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Source / episode info

  • Episode: 483
  • Title: Divine Intervention Episode 483: USMLE Step 2/3 Rapid Review Series 102
  • Published: 2023-09-20
  • Source: Episode page

One-liner

This episode provides a rapid review of high-yield infectious diseases (e.g., Leptospirosis, Schistosomiasis, Nocardiosis) and inflammatory conditions (Sarcoidosis, RA), emphasizing the importance of exposure history, specific diagnostic findings, and differential diagnosis traps on board exams.

High-yield summary

  • Sarcoidosis: Characterized by non-caseating granulomas and often presents with a triad: bilateral hilar lymphadenopathy, arthritis, and erythema nodosum (Lovegren syndrome). The mechanism of hypercalcemia involves activated macrophages converting 25-OH Vitamin D to active 1--hydroxylase.
  • Leptospirosis: A spirochetal infection acquired from animal/rodent urine exposure (e.g., post-flood, plumber). Key signs include fever, myalgia, and conjunctival suffusion; severe disease is called Weil's disease.
  • Schistosomiasis: Caused by Schistosoma species, typically associated with contaminated fresh water sources in endemic areas (e.g., Africa/Middle East). Manifestations include hematuria and can lead to liver failure/cirrhosis.
  • Environmental Infections: Earth disturbance or trauma suggests Coxiella burnetii (Q fever) or other environmental pathogens; diagnosis often involves interstitial infiltrates and erythema nodosum.
  • Acid-Fast Bacilli Traps: When encountering acid-fast positive organisms, always rule out non-tuberculosis mycobacteria (NTM) like Nocardia, which can cause multi-organ involvement (lungs, brain, skin).
  • Babesiosis: A bloodborne protozoal infection transmitted by ticks/mosquitoes that targets red blood cell precursors, leading to hemolysis and elevated indirect bilirubin.

Learning objectives

  • Differentiate between various tropical/environmental pathogens based on specific exposure history (e.g., water source, animal contact, soil disturbance).
  • Recognize the classic clinical and pathological features of Sarcoidosis, including its metabolic consequences (hypercalcemia).
  • Understand the key diagnostic clues for spirochetal infections like Leptospirosis and Schistosomiasis.
  • Master the differential diagnosis between common acid-fast organisms (e.g., Nocardia vs. TB) and environmental pathogens ( Coxiella ).
  • Correlate clinical findings with specific pathogen mechanisms, such as Babesia 's targeting of red blood cell precursors or Schistosoma 's ability to cause cirrhosis.

Board exam buzzwords

ConditionKey FindingAssociationBoard Exam Tip
SarcoidosisNon-caseating granulomas; Bilateral hilar lymphadenopathy1--hydroxylase activity -> Hypercalcemia/Low PTHRemember the Lovegren syndrome triad (BHL, arthritis, EN).
LeptospirosisConjunctival suffusion; Fever/MyalgiaAnimal/Rodent urine exposure; Weil's disease (severe)Treat with Penicillin due to spirochetal nature.
SchistosomiasisHematuria; Liver failure/CirrhosisContaminated fresh water sources (Endemic Africa); Schistosoma eggsManagement is Praziquantel. Do not forget the liver involvement!
NocardiosisAcid-fast positive, filamentous branching rodsImmunocompromised state; Multi-organ involvement (Lungs/Brain/Skin)Always rule out NTM when seeing acid-fast organisms that are not TB.

Rapid review table

TopicKey PointContextExam Relevance
SarcoidosisNon-caseating granulomas; HypercalcemiaActivated macrophages convert 25-OH Vitamin D to active calcitriol (1,25-(OH)₂D).High yield for mechanism questions and electrolyte abnormalities.
LeptospirosisConjunctival suffusion; Weil's syndromeExposure via contaminated water/soil from animal urine (e.g., post-flood).Must consider this in tropical or disaster settings.
SchistosomiasisHematuria, portal hypertension, cirrhosisChronic exposure to fresh water containing Schistosoma eggs.Remember that the pathology is not limited to the bladder.
Acid-Fast BacilliAcid-fast positive, filamentous branching rods (e.g., Nocardia)Immunocompromised patients; Multi-organ involvement.Never assume acid-fast = TB; consider NT Ms.

Board-speak -> diagnosis

Board-speak / Vignette phraseDiagnosis / ConceptWhy it fits
Patient who works with water or after a flood develops fever, myalgia, and conjunctival suffusion.LeptospirosisExposure to animal/rodent urine is the classic source; Conjunctival suffusion is highly suggestive.
A patient from an endemic area presents with hematuria and signs of liver failure.Schistosomiasis (Schistosome species)Associated with contaminated fresh water exposure, causing egg deposition in urinary or intestinal tracts.
Non-caseating granulomas found in the lungs, skin, and lymph nodes, often associated with hypercalcemia.SarcoidosisThe classic pathological finding; Hypercalcemia results from 1--hydroxylase activity by activated macrophages.
A patient who has been exposed to contaminated soil or after an earthquake presents with dry cough and interstitial infiltrates.Coxidiumicosis (Histoplasmosis/Coccidioidomycosis)Suggests inhalation of environmental spores following earth disturbance; Erythema nodosum is a common finding.
Acid-fast positive organism causing multi-organ disease (lungs, brain, skin), but not TB.Nocardia speciesMust differentiate from Mycobacterium tuberculosis because the clinical presentation and microbiology are distinct.
A patient with watery diarrhea following travel to an area with poor sanitation and low CD4 count.Cryptosporidium parvumHighly associated with waterborne outbreaks, especially in immunocompromised hosts (HIV).

Differential diagnosis / distinguishing features

Leptospirosis vs. Other Febrile Illnesses

Key FeaturesDistinguishing FindingsNext Step
Fever, myalgia, conjunctival suffusion (red eyes)Exposure to animal/rodent urine; often associated with water exposure.Serology (MAT); empirical treatment with Penicillin.
Typhoid feverGastrointestinal symptoms (diarrhea/constipation), systemic illness.Blood culture or stool culture for Salmonella Typhi.

Schistosomiasis vs. Other Hematuria Causes

Key FeaturesDistinguishing FindingsNext Step
Chronic hematuria, signs of portal hypertension, cirrhosisExposure to fresh water in endemic areas; eggs found in urine/feces (microscopy).Serology for Schistosoma species; Praziquantel treatment.
Bladder cancerGross blood in urine; often associated with chronic irritation.Cystoscopy and biopsy of the bladder lining.

Management pearls

  • Sarcoidosis: First-line treatment is usually corticosteroids (e.g., Prednisone). The hypercalcemia seen in sarcoidosis responds well to steroid therapy.
  • Leptospirosis: Treat empirically with oral or IV Penicillin, given the spirochetal nature of the organism and risk of severe disease (Weil's syndrome).
  • Schistosomiasis: Treatment is highly effective using Praziquantel. This drug targets the parasite itself.
  • Coxidiumicosis: Management involves anti-fungals; initial treatment with Itraconazole or Azole derivatives, escalating to Amphotericin B for severe disease.

Don't miss

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Sarcoidosis Mechanism: The hypercalcemia is due to activated macrophages expressing 1-\alpha-hydroxylase, which converts inactive Vitamin D (25-OH) into active calcitriol (1,25-(OH)₂D).
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Babesiosis: This protozoan targets red blood cell precursors and causes hemolysis. Look for the "multi-stross" pattern on a peripheral smear.
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Spirochete Warning: When encountering any spirochetal infection (e.g., Leptospira , Treponema pallidum ), consider Penicillin as the primary treatment, even if the specific organism is not named.
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Acid-Fast Traps: Never assume acid-fast positive = TB. Always test for NT Ms like Nocardia .

Integration & clinical reasoning

  • Infectious Disease & Epidemiology: The diagnosis of many tropical and environmental infections (Leptospirosis, Schistosomiasis, Coxidiumicosis) is fundamentally linked to the patient's travel history, occupation, or recent exposure (e.g., post-flood, contaminated water).
  • Pathophysiology & Metabolism: Sarcoidosis provides a classic example of how an inflammatory process can lead to systemic metabolic derangement (hypercalcemia/low PTH) via enzymatic activation (1-\alpha-hydroxylase).
  • Microbiology & Clinical Presentation: Understanding the morphology and life cycle of pathogens (e.g., Schistosoma eggs, Babesia merozoites, Nocardia filaments) is key to recognizing board-style vignettes.

OMM / COMLEX integration

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For COMLEX: know these viscerosomatics / Chapman points, but don't let OMM distract from emergent diagnosis and management.
  • Standard emergency management takes priority over OMMT/OMM. In cases of suspected severe infection (e.g., sepsis from Leptospirosis or Nocardiosis), aggressive supportive care, antibiotics, and fluid resuscitation are paramount.
  • The concept of "exposure history" is a key component in both clinical reasoning and OMT; understanding the source of contamination (water, soil, animal contact) guides differential diagnosis.

Concept connections / cross-references

  • For detailed review on general infectious disease principles: Divine Intervention Episode 37 .
  • For comprehensive coverage of autoimmune disorders and inflammatory conditions: Divine Intervention Episode 12 (or similar episode covering rheumatology).

High-yield association table

ConditionAssociationMechanismClinical Significance
SarcoidosisHypercalcemia; Low PTHActivated macrophages -> 1--hydroxylase activity on Vitamin D.Requires steroid therapy and monitoring of calcium/PTH levels.
LeptospirosisRodent urine exposure; Weil's syndromeSpirochetal infection causing vasculitis, renal failure, and jaundice.High suspicion in post-flood or animal contact scenarios.
SchistosomiasisFresh water contamination (Endemic Africa)Eggs deposited in urinary/intestinal tracts -> chronic inflammation/fibrosis.Can cause severe liver disease (cirrhosis), not just bladder issues.
BabesiosisRed blood cell precursors; HemolysisProtozoan infection transmitted by ticks/mosquitoes.Look for the "multi-stross" pattern and elevated indirect bilirubinemia.

Key terms glossary

TermDefinitionContextExample
Conjunctival SuffusionRedness of the conjunctiva without underlying inflammation (vascular engorgement).Leptospirosis; highly suggestive sign in this context.Seen in patients exposed to animal urine during a flood.
Non-caseating GranulomaGranulomatous tissue formation that lacks central necrosis/caseation.Sarcoidosis; distinguishes it from typical TB granulomas.Found pathologically in lymph nodes or lung parenchyma.
1--hydroxylaseEnzyme responsible for converting 25-OH Vitamin D to active calcitriol (1,25-(OH)₂D).Mechanism of hypercalcemia in Sarcoidosis; activated by macrophages.Deficiency leads to low calcium/high PTH; excess causes high calcium/low PTH.
HematuriaBlood in the urine.Schistosomiasis or other urinary tract infections; often chronic and intermittent.Suggests pathology involving the bladder or ureters (e.g., Schistosoma eggs).

Study optimization

TopicStudy ApproachPriorityResources
Tropical/Environmental InfectionsCreate a flow chart based on exposure history (Water -> Schisto; Animal Urine -> Lepto; Soil -> Coxiella).HighReview board vignettes focusing on travel and occupation.
Inflammatory DisordersFocus on the mechanism of complications (e.g., Sarcoidosis -> hypercalcemia via Vitamin D activation).Medium-HighCompare RA vs. Sarcoidosis pathology/mechanisms.
Microbiology TrapsCreate a differential list for acid-fast positive organisms and waterborne pathogens.HighPractice questions differentiating Nocardia, Babesia, Cryptosporidium, etc.

Question pattern recognition

  • Pattern: Water exposure + Hematuria: Think Schistosoma species (especially S. haematobium ) first, but also consider UTI/bladder cancer. Remember the risk of cirrhosis.
  • Pattern: Fever + Conjunctival Suffusion + Animal Exposure: Highly suggestive of Leptospirosis. Treat empirically with Penicillin.
  • Pattern: Non-caseating Granulomas + Hypercalcemia: Points strongly to Sarcoidosis, due to the metabolic activation of Vitamin D by macrophages.

Test yourself

Common mistakes to avoid

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Mistake 1: Assuming all acid-fast positive organisms are Mycobacterium tuberculosis . Always consider NT Ms like Nocardia when multi-organ involvement is present, especially in immunocompromised patients.
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Mistake 2: Confusing the cause of hypercalcemia. Remember that Sarcoidosis causes high calcium due to Vitamin D activation (1-\alpha-hydroxylase), leading to low PTH.
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Mistake 3: Forgetting Schistosomiasis's systemic effects. Do not limit your differential diagnosis for hematuria/GI symptoms to just the bladder; Schistosoma can cause severe liver disease and cirrhosis.

Common traps

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Trap 1 (Sarcoidosis): The hypercalcemia is often misinterpreted as primary hyperparathyroidism, but it is secondary to Vitamin D overproduction by activated macrophages.
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Trap 2 (Leptospirosis): Students may confuse the signs of Leptospirosis with other febrile illnesses; always remember the specific exposure source (animal/flood) and the sign of conjunctival suffusion.
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Trap 3 (Coxidiumicosis): The association between environmental disturbance (earthquake, archaeology) and fungal infections must be kept in mind for differential diagnosis.

Original transcript with highlights

Original transcript with highlights

Welcome, my name is Devani. This is episode 483 of the Divine Intervention Podcast. And in today's podcast we're going to be continuing the rapid review series for Step 3. It's going to be series 1, 2, 2. For those people that are trying to get in your Step 2 CK scores with the application cycle going on, I do have a review class for Step 2, Step 3 taking place next week from Monday to Friday. We're going to meet Monday Tuesday Thursday and Friday. It's a 20 hour course. And basically we're reviewing tons and tons of very high-year concepts that are classicly tested in the US and the exam. It is not going to be lectures. It's going to be almost exclusively in the air-based. And I'll really draw down on pathophysiology and also help you with making integrations across multiple disciplines. So if you're taking your exam soon, I think you should take advantage of the class. I think you'll get a lot from it. Okay, and the class is over. So if you're interested, just shoot me an email. So what if they give you a question about kindergarten teacher? And they tell you that for the past two days, she has been having like, you know, arthritis, like just pain and tenderness, a longer fingers, her knee joints, right? Then it's like symmetric. It's like a symmetric arthritis. I'm an involuntary feat. It involves her hands. I mean, they even tell you that, wow, they're a lot of MCP involvement. So you're made a couple of Alangio joint involvement.

And then, of course, what will the US military support as answers, right? So let's kind of work through some of this. They put us to arthritis as an answer. You know, probably don't pick that. Usual arthritis usually is asymmetric, right? And usually a much older people. The only time you're going to see a young-ish person, like a person, they have four days, for example, getting osteoarthritis. Is if they've had like really bad joint problems as kids. So let's see if they had like really bad septic arthritis, wasn't treated properly, right? Those people have a high risk of like acts like early on set. Osteoarthritis. But that's not going to be the case here, right? And again, you don't just get osteoarthritis, boom out of the blue. And then, of course, in their great wisdom, they're going to put rheumatoid arthritis as an answer. And I would hope that you don't pick rheumatoid arthritis because remember, RA in general, before you can make a diagnosis of rheumatoid arthritis, the person should have symptoms for at least six weeks. That's usually like a smart thing to kind of keep on the back of your mind on the USMELIS. Don't just pick RA when a person has had symptoms for like a day. It doesn't really make much of any sense, right? But again, you see this is a kindergarten teacher with like a symmetric acute arthritis. This is going to be pretty classic for parvo B19. Parvo virus B19, right? Parvo virus B19.

And again, remember, parvo B19, what are the different ways they test it? It can cause like any plastic crisis and people that have hemoglobin apathy, right? So they can give you a person that has sickle cell disease, that has parvo B19 crisis. They can give you a person that has thalacemia, that has parvo B19 crisis. So please don't think that parvo B19 is only for people that have sickle cell disease. It could not be further from the truth. It can absolutely cause any plastic crisis as well. In people that have other hemoglobin apathy's like thalacemia, alpha thalacemia, beta thalacemia literally does not matter. And then remember, if a mom gets parvo B19 and her fetus gets parvo B19, the fetus can have high drops of talus. That's something bad that could happen, right? But again, remember parvo B19 and also cause a symmetric arthritis in people that work with kids. So they can easily make it a question about like a kindergarten teacher, a D-care worker, stuff like that, right? Or a person that works in a nursery, just stuff like that. So just be mindful of it so you don't get screwed over with that on your exams. And for the most part, when people have this problem, right? The reason that they can get it like an apathy crisis, especially like the sickle cell disease and the phylasemia folks, is that they typically have parvo B19, you know, being a single stranded DNA virus. They can actually infect ribloxile precursors.

So you may be able to generate ribloxile cells, and they're not getting a lot of trouble. And I guess it may also be useful to just consider what are the other bugs that love to target ribloxile cells on the USML exams. Don't forget that Babysia microly likes to target ribloxile cells. So you see a person that, you know, new England, whatever, and you notice that they have like increased indirect bilirubin. They have like an anemia. They may even have jaundice. Think about Babysia microly. Because remember Babysiosus is carried by the exodistic, a multi-scross business. So he tortures your ribloxile cells, explodes them, right? As your ribloxile is explode, you have any molasses. They very have a lot of himolasses. You're going to generate a ton of indirect bilirubin, indirect bilirubin, right? So that can cause you to have jaundice, right? Don't forget the multi-scross pattern on a blood cell, right? And then another thing that targets ribloxile cells is going to be plus volume species, right? Maliria. Maliria. Maliria. Maliria. Maliria. So just want to keep that in mind. Okay. Well, what if they give you a question about a person? That's like a plumber. And they tell you that for the past five days, he has been having a significant writer per cordron pain. And they tell you that he has had decrees during production. And then they give you like, you know, this is going to be one of these video questions on your exams. So you see this person's eyes really red.

When you see something like this, what are you thinking about? I really hope you're saying, oh, divine. Sounds like this person has leptosperosis, right? Person sounds an awful lot like they have a leptosperosis. Remember, leptosperosis can cause lots and lots and lots of problems, right? So, but the classic thing that's going to tell you that, oh, you do leptosperosis is you're going to see quantum tables of fusion. That's a buzzword you may actually see on your exams, quantum tables of fusion. I mean, it's not really a buzzword because it's not something that many people recognize on exams, but basically just means that person's eyes are like super, super, super red, right? So how does leptosperosis present? You're going to see a person that's been exposed to animal like rodent urine, right? So it can be a person that's a plumber, it can be a person that's a lifeguard, believe it or not. It can be a person that works in a disaster area, like in a marion swamp environment. You can even give this as a post-horicain question, right? They can give it like a Katrina sort of question like after Hurricane Katrina, right? Just if you say a post-horicain question, don't neglect leptosperosis. So that's usually the exposure that gets you in trouble. And remember, they're going to have like fevers, they'll have like myalgyz, you know, they'll have the shakes, they'll be shaking a lot, they'll have headaches, they'll have this quantum tables of fusion, they can have cough, right?

And if you're looking for the two organs that leptosperosis, right, loves to torch, loves to torch the lever and the kidneys. Leptospiring tyrogens loves to torch what? The lever and what? The kidney is very good, very high up to know that, right? In fact, if they give you a question about leptosperosis, they are many ways they can honestly test this thing. And sometimes they don't put in leptosperosis as an answer, they just put spirochet as an answer. The USML is whenever a bog is a spirochet, for whatever bizarre reason, quite a number of times, they don't like to put the actual bog name, they'll just put spirochet as an answer. So be mindful of that warning with something like leptosperian tyrogens, be mindful of that warning with something like trapolymapalidam, be mindful of that warning with something like Borrelia Bokdofri, which causes lung disease. All these bogs are pretty high yield high value spirochetes to keep at the back of your mind. And remember, they can also, instead of putting leptosperosis, especially if they emphasize a question where you see many of these organ failures, like the liver that keep me failing. So putting leptosperosis is an answer, but if you're not, they can put wills disease as an answer, wills disease, W-E-I-L, apostrophe S, right? Wills disease. It's just basically leptosperosis when a person has like liver and keep me failure with that. So just be kind of mindful, kind of mindful about that, right?

So again, just keep in mind, you're going to see this in a lot of like, all these tropical climates, right? So something like New Orleans, something like Florida, Louisiana, stuff like that. So just kind of keep your ice peel for things like that, Mississippi, keep your ice peel for stuff like that on your, on your exams. Okay? So again, those are all the ways they can go after leptosperosis. And even if you want to treat leptosperosis, you can use an antibiotic like penicillin, right? You can use penicillin, just kind of like the way we treat syphilis. Because it's a spiral kit, it responds pretty well to penicillin. And I mean, what if they give you a question about the person being treated for leptosperosis? And you know, like a few hours after they get like IV therapy, they start shaking, their skin turns red and all these things. I would hope you're seeing old divine. This sounds a lot like the Jarish Hexheimer reaction, the Jarish Hexheimer reaction, Jarish Hexheimer reaction. Okay? So again, I just said that, again, leptosperosis is something that you're going to see as a, you can see it as a post-horicain question. Since we're talking about post-whatever's, don't forget like the post-earth disturbance question. So like earthquakes, for example, that should mean you think about coxidiumicosis, right? Remember coxidiumicosis? After you've disturbed the earth, you know, archaeological exploration or earthquake happened, stuff like that.

And you notice the person has like cough, like a dry cough, and they have like infiltrates on a chest x-ray, interstitial infiltrates, you have a luchosaid, you have a luchosaidosis, they may even have like a tender nodules on their, on their shanes, like erythema nodosa. Think of coxidiumicosis. And don't forget coxidiumicosis, we're going to manage that with etraconozol. We're going to manage it with an easel. We're going to manage it with an easel. But again, if that doesn't work, and they have like severe disease, maybe we want to go for amphoterrable, right? amphotericin B. Okay. Now, I think another thing that may be helpful to discuss. So, what if they give you a question about like 20... Okay, let's say 55-year-old male, how's that? Let's say they give you a version of 55-year-old male. And this guy, you know, like 18 months ago, had a keeping transplant. And then, for the last five days, this guy's been having like really high fevers, and he told you that, wow, that you do a dermatologic exam, and he has like multiple skin abscesses. And then, they tell you that you'll find this cavitarian feel-trading the lungs. And then, they tell you that you also see like fluid collections in the brain. You're like, wait, what? What is this? I would really hope. And then, they tell you that, you know, they're able to, you know, get a biopsy of the long lesion or whatever, or a sputum sample. And you see a seat-fast positive organisms.

You know, a seat-fast positive, filamentous branching rods. And you see something like this. What should you think about? What do you think of no cardio? Okay? What do you think of no cardio? No cardio is something that it doesn't show up all the time on exams. But when it shows up very reliably, people get it wrong. It's just one of those reliable things where you're like, yep, this person's gonna get it wrong. Right? So you have to be one of those people, right? So how does this stuff present? Many times it's gonna present in people that are immunocompromised. Right? It's gonna present people that are immunocompromised. And it loves to go after three places where lungs, brain, and skin. Okay? Lungs, brain, and skin. Lungs, brain, and skin. You're gonna see the lungs, right? You're gonna see the person that can have like a cafeteria lesion in the lungs. And of course, the USML is right there. Not stupid. One of the answers they're gonna put is they're gonna put TB as an answer. Right? Because they know people are like, oh, TB, they're really hearing the lungs. Oh no, it's not TB. Right? TB does not cause lung, brain, and skin problems together. Right? Right? So, and you know, even if it's acid fast positive, right? Don't fall for TB. Just kind of be careful there, right? So you see like long abs, you see like a like a cafeteria lesion in the lungs. You see the person has brain abscesses. They have skin abscesses. Right?

And they tell you that, oh, the biopsy one of these specimens. And you see acid fast positive, filamentals branching around. I really, really, really want you to think about an accordion. Right? I really want you to think about an accordion. Right? And the thing is this is a very, and it can also cause disease in people that are diabetic, actually, right? Just something when I keep in mind. The thing is honestly like, being a diabetic is not good. It's just one of these simple rules of thumb for life. Being a diabetic is not good because diabetes can cause you to be a little compromised. Right? It's kind of like a concept with a USML Es. They like to give like the worst of the worst infections to diabetics. Right? Like, and if somebody's pilot of arthritis goes to diabetics, gangrenoscholisis diodes, gastrodiabetics, ectema gangrenosum goes to diabetics. And these are all disease pathologists, they can test. Right? So just, but, but, but infections think of, think of a diabetics. Right? So how in the word, we're in the original cardio? Well, you're going to be on therapy for a long time. Don't tell you that. You can be on therapy for like six months. And most things you're going to be on in the bathroom when tremethoprimsulfomythoxazole, TMP-SNX, TMP-SNX. Okay? That's how we're going to manage our cardio. Right? So I think one thing that may be helpful to know is just kind of being conversant with some of these acid-fast organisms that are not TB.

Because many times people get, once people see acid-fast, they think, oh, it's got to be TB. No, it's not always going to be TB. You kind of need to keep your ice peeled. The USML Es, they kind of pride themselves in testing both that are acid-fast positive, but are not TB. Like, literally, just give you one nonocardium. Another one they could give you are your exams. Is they could give you a question about like a HIV patient with diarrhea, with watery diarrhea. That seems to be all-relenting. And usually you're going to see these same people that have like crazy low-CD4 accounts. When you see stuff like this, I want you to think about cryptosporidium parvo. Cryptosporidium parvo. Something where money for paramomysin or anitazoxanide, paramomysin or anitazoxanide. Okay. So let's maybe move on from this. So just, again, kind of be careful about that. Okay. Now, what do you think of your question about a patient that just immigrated from some African country? You know, sometimes they'll be kind and throwing the country out of the end. But I'm not going to do that right now because let me get a little too easy. But you just kind of throw in some African immigrant. Right? And then the person, they'll tell you that for the past like few weeks, per se has noticed like a lot of blood in his urine. And this person has been feeling fatigued, has been exercising tolerance. Right? Whenever you see something like this, think of a bog. Right?

The person immigrant from Africa was like radioring and like anemic symptoms. I want you to think of Shisto Somaises. Right? Shisto Somaises. Shisto Somaises. And they'll tell you that this person did a lot of water-based stuff when doing Africa. Right? Maybe they were like fishermen or the ordinary marine workers or the worked out of water treatment plant or something like that. Right? Again, the USMD is just very inventive with some of these stories. So you see that. Think of Shisto Somaises. So what's the deal with Shisto Somaises? Remember that Shisto Somai, especially Himatobium, right? Loves to lay on these eggs. Right? You know, eggs like they can take over your intestines, your liver, your bladder. Right? But you know, you're usually going to be exposed to like contaminated water and then you're going to get in getting in a lot of trouble. Right? So you're going to see these people, they're going to have like a hematuria. Right? So the urine will be red because again, it kind of torches the bladder. And sometimes even if you don't know, they can even have blood in their stools. They better not. They're not blood in their stools. Right? Now, the thing is many people know the bladder cancer, bladder cancer, is with this thing. But please don't forget that Shisto Somaises can actually cause liver failure, can actually cause cirrhosis. It doesn't just lay eggs in your bladder. It can also lay eggs in your liver. Believe it or not. So you can actually cause cirrhosis.

It's just one of these things that people don't emphasize enough on TV shows up on you exam. And then you're like, huh? Interesting. Right? So it's just something you want to kind of keep on the back of your mind on exams. And how do we manage the stuff? We're going to manage your crazy quantel. We're going to manage your crazy quantel. Don't worry about how crazy quantel works. Just know that crazy quantel is how we manage your Shisto Somaises on the USM in exams. And again, I said that I'm going to give off the country at the end. The country at the end is going to be Egypt. Right? But again, the USM is going to be very specific and see Egypt because they say Egypt. I know someone like, oh, of course, Shisto Somaises. They're always going to do that. So just going to be mindful about that. They just put like a non-descript African immigrant term. Now, what do they give you a question about a person that's from Mexico, right? Mexican immigrant. And for the last two weeks, it's a guy, right? Like 38-year-old male. And he's been having like pin on it, turn on his over his shins. Right? And he tell you that many has like that he's like he's been having like pin with movement of his lower extremities. Right? And he tell you that he has a dry cough. And when you see something like that, I would hope you're saying, oh, divine. This person has love green syndrome. Love green. You're like, love green what? Yeah, love green syndrome. Right? This person pretty much has sarcoidosis.

So here's the thing. People are used to women as the only recipients of sarcoidosis on exams. That's not true. Okay? Men can get sarcoidosis for sure. And I don't know for whatever reason, friends at the USMLE is the love to give sarcoidosis, not just to African Americans, but to people of Hispanic origin actually. So just something you want to kind of broaden your horizons too. So don't just think of African American females as the only people that can get sarcoidosis. Other demographics like Hispanics can also get sarcoidosis. And men can also get sarcoidosis. In fact, I know you may wonder, divine, how did you jump at sarcoidosis from here? Or how did you jump a love green syndrome? Love green syndrome is actually a triad. It's a, it's like a special kind of sarcoidosis where they have like the hyaluronic apathy, which we find in sarcoidosis. They have the acura thritis, which we find in sarcoidosis. And then they also have erythema nodosum. Erythema nodosum. Erythema nodosum. And you see that triad, right? Think of love green syndrome. Remember, we already talked about erythema nodosum as well in conjunction with coxidiumicosis, and immunosurcoidosis already. So think of love green syndrome. So remember, in sarcoidosis, if you suspect it, right, you're going to get a chest x-ray. You're going to see the bilateral hyaluronic apathy. And most times you can just give these people steroids and they're going to be fine, right? Now what are some other features of sarcoidosis?

Well, don't forget it. It's a granoloma disease. You're going to see non-key seeding granolomins. Don't ignore that. Maybe like, divine, that's just a factor for step one. I wish I was the best on your exam. It's a non-key seeding granoloma. You've got to know that stuff. Not just for step one, but for step two and step three. So non-key seeding granoloma, right? You're going to see high levels of AC Es and retention, converting, enzyme, right? And they remember the granolomins, these non-key seeding granolomins, they have epithelial histiocytes. They have macrophages that surround them. These macrophages express one alpha hydroxylase. One alpha hydroxylase is going to convert calcium dial, which we call 25 hydroxyl vitamin D, to calcium trial, which we call 125-dye hydroxyl vitamin D. And when you make that calcium trial, it's going to cause you to reabsorb a ton of calcium and force it from your GI tract. That's going to cause hypercalcemia. So again, when you're exams, they can see what's the mechanism, they can even give you a short-quake question and they make it all about the electrolytes. So what electrolyte problems do you expect? Well, they're going to have hypercalcemia. Obviously, they're going to have a low PT. They're going to have a reduction in their PT. Because of negative feedback from that hypercalcemia. And again, you're going to manage it with steroids.

In fact, the hypercalcemia that people that have short-quake doses has are response beautifully, beautifully, beautifully to a steroid therapy. Or they can even ask, what's the mechanism behind the hypercalcemia? Or they can see what's the mechanism behind the reduced PTH levels. They can put an answer that says hypervitalinosis D. So just be careful about that. This is the thing I tell many people in my review courses that see. The USML is just not like they just invent new knowledge that they test. They just think the same good old knowledge that we've always heard about. They just find unique ways to test it. So just be mindful of that on your exams. I mean, literally, I just talked about steroid doses. But I give like a few different weird things like, hmm, Hispanic instead of African-American, hmm, male, boom, instead of female. So just be mindful of that. And they are very, very descriptive these days. So just be smart. So don't get these things wrong on exams. Okay, I think I'm going to go ahead and stop here. Again, I offer one tiering for step one, step two, step three. I have review courses for step one. It's a 25 hour course and a 20 hour course for step three. And then I have some courses for step one to step three. It's a, I have a two and a half hour in being tested in strategy scores. A four hour bio stats class, five hour social sciences, all the team improvement, health care systems, and ethics class.

All these classes, tons of people have taken them, and found them to be profoundly helpful. So if you're interested in any of these, just shoot me an email. And these courses are not lectures. They're actually all based on clinical scenarios because that's what's going to be most true to the exam you're going to be taking. So just if you're interested, just shoot me, shoot me an email. And I have these podcasts on the major apps, Apple, Google, Spotify. And then I have a You Tube channel, Devine intervention, USM, really podcast and videos. That's where I post the videos that I make. And then I have a new website called Devine Intervention Lifelessens.com. That's where I post, you know, many people say, wow, I love your life lessons. So I just figured out, make a new website, devineinterventionlifelessens.com. There is actually an Apple podcast associated with that, the Devine intervention, life lessons podcast. And every week, I just really on Friday and Sunday, I post two podcasts. That's from a biblical perspective, address a common life problem. So check those out. I actually have more than 200 podcasts on there. So I'll see you in a piece of 484. Have a wonderful rest of your day. God bless you and bye for now. Thank you.

Practice questions — USMLE style

Question 1 — Immunology/Endocrinology

A 35-year-old woman presents with a history of recurrent episodes of polyarthralgia and has been diagnosed with sarcoidosis. On physical examination, she exhibits erythema nodosum on her shins and bilateral hilar lymphadenopathy noted on chest imaging. Laboratory studies reveal hypercalcemia (Ca > 10 mg/dL) and hypophosphatemia. The mechanism underlying this electrolyte imbalance is best explained by:

  • A) Increased parathyroid hormone secretion leading to bone resorption.
  • B) Direct renal tubular damage causing calcium wasting.
  • C) Activation of 25-hydroxyvitamin D by the granulomas, leading to excessive calcitriol production.
  • D) Decreased gut absorption of phosphate due to elevated levels of fibroblast growth factor 23 (FGF23).

Answer: C. Sarcoidosis is characterized by non-caseating granulomas. These granulomas contain activated macrophages that express 1-$\alpha$-hydroxylase, an enzyme that converts inactive vitamin D (25-hydroxyvitamin D) into the active form, calcitriol (1,25-dihydroxyvitamin D). Excess calcitriol leads to increased intestinal absorption of calcium and phosphate, resulting in hypercalcemia. The high levels of calcitriol also suppress parathyroid hormone (PTH), leading to secondary hypocalcemia/hypophosphatemia cycle that is often managed by steroids.

Question 2 — Infectious Disease

A 40-year-old male plumber presents to the emergency department after working in a flood-affected area following a major hurricane. He reports fever, severe myalgias, and headaches over the past week. On examination, his conjunctivae are markedly injected (conjunctival suffusion). Blood work is notable for mild anemia and elevated creatinine. The most likely diagnosis, given the clinical presentation and environmental exposure, is:

  • A) Leptospirosis
  • B) Lyme disease
  • C) Rickettsialpox
  • D) Coccidioidomycosis

Answer: A. Leptospirosis is a zoonotic infection transmitted through contact with animal urine (especially in flood-prone or contaminated water environments). The classic triad includes fever, myalgias, and conjunctival suffusion. It targets the liver and kidneys, leading to potential acute kidney injury and jaundice. While Coccidioidomycosis can also be acquired from environmental exposure (earth disturbance), Leptospirosis is strongly associated with flood/water contamination and presents acutely with this constellation of symptoms.

Question 3 — Hematology

A 28-year-old female, who has a known history of sickle cell disease, presents to the clinic with acute onset of joint pain and tenderness in her hands and knees over the last few days. She also reports generalized fatigue. Laboratory studies reveal severe anemia and evidence of an aplastic crisis. The most likely causative agent for this presentation is:

  • A) Babesia microly
  • B) Parvovirus B19
  • C) Epstein-Barr virus (EBV)
  • D) Cytomegalovirus (CMV)

Answer: B. Parvovirus B19 is notorious for causing transient, symmetric polyartharthritis in young individuals. Crucially, it can trigger an aplastic crisis by infecting and destroying erythroid precursors in the bone marrow. This mechanism of red blood cell destruction is not limited to sickle cell disease; any hemoglobinopathy (e.g., thalassemia) puts the patient at risk for a Parvo B19-induced aplastic crisis.

Question 4 — Microbiology/Environmental Medicine

A hiker returns from an area in the southwestern United States after disturbing soil during an archaeological dig. He develops a persistent dry cough, fatigue, and infiltrates on chest X-ray. Serology is positive for Coccidioides antibodies. The most appropriate initial management strategy for this patient is:

  • A) High-dose intravenous penicillin
  • B) Oral azithromycin
  • C) Systemic corticosteroids
  • D) Oral itraconazole

Answer: D. Coccidioidomycosis (Valley Fever) is a fungal infection acquired from inhaling spores, often after disturbing soil in endemic areas. The standard initial treatment for uncomplicated pulmonary coccidioidomycosis is oral antifungal therapy, typically itraconazole. Amphotericin B may be reserved for severe or disseminated disease.

Quick fire review

What condition presents with symmetric polyarthritis, especially involving hands, and can be linked to working with children?

Parvovirus B19 infection.

What are the three key organs targeted by Leptospira infections?

The liver and the kidneys (and sometimes the eyes/conjunctiva).

What is the classic triad associated with Löfgren syndrome, a form of sarcoidosis?

Bilateral hilar lymphadenopathy, acute arthritis, and erythema nodosum.

After what type of environmental exposure should one suspect Coxidiumicosis?

Post-earth disturbance (e.g., earthquakes or archaeological excavation).

What is the key finding in Babesia microti infection that suggests hemolysis?

Increased indirect bilirubin, due to the parasite targeting erythrocyte precursors.

If a patient has symptoms following contaminated water exposure and presents with hematuria, what protozoan should be considered?

Schistosoma species (e.g., S. haematobium).

What is the primary mechanism by which sarcoidosis causes hypercalcemia?

Macrophages within non-caseating granulomas express 1-$\alpha$-hydroxylase, converting 25(OH)D to active calcitriol (1,25(OH)$_2$D).

What is the key differential diagnosis for a patient with fever, myalgia, and conjunctival suffusion after exposure to animal urine?

Leptospirosis.

Which acid-fast organism causes multi-organ disease (lungs/brain/skin) but must be differentiated from M. tuberculosis?

Nocardia species.

What is the characteristic finding in Schistosomiasis that can lead to severe complications beyond urinary tract involvement?

The eggs can lodge in the liver, causing portal hypertension and cirrhosis.

Which specific type of hemolytic crisis can be caused by Parvovirus B19, regardless of the patient's underlying hemoglobinopathy?

Any hemolytic crisis (e.g., sickle cell or thalassemia).

What is the primary treatment class used for Coxidiumicosis?

Oral azoles (e.g., itraconazole/etraconazole); severe cases may require Amphotericin B.

Quick recall / Anki-style questions

What is the primary mechanism by which sarcoidosis causes hypercalcemia?

Macrophages within non-caseating granulomas express 1-$\alpha$-hydroxylase, converting 25(OH)D to active calcitriol (1,25(OH)$_2$D).

What is the key differential diagnosis for a patient with fever, myalgia, and conjunctival suffusion after exposure to animal urine?

Leptospirosis.

Which acid-fast organism causes multi-organ disease (lungs/brain/skin) but must be differentiated from M. tuberculosis?

Nocardia species.

What is the characteristic finding in Schistosomiasis that can lead to severe complications beyond urinary tract involvement?

The eggs can lodge in the liver, causing portal hypertension and cirrhosis.

Which specific type of hemolytic crisis can be caused by Parvovirus B19, regardless of the patient's underlying hemoglobinopathy?

Any hemolytic crisis (e.g., sickle cell or thalassemia).

What is the primary treatment class used for Coxidiumicosis?

Oral azoles (e.g., itraconazole/etraconazole); severe cases may require Amphotericin B.