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Episode Notes

Source / episode info

  • Episode: 256
  • Title: Divine Intervention Episode 256 – USMLE Step 2 CK Rapid Review Series 41 (and Step 2 CK 10 hr Course 9/5/20).
  • Published: 2020-08-24
  • Source: Episode page

One-liner

This episode is a high-yield review of basic science concepts for the USMLE Step 2 CK exam, emphasizing associations between malignancies and paraneoplastic syndromes (e.g., SIADH, H.O.A.), tumor markers (AFP, CEA), characteristic calcified masses in neuroimaging, and specific histological patterns (Burkitt lymphoma).

High-yield summary

  • EBV Associations: EBV is strongly associated with Burkitt Lymphoma (t(8;14)), Hodgkin's Lymphoma, Nasopharyngeal Carcinoma, and Primary CNS Lymphoma (especially in HIV+ patients).
  • HCC Risk: Chronic exposure to grains/aflatoxins leads to Hepatocellular Carcinoma (HCC), which is a critical association for liver pathology.
  • Perineoplastic Syndromes: Lung cancer can cause multiple syndromes: SIADH (hyponatremia, hypertonic urine >1.012 SG), Hypertrophic Osteoarthropathy (H.O.A.), and Lambert-Erythroasthenic Syndrome (LEMS).
  • Calcified Masses: Calcification in the meninges/brain is highly specific: Hemangioblastoma (cerebellum, calcified mass) vs. Craniopharyngioma (pituitary stalk, calcified mass) vs. Oligodendroglioma (frontal lobe, calcified mass).
  • Tumor Markers: Specific markers are associated with primary sites: AFP (Yolk Sac Tumor, HCC), CA-125 (Ovarian Cancer), CEA (Colorectal/Pancreatic), and PSA (Prostate Cancer).

Learning objectives

  • Identify the key associations between common malignancies and their associated paraneoplastic syndromes (e.g., SIADH, H.O.A.).
  • Differentiate the clinical presentation and imaging findings of various calcified intracranial masses (Hemangioblastoma vs. Craniopharyngioma).
  • Interpret tumor markers (AFP, CEA, CA-125, PSA) to suggest a primary site of malignancy.
  • Recognize the characteristic histology and genetics of lymphomas like Burkitt lymphoma.
  • Understand the pathophysiology of paraneoplastic hypercalcemia from various sources (PT HrP, Sarcoidosis, Multiple Myeloma).

Board exam buzzwords

ConditionKey FindingAssociationBoard Exam Tip
Burkitt LymphomaStarry sky pattern; t(8;14) translocation.EBV; Burkitt's macassar.Always link this triad together on the exam.
Small Cell Lung Cancer (SCLC)High urine specific gravity (>1.012); low cortisol response to dexamethasone.SIADH, Lambert-Erythroasthenic Syndrome (LEMS).Remember SCLC is highly neuroendocrine and often aggressive; treatment is chemo/radiation.
HemangioblastomaCalcified mass in the cerebellum or posterior fossa.Neuroblastoma (in infants); Arachnoid cyst (anterior midline).If calcification is seen, think of a differential diagnosis based on location.
HCCAflatoxin exposure; elevated AFP/ALT.Chronic liver disease (cirrhosis).HCC development must be considered in any patient with chronic liver disease and risk factors like aflatoxins.

Rapid review table

TopicKey PointContextExam Relevance
Burkitt Lymphomat(8;14) translocation; Starry sky pattern.B-cell lymphoma, highly proliferative.High yield for genetics and histology in board exams.
HCC/AflatoxinsAflatoxin exposure -> HCC.Chronic liver disease risk factor.Links environmental toxicology to malignancy development.
Paraneoplastic HypercalcemiaPT HrP (Squamous Cell Lung Cancer); IL-1 (Multiple Myeloma).Bone resorption; elevated serum calcium.Requires knowing the source of excess PTH action, not just high Ca++.
Calcified Brain MassHemangioblastoma in cerebellum; Craniopharyngioma near pituitary stalk.Differential diagnosis based on location and age/sex.Calcification is a major clue; always list differentials.

Board-speak -> diagnosis

Board-speak / Vignette phraseDiagnosis / ConceptWhy it fits
A child with a jaw mass, t(8;14) translocation, starry sky pattern.Burkitt LymphomaThe classic genetic and histological triad for this highly proliferative B-cell lymphoma.
Patient exposed to grains/aflatoxins develops liver mass on ultrasound.Hepatocellular Carcinoma (HCC)Aflatoxin exposure is the most common environmental risk factor leading to HCC, especially in endemic areas.
Lung cancer patient with joint pain and digital clubbing; next step is CXR/CT.Hypertrophic Osteoarthropathy (H.O.A.)H.O.A. is a classic paraneoplastic syndrome of underlying malignancy, requiring imaging to find the primary source.
Small blue cells positive for chromogranin and found in lung cancer.Small Cell Lung Cancer (SCLC)SCLC often has neuroendocrine features; Chromogranin positivity supports this diagnosis.
Calcified mass in the cerebellum causing morning headaches/nausea.HemangioblastomaThis is the classic location and appearance of a calcified tumor, often associated with subarachnoid hemorrhage risk.
A woman with an adnexal mass; CT suggests adrenal source for hyperandrogenism.Hyperinidrogenism (Adrenal Tumor)The initial workup must rule out adrenal sources (e.g., adenoma) before assuming ovarian origin, especially when testosterone is normal.

Differential diagnosis / distinguishing features

Hyperandrogenism Workup

Key FeaturesDistinguishing FindingsNext Step
Ovarian Source (e.g., Granulosa Cell Tumor)Estrogen production; precocious puberty in girls, or endometrial hyperplasia/cancer risk.Biopsy of the adnexal mass; measure estrogen levels.
Adrenal Source (e.g., Adenoma)High DHEA-S; adrenal tumor is the primary source of excess androgens.CT scan of abdomen/pelvis to image adrenal glands.

Management pearls

  • HCC Workup: In any patient with chronic liver disease, perform screening for HCC (ultrasound/AFP) due to high risk from aflatoxin exposure.
  • Paraneoplastic Hypercalcemia: Always determine the source of PTH excess: Primary hyperparathyroidism (PTH), Malignancy (PT HrP or IL-1), or Granulomatous Disease (Vitamin D activation).
  • SCLC Management: Due to its aggressive nature, SCLC is typically treated with chemotherapy and radiation; surgery is rarely curative.
  • Calcified Brain Mass Workup: The location of the calcification dictates the differential diagnosis (e.g., posterior fossa suggests Hemangioblastoma; suprasellar suggests Craniopharyngioma).

Don't miss

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EBV Association: Remember EBV's association with Burkitt, Hodgkin, and Nasopharyngeal Carcinoma.
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HCC Risk Factor: Aflatoxin exposure is a major risk factor for HCC development in the context of chronic liver disease.
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Paraneoplastic Syndromes: Be ready to link specific cancers (e.g., Squamous Cell Lung Cancer -> PT HrP) to their resulting endocrine/metabolic derangements.
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Tumor Marker Interpretation: Markers like PSA, CEA, and CA-125 are primarily used for monitoring response to therapy, not initial diagnosis.

Integration & clinical reasoning

  • Endocrine Integration (Hypercalcemia): The mechanism of hypercalcemia is often the most tested aspect: PT HrP mimics PTH action; IL-1/Osteoclast Activating Factor stimulates osteoclasts; Sarcoidosis involves activated macrophages producing 1-\alpha-hydroxylase.
  • Oncology Integration (Lung Cancer): Lung cancer is a major source of paraneoplastic syndromes, including SIADH (SCLC), H.O.A., and LEMS.
  • Neuroimaging Integration: Calcified masses are highly specific; the location dictates the differential diagnosis (e.g., posterior fossa vs. suprasellar).

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 OMM/OMT in acute crises (e.g., severe electrolyte imbalance from SIADH or acute liver failure).
  • The understanding of systemic inflammation and cytokine release (IL-1, TNF-\alpha) is relevant to the pathophysiology of Multiple Myeloma hypercalcemia and general inflammatory states.

Concept connections / cross-references

  • For detailed information on liver pathology and HCC screening, see [ Episode 12 ].
  • For comprehensive review of endocrine emergencies like adrenal insufficiency or hypercalcemia, see [ Episode 45 ].
  • For general oncology principles and tumor markers, see [ Episode 88 ].

High-yield association table

ConditionAssociationMechanismClinical Significance
Burkitt LymphomaEBV; t(8;14) translocation.High proliferation rate due to genetic instability.Classic triad (EBV/t(8;14)/Starry Sky) must be recognized.
Squamous Cell Lung CancerPT HrP production.Parathyroid hormone-related peptide mimics PTH, causing hypercalcemia and hypophosphatemia.Hypercalcemia is a common paraneoplastic finding in this type of lung cancer.
Small Cell Lung Cancer (SCLC)SIADH; Lambert-Erythroasthenic Syndrome (LEMS).Neuroendocrine activity leading to ADH excess or neuromuscular junction dysfunction.These syndromes are key diagnostic clues for SCLC.
Multiple MyelomaInterleukin-1 (IL-1) / Osteoclast Activating Factor.IL-1 stimulates osteoclasts, leading to bone resorption and hypercalcemia.Hypercalcemia is a common complication of plasma cell dyscrasias.

Key terms glossary

TermDefinitionContextExample
AflatoxinToxic mycotoxins produced by Aspergillus mold.Liver pathology; chronic exposure to contaminated grains.Causes HCC and is a major risk factor for liver cancer.
Hypertrophic Osteoarthropathy (H.O.A.)Joint pain, clubbing, and periosteal new bone formation in the long bones.Paraneoplastic syndrome of underlying malignancy (e.g., lung cancer).Requires imaging to find the primary source of cancer.
Interleukin-1 (IL-1)A pro-inflammatory cytokine/osteoactivator.Multiple Myeloma; bone pathology.Acts as an osteoclast activator, leading to pathological bone breakdown and hypercalcemia.
ChromograninNeuroendocrine protein marker.Small Cell Lung Cancer (SCLC); neuroendocrine tumors.Positive staining supports a diagnosis of neuroendocrine origin.

Study optimization

TopicStudy ApproachPriorityResources
Paraneoplastic SyndromesCreate flowcharts linking cancer type -> hormone/cytokine -> resulting syndrome.High (Board-level association questions).Review specific associations: SCLC -> SIADH; Squamous LC -> PT HrP.
Calcified MassesUse a differential diagnosis table based on the location of calcification in neuroimaging.Medium-High (Pattern recognition/Vignette traps).Memorize key locations: Cerebellum (Hemangioblastoma); Suprasellar (Craniopharyngioma).
Tumor MarkersUnderstand that markers are for monitoring, not diagnosis; know the primary source marker.Medium (Common trap question area).PSA is used to monitor treatment response in prostate cancer.

Question pattern recognition

  • Pattern: Calcified mass in the cerebellum/posterior fossa -> Hemangioblastoma. This is a classic location and appearance for this tumor, often associated with subarachnoid hemorrhage risk.
  • Pattern: Hypercalcemia + Malignancy -> Check PT HrP source first. If PT HrP is high, suspect Squamous Cell Lung Cancer or other malignancies; if IL-1/PTH action is suspected, consider Multiple Myeloma.
  • Pattern: Adnexal mass in a woman with hyperandrogenism and normal testosterone -> Rule out adrenal sources (CT abdomen) before assuming ovarian origin. This prevents missing an adrenal adenoma.

Test yourself

Common mistakes to avoid

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Mistake 1: Assuming all calcifications are benign. Calcification in the brain/meninges requires a differential diagnosis (Hemangioblastoma vs. Craniopharyngioma vs. Oligodendroglioma) based on location and age.
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Mistake 2: Confusing tumor marker utility. Never use markers like PSA or CEA to diagnose cancer; they are primarily for monitoring treatment response.
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Mistake 3: Reversing the hypercalcemia mechanism. Remember that PT HrP (Squamous LC) and IL-1 (Multiple Myeloma) both cause bone resorption, leading to high calcium, but their sources are different.

Common traps

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Trap 1 (Calcification): The location of calcification is key. Posterior fossa/cerebellum suggests Hemangioblastoma; suprasellar suggests Craniopharyngioma.
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Trap 2 (Tumor Markers): Do not assume that a positive tumor marker confirms the diagnosis or guides initial therapy—it is mainly for monitoring.
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Trap 3 (Adrenal Source): When hyperandrogenism occurs, always rule out an adrenal source (CT abdomen) before attributing it solely to ovarian pathology.

Original transcript with highlights

Original transcript with highlights

Okay, welcome. My name is Divine. This is episode 256 of the Divine Intervention Podcast. And in this podcast now we continue the Rapid Review series for the USMEL Step 2 CK exam. And this will be series 41. And in today's podcast before I start, I just want to send out a reminder. So this 10 a.k.a. Step 2 CK class I have. Again, it's been wearable received. It's now at this point being taken by probably almost 200 people, if not more. And again, for the most part, for the vast majority of people, I've got a very good feedback from it. So, and again, I update the course very regularly. So it's not going to be a course where you learn something and then it's stuck in the past. I try to make regular updates. Again, as I've said before, I think of the course as software. So just trying to keep like, kind of beyond the on the forefront of how the Indian is taking things in this in this day and age. So again, it's going to take place on the 5th of September. And it's going to be again 6 to 10 a.m. Pacific time in the morning, not to 4 p.m. Pacific time in the afternoon and 6 to 8 p.m. Pacific time in the evening. So there will be two outbreaks basically between each section and it's held over zoom. And remember the test-ticking strategies class is going to be a 2 to 2 and a half hour class is going to take place on the 10th of September. And then I have a 2d version of this 10 hour course taking place on the 11th and the 12th of September as well.

So if you're interested, just reach out to me through the website. On the website you see a contact whatever you can contact me through that. And then we'll kind of go from there. Okay, so let's go into the rapid review. So what if they give you a question? What if they give you a question about and to be honest, let's rapid review because I've been hearing a lot of stories from people saying that, you know, step 2, seek has been testing a lot of step 1 information, like some very heavy basic sciences stuff. So that's something I kind of want to actually focus on today. You know, just I mean, it will be clinical, but I will talk about it in a basic science context just to help people with those kinds of questions on exams. So what if they give you a question about the African kid like eight years old, has this big jaw mass? What are you thinking about? I would hope you're thinking about Brickett's lymphoma, right? Remember Brickett's lymphoma, right? Has that 814 translocation and that 814 translocation, right? Is going to ultimately lead to this amplification that makes cells like just keep proliferating, proliferating, proliferating, right? And remember, classically on histology, you'll find that starry sky pattern, right? And what is the bug that is linked with Brickett's lymphoma on MBA needs? I would hope you're telling me the abstin bar virus, right? EBV, right?

And the thing is, is actually generally high or for purposes of step 2, seek to know the malignancies that are associated with EBV, right? So remember EBV is associated with Brickett's lymphoma, right? As I've talked about already. It actually has an association with Hodgkin's lymphoma. Don't forget Hodgkin's lymphoma, right? You'll find those rates, tremor, excels, right? Remember, those are, you'll find all these lymphocytes that have like a bilob nucleus, right? And also Nizofarin, Joe Carcinoma has a stronger association with EBV, right? And then if you have a patient that has HIV, don't forget the primary CNS lymphoma. The primary CNS lymphoma has an association with EBV, right? And then, what if they give you a question about a person like a patient, they tell you that, oh, this patient, you know, he works in a barn, and they tell you that he has been working in this barn for that less say like his anemic grant, he's been working in this barn, you know, where these store all these knots and produce and greens and everything, right? And then they tell you that over the last six months, this person has lost 20 pounds, right? Has been having like John this, right? And then they give you some labs and you notice that this person's liver labs are out of whack, right? And then they tell you that on red-upocortin ultrasound, they find like a mass within the liver. If you see that, what are you thinking about?

I really, really hope you're thinking about a hepatocelular carcinoma, right? So remember, whenever you see all these people that deal with grains and all that stuff, right? Those things tend to contain aflatoxins and those things are very toxic to the liver, right? Ultimately, those things can give rise to hepatocelular carcinoma. Now, what if they give you a question about a patient and they tell you that, oh, this patient, over the last, you know, three, four weeks, this patient has been having like joint pain, like being in his knees, in his hips, in his fingers, right? And then they tell you that you see like a lot of like digital clubbing with his fingers and his toes. If you see that, and they ask, what's your next best step in management? What would you do for that patient? I will hope you're telling me that you want to go ahead and get some kind of chest x-ray or chest CT, right? This person has long cancer, right? Remember, this perneoplastic phenomenon that this person has, right? Is something called hypertrophic osteoarthropathy. Sometimes you may see it on exemptions referred to as hypertrophic pulmonary osteoarthropathy, right? So it's just this thing that happens in the cell in a long cancer, especially when people have like, at no cost, in a moment of the longs, right? So that's something you want to watch out for. And again, remember, you're other pulmonary perneoplastics, right? So remember, people can get, especially with small cell lung cancer, right?

People can get SIDH, right? So they can get like hyponitremia and the ayurin will be very hyprtonic, right? Or, and remember, when the person's urine is hyprtonic, instead of saying that the person's urine is hyprtonic, the MBME can basically give you the person having a urine-specific gravity that is more than 1.012, right? And that's like a sorrogate for very hyprtonic ayuric, right? And then don't forget, right? Ectopic CT should small cell lung cancer as well. Remember, that's the one where high duosdexamethosol does not suppress the cortisol the next morning, right? And then also don't forget that small cell lung cancer has an association with Lambert etymiaesthenic syndrome, right? So they'll give you a question about a person that has like decreased diptym-dangerive flexes, proximal muscle weakness, right? And they'll tell you that, oh, that when you repeatedly stimulate this person's, when you do a repetitive nerve stimulation, you observe an incremental response. If you see stuff like that, right? That's Lambert etymiaesthenic syndrome. Remember, Lambert etymiaesthenic syndrome for the most part of an exam is not affect the head and neck, right? It affects more of your appendicolytic skeleton as against the axial skeleton, right? And again, it's something that will classically find your lung cancer.

I mean, in lung cancer, you can also find like polyandromatomaiocyitis, believe it or not, those myopathies have a classic association, well-established association with lung cancer on exams, right? And then don't forget PT-HRP, right? So people that have lung cancers, especially the scrimocel lung cancer. And by the way, let me tell you this, scrimocel lung cancer loves to cavitate, loves to form a cavity, right? So if you see a person that has a lung, it's a question about lung cancer, and you see like air fluid levels in the lungs, that's going to be scrimocel. That's not going to be small cell, right? Scrimocel cancer, famously, cavytits, right? Scrimocel lung cancer, famously, cavytits, right? And again, remember, it produces a parathyride hormone-releafate peptide, right? So because it produces parathyride hormone-releafate peptide, right? That can essentially cause, basically, works like PT-HRP. So you'll raise the person's blood calcium, it'll tank the person's blood phosphate, right? So the person will have a hypercalcemia, right? Remember, the most common cause of hypercalcemia in the hospital is actually from a lignessy. Now, for some of these lung, for some of these malignancies, it's actually good to know like some tumor markers. It's actually good to know some tumor markers. So, for example, you may see a person having a material that, oh, this person has this malignancy, and it's positive for caretin.

Well, if a malignancy is positive for caretin, then that tells you that you're likely dealing with some kind of scrimocel cancer, right? And another one that we throw on a test, right? Especially those small cell lung cancer, you may tell you that, oh, you see like small blue cells that are positive for chromogramming, right? And then you see something that's positive for chromogramming, that's pretty classic, right? For small cell lung cancer. It just tells you that it's a tumor or a malignancy that is endocrine in origin, right? That is endocrine in origin. And I think one thing I would really like to emphasize here is small cell lung cancer. Many times people keep getting this wrong one example for whatever reason. You don't do radiation, you don't do surgery for small cell lung cancer, small cell lung cancer. When is diagnosed? It's already assumed to be stage four, right? So, you're not going to read it a whole human being or caught up a whole human being, right? You're going to do chemotherapy, right? Whenever a person has a systemic malignancy, you're going to do chemotherapy for that. And I guess thinking in terms of some of these tumor markers, right? So remember like GFAP, right? GFAP is a classic one that pops up on exams as well. Remember, that's what you find positive in people that have like these astrocytomas, right? Or people that have glioblastoma multi-forming, right? And then another one you may see, they love to do this one. Vimentin, right?

Remember, vimentin is a muscle marker, right? So, the person has a malignancy that is arising from muscle, right? So, you may give you a question about a person that has like tuberous sclerosis or something like that, right? And then they'll tell you that all the person has like a cardiac mass, right? And then they'll tell you that that mass is vimentin positive, right? That person, and usually people that have tuberous sclerosis, they have like a benign mass of the heart, right? But if you go to the moma lignan form, the rhodomaio sarcoma, they'll be vimentin, they'll be vimentin, they'll be, sorry, desmin. I don't know what you keep saying vimentin. They'll be desmin positive. So, desmin is a muscle marker. Vimentin is something you'll find in like sarcomas, right? So, if a person has like a lyomaio sarcoma, right? And those are things that tend to have a vimentin positivity, right? And then don't forget, right? Like melanomas, right? Or they tell you about a person that has lunger and cell histocytosis. Those things are all S100 positive, right? S100 positive. And if you're looking at some of these ovarian malignancies, right? So, for example, if a person has like hyperindrogenyzema and they tell you that the person has an adnexel mass, right? That's going to be a sertoli-ledic cell tumor. Remember, that's positive for testosterone, right?

If you see a woman half-science of hyperindrogenism, what you notice is that testosterone levels are normal and that's for your next best step. Go ahead and get a CT of the abdomen and pelvis to examine the adrenal glands, right? The person probably has some kind of adrenal tumor that's producing a ton of DHS that's causing most of those symptoms. And remember that if you see granulosa cell tumors, remember those things have those call external bodies when you're to perform histology, right? Granulosa cell tumors remember those things produce estrogen, right? So, you can shop in a kid, right? If you see that a kid will have like precocious puberty, especially a girl, right? Because she's seeing all this estrogen. But you know if it's like a postmanopausal woman, she'll have like a domicero hyperplegia and domicero cancer, right? Because she's basically getting unopposed estrogen. And please don't forget the biggest risk factor, right? For endometrial cancer, right? Is exposure to an oposed estrogen? And then don't forget those yolk sac tumors, right? Remember sometimes on the exams you see them refer to as endodermal sinus tumors, right? So those tumors tend to be positive for AFP. Another malignancy that's AFP positive, right? Is hepatocellulocarcinoma, right? Hepatocellulocarcinoma tends to be positive for AFP. And then if you're thinking in terms of choreocarcinoma, right? So choreocarcinoma, remember it loves to metas the size of the lungs.

And it's very responsive to methotrexate. That one tends to be better HCG positive, right? So that can present as hyperemesis gravidar, right? In a woman, I see a woman that has this malignancy, this long mass. And she has a lot of nausea and vomiting, right? You want to begin to consider choreocarcinoma, especially in detail you that, oh, she recently had an abortion or she recently had a molar pregnancy removed or she recently just delivered a baby. And then you see like a pulmonary mass, like hyperemesis gravidar, and stale symptoms. You want to think about choreocarcinoma in that circumstance. I remember that the beta HCG will be positive in those situations, right? And then obviously for presciense, prostate cancer, right? The PSA will be elevated. Although remember the PSA, you don't use it to meet the diagnosis, right? Use it to monitor response to therapy, right? Many of these tumor markers use them mostly to monitor response, response to therapy, and that's pretty much it, right? And then remember all these malignancies that I derive from neurocress cells, right? So like melanomas. Again, I think I've talked about this already, or like these vestibular neuromas, right? These are known as, that we find in people that have NF2. These things are all S100 positive, right? These things are all S100 positive. And then, I've kind of seen some more things about some of these cancer-related things, right?

So, say for example, what if they give you a question about a patient, right? And they tell you that, oh, this patient, you know, has, you know, for the last three months has been having like really bad morning headaches, right? And they're, you know, they get better throughout the day. And then they tell you that all that the obtain the image of the brain, and they find a calcified mass in the vernis, right? If you see that, I'll really hope you're thinking about a hemangioblastoma, right? Remember those hemangioblastomas, those things tend to be calcified. So if you see a calc, like whenever the NBME tells you that something is calcified, usually has meaning, right? It's like a, it's almost like a concept, right? So like, hemangioblac, if you see a calcified mass in the vernis of the cerebellum, that's a hemangioblastoma, right? Remember, those things can produce epoch in a perinoplastic fashion, right? And when you produce epoch in a perinoplastic fashion, right, that's going to cause a polycythemia, right? If you see a calcified mass, right? A calcified supercelemus in a child, and let's see, maybe this child has like a bite temporal hemianopsia. And you're thinking about a craniofarinjoma, right? You're thinking about a craniofarinjoma. Remember, those things that are right from oral electrode, right? Raffi's pouch. Again, it's calcified. We've detected that, oh, you see a calcified mass in the frontal lobe, right? That's an oligodendroglyoma, right?

Remember, those things have a fried egg appearance on the histology, right? And then, if you see like a calcified adnexomas, right, in a patient, right? And, oh, you see a calcified mass in the anterior medius thynum, right? You should be thinking about a bermoid cyst, right? You should be thinking about some kind of a teratoma, right? Remember, those things contain like multiple tissue types. And if they're shopping the medius thynum, they'll shop in the anterior medius thynum, right? Also, still continue with this topic of calcified masses, right? If you see a kid like less than a year old, has this calcified mass, you know, that crosses the midline, right? Then you want to think about a neuroblastoma, right? Although, remember, on like a teratoma that shows up in the anterior medius thynum, neuroblastoma will shop in the post-traumatic stynum, right? Because it's just, it's a neuroblastoma, right? So, if you see it anywhere, you'd likely see it in the post-traumatic stynum, right? And then, I guess with this hypercalcemia business, right? Remember, people that have sacroidosis, they can also have hypercalcemia as well, right? Because remember, sacroidosis associated with these nonchysin granolomas, these nonchysin granolomas, they contain all these epithelioid macrophages, right? These epithelioid macrophages, they produce a ton of one alpha hydroxylase. That one alpha hydroxylase, right? We'll convert calcium, diol, to calcium, trial, right?

So, that'll be why those people will have hypercalcemia. Although, an Indian is, they can also ask you about the mechanism behind hypercalcemia and like, a person will multiple myeloma, right? If a person has multiple myeloma, well, what's going to happen to those people? Those plasma cells, they secret a lot of interlooking one. And remember that another name for interlooking one, right? It's osteoclast-activating factor. So, because interlooking one is known as osteoclast-activating factor, it'll activate osteoclast-reserve bone, right? And when you reserve the bone, they'll ultimately give rise to a hypercalcemia, right? They'll ultimately give rise to hypercalcemia. And then, what if they give you a question about a person that has an exomas, right? And then they tell you that this person has lost like 15 pounds over the last three months. And this person is like tacky cardic, increased deep tendon reflexes, right? And the person even has like an irregularly irregular interval on an eKG. Well, that's pretty easy, right? If you see that, you're seeing who, who? This person has hyperthyroidism, right? So, just try to put those two things together. You see hyperthyroidism and an exomas, right? That's pretty classic for stromal viria, right? Prism and stromal viria. And when a person has stromal viria, right? Remember, it's a teratoma that contains thyroid tissue, a topic thyroid tissue. So, it's making a ton of thyroid hormone, right? And that's causing all those problems.

And why do you think this person has this irregularly irregular interval on an eKG? That's eFib. Remember, eFib is the most common eregment that we'll find in people that have hyperthyroidism. Although, remember, the biggest risk factor for eFib, right? He's having a histrava of mitro stenosis, right? Having a histrava mitro stenosis has the biggest risk factor for eFib, right? Does the biggest risk factor for eFib? And then, let's see. I'm just trying to think of any other big tumor markers I want to talk about today. I mean, if a person has an elevation in their C-in-199, right? That tells you that they know pancreatic cancer, right? Remember, calcium tonin, right? Is the tumor marker for medinary thyroid cancer, right? Especially, like, they can give you a question about a person that has a neck mass. And this person has a prolonged uterine interval on an eKG. That's hypocalcemia from calcium tonin, right? Remember, you're going to see that with medinary thyroid cancer, right? Another common one you miss your own exam is C-E-A, right? The carcinotembryonic antigen. Remember, that's found in many gem allegnancies, like colon cancer, pancreatic cancer, in some cases, can have that although. On embimic exams, think of pancreatic cancer as being mainly C-E-199, right? And then C-A-125, obviously, is ovarian cancer, right? C-A-125 is ovarian cancer. And then remember, the alchvoss, this alchvoss conundrum is something many people kind of fall for in exams.

But if alchvoss is elevated, it can be from a bone process, or it can be from a bone, or from a liver process, right? Like a callistatic process in the liver, right? But the way you tease those two apart, you're like, hmm, where's this alchvoss elevation coming from? Is it coming from bone or from the liver? Is you check the G-G-T, right? The G-G-T is elevated, and the alchvoss is elevated. It's something in the liver that's going on, right? But even if the alchvoss is going to elevate it, and the G-G-T is normal, that's probably a bone process, right? So, maybe the person has bone mets, or the person has osteoporosis, or has like patches of disease of the bone, right? And there's actually a kind of alchvoss called placental alchvoss that's actually elevated in people that have like semi-nomers, right? So, knowing these two more markers is not necessarily the worst thing in the world. If you know these things, these are like just easy points, easy points on an exam. So, I guess to wrap up, please don't forget to subscribe to the You Tube channel. It's called Divine Intervention US Mly Podcasts and Videos. That's where I put all my videos. But all the podcasts, all my slides, everything, you can find them on my website, right? Divine Intervention Podcast.com. And please also don't forget to subscribe to the podcast. I have it on Apple Podcasts, on Spotify and Google Play. So, again, please subscribe any little bit of support helps. So, thank you very much for listening.

I'll see you in the next podcast. Thank you and God bless you.

Practice questions — USMLE style

Question 1 — Oncology/Paraneoplastic Syndromes

A 55-year-old male smoker is diagnosed with small cell lung carcinoma (SCLC). He presents with chronic symptoms of fatigue, weight loss, and mild hyponatremia. Laboratory testing reveals a urine specific gravity greater than 1.012, indicating concentrated urine despite the low serum sodium level. Which paraneoplastic syndrome is most likely responsible for this electrolyte imbalance?

  • A) Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
  • B) Hypercalcemia due to PT HrP secretion
  • C) Eaton-Lambert Myasthenic Syndrome (ELMS)
  • D) Hypoglycemia secondary to tumor lysis

Answer: A. The patient's presentation—hyponatremia with a concentrated, hypertonic urine (urine specific gravity > 1.012)—is classic for the syndrome of inappropriate antidiuretic hormone secretion (SIADH). SCLC is strongly associated with SIADH due to ectopic ADH production. While PT HrP can cause hypercalcemia and ELMS affects muscle weakness, the combination of hyponatremia and concentrated urine points directly to SIADH.

Question 2 — Endocrinology/Metabolic Bone Disease

A 70-year-old man is diagnosed with multiple myeloma. He presents with generalized bone pain, fatigue, and laboratory findings showing hypercalcemia (serum calcium elevated) and elevated alkaline phosphatase. The underlying mechanism for the hypercalcemia in this patient is primarily due to:

  • A) Increased renal excretion of phosphate leading to secondary hyperparathyroidism
  • B) Direct stimulation of osteoclast activity by plasma cell secretions
  • C) Excessive production of 1-$\alpha$-hydroxylase by granulomatous tissue
  • D) Consumption of calcium via increased gut absorption stimulated by PT HrP

Answer: B. Multiple myeloma involves plasma cells that secrete various cytokines, notably Interleukin-6 (IL-6). IL-6 acts as an osteoclast-activating factor, stimulating the release of bone mineral and leading to hypercalcemia. This mechanism is distinct from sarcoidosis (which uses 1-$\alpha$-hydroxylase) or primary hyperparathyroidism.

Question 3 — Gastroenterology/Oncology

A factory worker who handles grains for a living presents with progressive weight loss, jaundice, and an abdominal ultrasound revealing a large mass within the liver parenchyma. The patient's history suggests chronic exposure to environmental toxins found in stored crops. Which diagnosis is most likely, and what is the primary risk factor associated with this malignancy?

  • A) Cholangiocarcinoma; Chronic bile duct obstruction
  • B) Hepatocellular Carcinoma (HCC); Exposure to aflatoxins
  • C) Metastatic adenocarcinoma; Primary gastrointestinal inflammation
  • D) Gallbladder carcinoma; Smoking history

Answer: B. The combination of liver mass, chronic exposure to grains/stored crops, and the associated risk factor points strongly toward HCC. Aflatoxins, produced by molds that contaminate stored grains, are potent hepatotoxins and are a well-established cause of HCC.

Question 4 — Neurology/Neoplasia

A pediatric patient is evaluated for recurrent headaches and has an MRI revealing multiple calcified masses within the cerebellum. The clinical picture suggests a primary CNS tumor. Given the location (cerebellum) and the finding of calcification, which diagnosis should be highly suspected?

  • A) Meningioma
  • B) Craniopharyngioma
  • C) Hemangioblastoma
  • D) Oligodendroglioma

Answer: C. Calcified masses in the cerebellum are classically associated with hemangioblastomas. While craniopharyngiomas can calcify and affect the pituitary region, hemangioblastomas are a common finding in the posterior fossa/cerebellum. The presence of calcification is a key diagnostic clue for several CNS tumors on board exams.

Quick fire review

What finding in a patient with lung cancer, especially when combined with joint pain and digital clubbing, suggests a paraneoplastic syndrome?

Hypertrophic osteoarthropathy (or hypertrophic pulmonary osteoarthropathy).

Which specific type of lung cancer is famously known for cavitating?

Squamous cell carcinoma.

What are the key features suggesting Lambert-Eaton Myasthenic Syndrome on an exam?

Proximal muscle weakness, decreased deep tendon reflexes, and an incremental response upon repetitive nerve stimulation (RNS).

Which tumor marker is positive in both Yolk Sac Tumors and Hepatocellular Carcinoma?

Alpha-fetoprotein (AFP).

What specific finding on a patient's EKG suggests hyperthyroidism?

An irregularly irregular interval, indicative of Atrial Fibrillation (Afib).

If a calcified mass is found in the anterior median sella turcica, what should be suspected?

A dermoid cyst or teratoma.

What tumor marker is elevated in pancreatic cancer and colon cancer?

CEA (Carcinoembryonic Antigen).

Which malignancy produces PT HrP, leading to hypercalcemia?

Squamous cell lung cancer.

Name three malignancies strongly associated with EBV.

Burkitt's lymphoma, Hodgkin's lymphoma, and Primary CNS Lymphoma (in HIV patients).

What is the classic finding on histology for a malignancy positive for Chromogranin?

Small cell lung cancer (indicating an endocrine origin).

Which type of tumor marker elevation requires checking GGT to differentiate between bone vs. liver source?

Alkaline Phosphatase (ALP) or Calcium (Alkaline phosphatase is often used in this context, but the principle applies to ALP/Calcium levels).

What specific finding suggests a diagnosis of Sarcoidosis-related hypercalcemia?

Elevated serum calcium due to 1-$\alpha$-hydroxylase activity by epithelioid macrophages within noncaseating granulomas.

Quick recall / Anki-style questions

What tumor marker is elevated in pancreatic cancer and colon cancer?

CEA (Carcinoembryonic Antigen).

Which malignancy produces PT HrP, leading to hypercalcemia?

Squamous cell lung cancer.

Name three malignancies strongly associated with EBV.

Burkitt's lymphoma, Hodgkin's lymphoma, and Primary CNS Lymphoma (in HIV patients).

What is the classic finding on histology for a malignancy positive for Chromogranin?

Small cell lung cancer (indicating an endocrine origin).

Which type of tumor marker elevation requires checking GGT to differentiate between bone vs. liver source?

Alkaline Phosphatase (ALP) or Calcium (Alkaline phosphatase is often used in this context, but the principle applies to ALP/Calcium levels).

What specific finding suggests a diagnosis of Sarcoidosis-related hypercalcemia?

Elevated serum calcium due to 1-$\alpha$-hydroxylase activity by epithelioid macrophages within noncaseating granulomas.