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Episode Notes

Source / episode info

  • Episode: 403
  • Title: Divine Intervention Episode 403 – USMLE Step 2/3 Rapid Review Series 79
  • Published: 2022-07-16
  • Source: Episode page

One-liner

This episode provides a high-yield review covering social services reporting protocols (child/elder abuse), the pathophysiology of hypercoagulable states triggered by malignancy or nephrotic syndrome, key differentiations among GI motility disorders (GERD vs. Achalasia), and advanced neurobiology topics like PML, Parkinson's disease, and Alzheimer's disease.

High-yield summary

  • Elder/Child Abuse: Suspected abuse in children requires contacting Child Protective Services (CPS); suspected neglect or abuse in the elderly requires contacting Adult Protective Services (APS). Intimate partner violence is managed through counseling and safety planning, not typically reported to APS/CPS.
  • Hypercoagulability: Any malignancy increases the risk of thrombosis due to cytokine release and procoagulant factors. Anticoagulation with Heparin or LMWH is generally preferred over Warfarin in cancer patients because it allows for rapid reversal if bleeding occurs.
  • PML Pathophysiology: Progressive Multifocal Leukoencephalopathy (PML) is caused by the reactivation of the JC virus, which infects and destroys oligodendrocytes, leading to demyelination in the white matter. This is common in immunocompromised states (e.g., advanced HIV).
  • GI Motility Disorders: Achalasia involves failure of the Lower Esophageal Sphincter (LES) to relax upon swallowing, presenting with a "bird's beak" sign on barium swallow. GERD is characterized by transient LES relaxation and acid reflux; initial management is PPI therapy.
  • Neurodegenerative Patterns: In Alzheimer's disease, pathology involves extracellular Amyloid plaques and intracellular neurofibrillary tangles (composed of hyperphosphorylated Tau protein). Parkinson's disease is associated with the loss of dopaminergic neurons in the substantia nigra pars compacta, visible post-mortem as Lewy bodies.

Learning objectives

  • Differentiate mandatory reporting protocols for suspected child and elder abuse.
  • Identify the pathophysiology and initial management of various GI motility disorders (GERD, Achalasia, Diffuse Esophageal Spasm).
  • Recognize the clinical presentation and underlying pathology of hypercoagulable states associated with malignancy or nephrotic syndrome.
  • Correlate neurological symptoms (e.g., progressive weakness, white matter lesions) with specific infectious/degenerative processes (PML, AD, PD).
  • Understand the role of PP Is in GERD management and when advanced testing (EGD, pH monitoring) is required.

Board exam buzzwords

ConditionKey FindingAssociationBoard Exam Tip
MalignancyHypercoagulability/ThrombosisCytokine release; Trousseau's syndromeAlways consider anticoagulation (Heparin/LMWH) in cancer patients.
PMLWhite matter demyelinationJC virus reactivation; OligodendrocytesThe key mechanism is viral attack on oligodendrocytes, not just general white matter damage.
Achalasia"Bird's beak" sign on swallowFailure of LES relaxationDistinguishes it from GERD (transient relaxation) and spasm (diffuse narrowing).
Alzheimer's DiseaseAmyloid plaques & Tau tanglesHyperphosphorylated Tau protein; Hippocampus atrophyRemember the two main pathological hallmarks: plaque deposition and tangle formation.

Rapid review table

TopicKey PointContextExam Relevance
Elder Abuse ReportingContact Adult Protective Services (APS)Suspected neglect/abuse in elderly populations.High-yield social services question; must know the correct agency for age group.
HypercoagulabilityHeparin preferred over WarfarinCancer, Nephrotic Syndrome, Factor V Leiden, HIT.Anticoagulation is critical when antithrombin levels are low or clotting risk is high.
GERD WorkupPP Is first line; EGD/24h pH monitoring for refractory cases.Persistent heartburn despite maximal PPI dose.Know the stepwise approach: empiric therapy -> endoscopy -> objective testing.
PMLJC virus targets oligodendrocytesImmunosuppression (e.g., advanced HIV).The specific cell type (oligodendrocyte) is the critical derivative detail to remember.

Board-speak -> diagnosis

Board-speak / Vignette phraseDiagnosis / ConceptWhy it fits
A 70-year-old woman with unexplained abrasions and poor nutrition is found by her son.Elder Abuse/NeglectThe key demographic (elderly) mandates reporting to Adult Protective Services (APS), regardless of the specific injury type.
A child presents with red NO hemorrhages and a subdural hematoma following non-accidental trauma.Child AbuseClassic signs requiring immediate mandatory reporting to Child Protective Services (CPS).
A patient with advanced gastric cancer suddenly dies in the ER, showing no obvious cause of death.Pulmonary Embolism (PE) / HypercoagulabilityMalignancy is a major risk factor for hypercoagulable states; PE must be considered first when sudden death occurs in a cancer patient.
A 40-year-old man presents with dysphagia, and the barium swallow shows a "bird's beak" appearance at the LES.AchalasiaThe pathognomonic finding of failure to relax the LES is key; this distinguishes it from GERD or spasm.
An immunocompromised patient develops progressive white matter lesions on MRI.Progressive Multifocal Leukoencephalopathy (PML)PML is a JC virus-mediated demyelination, requiring recognition in the context of immunosuppression (e.g., advanced HIV).
A 75-year-old man presents with multiple ulcers scattered across the duodenum and jejunum.Zollinger-cuvieres Syndrome / GastrinomaMultiple duodenal/jejunal ulcers suggest a gastrin-secreting tumor (Gastrinoma), which is often associated with MEN1 syndrome.

Differential diagnosis / distinguishing features

CNS Demyelination Syndromes

Key FeaturesDistinguishing FindingsNext Step
Multiple Sclerosis (MS)Optic neuritis common due to CN II derivation from optic nerve; white matter lesions on T2 MRI.Diagnosis of exclusion, often requires longitudinal evidence/McDonald criteria.
Progressive Multifocal Leukoencephalopathy (PML)White matter demyelination in immunocompromised patient; JC virus reactivation.High suspicion in advanced HIV or immunosuppression; repeat imaging to track progression.
Guillain-Barré Syndrome (GBS)Acute, ascending peripheral weakness/paralysis; affects Schwann cells.Nerve conduction studies showing demyelination of peripheral nerves.

Management pearls

  • For suspected child abuse: Mandatory reporting must be made to Child Protective Services (CPS) .
  • When managing GERD, always start with a trial of Proton Pump Inhibitors (PP Is) ; if symptoms persist, proceed to EGD and 24-hour pH monitoring.
  • In any patient with malignancy and signs of bleeding/thrombosis, prophylactic anticoagulation using LMWH is often indicated due to the hypercoagulable state.
  • For suspected gastrinoma (multiple duodenal ulcers), screening for MEN1 syndrome and administering PP Is are crucial steps.

Don't miss

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The key difference between primary AI (e.g., autoimmune) and secondary AI (e.g., steroid use) is the preservation of aldosterone in secondary AI, meaning hyperkalemia/Type 4 RTA only occurs in primary adrenal insufficiency .
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In PML, the target cell for JC virus reactivation is the oligodendrocyte , leading to white matter demyelination.
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The classic presentation of a gastrinoma involves multiple ulcers (duodenum/jejunum) and requires screening for MEN1 syndrome.

Integration & clinical reasoning

  • GI Motility & Acid: Understanding that both GERD and Gastrinomas involve excessive acid production (GERD via LES relaxation; Gastrinoma via histamine/acid stimulation of parietal cells) links motility issues to endocrine pathology.
  • Neurobiology & Immunity: The link between immunosuppression, JC virus reactivation, and PML highlights how immune status dictates the risk of opportunistic CNS infections.
  • Thrombosis & Systemic Disease: Recognizing that systemic diseases (Nephrotic Syndrome, Lupus, Cancer) can trigger hypercoagulable states emphasizes the need for a comprehensive workup beyond just bleeding/clotting symptoms.

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 assessment for acute GI obstruction, adrenal crisis, or severe bleeding.
  • When considering chronic neurological issues like Parkinson's or Alzheimer's, the focus remains on standard pharmacological and supportive care; OMT is not a primary treatment modality.

Concept connections / cross-references

  • For detailed information on adrenal insufficiency and mineralocorticoid deficiency: Episode 37
  • For general principles of GI anatomy and motility disorders: Episode 12 (Hypothetical reference)

High-yield association table

ConditionAssociationMechanismClinical Significance
MalignancyHypercoagulable stateRelease of procoagulant cytokines/factors; Trousseau's syndrome.Requires prophylactic anticoagulation (Heparin/LMWH); risk for PE/DVT.
PMLJC Virus reactivationLysis and destruction of oligodendrocytes in the CNS.Leads to progressive white matter demyelination, especially in advanced HIV.
AchalasiaFailure of LES relaxationLoss of inhibitory innervation (Auerbach's plexus).Requires definitive treatment like pneumatic dilation or botulinum toxin injection.
GastrinomaMEN1 SyndromeGastrin overproduction stimulates parietal cells via histamine/acid pathways.Must screen for other MEN1 components: pituitary adenomas, pancreatic NE Ts.

Key terms glossary

TermDefinitionContextExample
Adult Protective Services (APS)State agency responsible for investigating suspected neglect or abuse of elderly individuals.Social services reporting; mandatory when the patient is over 65 years old.Finding unexplained bruising on a home-bound senior citizen.
Progressive Multifocal Leukoencephalopathy (PML)Demyelination of white matter in the CNS caused by JC virus reactivation.Immunocompromised patients (e.g., advanced HIV, high-dose steroids).MRI showing multifocal, non-enhancing white matter lesions.
Bird's Beak SignPathognomonic finding on barium swallow indicating failure of LES relaxation.Achalasia; distinguishes it from other causes of dysphagia.Swallowing contrast material and seeing the narrowing at the gastroesophageal junction.
Trousseau's SyndromeMigratory thrombophlebitis associated with underlying malignancy.Cancer (especially GI/pancreatic); indicates a hypercoagulable state.Finding superficial vein thrombosis in multiple, non-contiguous locations.

Study optimization

TopicStudy ApproachPriorityResources
Social Services ReportingMemorize the correct agency based on age group (Child vs. Elder).High (Board trap question)Review guidelines for CPS/APS; practice vignettes.
GI Motility DisordersCreate a differential table comparing mechanism, physical exam findings, and initial treatment.Medium-HighFocus on manometry results and classic signs (e.g., bird's beak).
Neurodegenerative DiseasesUnderstand the pathology (plaques/tangles, Lewy bodies) rather than just the name of the disease.High (Derivative question focus)Use flowcharts to link underlying pathology -> clinical presentation.

Question pattern recognition

  • Pattern: Elderly patient with unexplained injuries and poor nutrition -> Suspect Elder Abuse; contact Adult Protective Services (APS) .
  • Pattern: Dysphagia for both solids and liquids, "bird's beak" sign on swallow -> Achalasia; next step is manometry/dilation.
  • Pattern: White matter lesions in an immunocompromised patient -> Suspect PML; requires high suspicion of JC virus reactivation.

Test yourself

Common mistakes to avoid

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Mistake 1: Confusing APS and CPS. Remember that age dictates the reporting agency (APS for elderly, CPS for children).
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Mistake 2: Assuming all hypercoagulable states are due to Factor V Leiden. While it is a cause, malignancy, nephrotic syndrome, and HIT are equally important triggers.
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Mistake 3: Misinterpreting PML pathology. Do not just say "white matter lesion"; specify that the target cell is the oligodendrocyte and the agent is the JC virus .

Common traps

⚠️
Trap 1 (GI Motility): Assuming GERD means LES failure. Remember, GERD involves transient relaxation , while Achalasia is a permanent functional obstruction .
⚠️
Trap 2 (Hypercoagulability): Choosing Warfarin for cancer patients. The risk of bleeding and the need for rapid reversal makes LMWH/Heparin superior choices.
⚠️
Trap 3 (Neurobiology): Confusing the pathology in PML (oligodendrocyte destruction) with general white matter demyelination seen in MS or other conditions.

Original transcript with highlights

Original transcript with highlights

Okay, welcome. My name is Divine. This is episode 403 of the Divine Intervention podcasts. And in this podcast I am going to be continuing the Rapid Review series for the USMELY step 2 CK and step 3 exams. Obviously this is also going to be helpful for people taking complex level 2 or 3 and this is going to be series 79. And just by a well-verminder if you're taking your USMELY exams anytime soon. I have a few courses that you may find to be helpful. I have an MBME Test Ticking Strategy course. It's going to be taking place next week Friday. That's the 22nd of July from 5 to 7 30 PM Pacific Standard Time. I've had lots of people take these courses and they've done really well on their tests. And then I also have a 20 hour review course. We go over internal medicine, PEEDS, OBGYN, psych, neuro, biostatistics, ethics, multi-system processes and disorders, communication, healthcare systems. Again many people have taken these courses. I've seen I get emails especially on Wednesday. Oh Divine, my 10 day of your course, my scores jumped 30 points. My scores jumped 40 points. I got in the 260s. Definitely this past week and I'm really grateful for it. I've got in emails from tons of people that got in the 260s on their exams. And these were people that took my course in one way or the other. And then I also have an MBME Biostatistics Slash Epidemiology bootcamp. It's going to be taking place on the 21st of July from 4 to 8 PM Pacific Standard Time.

Okay, from 4 to 8 PM Pacific Standard Time. Biostatistics is not a memorization B-science. It's a very conceptual science. So to get that, those concepts down, understanding has to be there. Most questions on MBME exams these days for biostatistics are not plug and chow do your math based. Their modules for reasoning based. So the class is going to be centered around using scenarios to help you get your thinking on biostatistics and epidemiology in the right place. And the 20 hour review course I mentioned is going to be taking place the week after the after the 22nd. Right? So it's going to be taking place from the 25th to the 30th of July, although we won't meet on the 27th. So Monday Tuesday Thursday Friday and Saturday from 4 to 8 PM Pacific Standard Time. So that'll be like 7 to 11 PM Eastern Standard Time. So if you're interested, again, just shoot me an email. The courses are all held over Zoom and you can register and we'll take things from there. So what if they give you a question about like an 80, 70 year old woman, you know, the tell you that oh, she comes to the physician because she has abdominal pain. Right? And the tell you that, you know, she lives with her with her son and his family. And the tell you that, you know, she has all these abrasions on her skin and her BMI is like 17. And you know, when you ask her questions, she's very invasive and things like that. What should you think about? I really hope you're thinking about elderly abuse, okay?

Think about elderly abuse. Remember when the elderly are being abused, you need to call adult, adult protective services. You need to contact adult protective services. You may not see that as an answer, but you may see some answer about like social services of some sort. You need to go ahead and inform those people so that the person gets help, okay? You need to, you need to go ahead and inform. And another thing that's also helpful is obviously if you see a child with like red no hemorrhages, sub-dural hematomas, weird fractures, a child that just doesn't seem to be well cared for, you want to worry about child abuse. And again, for child abuse, you're going to contact child protective services. That's pretty high yield to know, right? Or you see a child that has an STI, you know, child that shouldn't be sexually active, like a 70-year-old girl with a trichomon ISS, or you see like a 70-year-old girl, and she has these advanced sexual knowledge. That's pretty worrisome, right? That's child sexual abuse. So again, you need to contact child protective services. Right? Remember, even one child ends by proxy, where the proxy is the child, where you're literally the adult and you're inducing, like, dying in the child, giving the child laxatives and stuff. This is a psychiatric disorder that the parents have, but they're literally negatively affecting the child's health. You're going to call child protective services in those circumstances on exams. Okay?

So remember, calling social services applies to kids and the elderly, okay? But, you know, young people, people that are like, oh, like in the 30s, and let's say, they're being abused by their partner. You don't really report to any social services. That's just, that's just it. That's more intimate partner violence. That's just it. Right? So you can offer counseling, make a safe keep plan, but really you can be calling adult protective services or child protective services when you're not dealing with a kid or an elderly person. And again, I know some people would be like, oh, they find, can you tell me a specific age? Again, certain things like that just are not particularly helpful on exams. The key critical thing to just know is they're going to make it pretty obvious. For person is in their 80s, they are an elderly person. If a person is like 10 years old, they're a child, right? Just again, just simple straightforward things. I feel like many times people try to over complicate the end being is more than they actually need to be overcomplicated. Now, what if they give you a question about a patient that has some kind of malignancy? Let's say they have like long cancer or something like that. And then you notice that they just die suddenly. You just notice that, wow, within a few minutes, boom, they die. What is the thing that likely kill them? I'll really hope you're saying, oh, divine. This person probably died of a PE of some sort, right?

This person probably died of a PE of some sort. When you see very sudden, rapid death in a person that has a malignancy of some sort, always think about a PE. Well, at least that should be one of the first things you think about. I think one thing people kind of ignore is that having malignancy makes you hyperquagulable, having malignancy makes you hyperquagulable. So many times people that have cancer, they need to be placed on heparin, right? Usually for cancer patients, you try to not give them warfarin on NV Me exams. You think more about heparin. You try to put cancer patients on heparin so that you can protect them from forming plots, okay? Because cancer makes you hyperquagulable, okay? So those people need to be on anti-quagulation. So they don't get dv Ts, they don't get P Es, they don't get some of these strokes, okay? That's something you really need to keep at the back of your mind on exams, right? So cancer patients can have lx-wellin, you see lx-wellin, especially like a unilateral lx-wellin with cancer patients, that's a dv T question right there, right? So many times tumors can elaborate chemicals and cytokines and substances that can trigger coagulation. In fact, there are certain tumors that are pretty famous for that, like a left-atomic soma. Those things, little parts can just fly off and go to the brain and include one of your cerebral vessels, you know, very commonly a middle cerebral artery.

So you're just going to keep that at the back of your mind, right? So again, heparin, especially low molecular weight heparin, it's pretty helpful in people that have a malignancy, right? And then just again, make sure you also know many of your other hyperquagulable disorders, right? So for example, they can give you a question about a person like a young male that has hematuria, that is worse in the mornings, has all these thrombotic episodes, right? You want to think about PNH. PNH is a hyperquagulable disorder. People that have proxysmal noxinohymoglobinuria, just because they have this constant inflammation in their bodies that renders them hyperquagulable, okay? That renders them hyperquagulable. Or they can give you a question about a person that has like generalized edema, but you see the creatinine is really high and you see them developing a DVTURPE, right? That's nephrodic syndrome. And bring nephrodic syndrome and even in nephrodic syndrome, it's not just obvious when you're losing your urine, you're also losing antithromic, three. An antithromic being three is a powerful inhibitor of factor two and factor ten, okay? It'll factor two and factor ten, right? So if factor two and factor ten are not being inhibited, they're going to be running a mock and you're going to have hyperquagulable problems. That's why sometimes when people have nephrodic syndromes and whatnot, it's usually like a smart idea to put those people on anticoagulition, okay?

So that they don't develop issues, right? And then also remember if a person has factor five lighting, where factor five is resistant to degradation, right? It just hangs around for longer. That can make you hyperquagulable, right? If you're a bedbound, if you just have surgery, especially orthopedic surgery, those things that are spread, those people are especially prone to developing hyperquagulable events, right? When you see a long car ride, long plane ride, again, think of hyperquagulable events, right? That's these things are again just all pretty high to know, for example, even hit, happening in the uterine beside opinea is a hyperquagulable disorder, right? Because you know, yes, you found these antibodies against hyperinamplicated factor four. Those antibodies literally depleted your pleaklets. So maybe like, oh, my pleaklets are depleted. So more at risk of bleeding, yes, you are, but you also have high risk of clotting. Because those activated pleaklets are literally available for forming, you know, primary humus, stasis pleated plokes and things like that. So that's why when people have hit, they really want to give them a factor two inhibitor, right? So something like a guttural band, or a big guttural, bivalryrdic. Pretty helpful in these folks, right? Pretty, pretty helpful in these folks, right? So again, don't forget, people that have cancer, people that have cancer, they're hyperquagulable, okay? People that have cancer, they're hyperquagulable.

And then, what if they give you a question about a patient and you tell you that this patient, you know, has this burning chest pain that is really bad at night and lot of nights, right? You see that? I really hope you're saying, we're dividing this person has a gird, right? This person has a gird. So when a person has a gird, again, the thing is our friends at the MBM Es, they are very big on pathophysiology these days because they know that we live in an on-key generation, do something I tell people during the MBME testing and strategies class. But they know that we live in an on-key generation. So a lot of people, all they're very good at is just memorizing stuff, they don't really understand what it means. So they wonder they're like, wow, divine. The MBM Es, they're testing stuff I've never seen before. That's not true, right? So don't get me wrong. To the MBM Es test is that people have never seen before. Yes. But many people, when they walk out of an exam, they're like, oh, we're divine. They tested it. Like 80% of the exam is not in this, it's not in that, that's our eye. That's not true, right? It's just literally not possible, right? It's literally not possible, right? What's the problem with the Morris and MBME exams? The Morris and MBME exams, the big massive problem for many people is that there's just, again, a pretty extensive use of derivatives, right?

Derivative, again, is something where it's something you know just placed in terms you may not be familiar with. The most effective strategy for dealing with derivative questions is the ability to understand pathophys. If you understand pathophysiology, you'll be very well suited for dealing with derivative questions because there'll be novel like terms, but you can usually see right through those terms if you have an understanding of the underlying pathologies. So I'll just strongly encourage you to just be memorizing things, make sure you actually understand what in the world you're trying to memorize. Because again, a good question, they know that everyone can decipher what good is. So what can they do? They can just ask you about the pathophys, and really the pathophys behind GERD is that your lower suffragesal's fencer is just too relaxed. It's because it's supposed to relax every now and then, right? But sometimes it just relaxes too much or relaxes at inopportune times. That's what causes people to have GERD, because they have reflux of stomach acid to their lower suffigas and then it burns their suffigas. So usually when a person has GERD, remember you're going to try a PPI, a proton pump inhibitor in these people, right? Try your proton pump inhibitor. Try your proton pump inhibitor. Try your proton pump inhibitor. Try it first. Although if you don't see a PPI as an answer, you can try a H2 blocker. That's also acceptable.

But try those, usually for most people, it results to your problems. But if it doesn't, and you've increased the dose, you're giving them a maximum PPI therapy, then you need to get an EGD with biopsy, right? You need to get an EGD, right? You don't even necessarily have to do a biopsy, but you need to do that EGD to confirm that what in the world is going on, right? And also sometimes it's also pretty helpful. If the EGD is negative to do the 24 hour, it's of a JLPH monitoring, okay? The 24 hour, it's of a JLPH monitoring, right? So that's like the Gold Standard test for diagnosis, GERD in a patient, right? That's the Gold Standard test. Although if you remember, if a person has GERD and you have alarm symptoms like odinophagia, or you notice that they're having like weak loss, right? Or they're old, right? Let's see, we've had GERD for like 20 years, they're like over the age of 50, right? Just tells you that, huh? When this person that has had like long-standing GERD, which we'll probably just kind of check them out for, S-O-V-G-L-N-O, of course, no, okay? So those are kind of important things to know. And again, since we're kind of talking about this, acid business, right? Let's look at some other pathophysiologies behind acid-based diseases, right? So, well, you know, it's so-for-jil-ish, stomache-ish problems, right?

So if they give you a question about a person that, you know, especially it's going to be usually a younger person, the Kant-Swallow liquids are solid very well, they're regurgitated and digested food and they're young, what should you be thinking about? I really hope you're saying, oh, divine, this person has ecalisia. Now, remember, we said that for GERD, you have in a appropriate relaxation of your lower sub-jil-sfincter. When you're dealing with ecalisia, here your lower sub-jil-sfincter does not relax, right? Because after you swallow your lower sub-jil-sfincter is supposed to relax so that food can go through, right? And go in all the way to the stomach. But if it feels to relax, that's ecalisia, right? That's ecalisia. That's ecalisia. That's ecalisia, right? That's the bird's beak sign, right? Or you see a person and you have this feature to both solids and liquids, right? But you'll give it this presentation that they seem to have like these anginous symptoms, these weird anginous symptoms that come in tremendously, right? And it may not necessarily be effort-induced. When you see that think about the fuses of a gel spasm, right? The fuses of a gel spasm, you know, most times those people, you have like spasm of the mid-a-soft August, right? So you can almost have like an angina-like presentation. Most of those people respond beautifully to nitrates, okay? They respond beautifully to nitrates, right?

Or you see a person and they have like ulcers in weird parts of their stomach, right? Like in the jajunam. Or you notice that people, these people just have like a lot of ulcers in the duodenum, right? Because usually for pressing aspect, ulcer disease, you know, feel ulcers here and there. But if you see multiple ulcers, so many ulcers in the duodenum, that's not normal, right? This person has a gastronoma. They have a zoological elicin syndrome. And you know, you'll probably be prudent if a person is diagnosed with zoological elicin syndrome. So probably screen them for a meningin mutation. They probably have MEN1. Because remember, in MEN1, they have a thyroid problem, so they can have hypercalcemia. They can have pituitary adenomas, especially like prolectinomas. But they can also have pancreatic neuroendocrine tumors, like gastronomas, which you should have PPI, so glucadonomas. Don't forget your necrolitic migratoryory thema. Or you can have insulinomas, right? Where they have whipols triad, right? Hypoglycemia, they have clinical signs of hypoglycemia. And you know, the symptoms get better when you give them glucose, continium substances. So that's something that's kind of high yield to keep in mind, or you see a person, and you know, they have like, like again, like peptic ulcer disease, right? We're usually going to be thinking about each pylori, each pylori infection. Remember, that absolutely cause people to have peptic ulcer disease, right?

But in gastronomas, remember, you're making a lot of gastric. Gastric is one of the things that stimulates your parietal cells, because stimulator parietal cells, and those parietal cells within me get ton of acid, right? So you have peptic ulcer disease. And gastric ulcer stimulates your enterochromophine-like cells. Enterochromophine-like cells, they make histamine. So if they make histamine, histamine is a very powerful stimulant of your parietal cells, and that's going to cause you to make a ton of acid as well, right? So those are the two key primary mechanisms that gastrin uses to raise your gastric acid, right? Again, these are all things you kind of want to make sure you know for, you know for, for exams. And then, what if they give you a question of on a patient, and you tell you that this man, he's 75 years old, you know, he's been falling over every now and then, he's having trouble finding motor activity, and you tell you that he has seborrheedermatitis, what are you thinking about? This guy has Parkinson's, right? This guy has Parkinson's. Remember, both are have Parkinson's. The problem is they have a dopamine loss, right? They don't have an off-dupamine, right? So why don't they have an off-dupamine? They don't have an off-dupamine, because the substantioneigrioparous compacta just does not work, right? Just does not work. And again, the mbim is know that most people know about this whole deep pigmentation of the substantioneigri.

Do you know the people that people know that? And that's fine. That's fine. That's that's not a problem. That's not a huge deal. But one thing that's also kind of helpful to know is that if you biopsied those people's substantioneigri, that's probably something a dupe-post-mortem when they're dead. Now you're going to see Louis buddies, or you're going to see Louis buddies in the substantioneigri. When you see Louis buddies in the substantioneigri, you're dealing with Parkinson's disease, right? So remember, Louis buddies, you can find them in Parkinson's disease, but you can also find them in Louis buddy dementia. Remember, Louis buddy dementia is one of these Parkinson's plus syndromes, right? But what if they give you a question about a person, and they tell you that this person has like really bad HIV, and they tell you that for the past few weeks, they be having like, altered mental status, they be having like, progressive weakness and things like that. And then they tell you that, oh, you get an MRI of the brain, and you see like lesions all throughout the white matter. That's all you need. That person has a GC virus infection, right? They have progressive multifocal, luchoencephalopathy, progressive, multifocal, luchoencephalopathy. That's what's known as PML, okay? That's what's known as PML.

Remember, it's caused by the GC virus being reactivated, pretty common in HIV patients, where you can also find it in MS patients, you know, taking that at a lesion map, MS patients taking a not at a lesion map, okay? That's a monoplonal antibody against the integrates. It's a drug that can raise your risk of progressive multifocal, luchoencephalopathy. So again, you know, many people know GC virus reactivation, blah, blah, blah, blah. But again, what can be a derivative question that the NBME throws at you? Well, they can give you some question about, they can give you a question. You're reading the question, you know it's PML, you know it's GC virus. But then you don't see PML as an answer, you don't see GC virus as an answer, you don't see anything involving white matter as an answer, right? But then they decide to throw in something about oligodendrocytes, right? They decide to throw in something about oligodendrocytes. That's a derivative answer. That's what I'm trying to get at here, right? They throw in something about oligodendrocytes and people are like, wow, divine. This stuff I saw in the NBM Es I've never seen it before. Well, that's just because the understanding is not there, right? Again, I'm telling you, as you're memorizing things, make sure you're understanding it. That's one thing I try to do in my 20 hour courses, where I'm not just going to be throwing facts at you.

No, I'm going to make sure you understand stuff because that's the thing that will ultimately help you on exams, okay? That's the thing that will ultimately help you on exams. That's the thing that will ultimately help you on exams. So these people, right? What's the path of this behind PML? The thing is the GC virus will reactivate within your oligodendrocytes. If you reactivate within your oligodendrocytes, your oligodendrocytes will not work, okay? Because remember, your oligodendrocytes, they're supposed to, or they won't work well. They're supposed to help you mainly meet in the central nervous system, right? So again, you're going to see inclusions actually. If you were biopsy like the white matter or a person with PML, you're going to see inclusions of the virus within your oligodendrocytes, right? And don't forget the other key oligodendrocyte-related disease, right? MS. MS is a central demyelinitine disease, so your oligodendrocytes will be affected, okay? That's why again, you're going to see white matter changes on MR Is, usually T2-weighted imaging. You don't need to worry about that specific detail, right? But contrast that with Guillain-Barré syndrome that's more of a peripheral demyelinitine disease, so it's your shuan cells that are messed up, okay? Not your oligodendrocytes. And if you really think about it, there's a reason why people that have MS, they have a lot of cranial nerve two problems, right? Have you ever wondered why that's the case?

The thing is all your cranial nerves are part of your peripheral nervous system, except cranial two. A cranial two is actually derived from the dying cell phone, right? So because cranial two is not from your peripheral nervous system, it is it is mildly needed by oligodendrocytes, right? So when you have oligodendrocyte problems, like you do in multiple sclerosis, like your oligodendrocyte proteins or whatever are messed up, then you're going to have issues with with optic neuritis, for example, right? So just going to keep that kind of keep that stuff in mind or like internally up pharmacoplasia, these are all nerve pathways that are mainly needed by oligodendrocytes, okay? That are mainly needed by oligodendrocytes, right? Or again, let's maybe do a few more of these brain related derivative questions, right? Or they can give you a question about a person in 40s, they tell you that is that died at 49, but now he's having peripheral movements at these early 40s, what's going on? That's that's haunting tense, right? Remember, haunting tense, what's messed up? It's the codic nucleus, it's the codic nucleus, right? They have atrophy of the codic because they're literally losing those neurons, they're literally losing those neurons in the codic, right? Or they can even give you a question about a person that has Down syndrome, you know, they are becoming forgetful, you know, they are needing help with activities of daily living, right?

That's Alzheimer's, but again, what's happening in Alzheimer's? Alzheimer's is because you have these bidameloid plaques and these neurofibularity tangles, right? Within the neurons of the cortex, right? The thing is those neurofibularity tangles remember, they're their tau protein, normally tau protein, what it does is it helps you stabilize your microtubules, it has so sheet with microtubules, but when people, so tau is actually pretty normal in the brain, but you know, when people have Alzheimer's, sometimes they just have problems with their tau proteins and those tau proteins just disengage from the microtubules and then the tau proteins start coming together, they start forming aggregations and then that's how those people get in trouble, right? And then it begins to cause those codic neurons to begin to die and then those people have like atrophy of their cortex and things like that, right? Remember, they can even give you like an imaging question about an Alzheimer's patient and you notice that while the eventacles are pretty big and then you're like, hmm, why the eventacles big? Do they have hydrocephalus? No, they don't, they don't have a true hydrocephalus, they have something we call hydrocephalus, ex-vakua, hydrocephalus, ex-vakua, right? V-A-C-U-O, so, so hydrocephalus, X-E-X, then vaco, right? V-A-C-U-O, right?

So the thing is, I just kind of think of it as the neurons are getting smaller, they're getting lost, so it's almost like there's more space for your ventricles, so your ventricles are going to kind of spread out, so your ventricles look a little larger, right? Again, these are all things, they are all related to a classic pathology, Alzheimer's, but they are all derivative things you could see on an example. This is going a little long, so I'm going to stop shortly here, right? Or you see a person that has like HIV dementia or something like that, and then they say, oh, and they say the person dies, and then they say you're doing a knot-topsie, what are you going to find? Well, think about it, remember HIV, HIV, loves to go after immune cells, right? Well, it's like the big immune cell that you'll find in the central nervous system, it's your microglia, right? So your microglia, they're going to have all these modules and them, you're going to see all these more time-uclideate giant cells in your brain in a person that has HIV, okay? You've got to see your microglia being affected, and you'll see your microglia form, you know, you see all these more time-uclideate giant cells. I remember multi-glute nucleotide giant cells are basically like buns of macrophages. Well, guess what? The macrophage of your central nervous system is your microglia, okay?

So again, you may be wondering, wow, they're fine, so they can test HIV with microglia, they absolutely can, they absolutely can, so just make sure I'm just begging you, please, I don't like when people don't do well on exams, I don't like when people don't do well on exams, I'm begging you, just make sure you know your concepts, right? You can memorize, you can use Anki and everything, Anki is amazing, right? But just make sure, as you're making those Anki cards on buzzwords and whatnot, make sure you understand what in the world those buzzwords mean, that's very important, that's very critical for your success, I'm telling you, that's one of the most common reasons why people feel you are semilies, is not because they don't use Anki enough or they didn't do enough practice questions, it's just they don't have understanding, they don't have understanding, so they can see things in multiple dimensions. So I'm going to go ahead and pause here today, I do offer one on one tutoring, and I'm going to talk about a life lesson at the end actually, but let me see some things real quick first, right? So I do offer one on one tutoring for step one to step three, complex level one to three, the only thing I don't do there for, you know, OMM, I don't really tutor to OMM, I won't do this thing called longitudinal tutoring, where I work with people all through their first two years of med school, or their third year of rotations and curse ships I tutor them for their shelf exams.

Usually, by the time it comes around for those people step one exams or step two or step three exams, they feel super, super comfortable, because I will really on content, I will really on test taking strategies, I like using NBM questions to teach people the material and to teach them how to take NBM tests. And then I have these podcasts on Apple podcasts on Google podcasts and Spotify, at least the most recent 150, if you want everything from episode one, just go on the website, devineinterventionpodcast.com. If you actually have a Word Press account on your subscribe to my podcast with that, you'll get an email notification whenever I make a new podcast. And then I also help with your applications, right? So I've done this for years, there are many people that have worked with that are now attendants, people have worked within competitive specialties all over the country, California, New York, Boston, I've worked with people from many places, many disciplines, Durham, orthopedes, IAM, neurology, site, ENT, worked with tons and tons and tons of people, right? So I help with personal statements, rec letters, errors, applications, the supplemental application, mock interviews. So if you're interested in any of those things, just shoot me an email through the website and I'll point you in the right direction. And then I also have a You Tube channel, devineintervention, USMLE podcast and videos.

Again, I am going to mix some changes on the You Tube channel very soon to increase access to my podcasts. So be on the lookout for that. Just subscribe. Again, that little bit of support certainly helps. Devineintervention, USMLE podcast and videos. Devineintervention, look for that specifically because, they are fake out You Tube channels, but look for devineintervention, USMLE podcast and videos. That's where I put all the videos and stuff that I make. I'm going to be doing over the next few few weeks here. And then I also have a website, a new website called devineintervention, lifelessons.com. That's where I post the life lessons that I make. Many people say they love my life lessons. Many of you know I'm a Christian. So I said I'll make another website, just they would it specifically to life lessons that are based on the Bible. Most of the podcasts are like 10 to 15 minutes long. And I make like two every week. We have about 99 episodes right now. I even have a podcast on that on an Apple podcast. It's called the devineintervention life lessons podcast. So you know, hit that website up. You're going to find a lot of stuff there that's that's going to be pretty, pretty helpful. So I just have a quick life lesson today. That's the importance of being prepared. That is the importance of being prepared. The thing is, I'm telling you, many people try to wing it through life. And then they wonder why they're not successful. Right?

You can know the best way to approach life is to approach life prepared. The thing is, can you prepare for every scenario you see? No. What the fact that, oh, you may not be prepared for every scenario you see. There's nothing you should not be prepared. Okay? You see many people, they go into USML exams, they go into patient presentations, they go into things in the third year with no level of preparation. And then they wonder why they're getting poor results. The thing is, when you're prepared, when opportunity arises, you can take advantage of it. That's the truth, right? So I'll just encourage you today. Be prepared. You will gain a lot more from life when you are prepared. You get a lot more from life. You will take advantage of more opportunities when you're prepared. Sometimes preparation may seem useless. It may seem like, wow, why am I wasting all this time to get nothing done? Why am I wasting all this time? But sometimes that preparation you do can speak for you like 10 years down the line. You may just notice that, wow, this thing I really prepared for like 10 years ago. An opportunity just shows up that you're able to take advantage of very quickly because you were prepared. Right? If you look at the Bible, like Joseph and the Egyptians, they were ready for the famine that happened. Why? Because they were prepared. I'm telling you, many times people struggle through life just because they're not prepared. They're not prepared. Right?

Like, for example, you see people, they're, oh, they're USML exams coming up in a month. And that's when they start preparing. They're like, oh, my preparation is going to start doing my dedicated period. You're going to put yourself in a tough spot. Right? Where were all the years you spent during your preclinicals? What were you doing? What were you doing? What were you doing? Were on social media? You were watching a lot of streaming services? What were you doing? I'm not saying those things are bad. Where you've got to leave your life in balance. You need to prepare. You need to prepare. Right? You need to prepare. Or you're going through your third, like, let me tell you this, success on USML exams. I'm not determined by how well you use your dedicated period. They're determined many times by your habits before your dedicated period even starts. Right? Again, when you just make good decisions earlier on in life, right? Then your life is going to be good. Right? When you see, for example, like your physician, right? And at least you earn a descending comment. You earn a descending comment. And then you're just blowing it on this and that and this and that and this and that. And you don't plan for the future. Right? You can't work forever. That's the truth. Right? You got to plan for your future. So I'm telling you this. Again, I don't mean to sound harsh, but guys and girls listen to this podcast. You got to prepare. You got to prepare. Right?

Most good things, what many good things will come to you when you're prepared. Right? You don't prepare for the future when the future is arrived. You prepare for the future before the future arrives. So I'm encouraging you, prepare it and all be well. We feel. Until the next podcast have a wonderful weekend. God bless you. Thank you.

Practice questions — USMLE style

Question 1 — Hematology/Internal Medicine

A 68-year-old man with a history of metastatic lung carcinoma presents to the emergency department after collapsing suddenly. Initial workup reveals no obvious cardiac cause for death. Given his underlying malignancy and sudden demise, which complication is most likely responsible for his acute death?

  • A) Acute myocardial infarction due to hypercoagulability
  • B) Pulmonary embolism (PE) secondary to venous stasis
  • C) Disseminated intravascular coagulation (DIC) triggered by tumor lysis
  • D) Thrombotic microangiopathy caused by cytokine release

Answer: B. The transcript emphasizes that malignancy makes a patient "hyperquagulable," and when sudden death occurs in such a patient, one must always think of a Pulmonary Embolism (PE). Cancer can trigger coagulation cascades, leading to venous thromboembolism (VTE) like DVT or PE. Therefore, prophylactic anticoagulation (e.g., LMWH/Heparin) is standard care for cancer patients due to this increased risk. While DIC and MI are possible complications of malignancy, the most direct and emphasized high-yield concern regarding sudden death in a hypercoagulable patient is PE.

Question 2 — Neurology

A 45-year-old man with advanced HIV presents with progressive weakness, altered mental status, and signs of white matter lesions on MRI. The infectious workup is negative for common pathogens. Based on the clinical presentation and imaging findings, what is the most likely diagnosis?

  • A) Multiple sclerosis (MS), due to demyelination in the CNS
  • B) Creutzfeldt-Jakob disease, given rapid cognitive decline
  • C) Progressive multifocal leukoencephalopathy (PML), caused by JC virus reactivation
  • D) HIV encephalopathy, resulting from direct viral neurotoxicity

Answer: C. The transcript specifically details that PML is a common and high-yield complication in advanced HIV. It is caused by the reactivation of the John Cunningham (JC) virus, which infects and damages oligodendrocytes within the white matter of the central nervous system, leading to progressive multifocal leukoencephalopathy. While MS also causes demyelination, PML is directly linked to JC virus reactivation in immunocompromised states like advanced HIV.

Question 3 — Gastroenterology

A 25-year-old man presents with chronic dysphagia that affects both solids and liquids. On physical examination, he has a history of regurgitation of undigested food. Endoscopy reveals a "bird's beak" appearance at the gastroesophageal junction (GEJ). What is the underlying pathophysiological mechanism causing this patient’s symptoms?

  • A) Transient relaxation failure of the lower esophageal sphincter (LES)
  • B) Increased acid secretion due to gastrin-stimulated parietal cells
  • C) Failure of the LES to relax upon swallowing
  • D) Chronic inflammation leading to stricture formation at the GEJ

Answer: C. The "bird's beak" sign and dysphagia affecting both solids and liquids are classic signs of achalasia. Pathophysiologically, achalasia is characterized by the failure of the lower esophageal sphincter (LES) to relax properly when swallowing occurs. This contrasts with GERD, where the issue is often related to inappropriate relaxation or a weak LES.

Question 4 — Nephrology/Internal Medicine

A 55-year-old woman develops generalized edema and signs of nephrotic syndrome. She presents with new-onset deep vein thrombosis (DVT) in her calf. Given the underlying renal pathology, what is the primary mechanism contributing to her increased risk of thrombotic events?

  • A) Decreased synthesis of anti-thrombin III by the damaged kidney
  • B) Increased activation of Factor VIII due to chronic inflammation
  • C) Elevated levels of procoagulant factors like fibrinogen
  • D) Direct deposition of immune complexes leading to vasculitis

Answer: A. The transcript highlights that in nephrotic syndrome, not only is urine loss occurring, but there is also a significant loss of antithrombin III (ATIII). ATIII is a powerful natural anticoagulant inhibitor of Factor II and Factor X. This depletion leads to an overall hypercoagulable state, making the patient prone to DVT/PE.

Quick fire review

What is the key difference between GERD and Achalasia pathophysiology?

In GERD, the LES relaxes too much or at inopportune times; in Achalasia, the LES fails to relax completely.

When evaluating a patient with suspected child abuse, what specific agency should be contacted?

Child Protective Services (CPS).

What is the primary concern for anticoagulation when managing a patient with an active malignancy?

The malignancy makes the patient hypercoagulable, increasing the risk of DVT/PE.

If you see multiple ulcers in the duodenum and suspect MEN1 syndrome, what specific tumor types should you screen for?

Gastrinomas (leading to Zollinger-Crlitz syndrome) and insulinomas.

What is the most common finding on post-mortem biopsy of a patient with Parkinson's disease?

Lewy bodies in the substantia nigra.

Which type of demyelination affects the peripheral nerves, involving Schwann cells?

Guillain-Barré Syndrome (GBS).

What is the primary concern when seeing sudden death in a patient with known malignancy?

Pulmonary Embolism (PE), as malignancy causes hypercoagulability.

Which specific type of inhibitor should be given to patients with Heparin-Induced Thrombocytopenia (HIT)?

A factor II inhibitor (e.g., argatroban).

What is the name for the condition where a patient has multiple ulcers in the duodenum and jejunum, often associated with MEN1?

Zollinger-Crlitz syndrome (due to gastrinomas).

In PML, which virus reactivates, and what cell type does it primarily infect within the CNS?

JC virus; Oligodendrocytes.

What is the key difference in pathology between Multiple Sclerosis (MS) and Guillain-Barré Syndrome (GBS)?

MS affects myelin around axons in the CNS (oligodendrocytes); GBS affects peripheral nerves (Schwann cells).

Which specific finding, when seen on post-mortem biopsy of the substantia nigra, confirms a diagnosis of Parkinson's disease?

Lewy bodies.

Quick recall / Anki-style questions

What is the primary concern when seeing sudden death in a patient with known malignancy?

Pulmonary Embolism (PE), as malignancy causes hypercoagulability.

Which specific type of inhibitor should be given to patients with Heparin-Induced Thrombocytopenia (HIT)?

A factor II inhibitor (e.g., argatroban).

What is the name for the condition where a patient has multiple ulcers in the duodenum and jejunum, often associated with MEN1?

Zollinger-Crlitz syndrome (due to gastrinomas).

In PML, which virus reactivates, and what cell type does it primarily infect within the CNS?

JC virus; Oligodendrocytes.

What is the key difference in pathology between Multiple Sclerosis (MS) and Guillain-Barré Syndrome (GBS)?

MS affects myelin around axons in the CNS (oligodendrocytes); GBS affects peripheral nerves (Schwann cells).

Which specific finding, when seen on post-mortem biopsy of the substantia nigra, confirms a diagnosis of Parkinson's disease?

Lewy bodies.