DIP Episode 391 - USMLE Step 2CK/3 Rapid Review Series 75
Topic
Lung cancer syndromes; Postpartum hemorrhage; Anti-hypertensive nephrotoxicity; Cardiac arrhythmias (V-tach); HIV vaccine guidelines; Small bowel obstruction.
Key Takeaway
Understanding the specific paraneoplastic syndromes associated with different types of lung cancer, recognizing high-risk drug interactions (e.g., ACE inhibitors and bilateral RAS), and mastering acute cardiac rhythm management protocols are critical for board success.
Episode Notes
Source / episode info
- Episode: 391
- Title: Divine Intervention Episode 391 – USMLE Step 2 CK/3 Rapid Review Series 75
- Published: 2022-05-19
- Source: Episode page
One-liner
This episode provides a rapid review covering the clinical manifestations of lung cancer paraneoplastic syndromes, emergency management of postpartum hemorrhage, nephrotoxic effects of anti-hypertensives (AC Ei/AR Bs), acute cardiac rhythm recognition and treatment protocols, HIV vaccine guidelines, and common causes of small bowel obstruction.
High-yield summary
- Small Cell Lung Cancer (SCLC): Highly associated with paraneoplastic syndromes: SIADH (Hyponatremia), Hypercalcemia (PT HrP), Hypokalemic Metabolic Alkalosis, and LEMS (proximal weakness).
- Postpartum Hemorrhage (PPH): The most common cause is uterine atony; risk factors include polyhydramnios, large baby (>9 lbs), and diabetes. First line treatment is uterine massage followed by Oxytocin.
- ACE Inhibitors/AR Bs: Use with caution in bilateral renal artery stenosis (RAS) due to efferent arteriolar dilation, which decreases glomerular filtration rate (GFR). They are also useful for treating peripheral edema associated with CCB use by dilating veins.
- V-Tachyarrhythmias: Wide complex tachycardia requires immediate triage: stable/with pulse -> Materia Rate; unstable/pulseless -> Unsynchronized Cardioversion (Defibrillation). Defibrillable rhythms include V-fib and pulseless V-tach.
- HIV Vaccines: Live attenuated vaccines are contraindicated if the CD4 count is < 200 cells/mm³. The intranasal influenza vaccine should never be given, regardless of CD4 count.
- Anti-cholinergic Side Effects: Drugs like TC As and first-generation low-potency antipsychotics (e.g., Chlorpromazine) cause Anti-H1 (sedation), Anti-1 (orthostatic hypotension), and Anti-muscarinic effects.
Learning objectives
- Differentiate the clinical presentations of various lung cancer types, particularly recognizing paraneoplastic syndromes associated with SCLC.
- Master the immediate management protocols for postpartum hemorrhage, identifying primary causes and first-line pharmacological interventions.
- Analyze drug interactions involving RAAS blockade (AC Ei/AR Bs) in patients with pre-existing renal artery stenosis.
- Apply advanced cardiac life support principles to wide complex tachyarrhythmias, distinguishing between stable and unstable presentations.
- Recall contraindications for live attenuated vaccines in immunocompromised patients (e.g., HIV).
Board exam buzzwords
| Condition | Key Finding | Association | Board Exam Tip |
| Small Cell Lung Cancer (SCLC) | Hyponatremia, Hypercalcemia, Hypokalemic Metabolic Alkalosis | SIADH, PT HrP, Ectopic mineralocorticoid excess. | Remember the three main paraneoplastic syndromes: SIADH, Hypercalcemia, Electrolyte imbalance (Hypo K). |
| Postpartum Hemorrhage (PPH) | Uterine Atony | Polyhydramnios, Macrosomia, Diabetes. | First-line treatment is uterine massage followed by Oxytocin. |
| ACE Inhibitors/AR Bs | AKI with profound creatinine rise after initiation. | Bilateral Renal Artery Stenosis (RAS). | Suspect RAS and perform renal angiography; these drugs are nephrotoxic in this setting. |
| Wide Complex Tachycardia (V-tach) | Unstable, pulseless rhythm. | V-fib or Pulseless V-tach. | Requires immediate Unsynchronized Cardioversion (Defibrillation). Materia Rate is for stable rhythms. |
Rapid review table
| Topic | Key Point | Context | Exam Relevance |
| Lung Cancer Syndromes | SCLC -> Paraneoplastic Syndrome | SIADH, PT HrP, LEMS. | Must know the specific syndrome associated with SCLC (e.g., hypercalcemia via PT HrP). |
| Postpartum Hemorrhage | Uterine Atony is #1 cause. | Overdistension of the uterus (polyhydramnios, macrosomia). | Oxytocin causes uterine contraction to achieve hemostasis by compressing blood vessels. |
| ACE Inhibitors/AR Bs | Risk in bilateral RAS. | Efferent arteriolar dilation -> decreased GFR. | A profound rise in creatinine after starting an ARB is a major red flag for underlying renal artery stenosis. |
| V-Tach Management | Stable vs Unstable protocols. | Wide QRS complex > 3 small boxes. | Unstable/pulseless = Defibrillation; Stable/with pulse = Materia Rate. Never give Amiodarone if the rhythm is unstable. |
Board-speak -> diagnosis
| Board-speak / Vignette phrase | Diagnosis / Concept | Why it fits |
| Non-smoker with a peripheral lung mass, presenting with hyponatremia and euvolemia. | Adenocarcinoma (Non-small cell) or SCLC (if central). | Peripheral masses are often adenocarcinoma; SIADH is classic for SCLC but can occur in others. Hyponatremia suggests ADH excess. |
| Patient on a dihydropyridine CCB develops severe peripheral edema and signs of venous congestion. | ACE Inhibitor/ARB therapy. | CC Bs increase systemic capillary hydrostatic pressure, leading to fluid extravasation; AC Ei/AR Bs dilate veins (venous dilation), reducing venous pressure and thus lowering interstitial fluid pressure. |
| A patient with a history of bilateral renal artery stenosis develops acute kidney injury after starting an ARB. | Acute Kidney Injury (AKI) due to RAS + RAAS blockade. | Angiotensin II constricts the efferent arteriole; blocking this effect causes efferent dilation, dropping glomerular hydrostatic pressure and severely reducing GFR. |
| A patient with V-tach who is hemodynamically unstable and pulseless on ECG. | Defibrillation (Unsynchronized Cardioversion). | Unstable/pulseless rhythms require immediate unsynchronized electrical shock to reset the heart rhythm. |
| Postpartum hemorrhage following delivery of a large baby in a diabetic mother. | Uterine Atony. | The most common cause of PPH; risk factors include uterine overdistension (polyhydramnios, macrosomia) and diabetes. Treatment is Oxytocin. |
| Patient on Chlorpromazine presents with orthostatic hypotension and sedation. | Anti-cholinergic side effects. | First-generation low-potency antipsychotics block 1 receptors (causing OH) and H1/muscarinic receptors (causing sedation). |
Differential diagnosis / distinguishing features
Small Bowel Obstruction Causes
| Key Features | Distinguishing Findings | Next Step |
| Adhesions (Most Common) | History of prior abdominal surgery (hysterectomy, appendectomy). | Supportive care; NG tube decompression. |
| Crohn's Disease Stricture | Chronic diarrhea history; inflammatory markers. | Colonoscopy/Enteroscopy to visualize strictures; medical management. |
| Hernia | Visible defect in the abdominal wall (inguinal, umbilical). | Surgical repair (Hernioplasty). |
Management pearls
- SCLC Diagnosis: Always consider a metastatic diagnosis and perform thorough staging (CT chest, PET scan) before resection.
- PPH Management: If uterine massage fails, administer Oxytocin IV/IM to induce contraction and vasoconstriction.
- AC Ei Nephrotoxicity Workup: A significant rise in creatinine after starting an AC Ei/ARB mandates a renal angiography to rule out bilateral RAS.
- V-Tach Protocol: For unstable wide complex tachycardia (pulseless or hypotensive), immediate unsynchronized cardioversion is required; do not delay for rhythm diagnosis.
Don't miss
Integration & clinical reasoning
- Cardiology & Nephrology: The use of CC Bs (e.g., Nifedipine) increases systemic capillary hydrostatic pressure, leading to edema. AC Ei/AR Bs counteract this by dilating the venules, reducing venous pressure and thus lowering interstitial fluid pressure. This demonstrates a complex interplay between vascular resistance and fluid dynamics.
- Oncology & Endocrinology: SCLC's association with PT HrP secretion (mimicking PTH) causing hypercalcemia is a classic example of paraneoplastic endocrine mimicry.
- GI Surgery & Nephrology: The management of small bowel obstruction, whether due to adhesions or Crohn's strictures, requires initial supportive care (NG tube decompression), but the underlying cause dictates long-term treatment (surgery vs. immunosuppression).
OMM / COMLEX integration
- For any acute, unstable pathology (e.g., septic shock, massive hemorrhage, cardiac arrest), standard emergency medical protocols take absolute priority over OMT/OMT considerations. Stabilization must occur first.
- In the context of chronic conditions like Crohn's disease or severe hypertension, understanding the systemic inflammatory and vascular components is relevant to viscerosomatic pain patterns, but this episode does not emphasize specific points.
Concept connections / cross-references
- For detailed information on anti-hypertensive agents and their mechanisms: Episode 123 (Hypothetical episode number for RAAS/CC Bs).
- For general guidelines on managing acute abdominal pain and bowel obstruction: Episode 456 (Hypothetical episode number for GI surgery).
High-yield association table
| Condition | Association | Mechanism | Clinical Significance |
| Small Cell Lung Cancer | SIADH, Hypercalcemia, LEMS | Paraneoplastic syndromes; ectopic hormone production. | Requires aggressive screening for these metabolic derangements upon diagnosis. |
| ACE Inhibitors/AR Bs | Bilateral Renal Artery Stenosis (RAS) | Efferent arteriolar dilation -> decreased GFR. | A major cause of AKI in hypertensive patients; requires renal angiography workup. |
| Dihydropyridine CCB Use | Peripheral Edema | Increased systemic capillary hydrostatic pressure. | AC Ei/AR Bs are used to treat the resultant edema by dilating venules and reducing venous pressure. |
| First-Generation Low Potency Antipsychotics (e.g., Chlorpromazine) | Anti-cholinergic effects | Blockade of H1, 1, and muscarinic receptors. | Causes sedation, orthostatic hypotension, and dry mouth/constipation. |
Key terms glossary
| Term | Definition | Context | Example |
| Uterine Atony | Failure of the uterus to contract after placental delivery. | Postpartum Hemorrhage (PPH). | The most common cause of PPH; treated with Oxytocin. |
| PT HrP | Parathyroid hormone-related protein. | Hypercalcemia in malignancy. | Secreted by SCLC, mimicking PTH action to raise serum calcium levels. |
| Unsynchronized Cardioversion | Electrical shock delivered without timing relative to the cardiac cycle. | Pulseless V-tach or V-fib. | Used for immediate defibrillation when the patient is unstable/pulseless. |
| Anti-1 Blockade | Blocking of alpha-one adrenergic receptors. | Anti-cholinergic side effects (e.g., Chlorpromazine). | Leads to orthostatic hypotension due to impaired vasoconstriction. |
Study optimization
| Topic | Study Approach | Priority | Resources |
| SCLC Syndromes | Create a mnemonic/flowchart linking cancer type -> syndrome -> mechanism. | High (Board-level recall). | Review board questions focusing on non-smoker lung masses. |
| Vascular Pharmacology | Understand the hemodynamic effects of CC Bs vs. AC Ei/AR Bs. | Medium-High (Integration/Mechanism). | Practice drawing capillary pressure changes and their impact on edema formation. |
| Acute Cardiac Emergencies | Memorize the management algorithms for V-tach based on stability and pulse status. | High (Step 2/3 Clinical Skills). | Review ACLS guidelines; focus on Materia Rate vs Defibrillation indications. |
Question pattern recognition
- Non-smoker Lung Mass: Always suspect SCLC or Adenocarcinoma. If associated with SIADH, hypercalcemia, or LEMS, strongly favor SCLC.
- PPH Management: The sequence is always: Massage -> Oxytocin -> (If refractory) Methylergonovine/Tranexamic Acid. Never forget the underlying cause of atony.
- Anti-hypertensive AKI: If a patient with known RAS develops severe AKI after starting an ARB, immediately suspect that the RAAS blockade is exacerbating renal hypoperfusion.
Test yourself
Common mistakes to avoid
Common traps
Original transcript with highlights
Original transcript with highlights
Okay, welcome. My name is divine. This is the episode 391 of the divine intervention podcasts. And to this podcast, we're going to be continuing our rapid review series for the USMELIS that just decays that three exams. This is going to be series 75. If you're taking the USMELIS that tools that three exams or complex level two or three exams, I have a few courses coming up that may be of interest to you. I have the MBA Me Test against Strategy scores. It's tomorrow from 5 to 5 to 7 30 p.m. Pacific Standard Time. And then I have a 20 hour review course that's going to be taking place this Saturday. And next week Saturday, it's going to be 10 hours on each of those Saturdays. And then I have the 75 hours step 2 CK school, the disc school, the second version of it. The first version was extremely successful. The second version is going to be taking place in the first two weeks of the month of July. So if you're interested in any of these courses, shoot me an email through the website. I'll give you some more information. You can also listen to the podcasts that I meet on these specific courses. Okay, so let's begin. So what if they give you a question? About 62-year old female, they tell you that she has no history of smoking, but she presents over the last three months with weight loss, has this dry non-productive cough. And then they tell you that you see a mass in the lungs. What should you be thinking about?
And they tell you that she has no history of smoking and the MBM Es, you know, occasionally they write these questions where there is literally like no, no clues given. They just give you a question. Obviously, this person has a mass in the lungs, so they have lung cancer, but they don't give you many clues at all. And if I see stuff like that, always think in terms of what is the most likely in that situation. So for example, this person being a non-smoker and having a lung mass very likely has a no-carcinoma. A no-carcinoma is the most common kind of lung cancer in people that have no history of smoking. So that's something I want to keep in mind on the exams. Remember, a no-carcinoma tends to be a peripheral mass, a large cell carcinoma also can be a peripheral mass versus a small cell and a small cell that tends to be more central masses. Don't forget your pyrneoplastics with the lung cancers, right? Remember, both have lung cancers. They can have a topic-acity production. That's the one that does no suppress with hypodesythemethosol, that'll be small cell. They can have proximal muscle weakness in the context of lumbar etymisthenic syndrome. That's also found with small cell. They can also have hyponitremia, you know, seizures of that nature. They can have a hypotonic serum, hyper-tonic urine from the SIDH that again will also find with small cell lung cancer.
And then don't forget they can get bone pain, they can get hypercalcemia abdominal pain, you know, the stones, bones, grams, and psyche cover tons of hypercalcemia. That's going to be with squint cell lung cancer with a parathyroid hormone relief epiphyde production. And then do not forget that you could also find these are problems. You know, you could also find a person that has like this, you know, few, these few weeks, they have like this, the fuel joint pain, digital club in and all those things. Obviously, that's going to be the, that's going to be the hypertrophic pulmonary osteoarthropathy, right? You don't find that with many lung cancers, right? They can give you a person that has a lung mass and they have like facial swelling, neck swelling, and things like that. Obviously, that's going to be the super, super-refiniciva syndrome. For that radio therapies, what is indicated is one of those radiation oncology emergencies, right? So those are all things you can see with lung cancer, right? Those are all things you can see with lung cancer. And remember, lung cancer, you're going to get the chest CT is actually going to help you a lot with staging and surgical planning. And then many times you're going to get a PET scan, right? So you get the chest CT after that, you get the PET scan, and then typically you're going to go ahead and you're going to go ahead and do some kind of biopsy. You can get the biopsy many different ways.
You can do a mediascanoscopy, with biopsy. You can do it in the bronchial ultrasound, with biopsy. You can even do percutaneous CT guided biopsy, especially for the more peripheral lesions. So those are always you can obtain tissue, right? And again, remember a small cell lung cancer, once you diagnose it, it's teach four. So always consider a medastatic diagnosis. So that's just something I want to keep in mind. And obviously, before you take a person to reset part of their lungs for any kind of lung cancer, you got to remember to check the PF Ts, especially the FVV1, especially the FVV1. That's pretty important. Okay. But what if they give you a question about 32-year-old female, the tale is that she has a history of diabetes, the tale is that she delivered 9 pound, it was newborn at 37 weeks gestation, and the tale is that she delivered this child like two hours ago, which has been having copious amounts of blood emanating from her vagina. What do you think? What's the cause? What are we doing in this circumstance? Well, I would really hope you're saying all divine, this person has supposed bottom hemorrhage, right? What's the most common cause of post bottom hemorrhage? It's going to be uterine acne, right? And uterine acne is pretty common in people that are diabetics, right? I mean, look at this child she delivered, it's almost 10 pounds, baby's big, right?
So to accommodate that big baby or to push out that big baby, moms, uterus, most have contracted pretty significantly to get that baby out. So since moms, uterus, contracted pretty significantly, you can think of moms, uterus as kind of being tapped out, being tired, having no strength. So that's uterine acne, that's really the pathophysiology in this kind of person. Really anything that makes your uterus work harder than it needs to, or makes the uterus bigger than it needs to be, that's going to cause uterine acne. So say, for example, you have polyhydramneus, right? Your uterus just distains, distains, distains, almost think of it as like dilated with your therapy. I'm fairly certain that is not a term that exists, but I just think of it as like chronic volume overload. Again, I'm trying to make some parallel here with a person having a dilated cardiomyopathy and eccentric hypertrophy, I just going to think of it the same way. When a person has polyhydramneus for pretty long stretches of their pregnancy, the uterus has then had to deal with chronic volume overload. That kind of distains the uterus, makes it difficult for it to contract down to a normal size after delivery, right? So polyhydramneus is another risk factor in endymies for people having a postpartum hemorrhage. So for a person who has uterine acne, what are you going to do? Well, you're usually going to try a uterine massage first, right?
You know, that tends to work pretty well for many people, but if that's not caught in it, then you're going to go ahead and proceed to doing giving oxytocin, right? Because basically by giving oxytocin, you're going to squish the myo-leachum, when you squish the myo-leachum, the uterus will contract down. As it's contracting down, it's literally time of the blood vessels that produce its walls, so the person can stop bleeding. So that's something you kind of want to keep at the back of your mind with postpartum hemorrhage, right? The most common cause of postpartum hemorrhage is going to be uterine acne. It's going to be uterine acne. And then, what if they give you a question about the 55-year-old male, they tell you that she was recently pleased on an anti-hypertensive, and then you see she's creatinine just goes through the roof, it just goes from like, oh, it was one on baseline, and that was like three. What happened? Well, I'll really hope you're thinking about isynhibitors. Now, remember isynhibitors, one thing they love to do is they're not good in people that have bilateral renal adristinosis, because if you think about it, if you have renal adristinosis, you're not profusing your offering at your overalls really well. If you don't profuse those things really well, then there's not enough blood going to your glomerular capillaries.
If you don't have enough blood going to your glomerular capillaries, well, surprise surprise, you're going to have a decrease in hydrostatic pressure in your glomerular capillaries. If you have that decrease in hydrostatic pressure, then that's going to not favor filtration. So your GFR is going to be low to start, and then you decide to add on to that by giving an isynhibitor. Well, isynhibitors and R, you know, in just in two receptor blockers, they're very good dilators of the efferin arterial. If you dilute the efferin arterial, you're literally stealing blood away from the glomerular capillaries. You still blood away from the glomerular capillaries. Surprise surprise, you're going to bring those hydrostatic pressures down even more, and that's going to again lower your ability to filter out fluid, right? So you're going to ultimately have even further decreasing in GFR, and your creatinine is going to go up, right? So that's why many times a clue to bilateral orinolateral stenosis on nbimixams is a person that has a profound rise in creatinine after an isynhibitor or an ARB is instituted. That's very high you to know for tests. So it won't be like, oh, their creatinine was one, and then it became 1.3. Pretty much everyone that's placed on an isynhibitor for the most part within reason is going to have a mild bump in the creatinine, literally for the exact same mechanisms I just described.
But going out by a factor of 2, a factor of 3, anything like that is certainly not normal. In those circumstances, you want to perform some kind of renal angiography or renal arteriography, just to make sure the person does not have renal arterial stenosis. Because if you think about it, the stories are kind of linked together. The person was placed on an anti-hypertensive. So probably surprise is probably the renal arterial stenosis they had in the first place that caused that hypertension. So again, isynhibitors, they're kind of high you drugs to know for exams. Remember, you don't want to give them to a person that has a c1 esterase inhibitor deficiency, because when you have that deficiency, it can break down pretty kind. So isyn is going to help you out there. If you then take an isynhibitor, they're going to be in big trouble. Remember, that's an autosomal dominant disorder, hereditranjirigima. And in isynhibitors, they're also pretty good for treating the peripheral edema. That's associated with taking a dihydropereodine-cosm-channel blocker. Because those dihydropereodine-cosm-channel blockers, they're very powerful at terryola dilators. That's how they reduce systemic muscular resistance and bring down your blood pressure. So when you bring down your when you dilate those arterials, you're going to be sending more blood to your systemic capillaries. When there's more blood there, you're going to raise the hydrostatic pressures.
If you raise the hydrostatic pressures, that's going to cause you to have more fluidic extravacition. When you have fluidic extravacition, you're going to have peripheral edema. So how do you fix the problem? You're going to give something that dilates venials, like the isynhibitors. You dilate those venials. When you dilate those venials, that's going to draw more fluid away from those systemic capillaries. That's going to lower the hydrostatic pressures in those capillaries. And that's going to ultimately help the person's problems. So isynhibitors are the drugs of choice for treating the peripheral edema associated with taking a dihydropereodine-cosm-channel blocker. So something like, sorry, something like, I'm low-deepin, phylo-deepin, like phylo-deepin, and things like that. So just going to keep that in mind. Keep that in mind. Keep that in mind. Keep that in mind. That's very, very high yield to know, for example. So isynhibitors, you know, they're pretty useful drugs, the Improve survival in CHF, they're one of those drugs that actually Improve survival. And they also pretty helpful in people that have renal disease. For example, you have like a person that is hypertensive and their kidneys don't work great. Give an isynhibitor. Because again, by dilating those efferinaterials, you're literally exerting some renal protective effects. So that's pretty, pretty important to know for, for example.
Now, what if they give you a question about, what if they give you a question about 37-year-old male, you know, the tell you that he's birthed to the emergency room by his mom because he collapsed at home. And they tell you that, you know, he was recently placed on an anti-psychotic. He was placed on medication because he was hearing voices and all those things. He was placed on medication like five days ago. And then the bring him to the hospital and they give you an ekegi. The MBME says, you know, the following was obtained on ekegi. You see an ekegi and you see the QRS complex is like wide. And you see this person's, his heart rate is like 325 beats per minute or something really crazy. If you think about that, really hope you're thinking about the prolongation of the acute interval. This person took an anti-psychotic, prolonged the acute interval, give the person a V-tap. So you see a wide complex regular tachyorythmia. That's V-tap. Once you see something that is wide complex, so that means the QRS is more than three little boxes. It's a ventricular arrhythmia for the most part. So white QRS tachyorythmia, that's going to be V-tap. And this person is, you know, not doing well at all. I mean, obviously, for a person who has V-tap, you need to triage them into all three categories on exams. And I'll get back to the anti-psychotic part in a bit. But basically, what happened here? So this person has V-tap.
Well, remember, V-tap, you can either have no pulse or you can have V-tap and be hemodynamically unstable or you do have a pulse or you can have V-tap and be hemodynamically stable and have a pulse. For the people that are hemodynamically stable have a pulse, have V-tap. You're going to give them a mutatorate. A mutatorate is going to be the drug of choice in those circumstances. But for a person that has V-tap, they have a pulse and they're hemodynamically unstable. We're going to go ahead and do synchronized cardioversion. Synchronized cardioversion. Remember, synchronized cardioversion occasionally could have other names on in-beaming exams. For example, it could be called direct core-end cardioversion, it could be called direct core-end counter shock. Those are all names you'll be seeing on an exam for synchronized cardioversion. Now, if a person has V-tap and they have no pulse, that's obviously a bad situation. They're almost dead at that point. In those circumstances, you're going to go for the nuclear options. You're going to go ahead and do an un-synchronized. Notice I did not say synchronized. Un-synchronized cardioversion. Another name for un-synchronized cardioversion is defibrillation. Right? Defibrillation. Remember, there are two defibrillatable radios that you need to know for sure. For purposes of the USML exams, you need to know V-tap with no pulse gets defibrillation. And people that have V-fib also get defibrillation.
Again, another name for defibrillation is un-synchronized cardioversion. Un-synchronized cardioversion. Un-synchronized cardioversion. Now, what if they give you a question about a patient that has HIV? And then they give you a rundown of vaccines and the ask, which of these vaccines is going to be contraindicated in this patient? Again, that should be easy for you. You know that, in general, if you have a CD-4 count that is on the 200, you don't want to get any kind of live-atten with your vaccine. So, it's going to be things like the MMR vaccine, the measles, mumps, rebella vaccine, anything like the yellow fever vaccine. You don't want to give those things, right? Or even like the intranasal influenza vaccine, not a good idea in people that have HIV. Right? Now, the thing is there are some rooms that state that, you know, if the person's CD-4 count is sufficiently high, like let's say it's over 200 or something, you know, you can say we can give you the MMR vaccine, we can give you, you know, live-atteninivirus vaccines. But, that intranasal influenza vaccine should never be given regardless of CD-4 count to a HIV patient on MB Mexams. So, again, let me just make sure that I make this very clear. If your CD-4 count is over 200, in general, you can get live-atteninivirus vaccines. But, regardless of your CD-4 count, you should never get an intranasal influenza vaccine if you're a HIV patient on MB Mexams.
And the one quick thing I also wanted to say that I would discuss with antipsychotics is, again, the reason they pretty have the V-TAC from the VNF I just discussed was because they took the antipsychotic. Antipsychotics are very notable, prolongers of the QT interval, right? So, especially Ziprasi don't. Ziprasi don is like the big one of all of them. It's the one that prolongs the QT interval the most. But, you can also find that in every of the antipsychotics. So, what are the other things that actually can prolong your QT interval? Well, they're going to be things like hypochylemia, hypochalcemia, hypomagazemia, dejuoxin, and coscutiprolongation. So, there are many things that can cause QT prolongation. Even TCE is tricyclicontide presence. They can absolutely cause QT prolongation. Although, remember, tricyclicontide presence, they tend to cause more of a wide QRS on MB Mexams. Obviously, in those circumstances, you're going to give the person a sodium bicarbonate. You're going to give them sodium bicarbonate. Why? Because TCE is the very powerful sodium channel blockers. So, because the block sodium channels, you want to give something that will overwhelm that sodium channel blockade, like sodium bicarbonate. That's why it's helpful. And also, by giving sodium bicarbonate, you're going to be accelerating the loss of the tricyclicontide presence from the presence body. Now, it's pretty high you to know something though.
With tricyclicontide presence, the fact that they have these things that are called anti-harm effects, anti-harm effects. In fact, let me tell you this. The drugs that have anti-harm effects are pretty high you to know for MB Mexams. So, what in the world does anti-harm stand for? Well, the H stands for anti-H1. So, they have anti-histamine effects, so they can be sedated as a result of taking those drugs. The H stands for anti-alpha one. So, obviously, if you're blocking alpha one receptors, you can get orthostatic hypertension. And then the M stands for anti-muscularly, anti-muscularly. So, you can get an anti-cholinergic toxic drum from any of these medications. So, what are the two general drug classes that tend to be associated with anti-harm side effects? The first group are your tricyclicontide presence. So, it turns like things like imitryptoline, not tryptoline, imipramine, desipramine, things like that. And then the second group that have these anti-harm side effects are going to be your anti-psychotics that are first generation, but they are low potency. I'll say that again, your anti-psychotics that are first generation, but they are low potency. So, what are some drugs that fall in here? The big one on exams is cloprimazine, CHLR, P-R-O-M-E, Zi-N-E, cloprimazine. Cloprimazine is a first generation low potency anti-psychotic that has these anti-harm side effects.
So, they can tell you about a person that was placed on cloprimazine for nausea, because sometimes he's used for nausea. And then they tell you that the presence does have orthostatic hypertension. You want to think about that alpha one, anti-alpha one effect, right? And once those anti-harm side effects that ultimately causing the problem in the patient. So, again, just pretty high-youtube able to tie all these things together is just something I think is going to be profoundly helpful to you on exams. Profoundly, profoundly helpful to you on exams. And then what if they give you a question about 29-year-old female? They tell you that for the last three days, she has been having a lot of nausea, a lot of vomiting. She has been able to pass gas, but she has not had any bowel movements. And then they tell you that she has a history of like chronic diarrhea and they tell you that she has been on the immunosuppressive therapy for this diarrhea. And you know, the immunosuppressive therapy will stop or she forgot to refill her medication or something like that. When you see something like this, what should you think about? Well, the first thing you should think about is that this person likely has Crores disease of some sort. Now, Crores disease, remember, typically it's going to be in the younger crowd, although it can also be in an older person. So, again, always look at the context that you're giving on exams.
So you can find it in the younger crowd, you have like chronic diarrhea. And many times you're going to put them on some kind of immunos, you know, like something like Sofosalazine, Mesalamine as first line. Obviously, that doesn't work. You're going to go to the TNTF inhibitor. But when the person has a flare of disease, you're going to go ahead and give them steroids. So now that I've kind of got in that basic information out of the way, what's causing this person to have this almost like acute worst end of their symptoms? So you see them having like a lot of nausea, a lot of vomiting, no bowel movements. This is a small bowel obstruction. Remember, Crores disease can cause a small bowel obstruction on the exams. In what context is going to be in the context of strictures, strictures? Whenever you have chronic inflammation of the GI tract, your body can try to heal that inflammation with fibrosis. And when the fibrosis happens, that can cause strictures. And that's stricture can cause a bowel obstruction. It can cause a bowel obstruction. That is extremely high yield to know for purposes of exams. And obviously, we're going to treat this person like we treat a regular small bowel obstruction. We're going to place an ingy tube to try to decompress the person's bowel.
And remember, and then group of people that can get the same problem are people that, for example, have peptic ulcer disease, especially if they have like, do it long ulcers, those do it long ulcers can heal with the formation of fibrosis and strictures. And that can cause a small bowel obstruction. Although remember, the most common cause of a small bowel obstruction in general are adhesions from prior abdominal surgery, like a hysterectomy or something of that nature. And then the second most common cause are hernias. And the third most common cause is cancer. Those are the three top causes of small bowel obstructions in the row world. And also an in-be-me exams. But again, the treatment is the same. You're going to place an ingy tube. Remember, sometimes they can call an ingy tube nasogastric intubation on exams. So don't be thrown off by that kind of terminology. Okay. So since this has gone for more than 20 minutes, I'm going to go ahead and pause here. Again, as I do at the end of every podcast, I go for one one teeter in full. All the USMLA exams step one to step three, pre-clean cool minutes cool exams, 30-ish off exams, and also offer review courses. I'll offer a 20-hour review course for step two and step three, which also applies to complex level two and three. I'll offer an in-be-me test-taking strategy scores. And also offer a 75-hour step two CK school that has limited attendance.
So if you interested in any of these things, shoot me an email through the website and I'll be happy to give you some more information. And then I have these podcasts on Apple podcasts on Google podcasts so at least the most for 7150. But if you want everything from episode one, all the way to this present episode reaches episode 391, then go on the website, divineinterventionpodcasts.com. That's where you see every single podcast. You don't even have to sign up. Although if you sign up with your Word Press account, you get an email notification whenever I make a new podcast. And then I also have a You Tube channel. It's called Divine Intervention, USMLA podcast and videos. And that's a You Tube channel where I post the videos that I make. So if you're interested in any of those things again, just go on the You Tube channel and you can find all my shelf reviews and things like that. But again, if you want the slides, as you know, those shelf reviews, go on the website, on that those respective episodes. And then I also have a new website called divineinterventionlifelessens.com. Basically, the way the website works is many people have told me, oh, divine, I love the life lessons you put at the end of your podcasts. So I decided to make a separate website, divineinterventionlifelessens.com, where I post Bible based teaching, they're very short podcasts. If I believe I have about 82 of them right now. And for the most part, they're under 10 minutes long. Most of them.
And it just uses the Bible to talk about common problems that are faced by humanity. So I would encourage you if you're interested in those, check out the website. I even have the podcast on Apple podcasts. It's called the Divine Intervention Life Lessons Podcast. So if you're interested in any of those things, just head on to that website or head on to the podcast and you can definitely take advantage of those things. Now, the quick life lesson I just want to share today is don't be antsy. Don't be antsy. This is a big problem in medicine. Many people in medicine have a lot of trouble with focus. But the key thing you need to realize and understand is there's not many things you can accomplish in life if you cannot just sit in one place and focus for a while. So you see people, everything has to be all fun and games. It has to be wow. So a riveting for them to be able to focus. No. The thing is there are certain things in life that are pretty boring that you have to sit through. But after you sit through those boring things, you record great success. So I'll just encourage you to stop thinking after thrills. Things that are wow, so fun and exciting. Like don't get me wrong. Obviously, if you can have fun while you're doing something, the better. But again, I'm telling you this, there are many things in life that are not for an exciting but they are necessary.
In fact, again, you've probably heard me say this saying in many of my podcasts where one of the biggest is the same by a scientist from like back in the day, Blaze Pascal. He says, all of a man's problems can be traced to one thing. No being able to sit quietly and learn in a room. So the thing is, you see people, they're like, wow, they have to be jumping all over the place. They have to be doing it. No, sitting one place and just focus. I'm telling you this, a person that is focused is a person that is going to achieve destiny. But a person that is on focus just always jumping from one thing to the other because they cannot just sit with something for long and get the benefit from it. And people that are generally going to keep struggling in life. Like I'll give you an example. You see some of the students have seen this play out so many times. They get one resource. They know that, okay, this resource is good. But in the use for like three days and then they give up because they hear some of their friends talking about some new architectly found or something new that they found that they use. And then they jump to that thing. After three days they get bored and jump to the next thing. I'm sure some people listening to this podcast can release to exactly what I'm saying. I will encourage you just sit with something. The fact that something gets boring after three, four days does not mean that it's not the right thing for you to be doing in that moment.
So I'm encouraging you to stop being antsy. If you find the right target, focus hard on that target and keep shooting at it until you get the benefit that you want. So thank you for listening to me. I'll see you in the next podcast. God bless you. Bye for now.
Practice questions — USMLE style
Question 1 — Obstetrics/Pathophysiology
A 32-year-old woman is delivered via Cesarean section after carrying a macrosomic baby. Shortly after delivery, she begins experiencing copious vaginal bleeding. Her blood pressure remains stable, but her vital signs are concerning for significant hemorrhage. The most likely underlying cause of this postpartum hemorrhage (PPH) is uterine atony. Which of the following interventions represents the initial and most appropriate management step?
- A) Immediate administration of tranexamic acid
- B) Placement of a Foley catheter to measure urinary output
- C) Vigorous fundal massage
- D) Administration of erythropoietin-stimulating agents
Answer: C. The most common cause of postpartum hemorrhage is uterine atony, which results from the uterus failing to contract adequately after delivery. The initial management step for suspected uterine atony is vigorous manual fundal massage. If this fails, uterotonics such as oxytocin are administered; oxytocin stimulates myometrial contraction, which in turn compresses the blood vessels within the placental site, achieving hemostasis.
Question 2 — Nephrology/Pharmacology
A 55-year-old male with a history of bilateral renal artery stenosis is placed on an Angiotensin-Converting Enzyme (ACE) inhibitor for hypertension. Within days, his serum creatinine rises significantly from a baseline of 1.0 mg/dL to 3.5 mg/dL. Which pathophysiological mechanism best explains the acute kidney injury observed in this patient?
- A) The ACE inhibitor causes afferent arteriolar vasodilation, leading to decreased glomerular hydrostatic pressure and reduced filtration.
- B) The drug blocks aldosterone receptors, causing excessive sodium retention and subsequent tubular necrosis.
- C) The combined effect of RAAS blockade and efferent arteriolar dilation reduces the net filtration pressure in the glomerulus.
- D) The medication directly impairs proximal tubule reabsorption, leading to acute azotemia.
Answer: C. In patients with bilateral renal artery stenosis, the kidney relies heavily on maintaining adequate glomerular hydrostatic pressure for filtration. ACE inhibitors (and AR Bs) block the RAAS system. By dilating the efferent arteriole, they reduce the resistance downstream of the glomerulus, which lowers the overall glomerular hydrostatic pressure and significantly decreases the Glomerular Filtration Rate (GFR), leading to a profound rise in creatinine.
Question 3 — Cardiology/Emergency Medicine
A 37-year-old male collapses at home after being started on an antipsychotic medication five days prior. In the emergency department, he is found to be tachycardic with a wide QRS complex (suggesting ventricular rhythm). He is currently hemodynamically unstable and has no palpable pulse. What is the most appropriate immediate intervention for this patient?
- A) Administer IV amiodarone
- B) Perform synchronized cardioversion
- C) Initiate atropine drip
- D) Perform unsynchronized cardioversion (defibrillation)
Answer: D. The patient presents with a wide complex tachycardia and is hemodynamically unstable with no pulse. This scenario requires immediate defibrillation, which is synonymous with unsynchronized cardioversion. Synchronized cardioversion is reserved for patients who are stable or have a pulse. Amiodarone (A) is used for stable V Tach; atropine (C) treats symptomatic bradycardia.
Question 4 — Gastroenterology/Surgery
A 29-year-old female with a history of chronic diarrhea, managed by immunosuppressive therapy, presents to the emergency department with severe nausea and vomiting but has not passed any flatus or stool for three days. She is suspected of having an acute small bowel obstruction (SBO). What is the most likely underlying cause of this SBO in the context of her chronic inflammatory condition?
- A) Adhesions secondary to prior abdominal surgery
- B) Stricture formation due to chronic inflammation and subsequent fibrosis
- C) Pseudomembranous colitis leading to paralytic ileus
- D) Crohn's-associated malignancy causing luminal narrowing
Answer: B. While adhesions (A) are the most common cause of SBO generally, in a patient with Crohn's disease, the obstruction is typically caused by strictures. Chronic inflammation leads to fibrosis and scarring within the bowel wall, which narrows the lumen and causes mechanical obstruction. This mechanism is highly characteristic of chronic inflammatory bowel diseases like Crohn's.
Quick fire review
What is the most common type of lung cancer found in non-smokers?
Adenocarcinoma (or no-carcinoma).
Name two paraneoplastic syndromes associated with Small Cell Lung Cancer (SCLC).
SIADH (hyponatremia), hypercalcemia (PT HrP), or hypokalemic metabolic alkalosis.
What is the most common cause of postpartum hemorrhage?
Uterine atony.
What are the two primary interventions for managing uterine atony-related PPH?
Fundal massage, followed by Oxytocin administration.
Which class of antihypertensive drugs should be used with caution in patients with bilateral renal artery stenosis due to risk of AKI?
ACE inhibitors and AR Bs (due to efferent arteriolar dilation).
What is the key contraindication for giving live-attenuated vaccines to an HIV patient?
A $\text{CD}4$ count below $200 \text{ cells}/\mu\text{L}$.
Which specific vaccine should never be given to an HIV patient, regardless of their $\text{CD}4$ count?
Intranasal influenza vaccine.
What is the primary mechanism by which ACE inhibitors/AR Bs worsen renal function in bilateral renal artery stenosis?
They cause efferent arteriolar dilation, lowering glomerular hydrostatic pressure and reducing GFR.
List three drugs or conditions that can prolong the QT interval.
Anti-psychotics (especially Ziprasidone), hypokalemia, hypomagnesemia, tricyclic antidepressants (TC As).
What is the drug of choice for treating peripheral edema associated with Dihydropyridine Calcium Channel Blockers?
Angiotensin Receptor Inhibitors (AR Is) or ACE inhibitors (which dilate venules).
If a patient has suspected Crohn's disease and presents with signs of small bowel obstruction, what is the most likely underlying cause?
Strictures/fibrosis due to chronic inflammation.
What are the three top causes of small bowel obstruction in general?
Adhesions (most common), hernias, and cancer.
When managing V Tach with no pulse, which type of electrical therapy is indicated?
Unsynchronized cardioversion (Defibrillation).
Quick recall / Anki-style questions
What is the primary mechanism by which ACE inhibitors/AR Bs worsen renal function in bilateral renal artery stenosis?
They cause efferent arteriolar dilation, lowering glomerular hydrostatic pressure and reducing GFR.
List three drugs or conditions that can prolong the QT interval.
Anti-psychotics (especially Ziprasidone), hypokalemia, hypomagnesemia, tricyclic antidepressants (TC As).
What is the drug of choice for treating peripheral edema associated with Dihydropyridine Calcium Channel Blockers?
Angiotensin Receptor Inhibitors (AR Is) or ACE inhibitors (which dilate venules).
If a patient has suspected Crohn's disease and presents with signs of small bowel obstruction, what is the most likely underlying cause?
Strictures/fibrosis due to chronic inflammation.
What are the three top causes of small bowel obstruction in general?
Adhesions (most common), hernias, and cancer.
When managing V Tach with no pulse, which type of electrical therapy is indicated?
Unsynchronized cardioversion (Defibrillation).