kids, they have a metabolic alkylosis. So the body is going to try really hard to try to see if he can deal with that alkylosis problem. The thing is on many cells in the human body, there's a hydrogen potassium antiporter. It essentially works to try to maintain a charge balance of some sort. So if you're alkalotic in your blood, your body will try to neutralize that base by pulling out hydrogen ions from the intracellular environment. As is pulling out those hydrogen ions to maintain electron neutrality, potassiums will go in the reverse direction. So you're putting more potassiums intracellularly. So there is less in the bloodstream. So that potentiates the hypochylemia. And also, if you think about it, these people's hypochloremia is also potentiated. Because if you think about it, you tell yourself that, wow, these people have vomited a lot of acid. So they have a metabolic alkylosis. So the kidney is going to try really, really hard to compensate.
But the thing is, for your kidney to compensate for a metabolic alkylosis, you can try to excrete more bicarb. But you cannot just excrete bicarb because you decide to excrete bicarb. That's absurd. You excrete bicarb because you have an off chloride to excrete it. Here's the thing. Your body to excrete bicarb on one side needs to be reabsorbing chloride on the other side in the kidneys, in the distal nephron, in the collecting duct, especially with those intercolledate cells. So these people are already puking out a lot of chloride. So they don't have enough chloride that they can reabsorbing the kidneys so that they can safely excrete bicarb. So again, they keep holding, holding, holding onto that bicarb. They keep holding onto that bicarb. They keep holding onto that bicarb. And again, remember, our duster also makes you dump hydrogen ions in your urine. So because it makes you dump hydrogen ions in your urine, you literally dump it in acid as well. That's going to potentially eat that alcoholosis. Again, these are all high-yield things to know. So you may be surprised because the thing that many people, in fact, this is something that I teach people during the test-taking strategy's course. The NBA means it's not like they are just creating so many new pathologies that they are suddenly testing out of the blue. No. The thing they are doing these days is they are taking the regular pathologies that you pretty much always tested.
But they're just testing them in new lights. They are trying to see if people have a deep, solid conceptual understanding of what's going on. That's what I try to achieve with my review courses. My review course is not me, it's not me, spinning facts that you are going to be using examples. I'm going to be using clinical scenarios to both stress and explain pathology, physiology and pathophysiology. So these folks, right, again, it's very high-yield. They can literally give you like a table question with a lot of errors. You should recognize that because this pool of volume depleted, their reading is going to be high, their angiotensial one and two are both going to be high. The aldosterone is going to be high, their chloride is going to be low, right? Their bicarb is going to be high because they have a metabolic alkalosis. The potassium is going to be low. These are all things you want to make sure that you can pool together, right? They are all things you want to make sure you can pool together. And their PCO2, think about it, what do you think the PCO2 B? The PCO2 should be high in a person that has pyrolyxtonosis because again, they have this metabolic alkalosis, so the lung is going to try its best to balance things out by hypofentilating, retaining more CO2. So that they can have a respiratory acidosis to counterbalance that metabolic alkalosis.
And one other thing that I would say is pretty helpful to people is understanding how to differentiate pyrolyxtonosis from a gird. This is something that many people massively struggle with on exams. Because they are like, ah, you know, a lot of kids are happy spiders. So how can I differentiate gird? And you know, the MBM is your smart. They can give you a pyrolyxtonosis question and it can put gird as an answer for the child or they can put like gastroeths of a jewelry flux because we know that many newborns speed up. If you have a newborn, you know that they're pretty good at speeding up. So what are some key things to help you differentiate? The first thing is the fact that there will be electrolyte abnormalities. There will be electrolyte abnormalities in a child that has pyrolyxtonosis, which I've already discussed, but you will not necessarily have those electrolyte abnormalities in gird or in gastroeths of a jewelry flux. And also, you'll see a lot of hemodynamic consequence with pyrolyxtonosis in a child. You are very unlikely to see hemodynamic consequence of any sort in gastroeths of a jewelry flux in a child. And then another thing that tells you that you're dealing with pyrolyxtonosis is you'll see an acute change in baseline. You'll see an acute change in baseline. You'll see an acute change in baseline. You notice that this child over the last two or three days is just not doing well.
When you see stuff like that, that should get you thinking more about pyrolyxtonosis versus gird versus gastroeths of a jewelry flux. And then don't forget the physical exam findings. The physical exam findings are also pretty pretty helpful in differentiating one from the other. The thing is you can't really use time frame because kids tend to spit up quite a bit the first few months of life. Usually, around five to six months, that spitting up kind of goes away or it reduces in volume. But if you see a child, just a large volume, non-bilius vomit, really want to think about pyrolyxtonosis. And one thing I also want to comment on is just the time frame of disorders. This is something that again, I try to comment on a lot during my review course. Time frames of disorders matter on NV Me exams. If you think about it, if they give you a question about a two-year-old child, and you're picking pyrolyxtonosis, you are positioning yourself very nicely for getting the question wrong. Pyrolyxtonosis is something that almost always, again, are there exceptions to this rule? Yes. But almost always on exams is going to present in a child before six months of age. Most times, it's going to present within the first 12 weeks of life on exams. So that's a time frame thing you want to kind of keep at the back of your mind as you study for your tests. So since this podcast is almost 24 minutes long, I think I'm going to go ahead and pause.
But as I do at the end of every podcast, I do offer one or one tutoring for all the USMLA exams, step one, step two, seek in step three. I also offer one or one tutoring for the complex level one to three exams. I just don't tutor OMM and I don't really tutor the CCS cases on step three, except you have like special requests for those. But OMM, I definitely do not tutor for those. But the CCS cases I do occasionally when time permits offer tutoring for those. And then I offer the review courses. I have a 20-hour review course, I have an NV Me testing and strategy course, I've gone tomorrow. And then I have a bio-statistics bootcamp. And then, which is a four-hour class, the testing and strategy class is a two and a half hour class. The review course is 20 hours long. And then I also help with IRAS applications. So like personal statements, recommendation letters, mock interviews, supplemental applications, IRAS application itself, just in terms of making edits, giving recommendations, giving counseling. Again, I've been on an admissions committee before. And I've worked with tons of people that have much that a diverse area of residences like dermatology, orthopedic surgery, neurology, neurosurgery. I've worked with people from many different fields, a lot of internal medicine, family medicine, psych, OB-GYN. I've worked with many people from many disciplines. So the people I've worked with are literally attendants right now.
So if you're interested in any of those things, shoot me an email through the website and I'll give you some more information. And then I also have these podcasts on Apple podcasts, Google podcasts and Spotify, at least the most recent 150. You can find them, just find, look for Divine Intervention podcasts. Although I will say if you want everything from episode one to this present episode, which is episode 401, I would say that you should consider checking out the website, Divine Intervention podcasts.com, the podcasts as an S at the end. If you actually subscribe with a Word Press account, you'll get email notifications whenever I make a new podcast. And then I also have a You Tube channel called the Divine Intervention, USMLE Podcasts and Videos. That's a channel where I post the videos that I make. I'm going to be making some changes within the next few days with that You Tube channel. I'll encourage you to watch out for it. I think I'm going to be doing a few things that are going to make it easier for people to access these podcasts. You know, just creating another avenue for people to be able to access the podcast. So that's something I'm going to be doing. And then I also have a new website called Divine Intervention Life Lessons.com. It's a website where I post life lessons. I've heard many people say, oh, Divine, I really love the life lessons you put at the end of your regular podcasts.
So I made a whole new website, many of you that listen to this podcast on my Christian. So I make two podcasts every week. We have almost a hundred podcasts right now. Most of them are like 10 minutes long. And I just post them. I use the Bible to address a common problem that people face and then talk about practical strategies for countering those problems. So just go to Divine Intervention Life Lessons.com and you can find those. And then one other thing I will also say is I do have a podcast attached to that right. So if you go on Apple podcasts and look for the Divine Intervention Life Lessons podcast, you can easily, easily, easily, easily find, find those things. Now, a life lesson I want to discuss today is being contrary, being contrary. What do I mean by being contrary? Being contrary just means not necessarily following the crowd. I feel like a lot of a big problem we face in medicine, especially amongst medical students is just one jealousy. And when you see another person doing something, you then feeling your heart's that, oh, I must do this thing. And the thing is that's not very prudent at all. That is not very prudent at all. You don't always have to follow the crowd. The thing is there are times where following the crowd is not the wrong idea. There are times where the crowd is actually right. The crowd is actually making very correct, very cogent, very well-founded decisions. Not very wrong with that.
But the one thing I would say is there are certain times, actually quite a number of times, that the crowd is wrong. When you see people, they just blindly follow the crowd. The thing is again, it's really hard to stand out when you're a member of the crowd. You only stand out when you come out of the crowd. So don't always conform to the crowd. Don't always conform to the crowd. The crowd may be wrong. The thing is sometimes even the crowd may be right, but what is right for the crowd may not be correct for you the minority. There, for example, you see some people, they're like, oh, I want to study for step two. Oh, wow, everyone does this, this, this, and that. It may work for everyone, but it may very specifically not work for you. One of the biggest things I've learned from my one-on-one work with a lot of students is sometimes the classic resources that work for everybody does not work for a specific subset of students, a specific kind of student. That's the thing. So understand yourself, one of the best ways to not follow the crowd is understand yourself and clarify who you are. What are your values? Like, a person clarifying their values is, for example, in medicine is like, okay, how do I study best? So for some people reading a textbook may be the thing that makes the most sense for them. For some, listening to videos, listening to audio tapes, maybe the thing that works best for them. Like, for example, for me, I'm not a very big textbook creator.
Don't get me wrong. Have I read textbooks in the past? Absolutely. But textbooks, reading material has not always been my best method of learning. For me, that's one of the things that drove my formation of this podcast. For me, one thing that has always helped me is just watching videos and listening to audio tapes. I can read. Don't get me wrong. Actually, I read pretty heavily. It's just my reading is not textbooks. Many times I read like other kinds of materials. So these are just all things I will encourage you to keep in mind. Understand who you are. We live in a world where people always want to follow the crowd. And one of the reasons people want to follow the crowd is it's very comforting. Ooh, you know, I have other people that I agree with me or I have so many people that I agree with me. But many times the people that blaze trails, the people that break barriers, the people that break limitations, the people that accomplish great things, people that strike out from their own. They get there first before other people get there. So again, I'm not saying, oh, always strike out on your own or don't listen to the crowd. No, you can learn some very valuable lessons from the crowd. There are some times that, oh, the thing that the crowd is doing is what you're supposed to do. But again, just be able to sit down and think for yourself. Even the Bible says, come out from among them and be separate. Sometimes you need to be separate.
You need to not follow along with what everybody is doing. You need to not follow along with the popular thought of you, with the popular convention. So I really hope you find this life lesson to be helpful. I really hope you find this rapid review podcast to be helpful. I'll see you in episode 402. Thank you and God bless you. Bye for now.
Practice questions — USMLE style
Question 1 — Cardiology/Pediatrics
A 3-year-old boy is diagnosed with a large ventricular septal defect (VSD). Over several years, he develops signs of severe pulmonary vascular disease and respiratory distress. Physical examination reveals loud P2 heart sounds. The physician suspects that the initial left-to-right shunt has reversed due to chronic high pressure in the pulmonary circulation. Which complication best describes this physiological reversal?
- A) Patent Ductus Arteriosus (PDA)
- B) Tetralogy of Fallot
- C) Eisenmenger syndrome
- D) Coarctation of the Aorta
Answer: C. Explanation: The transcript details that chronic high pressures in the pulmonary circulation, resulting from a large VSD, can eventually lead to pulmonary hypertension. When the right heart ventricular pressures become so great that they overwhelm the left ventricular pressures, the shunt reverses from left-to-right (L $\rightarrow$ R) to right-to-left (R $\rightarrow$ L). This reversal of flow across a congenital defect is known as Eisenmenger syndrome.
Question 2 — Gastroenterology/Pediatrics
A mother brings her 3-day-old infant into the emergency department complaining of significant, non-bilious vomiting that has been projectile in nature. The vomit appears colorless and contains no bile. On physical examination, the examiner notes an olive-like mass palpated in the epigastrium. What is the most likely diagnosis?
- A) Gastroesophageal reflux (GERD)
- B) Hirschsprung's disease
- C) Malrotation with midgut volvulus
- D) Pyloric stenosis
Answer: D. Explanation: The classic triad for pyloric stenosis includes non-bilious, projectile vomiting in an infant, and the finding of an olive-like mass in the epigastrium. Non-bilious vomit suggests an obstruction proximal to the bile ducts (i.e., at or before the pylorus). GERD typically presents as less forceful spitting up, while Hirschsprung's disease usually causes distal bowel obstruction symptoms (e.g., abdominal distention, failure to pass stool) and often involves meconium ileus.
Question 3 — Nephrology/Pediatrics
A 4-month-old infant is diagnosed with pyloric stenosis and has been vomiting large volumes of gastric contents for several days. Laboratory analysis reveals the following findings: metabolic alkalosis, hypochloremia, and hypokalemia. The child also exhibits signs of volume depletion (low blood pressure). Which sequence best describes the primary physiological derangements leading to these electrolyte abnormalities?
- A) Loss of potassium $\rightarrow$ Metabolic acidosis $\rightarrow$ Hypocalcemia
- B) Loss of chloride $\rightarrow$ Metabolic alkalosis $\rightarrow$ Hypokalemia
- C) Loss of bicarbonate $\rightarrow$ Metabolic acidosis $\rightarrow$ Hyperkalemia
- D) Volume depletion $\rightarrow$ Metabolic acidosis $\rightarrow$ Hypochloremia
Answer: B. Explanation: Vomiting gastric contents (hydrochloric acid, H Cl) leads to the loss of chloride and hydrogen ions. The loss of acid results in a metabolic alkalosis. Furthermore, volume depletion activates the renin-angiotensin system, leading to increased aldosterone release. Aldosterone promotes potassium excretion by the kidneys, resulting in hypokalemia. This sequence—loss of $\text{Cl}^-$ causing metabolic alkalosis and subsequent potassium wasting—is characteristic of pyloric stenosis.
Question 4 — Cardiology/Auscultation
During a physical examination, you auscultate a patient's heart and note that the second heart sound ($\text{S}_2$) exhibits a fixed split, meaning the splitting is audible during both inspiration and expiration. The physician suspects an atrial septal defect (ASD). What physiological mechanism accounts for this finding?
- A) Increased venous return to the right atrium during deep inspiration, causing delayed closure of the pulmonic valve.
- B) A persistent left-to-right shunt that causes increased flow through the tricuspid valve regardless of respiration.
- C) The inability of the aortic and pulmonary valves to close simultaneously due to a defect in the interventricular septum.
- D) Increased systemic vascular resistance during expiration, which delays closure of the aortic valve.
Answer: B. Explanation: A fixed split of $\text{S}_2$ is highly suggestive of an ASD. The transcript explains that with an ASD, blood flows from the left atrium to the right atrium regardless of whether the patient is inspiring or expiring (a constant shunt). This increased volume flow through the right side of the heart means more blood passes through the pulmonic valve relative to the aortic valve, causing the pulmonic valve to close later than the aortic valve, resulting in a fixed split that does not change with respiration.
Quick fire review
What is a key physiological difference in VSD murmurs between utero and post-birth?
The murmur may not be appreciated at birth because right heart pressures are still elevated relative to the left side, limiting flow across the defect. It becomes louder weeks later as systemic pressures normalize.
Which type of S2 splitting is associated with an Atrial Septal Defect (ASD)?
A fixed split of S2, which is audible during both inspiration and expiration because blood always shunts from left to right regardless of respiration.
What are the three key electrolyte abnormalities seen in pyloric stenosis?
Metabolic alkalosis, hypochloremia, and hypokalemia.
If a cardiac murmur increases with inspiration, what does this suggest about the heart's circulation?
It suggests increased venous return (preload) to the right side of the heart due to decreased intrathoracic pressure during inhalation.
What is the preferred diagnostic imaging study for suspected pyloric stenosis?
Ultrasound.
When managing a child with pyloric stenosis, what must be addressed before surgery?
The electrolyte abnormalities (Metabolic alkalosis, hypochloremia, hypokalemia).
What is the most common cause of fixed splitting of S2?
Atrial Septal Defect (ASD).
Why does a small VSD murmur tend to be louder than a large one?
Smaller defects create higher velocity flow, which generates a louder sound (analogous to restricting water flow through a narrow hose).
What is the primary mechanism leading to metabolic alkalosis in pyloric stenosis?
Loss of hydrochloric acid (H Cl) via vomiting.
In the context of GI obstruction, what does non-bilious vomiting suggest about the location of the blockage?
The obstruction is proximal to the common bile duct/duodenum (e.g., Pyloric Stenosis).
What compensatory mechanism causes hypokalemia in pyloric stenosis patients?
Alkalosis triggers H+/K+ antiporter activity, causing potassium to shift intracellularly and leading to urinary wasting of K+.
If a child presents with non-bilious, projectile vomiting and an epigastric olive-like mass, what is the diagnosis?
Pyloric Stenosis.
Quick recall / Anki-style questions
What is the most common cause of fixed splitting of S2?
Atrial Septal Defect (ASD).
Why does a small VSD murmur tend to be louder than a large one?
Smaller defects create higher velocity flow, which generates a louder sound (analogous to restricting water flow through a narrow hose).
What is the primary mechanism leading to metabolic alkalosis in pyloric stenosis?
Loss of hydrochloric acid (H Cl) via vomiting.
In the context of GI obstruction, what does non-bilious vomiting suggest about the location of the blockage?
The obstruction is proximal to the common bile duct/duodenum (e.g., Pyloric Stenosis).
What compensatory mechanism causes hypokalemia in pyloric stenosis patients?
Alkalosis triggers H+/K+ antiporter activity, causing potassium to shift intracellularly and leading to urinary wasting of K+.
If a child presents with non-bilious, projectile vomiting and an epigastric olive-like mass, what is the diagnosis?
Pyloric Stenosis.