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Source / episode info

  • Episode: 638
  • Title: DIP Ep 638: USMLE Step 2/3 Rapid Review Series 134
  • Published: 2026-03-05
  • Source: Episode page

One-liner

This rapid review emphasizes recognizing alternate names and classic associations across multiple systems, covering GI motility disorders (Toxic Megacolon, Hirschsprung), dermatophytosis (Tinea corporis), gynecologic pathology (Asherman's syndrome), neuro-autonomic syndromes (Multiple System Atrophy), calcification patterns (Samoydes), and drug management principles (Ethacrynic acid, Sulfonylureas).

High-yield summary

  • Toxic Megacolon: Strongly associated with Clostridioides difficile colitis. Also consider other causes of severe colonic dilation/ileus in the setting of opioids or bowel obstruction. Transverse colon diameter > 6 cm is highly worrisome.
  • Multiple System Atrophy (MSA): A Parkinson's plus syndrome characterized by a triad: autonomic dysfunction, parkinsonism, and orthostatic hypotension. Key signs include poor sweating (anhidrosis/hypohidrosis) and significant drop in systolic BP (>20 mm Hg) upon standing.
  • Tinea Infections: The most common cause of Tinea corporis is Trichophyton species. For scalp or nail involvement, systemic therapy (Terbinafine or Griseofulvin) is required; topical agents are insufficient.
  • Asherman's Syndrome: A cause of infertility resulting from intrauterine adhesions/synechiae, typically following multiple D&C procedures. Treatment involves hysteroscopic lysis.
  • Ethacrynic Acid: Must be considered as a loop diuretic alternative when a patient has a history of severe sulfur drug allergy (e.g., to Trimethoprim-sulfamethoxazole).
  • Samoydes Calcifications: Associated with four classic malignancies: Papillary thyroid cancer, Mesothelioma (risk factor: asbestos), Serocystadenocarcinoma of the ovary, and Germ cell tumors (GCT).

Learning objectives

  • Identify and differentiate various types of colonic pseudo-obstruction syndromes (e.g., Toxic Megacolon vs. CD).
  • Recognize the classic clinical triad and associated complications of Multiple System Atrophy (MSA).
  • Differentiate between the etiologies, names, and management strategies for uterine adhesions (Asherman's syndrome) and congenital megacolon (Hirschsprung disease).
  • Apply knowledge of drug allergies to select appropriate alternative medications (e.g., Ethacrynic acid for loop diuretic effect in sulfur allergy).
  • Correlate specific calcification patterns with underlying malignancies (Samoydes pattern).

Board exam buzzwords

ConditionKey FindingAssociationBoard Exam Tip
Multiple System Atrophy (MSA)Orthostatic hypotension; Poor sweatingParkinsonism, Autonomic failureLook for a triad of autonomic dysfunction + parkinsonian features. Prognosis is poor.
Tinea corporisAnnular/ring-shaped rashTrichophyton species (most common cause)If the infection involves scalp or nails, systemic therapy is mandatory.
Ethacrynic AcidLoop diuretic effectSulfur allergy to Furosemide/loop diureticsUse this drug when a loop diuretic action is needed but sulfur drugs are contraindicated.
Angiogenin Sensitivity Syndrome (AGSS)46 XY karyotype, female phenotype; Poorly developed pubic hairTestosterone receptor defectRemember the key finding: failure to respond to testosterone despite having male chromosomes.

Rapid review table

TopicKey PointContextExam Relevance
Toxic MegacolonTransverse colon > 6 cm diameter; signs of ischemia/perforation.History of C. difficile colitis or opioid use.Requires immediate surgical consultation due to high risk of perforation.
Hirschsprung DiseaseProfuse stool expression on rectal exam (not "poop splatter").Congenital agangliosis; failure of enteric nervous system development.Alternate names include congenital megacolon or colonic aganglionosis.
Multiple System Atrophy (MSA)Systolic BP drop > 20 mm Hg upon standing.Autonomic neuropathy affecting multiple systems (cardiovascular, sweat glands).The definitive sign for orthostasis is a drop of 20 mm Hg in systolic BP.
Samoydes CalcificationsAssociated with Papillary thyroid cancer, Mesothelioma, Serocystadenocarcinoma.These calcifications are often found in the abdomen/pelvis and suggest underlying malignancy.Must recall the four classic associated cancers to avoid missing a high-yield pattern question.

Board-speak -> diagnosis

Board-speak / Vignette phraseDiagnosis / ConceptWhy it fits
A patient with a history of multiple D&C procedures presents with infertility.Asherman's Syndrome (Intra-uterine adhesions)Multiple uterine dilations/curettages can cause scarring, leading to poor implantation or tubal blockage.
Profuse expression of stool noted after rectal examination in an infant.Hirschsprung DiseaseThe classic physical exam finding that suggests a functional obstruction distal to the rectum (aganglionosis).
A 50-year-old male presents with unexplained orthostasis, poor sweating, and erectile dysfunction.Multiple System Atrophy (MSA) / Shy Drager SyndromeThis constellation points to severe autonomic failure affecting multiple systems (cardiovascular, endocrine, motor).
Finding of "world calcifications" on imaging in a patient with ovarian cancer.Samoydes CalcificationsThe term is used as a surrogate for classic associations like those seen in mesothelioma or papillary thyroid carcinoma.
A diabetic patient who has a known sulfur allergy requires oral hypoglycemic therapy.Meglitinides (e.g., Repaglinide)These drugs are an alternative to sulfonylureas and do not contain sulfur, making them safer for allergic patients.
A 19-year-old female presents with poorly developed pubic/axillary hair but has well-developed breasts.Angiogenin Sensitivity Syndrome (AGSS) / Testicular Feminization SyndromeThe underlying defect is in the testosterone receptor, leading to impaired androgen response despite normal XY karyotype.

Differential diagnosis / distinguishing features

Angiogenin Sensitivity Syndrome (AGSS) vs. Androgen Insensitivity Syndrome (AIS)

Key FeaturesDistinguishing FindingsNext Step
46 XY karyotype; Poorly developed pubic/axillary hair; Well-developed breasts.The defect is specifically in the testosterone receptor gene, leading to poor response to androgens.Confirm diagnosis via genetic testing (Androgen Receptor mutation). Management involves hormone replacement therapy.

Multiple System Atrophy (MSA) vs. Pure Parkinson's Disease

Key FeaturesDistinguishing FindingsNext Step
Autonomic dysfunction (orthostasis, poor sweating); Severe autonomic failure.The presence of significant orthostatic hypotension or anhidrosis points strongly toward MSA.Management is supportive; prognosis is extremely poor. Focus on recognizing the constellation of symptoms.

Management pearls

  • Toxic Megacolon: Immediate stabilization and monitoring are paramount. If signs of perforation (peritonitis, systemic toxicity) develop, surgical intervention (colectomy) is required.
  • Tinea Infections (Systemic): For tinea capitis or onychomycosis, topical agents are insufficient; systemic antifungals like Terbinafine or Griseofulvin must be used.
  • Orthostasis: If a patient presents with orthostatic hypotension, measure the change in systolic BP (SBP) and diastolic BP (DBP). A drop of \ge 20 mm Hg SBP is diagnostic for significant orthostasis.
  • Sulfur Allergy Management: When loop diuretic action is needed in a sulfur-allergic patient, use Ethacrynic acid as an alternative to Furosemide or Bumetanide.

Don't miss

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The most common cause of Tinea corporis is Trichophyton species.
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MSA involves the triad of autonomic failure, parkinsonism, and orthostasis; it has a very poor prognosis (death within 6–10 years).
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When evaluating calcifications in abdominal/pelvic malignancies, always consider the Samoydes pattern: Papillary thyroid cancer, Mesothelioma, Serocystadenocarcinoma, GCT.
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The key difference between sulfonylureas and meglitinides is that meglitinides (e.g., Repaglinide) are preferred if a sulfur allergy exists due to their faster action and reduced hypoglycemia risk.

Integration & clinical reasoning

  • GI Motility: Understanding the spectrum of colonic pseudo-obstruction syndromes (from functional ileus/opioid use to primary motility disorders like Hirschsprung or toxic megacolon) requires correlating clinical signs (dilation, obstruction pattern) with potential triggers (toxins, surgery).
  • Endocrinology & Genetics: The AGSS case highlights how a single receptor defect (testosterone receptor) can lead to profound sexual dimorphism and developmental issues in an otherwise chromosomally male individual.
  • Pharmacology & Allergy: Recognizing the need for alternative drug classes based on allergies (e.g., Ethacrynic acid for loop diuretics, Meglitinides for sulfonylurea alternatives) is a critical step in patient safety management.

OMM / COMLEX integration

🦴
For COMLEX: know these viscerosomatics / Chapman points, but don't let OMM distract from emergent diagnosis and management.
  • Standard emergency management takes priority in acute GI crises (e.g., Toxic Megacolon perforation, septic shock). OMT is adjunctive only after stabilization.
  • For neurodegenerative syndromes like MSA, the focus remains on supportive care and managing autonomic symptoms; there are no specific OMM/OMT procedures that alter the underlying pathology.

Concept connections / cross-references

  • For detailed review of GI motility disorders and specific colonic pseudo-obstruction syndromes, see Episode 637 .

High-yield association table

ConditionAssociationMechanismClinical Significance
Multiple System Atrophy (MSA)Autonomic failure; OrthostasisDegeneration of autonomic ganglia/nerves.Poor prognosis; requires careful management of blood pressure and fluid status.
Tinea corporisTrichophyton speciesDermatophytosis (fungal infection).Most common cause; systemic antifungals are needed for deep infections (nails, scalp).
Samoydes CalcificationsPapillary thyroid cancer, MesotheliomaDeposition of calcium salts in the peritoneal cavity.Suggests an underlying malignancy and requires thorough workup for primary source.
Angiogenin Sensitivity Syndrome (AGSS)Testosterone receptor defect; 46 XY karyotypeFailure to respond to testosterone due to defective receptor binding.Leads to ambiguous genitalia/poorly developed secondary sexual characteristics in males.

Key terms glossary

TermDefinitionContextExample
Toxic MegacolonAcute, severe dilation of the colon with risk of perforation.Usually triggered by C. difficile or opioid use.Transverse colon > 6 cm diameter is a major warning sign.
Intra-uterine Adhesions (Synechiae)Scar tissue within the uterine cavity.Caused by repeated D&C procedures; leads to infertility.Treated via hysteroscopic lysis.
Multiple System Atrophy (MSA)A progressive neurodegenerative disorder affecting multiple organ systems, especially autonomic function.Characterized by orthostasis and poor sweating alongside parkinsonism.The constellation of symptoms is key for diagnosis.
Ethacrynic AcidLoop diuretic agent.Used as an alternative to furosemide in patients with sulfur allergies.Provides the necessary loop diuretic effect without the sulfur moiety.

Study optimization

TopicStudy ApproachPriorityResources
GI Motility DisordersCreate flowcharts: Trigger -> Diagnosis -> Management (e.g., Opioids -> Toxic Megacolon -> Surgery).HighReview board-specific thresholds (e.g., 6 cm diameter).
Neuro/Endocrine SyndromesUse mnemonics and triads: MSA triad, AGSS findings, Samoydes cancers.Very HighFocus on the most common cause or the most critical finding for each syndrome.
Pharmacology & AllergiesCreate comparison tables: Drug A vs. Drug B (Mechanism, Allergy Profile).Medium-HighPractice selecting alternatives based on specific drug class contraindications (e.g., sulfur allergy).

Question pattern recognition

  • GI Obstruction/Dilation: Profuse stool expression after rectal exam -> Think Hirschsprung disease (or congenital megacolon).
  • Autonomic Failure: Orthostasis + Poor sweating + Erectile dysfunction -> Highly suggestive of Multiple System Atrophy (MSA).
  • Calcification Pattern: Abdominal calcifications associated with ovarian/thyroid cancer -> Consider the Samoydes pattern.
  • Drug Allergy Management: Need for loop diuretic effect in a sulfur-allergic patient -> Ethacrynic acid is the preferred alternative.

Test yourself

Common mistakes to avoid

🚫
Mistake 1: Confusing GI Obstruction vs. Colonic Pseudo-obstruction. Remember that while both cause dilation, Hirschsprung is a congenital agangliosis (functional obstruction), and Toxic Megacolon is an acute process often triggered by toxins/opioids.
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Mistake 2: Misidentifying the most common Tinea pathogen. Do not assume Microsporum or Epidermophytin ; always default to Trichophyton for tinea corporis unless otherwise specified.
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Mistake 3: Forgetting the specific BP threshold in MSA/Orthostasis. The drop must be \ge 20 mm Hg SBP change, not just general dizziness upon standing.

Common traps

⚠️
Trap 1 (Toxic Megacolon): Assuming that all severe colonic dilation requires immediate surgery; monitoring and supportive care are often the first steps unless perforation is imminent.
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Trap 2 (Tinea Treatment): Using topical antifungals for tinea capitis or onychomycosis, which will fail because systemic penetration is required.
⚠️
Trap 3 (MSA Diagnosis): Mistaking general fatigue and dizziness for MSA; the diagnosis requires demonstrating a specific constellation of autonomic failure and parkinsonian features.

Original transcript with highlights

Original transcript with highlights

All right, welcome. My name is divine. This is episode 638 of the divine intervention podcasts. In today's podcasts, we're going to be continuing the rapid review series for the USM list step two, CK and step three exams. This is going to be series number one thirty four, one thirty four. We've made a lot of these again. The USM is they just keep expanding and content. So unfortunately, we need to keep covering this material. So what if they give you a question about a patient and they tell you that this patient, you know, for the last you know, 24 hours has been having very, very severe abdominal pain. And you're told that this patient was recently diagnosed with malignancy and that the patient has been placed on was recently initiated on opioids. And then they tell you that they perform radiographic mission of the abdomen. And you notice that the person's transverse colon is massively dilated. When you see something like this, I really hope you're going to pick the answer and the answer for the diagnosis. I really hope you're picking the answer that talks about a toxic mega colon. Right. So the thing is, I know some of you may be like divine what are you talking about toxic mega colon with a person that is on opioids. Again, our friends at the MBM is they're very, they're very smart. Right. So they know that everybody has memorized that toxic mega colon has a very strong association with a CDF collitis. Right. You know, so CDF, right.

Whenever you see a person that has CDF and you notice that while the abdominal pain just takes like a big step up, you want to think about toxic mega colon and do those as circumstances. Right. But there are other people that can certainly get toxic mega colon on the USMEL exams. Right. So you want to think of it in the context of a person that for whatever reason may have like alias, right. They may have like alias and that can be superimposed with some kind of infection. Right. And then the transverse colon just does dilating, dilating, dilating, and I crazy. Right. So in fact, if it's more than if your transverse colon is more than six centimeters in diameter, that's really worrisome for toxic mega colon. Those people have to be watched very, very, very closely. Right. They have to be watched very closely. They have to be made in PEO. Right. And again, if you notice that they are beginning to have signs of bodily schema or infarction, then those people are going to need surgery. They're going to need surgery. Right. So keep that at the back of your mind for exams. Right. So toxic mega colon. Yes, there is the classic city for association, but it can also be associated with inflammatory bowel disease. Right. It can be associated with situations where your GI tract basically does not move. And then an opportunity is created for a bog to proliferate or for infection or whatever to happen.

So just keep that at the back of your mind as you prep for your, as you prep for your exams. Right. As you prep for your exams. Right. So and sometimes on your exams, again, they can use surrogate names. Right. So it's like, Hey, in every onky deck known to mankind, the term toxic mega colon is there. So it's like, Hey, why put toxic mega colon? Well, we can put something like inflammatory colonic dilution. Right. So that's a term you may see on your exams in inflammatory colonic dilution. Right. And I guess since we're talking about things that are mega, things are big. I think I maybe want to go ahead and just mention a few more mega things that we may see on the US Emily exams. Right. So we know that there's this bog known as tripanosuma cruzii, right. That likes to cause big problems. Right. So you can cause a big esophagus. It can cause a person to have ecalysia. Right. It can cause a big heart. It can cause a person to have a diluted cardiomyopathy. Right. So you can cause big things. Right. Another big thing that you want to think of on your exams, right. Is if a person has like a big, you know, a big colon, especially like a little child, right. And then they tell you that you do a rectal exam and that causes a profuse stool expression, right. Profuse stool expression. Again, the US Emily's, they're not stupid. They're not going to say, you know, you did a rectal exam and you had a poop splatter. Come on, they're not going to poop splatter on your exam.

That's insane, right. No, what they're going to do is they're going to tell you that, hey, but you did a rectal exam and there was a profuse expression of stool, a profuse expression of stool. When you see something like that, you absolutely positively want to think about a person with hers, prongs disease, right. Hers, prongs disease. Now the thing is again, our friends at the NBA, they know that the word, hers, prongs is in every onky dekno to mankind. So what's the alternate term they use for this on the exams? They can use trumps like congenital mega colon, right. Congenital mega colon is a term you may find for hers, prongs disease on your exams or sometimes they'll call it colonic egg ganglionosis colonic egg ganglionosis colonic egg ganglionosis, right. So again, keep this at the back of your mind as you're preparing for your exams. Again, the US Emily's, that's just one classic pattern, right. Again, if you remember the last podcast I made and by the way, if you missed my last podcast, you absolutely should listen to it. That podcast is one of these kind of like weird obscure podcasts, but it's very, very high yield for your exams, right. Especially the recent exams, right. So this is like the stuff that's been taken in 2025, 2026 going forward, right. The US Emily is there are certain rules and regulations they obey in obfuscating questions to get people down the wrong track, right.

So again, if you understand those patterns, then you're going to be able to catch on to what they're trying to do. And it's also going to help guide your study. So you should definitely listen to episode 637. It's a very, very worthwhile podcast to listen to, right. So again, a common pattern on the US Emily's is, hey, let's take what you know and present a surrogate. I talked about that in 637, talked about it in a different way, right. So again, kind of like how we've talked about toxic mega colon being the same thing as inflammatory colonic dilation. That's what we can present it, right. Or herchprom's disease being like a congenitome, like a colon or colonic iganglionosis, right. These are always that they present these things on on exams, right. Now, what if they give you a question about a patient and you're told that this patient, you know, for the last two weeks has been having this rush on his upper forearm, right. And it's circular, you know, looks clear, you know, looks pale in the middle, right. And it has like surrounding scale and it's been very itchy, right. And then they ask you which of the following pathogens is the most likely cause. And then let's say they give you an answer that talks about a micro-sporam canus and then they give you an answer that talks about trico-fighting tonsurons. And then they give you an answer that talks about epidermal fighting. They give you an answer that talks about staphoreus.

They give you an answer that talks about strep pyogenes. Which one should you pick on you exams? I'd really hope you're saying, oh, divine. I should pick the answer that talks about trico-fighting tonsurons, trico-fighting tonsurons. So what does this person has? Half, this not has, right. Half. So what does this person have? Well, this person has tiniacorpers, right. This is one of those fun gold or metal fight infections, right. So this person has tiniacorpers. And remember, you know, the USML is again a classic question pattern that he loved on exams. If you give you multiple correct answers to the same thing, right. So this is why podcasts like My Risk Factor's podcast, episode 37 and 97, 184 and 239 are super important, right. This is why knowing the epidemiology of certain diseases and disorders is extremely important. Why? Because the thing is they will give you multiple things that work and then you have to pick up on the one that is most common, right. So like, for example, we know that these tiniacs, right. Like tiniacorpers, you know, which involves the skin, tiniacapides, which involves the head, right. Or only comicosis, which involves the nails, right. This can be caused by the trico-fighting species, the micro-sporam species or the epidermal fighting species, right. So trico-fighting, micro-sporam, epidermal fighting, right. Trico-fighting, micro-sporam, epidermal fighting, right.

But the most common cause of tiniacorpers, very high yield, the most common cause of tiniacorpers is going to be a trico-fighting species. That's number one. Number two, are your micro-sporam species. Number three, are your epidermal fighting species, right. So in that, in this case, we're going to go ahead and pick a trico-fighting, a tonsuron. And remember, the way we're going to treat these things, especially if it's tiniacorpers, is you can use a topical iso. That is perfectly fine for this. But remember, remember, if it involves your head, tiniacapides, or involves your nails, only comicosis, again, it's the same most common cause, second most common cause, and third most common cause. But in those circumstances, you cannot use topical agents. You need systemic therapies, you know, you need systemic therapies, right. So you're going to need something that can penetrate caret in. So it can be something like an oral, an oral iso, or you can use grizzio-fulvin, or you can use a tribinofin, right. Classically, on the USMD exam, the Guafter Tribinofin or grizzio-fulvin. Although many times, the preferred that you use tribinofin or grizzio-fulvin, because grizzio-fulvin is a drug interactor, right. It's a cytochrome P415-ducer. It can cause a bunch of problems, right. But remember, it's a CP415-ducer. What are the other CP415-ducers you need to know for your exams? Without hope, you're saying that, hey, divine grizzio-fulvin, right. Kabameezapin, right. Phampin, right.

Babiterites, right. Phenetoin, right. St. John's worked. Herbs supplement a person takes for depressive symptoms, right. All those things can cause a person to, you know, their cytochrome P415-ducer, right. So they will reduce the half-life of the drugs. Although the other drugs the person is taking, right. So just going to keep that at the back of your mind in your prep for your exams. You know, I don't know why today my brain is really swirling with these alternate names for things, right. So again, please make sure you know your alternate names for disorders. It will really come in very, very clutch on your exams, coming very, very clutch on your exams. All right. Now, what if they give you a question about a patient? You told that this is a 32-year-old female and that for the past 18 months, she has been having unprotected sex with a husband, but she's unable to conceive, right. And they tell you that she has a history of multiple abortions in the past that have been treated with dilations and curatages. If you say something like this, what should you be thinking about? What should you be thinking about? I'm giving you some time to think. I hope you're saying divine. This sounds an awful lot like Ashremens syndrome, right. I remember what's an alternate name you may see on your exams for Ashremens syndrome. Ashremens syndrome, it may be called a uterine sineki, uterine sineki, right.

So what's the, or sometimes they can even call this intra-uteroine adhesions on your exams, intra-uteroine adhesions, intra-uteroine adhesions. So let's talk about the pathophysiology, right. So Ashremens syndrome is going to be a cause of infertility. And typically on your USMEL exams, you're going to see it in people that have had a lot of DN Cs, right. Because the thing is when you're having all these multiple dilations and curatages, you know, probably for like abortions or whatever, one thing that you can script the desigirabesalis, the desigirabesalis, the desigirabesalis contains the stem cells of the uterus, right. So if you script with those stem cells, I don't know how you want the uterus to proliferate, right. So that's going to be a problem with things like pregnancy and mences and things like that, right. So that's going to be Ashremens syndrome, also called intra-uteroine sineki, also called intra-uteroine adhesions. Typically the way you're going to fix that is you're hysteroscopically lysed those adhesions. You're going to hysteroscopically lysed those adhesions to fix the person's problem. So keep that at the back of your mind for your exams. And then what if they give you a question about a 50-year-old male? And you're told that for the past six months, this guy has been having a lot of trouble, you know, they tell you that he's having a lot of chills, right, that he is, you know, he's very intolerant of cold weather, right.

And then you're told that he's also been having marital problems because he has, you know, he has erected out his function, right. And you're told that he has like blottering continents and things like that. And then you're also told that this person has like some movement of normalities and that he's very and the, you're told that on physical exam, when he's gay, he's assessed that he takes a considerable amount of time to arise from a seated position. And when he arises, he feels dizzy upon arising. So he has basically like, you know, he feels dizzy upon arising and he can tell you that, oh, his blood pressure sitting down is like 130 over 85. And then his blood pressure upon arising is like 85 over 65 or something like that. So we're seeing orthostasis. If you put all these things together, what should you be thinking about? What should you be thinking about? I really hope you're saying that divine. This sounds a lot like multiple systematrophy, multiple systematrophy, multiple systematrophy. Remember many times this is one of those Parkinson's plus syndromes, right. Sometimes on the exams, though, what's an alternate name you may see an alternate name you may see on your exams with this is something called shy drigger syndrome shy dr dr ag r shy drger syndrome. So when you see something like this, I want you to think of multiple systems atrophy, right. So what's going to be the classic presentation? Well, these are going to have issues with sweating, right.

They're going to have they have a lot of autonomic problems and they have what sort of kind of looks like Parkinson's, right. So they'll have like a positive sweating. So they're going to struggle to sweat. That's number one. And that thing we also see is orthostatic hypotension, right. Orthostatic hypotension. So the me tell you again, if the US Emily's want to be kind, they'll say, oh, the person has orthostasis or they'll give you the values and then you're supposed to deduce that the person's orthostatic. So like what exactly will that be? Well, there'll be something along the lines of, ooh, the person in a seated or supine position, the blood pressure is X. And then when they stand, right. So in a supine or silly position, blood pressure is X. And when they stand, you notice that their systolic blood pressure is some number that is X minus 20 or something like that. When you see something like that, so minus 20 or greater, think of a person with orthostasis, right. That's like your systolic blood pressure like drops by like more than 20 millimeters of mercury with changes in position, you know, going from being supine to standing. When you see something like that, think of a person having orthostatic hypotension, right. And also those people tend to have erectile dysfunction, they tend to have issues with controlling their bladder, right. They tend to have issues with controlling their bladder, right.

So when you see something like that, think of a person having a shy trigger syndrome, which is also called multiple system atrophy. And then our friends at the MBM is one thing they love to do is to test prognosis, right. So they can ask you, what is the most likely outcome? The most likely outcome is going to be death within about six to 10 years, right. Has a very poor prognosis. Treatment is extremely challenging. There's not really much you can do for these people, unfortunately. So can I keep that at the back of your mind as you're preparing for your exams, as you're preparing for your exams, right. So shy trigger syndrome also called a multiple system atrophy, right. Now, one thing I just want to say that I think will be helpful to you on your exams is what are the malignancies that are associated with world calcifications on histology? What are the malignancies that are associated with world calcifications on histology? I really hope you're saying divine. It can be misothelialoma, or it can be meningeoma, or it can be papillary thyroid cancer, or it can be a serocystadinocorsidum of the ovaries, right. So what am I referring to by world calcifications? And so world, not WORLD, no, it's WHOR LED world in worlds, right. World calcifications, right. That's going to be a person that has a Samoma buddies. Again, the thing is our friends at the MBM is they're beginning to evolve, right. So they know that many people have memorized the terms Samoma buddies.

They also know that many people have memorized the term laminated, right. So L-A-M-E-W-L-A-T-E-D laminated calcifications. They know that many people have memorized those. So what do they do these days? They're like, hmm, okay. Well, maybe let's try a new term, right. So these days, you know, instead of calling it Samoma buddies or laminated calcifications, they may call it a world calcifications. When you see something like that, think of Samoma buddies, right. Remember, Samoma buddies are sort of four classic malignancies, right. Popularity thyroid cancer. Remember, that's the most common thyroid cancer. Remember, that spreads through lymph nodes. It doesn't spread to my toe genocally. Right. And the biggest risk factor there is going to be exposure to radiation. Number two, misotheliuma. Misotheliuma is also a suitor of Samoma buddies. Remember, the biggest risk factor from misotheliuma on the USM is going to be asbestos exposure. Right. And that typically is a suitor with hemorrhagic plural effusions. That also has Samoma buddies. And then number three, don't forget your serocyst adnocorsinomas of the ovaries. Right. Those things are probably one of the most common kinds of epithelial ovarian cancers. Right. And they're also associated with Samoma buddies. And then number four, do not forget, um, uh, I mean in Jiuma. Remember, many Jiuma has very strong associations with, um, you know, growing around cerebral convexities like your folks cerebride or your folks cerebelli.

Right. Remember, it's more common in women because it expresses estrogen receptors, right. It expresses estrogen receptors, right. And also we tend to find it in association with NF2 with neurofibromatosis type two, NF2, right. NF2 has a strong association of meningiomas, schwannomas, uh, uh, and they can also have ependymomas as well, right. And one other thing I, I guess I want to say about meningiomas is that on the USM, they don't only present at cerebral convexities. You may also find them at the cerebellopontine angle. That's very high you to know for your exams, right. The cerebellopontine angle on the USM is there two classic things that show up there. Either a meningioma or, uh, um, or come on, divine ecosystem. That's really in your brain. Um, so either a meningioma or schwannoma, yes, exactly a schwannoma, which is also known as an acoustic neuroma, right. So those things tend to be found at the cerebellopontine angle. Literally the junction between the cerebellum and the ponds, right. That's something that can be very easily visualized on brain, brain imaging. So keep that at the back of your mind as you're preparing for your exams, right. Now, what if they give you a question about a patient and they tell you that this patient, um, uh, you know, is a 19 year old female and she has never had mencies, right. And then you're told that, uh, uh, uh, uh, uh, vaginal exam is performed and it ends in a, you know, it, you know, it ends in a blind pouch, right.

And then you also notice that the patient's polydeveloped pubic and axillary hair. If you see something like this, what should you be thinking about? I'll really hope you're thinking of angiogenin sensitivity syndrome. But again, the USML is they know that everybody and their relatives know about angiogenin sensitivity syndrome. So what do they do on the USM Ls? Uh, one thing they love to do on the USML is instead, instead is to, uh, write an answer that says a testosterone receptor mutation or they can put an answer that says, uh, testosterone insensitivity, right. Another way they can also write this phenolue exam is they can call it a testicular feminization syndrome. You're like, define, are you serious? Yeah. So let's talk about all the names for angiogenin sensitivity syndrome, right. So again, on your exams, angiogenin sensitivity syndrome may be called angiogenin sensitivity syndrome, that's the easy one, or they can call this testosterone receptor defect, right. They can call this, testosterone insensitivity, right. Or they can call this testicular feminization syndrome. Those are all names for the exact same thing on the USML exams, right. But again, basically the problem here is that the testosterone receptor does not work. And if the testosterone receptor does not work, you're gonna get in a lot of trouble, right. Because again, basically you will not, you will not respond to testosterone, embryologically, right.

So many of the members of your Wolfian doctor are gonna get degraded, right. But the pressing genotypically is gonna be 46 XY, but phenotypically they're gonna be female, right. And you'll have poorly developed pubic and axillary hair because again, testosterone controls those things, but you'll have well developed breasts because estrogen controls those things, right. So keep that at the back of your mind as you are preparing for your exams. Keep that at the back of your mind as you're preparing for your exams. And then what if they give you a question about a patient? And you're told that this patient you know comes in for the last three days, has been having severe significant shortness of breath and they tell you that you hear crackles on pulmonary examination. And the person has you know three plus a dim of the bilateral or extremities. And you're told that this person you know chest radiography shows a cardiomegaly. And you're told that you know medical history is significant for asthma and COPD. And then you're told that the person has previously had respiratory failure requiring intubation. When they were giving a, when they were giving trimethyropram sofamethoxazone, right. And then they asked you what's the most appropriate next best step in management. I would really hope you picked the answer that talks about the administration of ethyrchrinic acid. You're like, what? Ethyrchrinic acid? Divine ready that come from. Okay, so let's let's unpack this, right.

Again, remember mechanisms of memorization and the USML Es, they're very, very big. They're very, very big on integration, right. So this person clearly has a CFF exacerbation, right. And then I give this extra history that hey, this person has a history of respiratory failure requiring intubation. When they got trimethyropram sofamethoxazone for some infection, that's kind of like an aphylaxis, right. So this person has an aphylaxis with sulfur drugs. So I would really hope that you don't pick the answer that talks about furostamide for this person, right. Again, remember when a person has an acute CFF exacerbation, typically you're going to give them a loop diuretic. Well, the thing is loop diuretics are associated with sulfur allergies, right. So if you have a history of a really nasty sulfur allergy like this person clearly has, it will be very unwise to give that person a furostamide. And I can promise you, a friend at the MBM is do put furostamide as an answer. Well, don't don't pick that, right. Pick the answer that talks about ethyrchrinic acid. If you want to loop diuretic function in a person that has sulfur allergies, then it is not necessarily a bad idea to consider ethyrchrinic acid. Ethyrchrinic acid is a loop diuretic, but it's not associated with sulfur allergies. So if you want a loop diuretic effect without the sulfur allergy to boot, consider getting ethyrchrinic acid, right.

Now, one other classic exam scenario you may see, although I guess before I jump to that scenario, let me just talk about this. Ethyrchrinic acid, though, remember there is a very good reason why you don't see it commonly used in the hospital. Why? Because of all the loop diuretics, it is the most auto toxic of all, right. It is the most auto toxic of all the common loop diuretics, you see tested on the USMEL exams, right. So keep that at the back of your mind as you prep for your test. And what are the other auto toxic drugs that you may see on your test? Well, don't forget vancomycin, right. Don't forget your platinum drugs like cisplatin. Don't forget your amino glycosides like gentamysine, you amysine, amicaseine, tubramysine, streptomysine, right. Those things are also auto toxic, right. And then the thing I wanted to jump to is like, hey, what are situations where if something is associated with sulfur allergy, try something else. Well, again, the classic situation is going to be a person that, again, you need loop diuretic effect. The person has had like a really bad enough elaxis to a sulfur drug. Right. So you don't do fear or some might do you do it. A chronic acid. But under classic situation, they love to test on the examples is like the difference between a sulfonyl urea and a meglith night, right. So remember your sulfonyl urears are going to be drugs like gliburite, glipyzite, glimiprite. We use them to control diabetes.

But another drug class that works just like the sulfonyl urears are your meglith mites. It is spelled M-E-G-L-I-N-I-T-E-S, right. M-E-G-L-I-T-I-N-I-D-E-S. You make glith mites. These include drugs like repaglinite and nuteglinite, right. They work identically to sulfonyl urears. But they have certain benefits. If you have sulfur allergies, well, take a meglith night instead of a sulfonyl urea, that's number one. Number two, these drugs, they are more rapid acting than the sulfonyl urears, right. So if you're trying to avoid the dangerous hypoglycemia that you may sometimes get with sulfonyl urears, your meglith mites are not a terrible idea on that those circumstances, right. So please keep that at the back of your mind as you prepare for your test, as you prepare for your test. Okay, so this is supposed to be a rapid review series. So I think I'm going to go ahead and call it here. But honestly, thank you for joining me today. If you love the way I teach, you love the way I explain mechanisms, you love the way I emphasize mechanisms over memorization, you love the way I make integrations, you're going to love my classes, right. So starting on the 16th of this month, I do have a bunch of classes I have for step one to step three. I have a two and a half hour test taking class, a four hour biostatistics class and a five hour social sciences, quality improvement, healthcare systems and ethics class.

And then first step two and three specifically, I have a 20 hour course that is five days, four hours each day. I have a last minute review that's three hours long. And then I in the month of June, the first weeks of June, I have like my mother load course, right. It's a 50 hour step two, step three class, extremely comprehensive, extremely detailed, just an amazing, amazing, amazing class. Very limited spots available for that. If you're interested, shooting an email, I can give you some more information. And then in the second week of May, I, you know, like between the 11th to the 15th of May actually, I have a 25 hour step one class, right. Very good for post studying for step one or level one or people studying for step two or step three level two level three that have very poor basic science foundations because believe it or not, a lot of basic sciences have started showing up on step two and step three. So I think many people do actually benefit from that class. Many people end up taking it in tandem. So they take the 20 hour step two, step three class and also find it very beneficial to take the step one class actually. So if you're interested, just shoot me an email. It's not some teaching assistant or some tutor or employee that teaches these classes. No, it's literally me. So it's me divine. I'll be teaching and it's me divine. I'll be answering your questions, right. The classes are over zoom.

And then I also offer one or one tutoring for all the US Emily and complex exams. And I help with a mock interviews, personal statements, you know, editing and all those things. So if you're interested in any of those things, just shoot me an email. I can give you some more information. And I have these podcasts on Apple Google and Spotify. So check those out. I put all the podcasts on divine intervention podcasts.com, right. And also every week I post like one or two podcasts, we're from a biblical perspective address, a life lesson. But that's on a separate website called a divine intervention life lessons.com. I'm a Christian, right. So I meet these podcasts and actually many people find them to be very helpful. I have like almost 400 podcasts on there. There's actually an Apple podcast associated with that called the divine intervention life lessons podcast. So thank you for listening to me today. I will see you God willing in episode 639. But share this with your friends with your colleagues. Again, I'm sure they're going to find this to be super super helpful. Well, until next time, have a wonderful day. God bless you and bye for now. Thank you.

Practice questions — USMLE style

Question 1 — Neurology/Endocrinology

A 50-year-old male presents with a six-month history of progressive symptoms including difficulty maintaining erections, unexplained episodes of dizziness upon standing, and generalized fatigue. On physical examination, he exhibits signs consistent with Parkinsonism (e.g., rigidity, bradykinesia). Vital signs reveal that his blood pressure is 130/85 mm Hg when supine but drops to 85/65 mm Hg when standing. He also reports poor sweating ability and difficulty controlling his bladder. Which diagnosis best explains this constellation of autonomic failure and movement disorder?

  • A) Parkinson's disease
  • B) Essential tremor
  • C) Multiple system atrophy (MSA)
  • D) Paraneoplastic syndrome
  • E) Primary adrenal insufficiency

Answer: C. Multiple system atrophy (MSA), also known as Shy-Drager Syndrome, is a progressive neurodegenerative disorder characterized by autonomic failure and parkinsonian features. The classic triad includes orthostatic hypotension (a drop of $\geq 20$ mm Hg in systolic BP upon standing), erectile dysfunction, and bladder dysfunction. This pattern distinguishes it from typical Parkinson's disease or other movement disorders.

Question 2 — Gynecology/Obstetrics

A 32-year-old female presents to the clinic for evaluation of chronic infertility. Her medical history is notable for multiple previous abortions that were managed with dilation and curettage (D&C). On pelvic examination, there are no obvious masses, but she has a history suggestive of uterine scarring. Which diagnosis should be suspected, and what is the typical initial management?

  • A) Asherman syndrome; hysteroscopic lysis of adhesions
  • B) Endometriosis; hormonal suppression therapy
  • C) Pelvic inflammatory disease (PID); broad-spectrum antibiotics
  • D) Adenomyosis; supportive care with NSAI Ds
  • E) Uterine fibroids; myomectomy

Answer: A. Asherman syndrome is the most common cause of acquired uterine infertility. It results from intrauterine adhesions or synechiae, typically following multiple D&C procedures (especially those involving aggressive scraping). The definitive treatment is hysteroscopic lysis of these adhesions to restore uterine cavity integrity.

Question 3 — Gastroenterology

A patient undergoes a colonoscopy and the pathologist notes calcifications within the bowel wall that have a characteristic "whirlpool" or whorled appearance. Clinically, this finding is most strongly associated with which malignancy?

  • A) Colorectal adenocarcinoma
  • B) Inflammatory bowel disease (Crohn's disease)
  • C) Mesothelioma
  • D) Diverticular abscess
  • E) Carcinoid tumor

Answer: C. Whorled calcifications are a classic, though sometimes evolving, finding associated with several malignancies. The most common associations include papillary thyroid cancer, mesothelioma (especially linked to asbestos exposure), serocystadenocarcinoma of the ovaries, and germ cell tumors/meningiomas. Mesothelioma is a key association that must be recognized on board exams.

Question 4 — Nephrology/Pharmacology

A patient with acute exacerbation of COPD presents with severe shortness of breath and bilateral pitting edema. The patient has a known history of asthma and also reports a previous anaphylactic reaction to trimethoprim-sulfamethoxazole (a sulfonamide). Given the need for a loop diuretic, which agent is the safest choice for this patient?

  • A) Furosemide
  • B) Bumetanide
  • C) Ethacrynic acid
  • D) Torasemide
  • E) Spironolactone

Answer: C. The primary concern in this scenario is the patient's history of anaphylaxis to sulfonamides. Furosemide, bumetanide, and torasemide are all loop diuretics that contain sulfur atoms and carry a risk of cross-reactivity or allergy. Ethacrynic acid is an alternative loop diuretic that achieves the necessary diuresis without containing sulfur, making it the safest choice in this specific clinical context.

Quick fire review

What are the three classic alternate names for Asherman syndrome?

Intrauterine synechiae, intra-uteri adhesions, or uterine synechiae.

What finding on a rectal exam is highly suggestive of Hirschsprung's disease?

Profuse expression of stool (or "poop splatter").

Which specific location in the brain is classically associated with either a meningioma or a schwannoma (acoustic neuroma)?

The cerebellopontine angle.

What are the three most common causes of tinea corporis, ranked by frequency?

1) Trichophyton species (most common), 2) Microsporum species, 3) Epidermophyton species.

If a patient has an orthostatic blood pressure drop greater than 20 mm Hg systolic upon standing, what syndrome should be suspected?

Multiple System Atrophy (MSA).

What is the key difference in mechanism and usage between sulfonylureas and meglitinides for diabetes management?

Meglitinides are preferred if a patient has a sulfur allergy or requires faster action than sulfonylureas.

List three malignancies associated with "world calcifications" (or ammonite bodies).

Papillary thyroid cancer, Mesothelioma, and Serocystadenocarcinoma of the ovary.

What is the most common cause of tinea corporis?

Trichophyton species.

If a patient has Tinea capitis or Onychomycosis (nail fungus), what systemic antifungal agents are preferred over topical treatments?

Oral ITRACON, Griseofulvin, or Terbinafine.

What is the defining characteristic of Multiple System Atrophy (MSA) that differentiates it from primary Parkinson's disease?

Severe autonomic failure, specifically orthostatic hypotension and bladder dysfunction.

For a patient with suspected Asherman syndrome, what is the standard treatment approach?

Hysteroscopic lysis of adhesions.

What are the three classic names for Androgen Insensitivity Syndrome (AIS)?

Angiogenin sensitivity syndrome, Testosterone receptor defect/insensitivity, or Testicular feminization syndrome.

Which drug class must be used cautiously in a patient with a history of sulfa allergy while needing loop diuretic function?

Ethacrynic acid (as an alternative to furosemide).

Quick recall / Anki-style questions

List three malignancies associated with "world calcifications" (or ammonite bodies).

Papillary thyroid cancer, Mesothelioma, and Serocystadenocarcinoma of the ovary.

What is the most common cause of tinea corporis?

Trichophyton species.

If a patient has Tinea capitis or Onychomycosis (nail fungus), what systemic antifungal agents are preferred over topical treatments?

Oral ITRACON, Griseofulvin, or Terbinafine.

What is the defining characteristic of Multiple System Atrophy (MSA) that differentiates it from primary Parkinson's disease?

Severe autonomic failure, specifically orthostatic hypotension and bladder dysfunction.

For a patient with suspected Asherman syndrome, what is the standard treatment approach?

Hysteroscopic lysis of adhesions.

What are the three classic names for Androgen Insensitivity Syndrome (AIS)?

Angiogenin sensitivity syndrome, Testosterone receptor defect/insensitivity, or Testicular feminization syndrome.

Which drug class must be used cautiously in a patient with a history of sulfa allergy while needing loop diuretic function?

Ethacrynic acid (as an alternative to furosemide).