DIP Episode 128 - USMLE Step 2CK Rapid Review Series 9 (IM) and a small update on the newer Step 2CK Questions
Topic
Multiple Myeloma; Acute Leukemias (ALL, CLL, AML); Systemic Vasculitis (GPA vs MPA); Scleroderma; Cardiac Murmur Workup.
Key Takeaway
The USMLE Step 2CK emphasizes pattern recognition and differential diagnosis across multiple systems, requiring students to synthesize findings from hematology, rheumatology, and cardiology rather than simply recalling isolated facts.
Episode Notes
Source / episode info
- Episode: 128
- Published: 2019-07-28
- Source: Episode page
One-liner
This episode reviews high-yield patterns in hematologic malignancies (Myeloma, Leukemia), systemic vasculitis (GPA/MPA), connective tissue diseases (Scleroderma), and cardiac physical exam findings, emphasizing differential diagnosis over rote memorization.
High-yield summary
- Multiple Myeloma: Classic triad includes hypercalcemia, renal insufficiency, anemia, and bone pain due to osteoclast activation; lytic lesions are common. The mnemonic for associated cancers causing lytic lesions is L-T-R (Lung, Thyroid, Renal) + Multiple Myeloma.
- Acute Leukemias: Remember the age extremes: ALL in childhood/young adults; CLL in elderly patients. Smudge cells are pathognomonic for CLL.
- CML Management: CML is associated with the Philadelphia chromosome ({t}(9;22)) and BCR-ABL fusion protein, treated with a tyrosine kinase inhibitor (TKI) like Imatinib.
- Vasculitis Differentiation: Granulomatosis with Polyangiitis (GPA) is strongly associated with c-ANCA positive findings. Microscopic Polyangiitis (MPA) and other ANCA vasculitides are typically p-ANCA positive.
- Scleroderma Diagnosis: The limited form is characterized by the CREST criteria (Calcinosis, Raynaud's phenomenon, esophageal dysmotility, Sclerodactyly, Telangiectasia). Anti-centromere antibodies are associated with the limited form.
- Cardiac Murmur Workup: Any systolic murmur 2/6 or any murmur needs workup (Echo), unless it is a very faint systolic ejection murmur (1/6).
Learning objectives
- Differentiate between various acute and chronic leukemias based on age of onset, peripheral smear findings, and immunophenotype.
- Apply the mnemonic L-T-R to identify potential sources of lytic bone lesions in multiple myeloma.
- Distinguish between primary systemic vasculitides (e.g., GPA vs MPA) using specific ANCA antibodies and clinical presentations.
- Recognize the key features and associated antibodies for limited versus diffuse cutaneous systemic sclerosis.
- Interpret physical exam findings, particularly cardiac murmurs, to determine the necessity of advanced imaging (Echo).
Board exam buzzwords
| Condition | Key Finding | Association | Board Exam Tip |
| Multiple Myeloma | Lytic bone lesions; Hypercalcemia | Osteoclast activation; Plasma cell proliferation | Remember the mnemonic: Lung, Thryoid, Renal + MM. |
| Chronic Lymphocytic Leukemia (CLL) | Smudge cells on peripheral smear | Age-related accumulation of mature B-cells | CLL is an "old person's disease." |
| Granulomatosis with Polyangiitis (GPA) | c-ANCA positive; Sinusitis, Hemoptysis | Type III hypersensitivity reaction | GPA classically involves the upper airways. |
| Limited Systemic Sclerosis | CREST criteria; Anti-centromere antibodies | Calcinosis, Raynaud's, esophageal dysmotility, Sclerodactyly, Telangiectasia | The anti-Scl-70 antibody is associated with the diffuse form. |
Rapid review table
| Topic | Key Point | Context | Exam Relevance |
| Multiple Myeloma | Plasma cell infiltration of bone marrow; Lytic lesions | Hypercalcemia, renal failure, anemia (CRAB criteria) | Must differentiate from other causes of lytic bone disease. |
| CML | {t}(9;22) translocation; BCR-ABL fusion protein | Chronic myeloproliferative disorder; progressive phase | Treatment is a TKI (Imatinib). |
| GPA vs MPA | GPA = c-ANCA positive; MPA/other = p-ANCA positive | Systemic vasculitis presenting with glomerulonephritis and airway disease. | Knowing the specific ANCA type helps narrow the diagnosis significantly. |
| Scleroderma Crisis | Vasospastic episodes (Raynaud's); Scleroderma Renal Crisis (SRC) | Anti-centromere/Anti-Scl-70 antibodies; Fibroblast dysregulation | Avoid vasodilators and Triptans during crises due to risk of vasospasm. |
Board-speak -> diagnosis
| Board-speak / Vignette phrase | Diagnosis / Concept | Why it fits |
| Elderly patient with pancytopenia, dry tap on bone marrow aspiration, and history of myeloproliferative disorder. | Primary Myelofibrosis (PMF) or Aplastic Anemia | Dry tap suggests fibrosis/replacement; PMF is a key differential for this triad. |
| Young child presenting with fever, weight loss, and positive T-cell immunophenotyping on flow cytometry. | Acute Lymphoblastic Leukemia (ALL) | ALL is the most common childhood leukemia, often associated with Down syndrome. |
| Middle-aged man with elevated WBC count, smudge cells on smear, and recurrent infections. | Chronic Lymphocytic Leukemia (CLL) | CLL is characterized by mature B-cell accumulation, typically seen in older adults, and smudge cells are classic findings. |
| Patient presenting with hemoptysis, sinusitis, and glomerulonephritis; c-ANCA positive. | Granulomatosis with Polyangiitis (GPA) | GPA classically presents with upper airway/sinus involvement and is associated with c-ANCA antibodies. |
| 35-year-old female with Raynaud's phenomenon, esophageal dysmotility, and anti-centromere antibodies. | Limited Systemic Sclerosis (CREST Syndrome) | The constellation of symptoms and specific antibody profile define the limited cutaneous form. |
| Patient presenting with a systolic murmur 2/6 at the apex during an annual physical exam. | Mitral Stenosis workup required | Any significant or concerning murmur requires further investigation, typically starting with TTE (Transthoracic Echocardiogram). |
Differential diagnosis / distinguishing features
Dry Tap on Bone Marrow Aspiration
| Key Features | Distinguishing Findings | Next Step |
| Primary Myelofibrosis (PMF) | Pancytopenia, dry tap; Often associated with a myeloproliferative disorder. | Rule out other causes of marrow failure/fibrosis. |
| Aplastic Anemia | Pancytopenia, dry tap; Bone marrow hypocellularity. | Determine underlying cause (e.g., nutritional deficiency). |
| Osteosclerosis/Infection | Localized bone pathology or infection. | Perform appropriate imaging and cultures. |
Cardiac Murmur Workup
| Key Features | Distinguishing Findings | Next Step |
| Systolic murmur 2/6 (or any murmur) | Suggests structural heart disease; Mitral Stenosis often presents with a diastolic rumble and opening snap. | Transthoracic Echocardiogram (TTE) is mandatory. |
| Faint systolic ejection murmur (1/6) | Usually benign; Low suspicion of significant valvular pathology. | Reassurance, but always consider the patient's risk factors. |
Management pearls
- For suspected Multiple Myeloma, perform SPEP and UPEP to look for a monoclonal spike (M-spike). A bone marrow biopsy showing >10\% plasma cells is required for diagnosis.
- In CML, the \text{t}(9;22) translocation leads to BCR-ABL protein, which must be inhibited by TK Is like Imatinib.
- When managing scleroderma renal crisis (SRC), Angiotensin II Receptor Blockers (AR Bs) or Endothelin Inhibitors are preferred agents over vasodilators due to the risk of inducing further vasospasm.
- If a patient has an asthma history, avoid adenosine analogs (e.g., Regadenoson) and nonselective beta-blockers during cardiac stress testing due to risks of bronchoconstriction/bronchospasm.
Don't miss
Integration & clinical reasoning
OMM / COMLEX integration
- Hematology -> Nephrology: Multiple Myeloma causes kidney failure via light chain deposition (cast nephropathy).
- Rheumatology -> Pulmonology/Nephrology: Systemic Sclerosis can cause pulmonary hypertension and renal crisis (SRC).
- Immunology -> Airway/Kidney: ANCA vasculitides target small vessels, causing glomerulonephritis (nephritic syndrome) and often affecting the sinuses/airways.
Concept connections / cross-references
- For detailed review on connective tissue disorders and their specific antibodies: [Link to Scleroderma Episode]
- For comprehensive coverage of hematologic malignancies and bone marrow pathology: [Link to Hematology Episode]
- For general principles of vasculitis classification and management: [Link to Vasculitis Episode]
High-yield association table
| Condition | Association | Mechanism | Clinical Significance |
| Multiple Myeloma | Lytic Bone Lesions | Osteoclast activation by plasma cells; Plasma cell infiltration. | Leads to CRAB criteria (Hypercalcemia, Renal failure, Anemia, Bone pain). |
| CML | Philadelphia Chromosome ({t}(9;22)) | BCR-ABL fusion protein creates a constitutively active tyrosine kinase. | Requires specific TKI therapy (Imatinib); prognosis improves dramatically with treatment. |
| GPA | c-ANCA positive | Autoantibodies targeting cytoplasmic components of neutrophils/granulocytes. | Strong association with upper airway involvement and necrotizing vasculitis. |
| Scleroderma | Anti-centromere antibodies | Associated with the limited cutaneous form (CREST). | Indicates a specific subset of systemic sclerosis requiring targeted management. |
Key terms glossary
| Term | Definition | Context | Example |
| Smudge Cells | Fragile, discoid lymphocytes seen on peripheral smear. | Chronic Lymphocytic Leukemia (CLL) | Pathognomonic finding for CLL; due to cell fragility during blood collection. |
| c-ANCA | Cytoplasmic anti-neutrophil cytoplasmic antibody. | Granulomatosis with Polyangiitis (GPA) | Highly specific marker for GPA, suggesting upper airway involvement. |
| CREST Syndrome | A limited form of systemic sclerosis defined by five criteria. | Connective Tissue Disease | Calcinosis, Raynaud's, esophageal dysmotility, Sclerodactyly, Telangiectasia. |
| BCR-ABL Fusion Protein | Abnormal protein formed by the {t}(9;22) translocation. | Chronic Myeloid Leukemia (CML) | The molecular target for tyrosine kinase inhibitors like Imatinib. |
Study optimization
| Topic | Study Approach | Priority | Resources |
| Hematologic Malignancies | Use algorithms: Age extremes, smear findings, and specific translocations/antibodies. | High | Review flowcharts comparing ALL vs CLL vs AML; memorize the L-T-R mnemonic. |
| Systemic Vasculitis | Focus on ANCA specificity (c-ANCA -> GPA) and clinical presentation (airway involvement). | Medium-High | Create a comparison table of vasculitides, linking symptoms to antibodies. |
| Cardiac Murmur Workup | Apply physical exam rules: Use the murmur grade/type to determine if an Echo is needed; know stress test contraindications. | High | Practice interpreting murmurs and correlating them with underlying pathology (e.g., opening snap -> MS). |
Question pattern recognition
- The "Best Answer" Trap: In multiple choice questions, do not choose the answer that seems most obvious (e.g., just because there is bone pain, assume osteoporosis); instead, select the diagnosis that best explains all given lab and clinical findings (e.g., Multiple Myeloma).
- The "Age Extreme" Pattern: When diagnosing leukemia, always consider age: young -> ALL; old -> CLL.
- The "Specific Antibody/Organ System" Link: High-yield questions link specific antibodies to specific organ systems or diseases (e.g., Anti-centromere -> CREST).
Test yourself
Common mistakes to avoid
Common traps
Original transcript with highlights
Original transcript with highlights
Okay, welcome. My name is Devine. I am a PGUI Tour resident. This is the 128th episode of the Devine intervention podcast. And in this podcast, I will be continuing my rapid review series for the USM list of one exam. And my focus will be on internal medicine as that constitutes the bulk of the exam. But before I jump into the topic, I will just want to say a few words about the USM list of 2 CK. I've got a lot of emails recently about this and I've seen a lot of people comment on Reddit about how tough the new USM list of 2 CK exams are. So there are certain things I would say to that. The first thing I would say is if you in the process of preparing for your step 2 CK exam, right now a smart play is to strongly consider taking the new practice exams that have been released. So the new MBME 5s and 6s for the different disciplines, right? So like there is internal medicine, there is psych, there is neuro, there is peds, there is surgery, there is OB-GYN, right? I would strongly encourage taking those new exams. They are very close and very representative to what I suspect the MBME will throw on step 2 CK. That's one. Second thing I will say is I understand where you are coming from seeing the new exam is hard, right? The thing is, and again, like I remember back in the day, right, this was way back when I took step 2 CK. I remember that that exam was tough, right? It's not, basically if anyone tells you the USM list is easy, right? They are probably lying to you, right?
So I understand where you are coming from. The USM list is difficult, but here is one thing I would want you to keep at the back of your mind, right? You really need to understand that a lot of the difficulty, right? So the first thing is assuming that you have a good knowledge base, right? Again, I'm not saying this as a robot or anything like that, right? Again, at the end of the day, you do have to buckle down, put in work and study, right? But one thing you need to realize that the thing is, is not like, here we are having a few additions to knowledge every now and then and the MBME test this new concept and that new concept. But the one central thing I would really want you to realize is that the USM list in general, they tend to test the same array of things just in general. Again, I'm not saying this as like, oh, for sure, for sure, but just in general, right? It's not like the MBME suddenly decided, starting in the month of June, July to just completely change the exams that they throw out, right? Like to like completely source out new pulmonary knowledge, new cardiovascular knowledge, new renal knowledge and all that stuff and then test it on the exam. No, right? The only thing is the question styling, we have changed quite a bit, right? So I suspect, because again, I see this from the standpoint of, yes, obviously, there's no way I'm eligible to take the current USM list to CK's, I've taken that exam longer ago, right?
But I have other chance to, you know, review a lot of the new MBM Es with the students that I tutor and I can tell you that those questions are, they kind of have a different flavor to them. So the thing I will say is, when you review your MBME exams, don't just pay attention to the concepts that are being tested, pay attention to the principles behind how the MBM Es test questions, right? So this is something I tell the students that I tutor every time, right? It's not necessarily about the difficulty of the question. Again, assume your knowledge base is good. And again, there are good resources out there that you can use to build up your knowledge base. Assuming your knowledge base is good, it is really not the difficulty of the MBME questions that ends up mattering the most. The thing that ends up mattering is the way you approach the questions, right? So the thing is at the end of the day, right? There are principles that you sort of kind of need to follow. And these are things you can abstract as you, if you review your MBME exams thoroughly, there are just certain patterns that the MBME tends to follow in the way they work questions, in the way they demand answers, in the way they write answers that are right answers that are wrong. So this is something that in my experience, these are something that people don't devote as much time to question analysis. So that's one thing I would really want you to keep at the back of your mind.
I mean, like literally I tell my students like, guys, it's not necessarily the difficulty of the exam that matters at the end of the day. It's like just ask yourself, at this certain common rules that you should just follow in general as your answering MBME questions that would help you get this question right under whatever circumstance. And the thing is just in my tutoring experience, if you look at the old MBME questions, right? So the MBME ones and two that are no longer being sold and the current ones, the fives and sixes. Yes, the question difficulty may have changed, the question flavor may have changed, the question style may have changed, but for the most part, those MBME questions still will be certain core principles, like they are just certain. And I'm not necessarily saying like, or core principle in terms of knowledge, the test. It's just core principle in terms of how they test and how you should approach those questions. So I will encourage you spend good time do those new MBM Es, review them thoroughly, right? And as you're taking those exams, try to ask yourself, what are some key principles that the MBME details that like because again, this is something that comes with experience but I guess some key principles you can abstract that the MBME seems to be following this particular pattern in the way the word questions. If you can do that, that can make a very significant impact on how you do question wise.
So that is just the sidebar sort of wanted to talk about. But again, the big thing is, if you especially if you disregard the second part of what I said, try to take the new MBM Es, the fives and sixes. I do think that they are very high yield and they are very good questions that are somewhat representative of how the exam feel. Okay? So let's jump right into the content. So what if you get a question about like 70 year old female, she comes to a PCP, she says, I've been having like really bad shoulder pain for like the past week. And she tells you that over her left shin, right over extremities, she's been having all this pain. And you check the shoulder. So you check the shoulder that she's having pain with and you see like a step off or something, right? And then they tell you that you know, a vital signs are normal. You get some labs. You notice that a white cone is 8500. So that's normal, right? A hematocritic 28% that's slow, right? And then they give you a plate, let's 1, 92,000. Nothing major there. Sodium is 130. Potassium is 3.9. Chloride is like 100. calcium is like 12.7. So that's somewhat elevated, right? And her phosphorus is 2.6. Bun is like, let me make up some number like 40. And her creatinine is 3. Right? So that's quite elevated. So they tell you every other lab is unremarkable. Last pap smear was like, I don't know, like two years ago. And again, they tell you that she has no history of abnormal pap smear.
And you know, she follows her yearly screenings, preventive guidance, and didn't be asked, what's the next best step in management in this question? So all your next step in management before this person. The first thing I would encourage you to ask yourself is, what do you think this person has? So look at the things I highlight it. This person has bone pain, her creatinine is elevated. She has a low hematocritic and she has high calcium. What am I going after there? I'm going after multiple my Loma. Right? Multiple my Loma. Right? So obviously, you would want to perform your S-PEP and your U-PEP. Right? And say, for example, if your friends or the MBM wanted to mess with your head, right? They would potentially give you an answer choice that says, what is the, you want to do like a dual energy extra abs of chiametry, right? So like a dexascane, or they may give you an answer choice that involves giving a bisphosphonite. Right? Or they may say, oh, you know what go ahead and transfuse like Pact Red blood cells, right? Or they may say, you know what go ahead and give broad spectrum antibiotics. Right? So let me sort of focus on this kind of question and how you may approach it. Right? So because all these other answer choices like dexascane, those are things that the MBM, right? Just again, just based on again, my experience with tutoring and taking MBM exams, like those are potential answers that your friends at the MBM want to throw on a question. So think about it.
First things first, this woman's hemoglobin is 28%. So that means a hemoglobin is a little above nine. Remember your hemoglobin divided by three is roughly your hemoglobin. So this woman's hemoglobin is not less than seven. So it makes no sense to transfuse. With regards to the dexascane option, right? So the thing is you do a dexascane if you suspect the person has osteoporosis. But if you notice, most of the question, yeah, even if there is a part of the question that says this person has a palpable step off when you pop it, the left shoulder and all that, making you think of a fracture. You don't want to just use that as your only thing you're going off of to say, oh, you know, this is the right answer to the question, right? If you notice, most of the question seems to be pointed about these disparate things and of all of them, the thing that seems to match with most of the question, right, is multiple myeloma, right? So a dexascane will not be appropriate. That's a very good trick answer that the MBM could slot in on an exam, right? And then they may say like resedron therapy, right? Resedron it is again, for people that have osteoporosis, you've not confirmed that the person has osteoporosis, right? So again, at the end of the day, you shouldn't just jump straight to therapy. And again, if you get led astray that this question, so I imagine some people listening to this podcast, probably got led astray that, oh, palpable step off, old person, blah, blah, blah, right?
Maybe osteoporosis, but again, if you're listened to the rest of the question, right? Between osteoporosis and multiple myeloma, if you listen to all the question I give you, which one seems to have the most backup for it? It's multiple myeloma, right? So again, that's kind of like a way you want to think when you're approaching MBM questions. So this person, right, obviously has multiple myeloma, remember, multiple myeloma, right? You have like the classic crap symptoms, right? So like hypercalcemia, right? Because those plasma cells secret into looking one, and another thing for interlooking one is osteoclast activated in factor, so that can cause hypercalcemia, right? They have like renal insufficiency because remember, those like chains, right? Can deposit and scrub the person's kidneys. They can have an anemia because again, those cells are just proliferating and ticking over the bone marrow. So they have in efficient or hematopoesis, and then they typically have bone pain, right? From like pathologic fractures. And remember that multiple myeloma is an example of something that causes like lyrical lesions, right? What are the other, I mean, what are the other cancers that make cause lyrical lesions on an exam? It may be things like renal cell carcinoma, lung cancer, thyroid cancer, right? And breast cancer can also cause lyrical lesions, but it can also cause blastic lesions at the same time. And the way I remember what cancers secret what?
Like lyric, I remember the word, I remember the word litter, right? So like litter, like a cat litter, right? So the L, right, tells you lung cancer, the T tells you thyroid cancer, the R at the end tells you renal cell carcinoma, right? And then you just kind of have to remember that multiple myeloma causes are the lyrical lesions. And remember, multiple myeloma, right? They may have like a ru-low antibodies on a, I mean, ru-low, like a ru-low formation of the array blood cells when you do a peripheral smear. So that's kind of how you know, right? And then remember again, you do a bone marrow biopsy to make the diagnosis. I mean, to scream, you'll do your S-pep and your U-pep, you'll find a monoclonal spike, right? And then the next thing you want to do afterwards is to, you know, get a, get a bone marrow biopsy, you'll find that they have more than 10% plasma cells, and that helps you establish the diagnosis. Okay, so now let me talk about some pathonomonic findings in diseases. And then you tell me, I'll give you like a vignette and you tell me what you think is going on here, right? So let's, or you tell me like a diagnosis or something, right? So let's assume you have like a 65-year-old guy, right? Tells you that he has like, they tell you in the question like, or, I mean, they won't tell you he has pancidopenia. That's too easy, right?
One of your friends that the NBMU would do is they'll show you a CBC, you'll see that the person's plate count is like 50,000, their white count is like 2000, their hemoglobin is like 8. So that tells you that they have pancidopenia, everything is low. And then they tell you that a peripheral smear reveals like tear drop shaped red blood cells, right? So tear drop shaped red blood cells, or they literally show you like a slide, and you see like a red blood cell shaped like a tear drop. I believe those are known as dachro sites. I'll encourage you to look up a picture. What kind of hematologic problem does this person have? Well, I hope you're telling me about primary mylofibrosis, okay? That's a high-yield thing you want to keep at the back of your mind, okay? Now, what if you get a question about like, you know, like an if-something-yield female, you know, she has a six-month history, recurring infections, the tell you a white count is like 87,000, right? That's already abnormal. And then let's say that this person has like, again, very low hemoglobin, has very low platelet counts, and she's been, again, having a recurrent like pneumococcal infections, for example. What are you thinking about here? I really hope you're telling me about CLL, right? CLL, right? So chronic lymphocytic leukemia, and what is the pathonomonic cell that you may find on a blood smear? It's a smudge cell, right? It's a smudge cell, right?
So let me essentially give you guys a trick for getting these hematologic malignancies correct, right? I call this like the hematologic malignancy algorithm, right? So the first thing you want to remember is that the LL lie at the extremes of age, right? So LL is at the young extreme of age, CLL is at the old extreme of age, okay? And I mean, a kind of nice way to remember that is that A comes before seeing the alpha-better, so that's a nice way to think about that. And the LL is at the extreme of age, right? So if you see like a young kid, right? This young kid has like a fairly high white count, right? Like it'll be like a 5, 6, 7 year old on NBM is fairly high white count, and again, every other thing is low platelets, a low hemoglobin is low, right? Then you want to think about ALL, especially if it's a kid that has a history of Down syndrome. Remember Down syndrome is very common in kids that have, I mean, ALL is very common in kids with Downs, right? So if you see those things, you want to think about ALL, right? And ALL, because one thing that kind of messes with people's heads on examples is they think that ALL has to be a problem that has been brewing over a month. No, okay? ALL from symptom onset to death is actually a very short period. It's one of those diseases that if you don't nip it in the butt early, those kids can die pretty quickly.
So on NBM is you may see these people like they've gone from normal or they just tell you that over a couple of weeks they've been having symptoms. Don't be afraid to choose ALL. Again, especially if you see the classic presentation on them describing here. And then if you look at the other end of the spectrum CLL, if you essentially see a person that is young on your exam, they can't have CLL. I'll just tell you that right now. CLL on NBM is an old person's disease. It's something that shows up in people that are like in their 70s or 80s. And the classic way it almost always presents is that they have recurrent infections. And you may say, hmm, defiance kind of weird. How do you have a high white count like white count of like 80, 70,000, but they're still not doing well, right? Well, the thing is they have this B cell malignancy. B cells are proliferate in a ton, right? But the thing is those B cells either don't make antibodies or the antibodies they make are not effective, okay? So CLL is almost like a functional immunodeficiency disease, okay? And remember again, smudge cells on histology. That's like a big thing. You want to keep at the back of your mind because your friends at the NBM is right. They love to put pictures occasionally on these exams. And then if you're thinking like middle aged, right? So if you're thinking about a middle age person, if they show you our rods, right? So notice I've gone away from the extremes. Now I'm in middle age people, right?
If they show you like our rods, you know it's AML, right? There are many kinds of acute leukemia, but the only one that they usually test on exams, right? Is acute promylocytic leukemia. Remember that with the our rods that can cause the IC, right? So if they describe a person like an AML and the person suddenly becomes, becomes unresponsive during surgery or whatever, right? You want to think about the IC from those our rods spilling into the circulation, right? And remember that that has an association with the 15, 17 translocation and you obviously want to go ahead and I give those people a trough, right? So all trans retinoic acid, again, nutrient that the NV Me seems to be using quite often, especially with the newer exams, appears to be that they will take what you know and just give it a different description, right? So instead of saying all trans retinoic acid, demisi like vitamin A derivative as an answer choice. So that's something you want to keep at the back of your mind. And then if you see again middle-aged person, but they show you like BCR able fusion protein or they tell you something about the Philadelphia chromosome or they give you like a CBCI, you notice that it's kind of like weird cells that are proliferated, right? So they tell you that oh, you're seeing like high numbers of like myelocytes and metamylocytes and all that stuff. That's essentially code word on NV Me's for for CML, okay?
And remember CML obviously again like I said BCR able BCR able fusion protein, right? Philadelphia chromosome, what's the chromosomal translocation? What is the chromosomal translocation that relates to CML? I hope you're telling me the 922 translocation, okay? So again you want to keep that at the back of your mind, right? And then remember you treat it with a macnip, it's a tyrosine Chinese inhibitor, just as a general trick on exams. If a drug ends in nip, it's a tyrosine Chinese inhibitor, end of story, okay? And then so let's go on to our next next scenario, right? So what if you get a question about you know like a 17 year old guy, they tell you that you notice that on a peripheral smear you see red blood cells that are stuck like coins. What am I describing? Well I hope you're telling me the rule of formation, right? That's obviously multiple myeloma as I already described. Okay now what if you get a question about a 78 year old guy again he has pancylopenia, everything is low and then they tell you that when you try to aspirate the person's bone marrow, you observe a dry tap. So dry tap on aspiration of the bone marrow whenever you see that actually want you to think about three things on your exam. The first thing I want you to think about is primary mylo fibrosis, okay? That's one high-yield thing you want to keep in mind. The second thing you want to keep in mind with that is essential thrombocytemia.
Remember essential thrombocytemia is one of those myeloproliferative disorders that has an association with like a jack-to-mutation. And then the third thing you want to think about is a plastic anemia. So again dry tap on a bone marrow aspiration or biopsy or whatever that tells you that you're dealing with one of those three disorders. Now what if they give you a question about like a 78 year old female over the last six months she's been having like recurrent infections. They tell you that how wide blood cell count is like 47,000. So you notice it's not crazy high like the others like said for CLL like 80, 70, even a hundred thousand right? And then they tell you that you see different like many cells in different stages of maturation right? And then maybe they tell you on the exam that oh these cells are like myeloproxidase positive and they tell you that these cells have like reduced activity of leukocyte alkaline phosphatase. What am I going after here? I hope you're telling me CML, okay? I hope you're telling me CML right again. Remember at 922 translocation, Philadelphia chromosome you give a magnet right? And remember right there's this weird thing that your friends at the NBME may love to throw on an exam right? So because if you have a white kind of like 50,000 it could actually be from just a severe region infection right where you have like a locomoid reaction to that. But remember that locomoid reaction you have like good legit white blood cells.
So a legit white blood cell marker like leukocyte alkaline phosphatase will be elevated in people that have a locomoid reaction. What amortical I mean in CML they tend to have low levels of leukocyte alkaline phosphatase because again those cells are abnormal. They don't function like normal B cells. So that's something again you kind of want to keep at the back. I mean not B cell sorry. They don't function like normal myelocytes. So that's something you want to keep at the back of your mind for tests. And then what if you get a question about you know like a 55 year old guy you know he's like status post day five from like you know some kind of treatment of a hematologic malignancy. They tell you that his platelets are like 40,000. His D dimers are markedly elevated. He's bleeding from every venue puncture site. What are you thinking about? What kind of hematologic malignancy are you thinking about? I really hope you're thinking again about acute promo elocytic leukemia. Again you will find our odds on on histology right. And remember those hours again like I said they can trigger DIC right. So they can easily make this a numbers game on the exam right. So notice instead of just telling you DIC right notice I'm giving you lab markers that tell you that you're dealing with DIC right. So like again like low platelets those people have like high fiber indigreduceant product right like they also have like high ptptt right.
And again you give all trans retinoic acid and again remember basically the thing that's going on here is that whenever a person has DIC all their all their platelet markers all the accolvolution markers just go out of whack right. And then what if you get a question about you know five-year-old again I'm just using this to reiterate because these are again all high yield things to know for exams. So what if you get a question about like a five-year-old female over the last six weeks she has lost a ton of weight she's having like daily fevers. You check a CBC you notice that she's hemoglobin and a platelet are low but you notice that a white count is like 45,000 right. And then they tell you that oh they did some cytologic testing and they found cells that are positive for TDD what are you thinking about. I hope you're telling me again Aila and again remember the astrogion Down syndrome right. Remember that thing where they say they all fall down right that's a nice nomonic there. So fall down Down syndrome Aila. And then what if you get a question about like some guidance 50s is again been having fever weight last night sweats and then they tell you that a peripheral smear reveals B cells with a bilobit nucleus. So B cells with a bilobit nucleus what kind of cell am I describing here.
Well I hope you're telling me the rich tremor cells remember those rich tremor cells you tend to find them in Hodgkin's lymphoma right and you see um device kind of weird how can I press in the 50s get Hodgkin's lymphoma remember your friends at the MBM right I don't know if again if you remember this from step one way we talk about diseases that have like a by like a bymodal distribution Hodgkin's lymphoma is one of them so it presents in young people but there's also this big optic around people in their 40s 50s 60s okay so it has a bymodal distribution so you can already see how they can infuse this with a bio stats question.
Another way they can also kind of integrate that whole bymodal concept is people that metabolize isonize it right there are people that are slow acid leaders and they are people that are fast-asseted leaders right those are always they can test those concepts and again remember Hodgkin's lymphoma you're dealing with rich tremor cells and those cells in general are CD15 and CD30 positive again kind of high up to know those things right and then if they give you a question about a person that has had like you know they have like a known history of CML okay and then they tell you that over like a three week period they're having like very high daily fevers a ton of weak loss they have like extensive diffusal infodanopathy what are you thinking about I really hope you're thinking about progression of the CML to EML so this people have had something called a blast crisis okay so that's something you want to keep out the back of your mind that's usually as you're there with like pretty bad mortality without like immediate treatment okay now let's go over a few more high yield scenarios right so what if you get a question about like a 45 year old female she has like a six month history intent providers and then they tell you that you get a BMP and you notice that she has like a conjugated hyperbiliar bineumia right and then they tell you that oh an ultrasound you notice that haj ha intra hepatic bowel dots are dilated what are you thinking about well I hope you're thinking about PVC right so primary bilayery colonjaites it was previously known as a primary bilayery cirrhosis right one thing you kind of want to keep at the back of your mind there is that PVC right is as such the anti-mide o'conjural antibodies and again you'll shop in a female that's like in her 40s or 50s or thereabouts and she has like itching peridots and a conjugated hyperbiliar bineumia right and really
the only definitive treatment is liver transplant but to temporized symptoms in the meantime to help with like the itching and all that stuff and the jaundice you can give them also dial right so instead of putting also dial you know friends at the mbmi put also the oxycolic acid it's the same thing and again liver transplant definitive treatment and if you're asking your question specifically about the itching one thing you may want to consider on a test is to give diphen hydramine okay that's an unusual way they can present this PVC concept okay now what if you get a question about like a 45-year-old guy he has a history of old redif colitis and then they tell you that again he's had like a six month history of peridots and then they tell you that they get an ultrasound and you see the elation of the intra and extra hepatic bowel dots what are you thinking about again I hope you're thinking about PSC right so primary sclerosis colangitis right and remember that this is like p-enca positive right the thing I tell people is oh divine it's so hard to memorize which is p-enca c-enca on all that crap here's basically what you should do the only thing that you probably ever be responsible for at least now as far as I know right now again remember divine does him know everything just a just a student like all of you right so the only thing that I will say that in general you should reasonably expect on the usml step 2c k exam with regards to c-enca is wegners right every other thing you're going to learn about is p-enca positive so that's kind of like a nice would remember to just remember this only thing that c-enca positive and then you know that every other thing that is anca positive has to be p-enca and the high-yield p-enca things you want to remember for step 2c k right you want to remember things like you want to remember things like a trox trowel syndrome right so
like using ophilic granulomatosis with polyngitis right trox trowels and then microscopic polyngitis is also p-enca positive and then you should also not forget that primary sclerosis in colngitis is also positive for p-enca okay remember p-enca deals with anti myeloperoxidides antibodies okay so that's something I want to keep at the back of your mind and again if you're comparing psc and pbc you kind of want to be able to compare and on contrast what I just said in psc those people have dilution of their intra and extra hepatic bowel dots in pbc people have dilution of just their intra hepatic bowel dots okay and really for the most part for psc you're going to need a liver transplant also dial really doesn't help it really doesn't improve survival in psc unlike what it does in in pbc and I mean occasionally you can use like endoscopy to dilute the structures but ultimately those people are going to need a they're going to need a liver transplant and then just as a throwback here if you see a conjugated hyperbilior bimemia in a newborn on an mbmexam what are the things you should be thinking about I really hope you're saying back to me things like biliria trisha right that's like the big big one but if your friends at the mbm you decide to not throw biliria trisha in as an answer choice then you want to think about like a colidocal cyst okay a colidocal cyst if they want to be like really really mean demipoda like something called like caroliz disease caroliz disease is a kind of colidocal cyst it's like a fairly common one with some unique features so occasionally you may see that thrown in on an exam okay now what if you get a question about a 25 year old guy they tell you that over the last couple of years so again notice a young person he's been having a lot of like sinusitis he's been having a hemoptysis and then they tell you that you occasionally notices a b
lood in his urine what are you thinking about well I hope you're thinking about Wagner's right again they mean not necessarily colli Wagner's or they may put the word Wagner's in parenthesis the new name right is granolomatosis with polyangitis so please please please here's the deal do not confuse granolomatosis with polyangitis which is Wagner's with eocenophilic granolomatosis with polyangitis which is drugstrafts okay those are two totally different diseases right so Wagner's right again C-Anca positive again he could present as like a rapidly progressive a glomerular fridus and again those people have kidney problems and sinus problems right and long problems if you see that think about Wagner's right think about Wagner's you may say oh divine but that's kind of like the way that good pastures presents yes I understand good pastures presents the same way well people that have good pastures are not going to get sinusitis okay they are not going to get sinusitis and another kind of like we're thinking you want to keep in mind is that good pastures syndrome for the most part good pastures is a type of type right good pastures syndrome is a type of it's a type two hypersensitivity reaction right because you're making antibodies against a fixed antigen contrast that with Wagner's right where you're making antibodies against it's like an antigen antibody complex that's causing all this trouble right so in Wagner's that's more of a type three hypersensitivity reaction yeah the hypersensitivity that things the NV Me seems to be again be a little more focused on these days so that's something I want to keep keep at the back of your mind and again Wagner's right you can feel like steroids and cycrophosphamide now what if you get a question about again 25-year-old guy you know you onset asthma you forget your analysis you are seeing like this morphic erythrocytes again inste
ad of same white blood cell I mean red blood cell casts your friends at the NV Me wanting to breed that as dysmorphic erythrocytes so that's something you want to keep in mind so what does this person have right this person obviously has strokes trials right remember strokes trials they'll have like asthma right you see a ton of eocenophilia right so if you see not one of these like anca vasculidides and you see like asthma as a component a ton of eocenophils as a component the first thing I want you to think about is strokes trials and again remember a stroke trials is also known as egpa eocenophilic granolomatosis with with polyngitis and again remember it's again pianca positive kind of like microscopic polyngitis and those are again the big things you want to keep in mind and really these rapidly progressive glomerulone fridides they present as nephritic syndrome so NB Ms they present as nephritic syndrome okay now what if you get a question about like a 35-year-old female um they tell you that she she comes in she says yeah doc I've been having like you know like in termithane discoloration of my fingers and then they tell you that physical exam is notable for like defuskin thickening what are you thinking about here right I hope you're thinking again about scleroderma right remember uh scleroderma there's like the limited kind right so like the lcss limited cutaneous a systemic sclerosis and then there's the diffused one right the limited one you want to know your antibodies remember like your crest antibodies right um I mean your anti-central mayan antibodies because it's known as like crest scleroderma right and what does the crest stand for it's like calcinoces right um renalz phenomenon is the r the e if I'm not mistaken is um esophageal dysmortality right the s stands for like sclerodactyl right so like the finger problems they have and then the t stands for
telangectatious okay so remember anti-central mayan antibodies versus the one that's more diffuse right where you're thinking about like anti scl 70 antibodies right like your anti-tipus and summaries antibodies and remember that if a person has scleroderma renal crisis right so they describe a person very high creatinines very elevated blood pressures histiose scleroderma for those people you obviously want to strongly consider giving them um you want to strongly consider uh giving them uh uh an es inhibitor es inhibitors are the drugs of choice in the treatment of a scleroderma renal crisis and remember that um scleroderma right there are certain drugs you'd want to avoid in those people right you want to avoid drugs that are visospastic so if for example a person that has a histiose scleroderma they give you a question about them beginning to have migrates right for those people right they gain in this would be a wonderful new style kind of mbm equation it doesn't make sense to give those people so much triptan right remember so much triptan is one of those drugs that are contraindicated in people that have a histiose like visospastic disease right so if for example a person has a histiose like renal sphenominon in the context of our scleroderma you don't want to do that right and other set of people that you don't want to give um uh so much triptan to people that have a history of um like a prince metal engine i think these days it's called variant engine you want to avoid visospastic drugs like so much triptan okay because remember so much triptan is a serotonin receptor agonist right so it can trigger visospasm right so it's not good remember in general just as a cliff snorts again this is super oversimplified but in general the presence of visodilation is associated with headache so when you give a viso constrictor headache tends to abate i mean think about it
ibuprofen your n-sets what do your n-sets do in hebitcycloxigenis if in hebitcycloxigenis you have low levels of firstaglandins so you're having low levels of a visodilion again that seems to help with headaches again there's a lot more pathophys but this is a rapid review so i'm not gonna going any further than that now my last scenario right so let me pose this as a multiple choice question so let's assume you get a question about like a 35 year old female she comes to a PCP in um april you know she's coming for an animal physical she's in good health she's enjoying her daily job a blood pressure is just fine 120 over 80 heart rate 79 respiratory rate 14 and then they tell you that all the vital signs for cbc labs everything out they're all within normal limits right she doesn't have gvd doesn't have peripheral edema i'm just trying to make this an mbm style question right because again they'll give you all these details and all this fun stuff right and then they tell you a peripheral pulses two plus bilaterally um she doesn't have any evidence of respiratory distress she had a flu shot last year and again notice she's coming in april for her anophysical and then they tell you that you know she's up to date on all her vaccinations and they tell you that when you listen to a chest you hear you know like a b9 two other six that's tolic murmur with an opening snap at the apex okay and then they tell you that a break sounds are equal bilaterally she has good air floor no whizzing no crackles nor on chai and then they ask what's the next best step in management and then they offer you a few options right the first one they tell you influenza vaccination option b they tell you reassure the patient like reassurance option c they tell you trans thoracic acochordiography option d they tell you to do like a vq scan so like a ventilation profusion scan to rely on p and then op
tion e they tell you to start her on plothalidone therapy right so what kind of answer would you want to go with here so again first in figure out what what am i trying to test with this question again i hope you're telling me that this person has uh has a murmur right because again everything is normally in the question but you see notice that this person has a two out of six that's tolic murmur right remember if a person has a murmur that is systolic that's that's three out of six of greater you need to get an echo right and if a person has any kind of that's tolic murmur you need to work it up or if a person has any murmur that is symptomatic you need to work it up as well so that's what i'm going after here and then you uh for those that we're considering the other answers this lead is coming in in april when do people get the influenza vaccine usually kind of like in the fall right so that's kind of like wrong timing there and then you're not going to reassure this woman she has like an actual problem right i mean if you even think about it she has like a systolic murmur her best at the apex opening snap um that's likely like mitral stenosis right that's likely like mitral stenosis and then you don't want to do a vq scan because she doesn't have any evidence of a pone embolus and plothalidone will not be appropriate remember plothalidone is an example of a thiazide diuretic right it's not appropriate in this patient because she's not hypertensive a blood pressure is 120 over 80 so this person again mitral stenosis right again if you have a any kind of the astolic murmur any systolic murmur that is three out of six or greater so if you have a systolic murmur that is two out of six one out of six you don't need to get an echo for those okay you absolutely do no need to get an echo for those the only exception to that rule is if a person has a murmur that is symptom
atic so if a person has like a one out of six systolic ejection murmur and the astolic ejection murmur and the astolic ejection murmur and the astolic ejection murmur and the astolic ejection murmur and the astolic ejection murmur and the astolic ejection murmur and the astolic ejection and the astolic ejection murmur and the astolic ejection murmur and the astolic ejection murmur and the astolic ejection and the astolic ejection murmur and the astolic ejection murmur and the astolic ejection murmur and the astolic ejection that the person has like some EKG problem like a left wonder branch block inferior q waves whatever awareness they put then you cannot do any kind of stress test that involves EK Gs right so that's again a high-youthing one to keep in mind if a person has a pre-existing EKG abnormality then you really should not be doing any kind of stress test that involves EK Gs you can do like a stress echo you can do an exercise echo and all that stuff if a person cannot exercise or they have like severe osteoarthritis and all that stuff then you cannot do a stress test that involves exercise right you want to proceed with the pharmacological stress test and those pharmacological stress tests right you can you can give something that can speed up the heart right so you can give like a bit of one agonist like a dobutamine right you can give something like dobutamine that can help another thing you can do is you can take advantage of the coronary steel principle if i'm not mistaken i believe i described that thoroughly in my in my um shelf medicine video so the coronary steel principle you can sort of take advantage of that so you can use like an adenosine analog like regadenosine apadenosine or you can use like a forceful diesterase inhibitor right like diperidomone okay and you may say oh define what if the mbm gives me a question where i see regadenosine as an a
nswer choice and i see dobutamine as an answer choice the thing is the thing is remember is that every mbm question is written with one there's i mean you can never have two correct answers to an mbm question even if you may see certain questions you're like man both of these things are pretty close right the thing is you need to go back to the question there has to be information there that will lead you towards one answer versus the other right so for example if you're trying to choose between those two things and the person has like a history of asthma right or like reactive area disease then it doesn't make sense to give an adenosine analog or diperidomone right because the thing is those people um if you give them adenosine they will have like bronchospasin and that'll be bad right that'll be really bad i remember that adenosine can cause a bronchoconstriction okay so that right there that will tell you that okay it's probably not a smart idea to give those people those drugs and remember i mean the mbm again they can even write questions where again you're deciding between like a beta blocker and some other drug right for president has a history of asthma a nonselective beta blocker is not a smart idea right it's not a smart idea so those are things you want to keep in mind if the person has drunk caffeine that morning then doing an adenosine based cardiac chemico stress test like the pharmacologic stress test again also makes no sense because remember that caffeine or like fioffelene right your methods and things they antagonize the effects of adenosine so again i apologize this has probably gone on a little long so i'm gonna go ahead and stop here um remember um as i say at the end of every podcast i'd offer one on one twitter and for all the usml exams right so step one step two ck step two cs step three um the preclinical medical exams the third year shelf e
xams um and then if you're a medicine resident i do twitter believe it or not for the medicine in train exam and also the internal medicine boards uh like the abiam aboard exams i tutor for all those things and then if you're a college student i need tutoring for physics gen cam ocham biochemistry physiology over tutoring for all those things and then if you're a med student applying to residency i know this is kind of application season so like ira's applications with like personal statements your entire ira's application um recommendation letters mock interviews and all those things i do a lot of consulting and advising with that i do it on a one on one basis um and also if you're a med student um i mean if you're a college student applying to med school so like an amcass app again i've been on an admissions committee had a top two med school i've read tons of high quality applications so i have a lot of experience with this i mean i worked with a ton of people this last cycle and essentially everyone i worked with matched most people matched to their to their first choice so take that forward you will so if you need any of those things i reach out to me through the website or send me an email so i wish you a very wonderful rest of your night i hope you all have a good sleep and feel free to reach out to me and have a wonderful sunday god bless you thank you so
Practice questions — USMLE style
Question 1 — Internal Medicine/Hematology
A 70-year-old female presents to her primary care provider with a one-month history of progressive bone pain and fatigue. Physical examination reveals palpable step-offs over multiple bones. Laboratory studies are notable for hypercalcemia (Ca 12.7 mg/dL), renal insufficiency (Cr 3.0 mg/dL, BUN 40 mg/dL), anemia (Hgb < 9 g/dL), and a peripheral smear showing numerous "railroad track" or pencil-shaped red blood cells. Initial workup is negative for infection. Which of the following is the most likely underlying diagnosis?
- A) Metastatic carcinoma
- B) Primary myelofibrosis
- C) Multiple myeloma
- D) Chronic lymphocytic leukemia (CLL)
Answer: C. The constellation of symptoms—bone pain, renal failure, hypercalcemia, anemia, and lytic bone lesions (implied by the step-offs and peripheral smear findings)—is classic for multiple myeloma. MM is characterized by plasma cell proliferation leading to osteoclast activation, which causes both hypercalcemia and bone destruction. The finding of pencil-shaped red blood cells on a peripheral smear is also highly suggestive of MM.
Question 2 — Rheumatology/Infectious Disease
A 35-year-old male presents with a six-month history of recurrent sinusitis, hemoptysis, and gross hematuria. He has no significant past medical history other than seasonal allergies. Physical examination reveals nasal polyps. Laboratory testing is positive for anti-neutrophil cytoplasmic antibodies (ANC As) with an enzyme-linked immunosorbent assay (ELISA) demonstrating a pattern consistent with cryoglobulinemia. Renal biopsy shows necrotizing glomerulonephritis, and the pulmonary evaluation suggests small vessel vasculitis. Which of the following ANCA patterns is most strongly associated with this clinical presentation?
- A) Anti-proteinase 3 (PR3)-ANCA
- B) Anti-myeloperoxidase (MPO)-ANCA
- C) Anti-Smith antibodies
- D) Anti-ds DNA antibodies
Answer: A. The classic triad of sinusitis, pulmonary involvement (hemoptysis), and glomerulonephritis in the context of positive PR3-ANCA is highly suggestive of Granulomatosis with Polyangiitis (GPA). GPA is strongly associated with anti-PR3 antibodies. In contrast, MPO-ANCA is more commonly associated with Microscopic Polyangiitis (MPA) or Eosinophilic Granulomatosis with Polyangiitis (EGPA), and Anti-Smith/Anti-ds DNA are markers for SLE.
Question 3 — Gastroenterology/Hepatology
A 45-year-old female presents with a six-month history of pruritus, jaundice, and fatigue. Laboratory tests reveal elevated alkaline phosphatase and conjugated bilirubin. Ultrasound imaging demonstrates marked dilation of the intrahepatic bile ducts. The patient has no known history of primary sclerosing cholangitis (PSC). Which of the following statements best differentiates this condition from Primary Sclerosing Cholangitis (PSC)?
- A) This condition is associated with anti-M2/anti-CCP antibodies and typically involves only intrahepatic ductal dilation.
- B) The definitive treatment for this condition is liver transplant, while PSC can be managed by endoscopic stenting.
- C) Both conditions are strongly correlated with inflammatory bowel disease (IBD), but PBC requires a more aggressive immunosuppressive regimen.
- D) This condition is characterized by the presence of extrahepatic ductal strictures and is associated with p-ANCA antibodies.
Answer: A. The clinical picture described—pruritus, jaundice, elevated ALP, and intrahepatic bile duct dilation in a female—is characteristic of Primary Biliary Cholangitis (PBC). PBC is strongly associated with anti-M2/anti-CCP antibodies. PSC, conversely, involves strictures of both intrahepatic and extrahepatic ducts and is typically associated with p-ANCA antibodies.
Question 4 — Hematology
A 78-year-old male presents to the emergency department after a fall. He has pancytopenia (low hemoglobin, low white count, low platelets) and appears acutely ill. When attempting bone marrow aspiration, the physician encounters significant resistance and obtains only a small amount of blood, leading to a "dry tap." Which of the following diagnoses must be considered in the differential diagnosis for a dry tap on bone marrow aspiration?
- A) Acute promyelocytic leukemia (APL)
- B) Myelodysplastic syndrome (MDS)
- C) Primary myelofibrosis
- D) Aplastic anemia
Answer: C. The three high-yield conditions associated with a "dry tap" during bone marrow aspiration are primary myelofibrosis, polycythemia vera, and essential thrombocythemia. These are all myeloproliferative disorders that cause fibrosis or hypercellularity in the marrow space, making aspiration difficult. Aplastic anemia typically presents with pancytopenia but does not inherently cause a dry tap due to fibrotic changes.
Quick fire review
What are the classic findings in Multiple Myeloma?
Hypercalcemia, renal insufficiency, anemia, and bone pain from lytic lesions.
What mnemonic is used for cancers causing lytic bone lesions?
L-T-R (Lung cancer, Thyroid cancer, Renal cell carcinoma).
Which hematologic malignancy presents in the oldest age group and has smudge cells on peripheral smear?
Chronic Lymphocytic Leukemia (CLL).
What is the key finding that differentiates Primary Sclerosing Cholangitis (PSC) from Primary Biliary Cholangitis (PBC)?
PSC involves dilation of extrahepatic bile ducts, while PBC primarily affects intrahepatic ducts.
What are the three conditions associated with a "dry tap" on bone marrow aspiration?
Primary myelofibrosis, Essential thrombocythemia, and Aplastic anemia.
Which drug class should be avoided in patients with Systemic Sclerosis (S Sc) due to risk of vasospasm?
Triptans (or other serotonin receptor agonists).
What is the key chromosomal translocation associated with Chronic Myeloid Leukemia (CML)?
The t(9;22) translocation, resulting in the Philadelphia chromosome and BCR-ABL fusion protein.
Which type of vasculitis is strongly associated with anti-cANCA antibodies and presents with sinusitis/hemoptysis?
Granulomatosis with polyangitis (GPA).
What are the characteristic findings on a peripheral smear for Primary Myelofibrosis?
Tear drop shaped red blood cells (dacrocytes) and sometimes reticulin fibrosis.
In Systemic Sclerosis, what does the acronym CREST stand for when describing limited cutaneous involvement?
Calcinosis, Raynaud's phenomenon, esophageal dysmotility, Sclerodactyly, Telangiectasia.
What is the definitive treatment for Primary Biliary Cholangitis (PBC)?
Liver transplant.
Which type of hypersensitivity reaction characterizes Goodpasture syndrome?
Type III hypersensitivity reaction (antibody-antigen complex deposition).
Quick recall / Anki-style questions
What is the key chromosomal translocation associated with Chronic Myeloid Leukemia (CML)?
The t(9;22) translocation, resulting in the Philadelphia chromosome and BCR-ABL fusion protein.
Which type of vasculitis is strongly associated with anti-cANCA antibodies and presents with sinusitis/hemoptysis?
Granulomatosis with polyangitis (GPA).
What are the characteristic findings on a peripheral smear for Primary Myelofibrosis?
Tear drop shaped red blood cells (dacrocytes) and sometimes reticulin fibrosis.
In Systemic Sclerosis, what does the acronym CREST stand for when describing limited cutaneous involvement?
Calcinosis, Raynaud's phenomenon, esophageal dysmotility, Sclerodactyly, Telangiectasia.
What is the definitive treatment for Primary Biliary Cholangitis (PBC)?
Liver transplant.
Which type of hypersensitivity reaction characterizes Goodpasture syndrome?
Type III hypersensitivity reaction (antibody-antigen complex deposition).