- Get CME-MOC credit with ACP!
- 00:43 Case presentation Part 1
- 04:55 Case presentation Part 2
- 06:50 Expert discussant
- 28:52 Framing bias
- 33:38 Concluding thoughts
- Hypereosinophilia is defined as an absolute eosinophil count > 1.5 x 109/L (or >1500 cells/microL) in the peripheral blood on two examinations separated in time by at least one month and/or pathologic confirmation of tissue hypereosinophilia.
- Hypereosinophilic syndrome is defined by the association of hypereosinophilia with eosinophil-mediated organ damage and/or dysfunction.
- Hypereosinophilia in malignancy can be reactive or secondary in solid tumors, versus primary or clonal from myeloproliferative neoplasms.
- Mnemonics and schemata are both mental tools that can aid memory formation, organization, and retrieval.
- Mnemonics are useful for quick recall of information especially in a large quantity
- Storage of data using schemata is bound by meaning and often provides a systematic approach to a clinical problem
- While mnemonics are powerful tools in early medical education and can pack a lot of information, it is important to remember to explore material not limited to existing mnemonics if we wish to master the particular subjects
- Framing bias in medicine is often loosely defined as:
- “The manner in which data is presented can affect decision making.”
- While a data value lands on the extreme end of the spectrum, it often but not always carries significant clinical importance.
- We tend to be intrinsically sensitive to rare findings, caution is needed when we assign such findings appropriate diagnostic weight.
Cindy: Hi everyone, Cindy Fang here. Welcome back to another episode of Hoofbeats, where we challenge you to solve diagnostically difficult, real world cases alongside experienced clinicians. And as always, I’m joined by my co-host Dr. John Hwang.
John: Hello all. It’s been a few months since our last episode, it’s good to be back! Let’s hear the case from one of our colleagues here at Core IM, Solon Kelleher.
Solon: Our patient is a 29 year-old man whose chief complaints are cough, abdominal pain, and fever. His illness began with the onset of a cough six weeks before his admission to the hospital. The cough was non-productive and associated with chest pressure and dyspnea, but seems unrelated to exertion. Three weeks later, he also developed a dull, nagging left-sided abdominal pain. He had no associated nausea, vomiting or diarrhea, but he did notice a whitish streak in his stool a few days earlier, a detail he could not elaborate on much further. His fevers began the following week.
He recalls that he ate raw tuna and other fish from a local store about two weeks prior to the onset of his illness. Otherwise, he does not remember any unusual ingestions recently. Around the time his illness began, he had traveled to Taiwan, but he cannot recall precisely whether his cough began shortly before or shortly after his arrival there. He returned to the US one week before admission. His travel history was also notable for trips to France, Hong Kong, and Canada earlier in the year.
He has no known medical, surgical or family history. He is sexually active, monogamous. He lives in Queens, NY with his wife; they keep two adult cats at home. He has no other contact with animals, domestic or wild. His only medication is Percocet, prescribed when he visited an urgent care for these symptoms one week prior to admission.
Cindy: So I know this is not a lot of information to go on, but while you take a second to think about our patient, I’ll use this chance to introduce our expert discussant today. Please welcome Dr. Anand Viswanathan, a fellow hospitalist at NYU. Every time I have a question in the office, whether it’s “What do you think I should do with this post-op fever?” or “How do I fix this stupid computer?” I run to Dr. V for help.
Viswanathan: I see that it’s a 29 year-old with six weeks of dry cough and two weeks of fever. And of course you think TB right off the bat, because that’s what you do with dry cough and fever. But it seems to be that there’s a subacute process, just from the chief complaint itself. Then when I look into the HPI.. the dry cough, the abdominal pain, specifically left sided. No diarrhea… and then this whitish streak… My perspective is as an inpatient hospitalist, so patients are coming in… You know, this guy has been dealing with a lot of things — three weeks of abdominal pain, two weeks of fever. I can understand not wanting to come to like a hospital for the dry cough, but there was something that at some point… why did they come in now? What really changed in their presentation? Were things getting worse? That’s what I usually try to elicit from patients. What has changed now?
Cindy: As best as I could tell, he come to urgent care a week prior to the current admission for the abdominal pain and was prescribed some Percocet. He probably re-presented to the same urgent care when he ran out of the meds; this time lab work was performed, and because of the test results he was referred to the emergency room.
John: And what lab result could have earned him an instant referral to the ER?
Cindy: Before we move on to that, I want you to know Dr. Viswanathan also asked for: sick contact, hemoptysis/B symptoms, bowel pattern, characteristics of his abdominal pain, CVA tenderness, and if the patient was taking any over the counter medications. I answered based on the admission H&P documented to my best ability, and the answer to a lot of these questions was “I don’t know, it was not available in the chart”. At one point Dr. V asked me if the patient’s cats were having diarrhea…I’m sure he was just messing with me because of my general unhelpfulness.
John: I’m sure he wasn’t trying to be mean.
Solon: On examination, the patient appears comfortable and generally well, but is febrile to 101.8, and tachycardic to 110. His blood pressure is 120/60, his respiratory rate is 16, and he is saturating 96% on room air. He is mildly tender over the left upper quadrant. His exam is otherwise unremarkable; his heart sounds are normal, his lungs are clear, and there is no visible rash nor joint effusions.
His labs are notable for a white blood cell count of 33, including an absolute eosinophil count of 17, a hemoglobin of 10, and a platelet count of 562. His serum sodium is 132, and glucose is 294. The BUN, serum creatinine, and remainder of his metabolic panel are normal. His chest X-ray is read as clear, and his ECG shows sinus tachycardia.
John: Absolute eosinophil count is 17 — as in seventeen thousand?
Cindy: Correct, 17,000. Now, that’s all the data we are going to get so far. We have a 29 year-old man with a good travel history, who eats raw tuna from a supermarket, here with significant leukocytosis and an eosinophil count of 17,000.
Listeners, please pause here and think about this patient. What do you think it is? What tests do you want to order? When we come back, we will hear more from our discussant.
Viswanathan: The next piece of data we have is this wonderful white blood cell count of 33, which to me immediately like sets off all sorts of red flags. Thinking about anything from C. diff to tissue ischemia to a leukemoid reaction, so severe infection, versus malignancy. Those are the things I tend to think of. And the next real “home-hitting” thing is this eosinophil count. Which, you can look at absolute eosinophils — is this a percentage or absolute? [Cindy: Absolute.] So that’s 1,700, or is that 17,000? [Cindy: 17,000.] So this, I believe goes into the area of hypereosinophillia, as opposed to just your standard regular eosinophilia. So I think this may push you toward one particular range of diagnoses as opposed to others.
John: Er, just to pre-empt any objections here: Hypereosinophilia does have a more formal definition, right? At least two measurements >1500 one month apart (in other words, it has to be both severe and sustained), or you demonstrate extensive eosinophils in a tissue biopsy. (And hypereosinophilia is also distinct from hypereosinophilic syndrome, which is when the hypereosinophilia is demonstrably leading to end-organ damage.) So our discussant is using the term loosely here, but his point is that the severity of this patient’s eosinophilia has some diagnostic meaning to him.
Viswanathan: Traditionally, I think back in medical school, you think of eosinophilia, you think of the mnemonic NAACP: neoplasia, allergy, atopy, asthma, Churg-Strauss, connective tissue diseases, and parasites, right? But with hypereosinophilia, well… You can see certain parasites like schisto and strongyloides. You can see Hodgkin’s lymphoma, because the Hodgkin’s generates IL-5 by the Reed-Sternberg cells. You can have ALL, cutaneous T-cell lymphoma. And for the solid tumors, you can have any number of different malignancies: both large cell and squamous cell lung cancer, GYN cancers and adenocarcinomas of the stomach, large bowel, and even transitional cell cancer of the bladder. There’s something known as mastocytosis, where mast cells accumulate in the skin and internal organs. And we can go even further.
Cindy: Our discussant refers to “NAACP” as a mnemonic for eosinophilia, so I have a perfect excuse to talk mnemonics for a second. Now, the formal definition of a mnemonic is, “a technique or strategy that assists in the creation, retention and retrieval of information from memory.” Acronyms are the most familiar type of mnemonic, but they aren’t the only type. Using hand gestures to quickly determine the axis of an EKG, that’s a “kinesthetic” mnemonic. Drawing a picture to incorporate all the causes of splenomegaly would be a “visual” mnemonic. Rhymes and songs are “auditory” mnemonics. While I was doing research on this, I even came across a poem that was written to help people remember different types of heart blocks.
John: A poem? How many types of heart blocks are there? (Is it a limerick? A Shakespearean sonnet? A Homerian epic ballad? Just show me later.)
Cindy: But the issue I want to highlight is this. Mnemonics, we’re saying, are mental constructs that we use to organize and remember information. But… Doesn’t that sound an awful lot like the concept of a diagnostic schema?
John: I’ve observed a lot of people seem to treat these concepts interchangeably. And I’ve had some people ask me directly whether there’s even any difference.
Cindy: So how do you answer them?
John: I think using an example might be helpful. As Dr. V was saying, in med school we learn the mnemonic “NAACP.” But these days, when my students ask me how I approach eosinophilia, I tell them I start with the phrase, “worms, wheezes, and weird diseases.” So let me just ask you folks, which of these two is a schema? Which is a mnemonic? Or are they both? And why? What do you think Cindy?
Cindy: Well, I would argue that “worms and wheezes” has a layer of MEANING that NAACP does not. Think about it: In NAACP, there is really no reason why neoplasm comes first, even though it’s among the rarer causes. There’s no reason why adrenal insufficiency is up there with allergy, even though the latter is a thousand times more common. There’s no reason for an important cause like drug-induced eosinophilia, i.e. DRESS, not to be on that list, except that there’s no D in NAACP.
Meanwhile, think about the sentence “worms, wheezes and weird diseases.” It divides the problem space of eosinophilia into three big regions based on statistical likelihood. Parasites are the most common group of causes in the developing world. Autoimmune and allergic disorders are the most common group of causes in the developed world. And there is a large and diverse group of rare illnesses to consider after the first two.
So to answer your question, I would argue that both of these are mnemonics, because they both help us remember something about the causes of eosinophilia. But unlike NAACP, “worms/wheezes” is also the start of a proper diagnostic schema.
John: And I agree with you, I think meaning is the key. Also, just to be careful here, I worry it sounds like we are arguing schemata are better than mnemonics, but that’s not true. Mnemonics are useful in certain situations, like where you need to recall something very quickly — at a code, your patient is asystolic, so what do you do? You shout out the H&Ts. In general, mnemonics are good solutions when we need to quickly memorize a large amount of information. They don’t take a lot of time to commit to memory, and they don’t require that you have a deep, intimate understanding of the clinical problem you’re dealing with. And that’s probably why we use it so much early in our medical training. A proper diagnostic schema though, it provides a systematic approach to thinking about a clinical problem in a meaningful way; it’s not simply a method of remembering things easily.
Cindy: And that’s why when I hear someone use a clever diagnostic schema that explores a problem space in a way I have never even thought of before, they instantly gain so much respect from me. That immediately tells me that this person’s fund of knowledge in the particular subject is, not surprisingly, much deeper than mine.
My next question for you is, when I hear someone on teaching rounds use a mnemonic to recall a list of causes without systematically thinking through a clinical problem, should I discourage or encourage their use? Are mnemonics a natural step in learning? Or should I prompt them to start thinking about the clinical problem at hand in a different way?
John: I think it depends, right? I definitely don’t think we should categorically discourage mnemonic use as part of the learning process — any more than I would yell at my four year-old for using training wheels. Actually, I might even encourage him to do those things, to let him find some early success at doing those things that he couldn’t have otherwise. But what happens later? Well, if biking doesn’t interest him, it doesn’t matter. But it’s dangerous if he does want to bike, if he tries to bike to work everyday — but he never learned how to bike without training wheels. And I think that’s really the source of my unease with mnemonics: When you first learn to navigate a new problem unfamiliar to you with a large amount of material, mnemonics are useful to help you get started. And honestly, for a clinical problem we encounter infrequently or don’t need to achieve mastery in, that might be enough! A simple mnemonic may be enough to get us through.
Cindy: But it’s easy to get too comfortable – When we rely on mnemonics too much and fail to re-think, re-learn, re-examine a specific clinical topic and develop a more intimate knowledge… If it limits my growth, an aid can become a crutch.
John: Yeah, that’s what I think too. So to get back to your question… When I see my learners rely on a mnemonic like NAACP for eosinophilia, first and foremost, it’s a sign, right? It’s telling me something about the way in which their knowledge about that problem is organized in their head. And I need to decide — if I think eosinophilia is a topic they need to master, it means at that point I need to step in and help them recognize the need to develop a deeper understanding of the material. And that might entail maybe pointing out the inadequacy of a mnemonic, like NAACP, or helping them distinguish which of their mnemonics have the potential to be the nuclei of mature, helpful schema, versus those that are just destined to become textbook fodder.
Cindy: Well, that was quite the digression on mnemonics. And all because Dr. Viswanathan said “NAACP” out loud once. Let’s come back to the case. So Dr. V went through a long list of possible causes in his mind. At this point he’s basically thinking two things: parasitic infections versus malignancy. He also ordered an HIV serology, a hepatic panel, ESR/CRP. He asked whether stool was sent for culture, ova and parasites, and GI pathogen PCR. He also asked for abdominal imaging. Before we give you all that data, I forced him to only choose one single test with the highest diagnostic value. You know, the question I see on CPC and get angry every time (WHY DO I ONLY GET TO ORDER ONE TEST?!) To my surprise, he asked for an abdominal imaging to pursue that focal abdominal pain further.
Viswanathan: Parasites and malignancy are the two things that somewhat scream at me. No diarrhea, but then this whitish streak, which seems to me a bit of a red herring. And, if you look at the countries this guy went to. France, Hong Kong, Taiwan, and Canada. I’m not thinking he was going barefoot and then some worm went up his feet.
So it’s interesting, when I think about this. Six weeks of dry cough, you think of something pulmonary related. You have three weeks of abdominal pain that seems a little more focal, and two weeks of fever — is there inflammation that’s going on in the left abdominal side, that’s maybe causing some inflammation and sort of pleuritic pain…? Just trying to tie together the dry cough and the abdominal pain.
I would say my impression now is that it’s likely that there’s a process that’s more pronounced in the abdomen. In choosing my diagnostic testing, I want to maximize the yield of each test. So I think abdominal imaging would be my go-to first.
Cindy: So if you remember, at the beginning of the discussion, Dr. V was leaning heavily toward infection, and he seemed to be sufficiently intrigued by the eosinophilia, as you can see by the long differential. But as the discussion went on, he got more and more interested in the focal abdominal pain. I tried to press him more, but he refused to comment further and insisted on obtaining the CT first.
Alright, fine. The abdominal CT revealed a 11x 10 x15 cm left renal mass most compatible with neoplasm.
John: Ah, Dr. V…
Cindy: So I asked him one more time about his interest in the patient’s abdominal pain.
Viswanathan: I think I anchored on certain things, certain items like the eosinophilia. I took each piece of data, and I thought, how important is this? You know, How important was that whitish streak? Not so important. When we’re looking at cases, we’re trying to form, we’re trying to solve a puzzle, right? So we’re putting all the pieces together, and then we’re taking each bit of information and asking, How important is this? How important is that this patient went to France recently? How important is it that he lives with two cats. So taking all those bits and pieces of information and thinking about, okay, Is this important? No. Or Yes. And then trying to sort of taking additional information and then re-prioritizing everything. So it’s almost like a constant inventory that is being removed so that way I can then solidify things.
I think in this patient I would be concerned about something in the GI tract specifically that’s causing this patient’s symptoms. The eosinophilia… It is the most interesting data, but it’s too vague. The differential for this is too much.
John: In short, he feels that eosinophilia, although very exciting and interesting, at this juncture of the reasoning process, does not help him narrow his differential further. It is time to focus on the focal abdominal pain.
Cindy: That decision in itself is interesting. If this case came in as an overnight admission, I definitely would spend the whole teaching rounds talking about that eosinophilia. Who cares about this guy’s abdominal pain?
John: Oh yeah, that’s me. Totally 100%. I mean, it’s intellectually exciting when we encounter a relatively rare finding, right? Psychologically we are naturally attracted to, and think of rare things as valuable.
But it didn’t get him all the way to the diagnosis, so he did something I honestly don’t think I could have done — he set the eosinophilia of SEVENTEEN THOUSAND aside. Much respect.
Cindy: I didn’t catch this on tape, but Dr. V also told me later that he thought the case was written in a way to guide him toward parasites. Knowing me, that made him more cautious and felt the need to not go down the parasite route too early.
John: Oh, I see, the gamesmanship. Well, you did emphasize the eosinophilia and travel history. And the tuna. Experienced discussants can smell a trap.
Cindy: To be fair, I actually did not twist the case that much. Remember how we said the patient presented an urgent care, got blood work, and then came in? So when he came to the ER, his eosinophilia was already known. So I intentionally kept my HPI very similar to the initial note written by the medical student in the ED who knew about eosinophilia. And you can tell he or she was thinking “OMG IT’S A PARASITE”. They probed all that ingestion and travel history out of the patient, right? I wanted to maintain the same framing effect that all the providers later were exposed to.
John: I see, so you’re saying there’s a certain realism to what you did. You mean you tried to tell him the same “story” that this patient’s real-life attending must have gotten — preconceptions and all.
Cindy: Yes, obviously I know the outcome of the case… I looked up the whole course and retrospectively and perhaps selectively put it together for presentation. But in real life, you can easily encounter a presenter who really wants a theory to be real, they end up presenting the story a bit differently.
John: This might be a bit of an aside, and I might be biased as an internist, but I feel I might go so far as to say that storytelling is the second most important function of a clinician? [Cindy: What’s the most important function?] Uhh… Oh God. That was a loaded sentence. …I’ll have to think about that. I just know it’s not the most important thing — if storytelling was our most important function, we’d be bards. It can’t be the most important thing… [Cindy: Fine.]
What I’m trying to say is that, yeah, the patient tells you their story, but you extract data from that telling, you combine it with your objective data from your tests, and you construct a new story, right? A new story, a more consistent story, one that fits what you think is going on. And when you call a consult, you tell a shortened version of that story. And a lot of training in residency, like writing HPIs, learning how to create one-liners and craft nighttime hand-offs, it’s all about honing our storytelling skills. Every time we’re hearing a story, it’s someone’s version of that story, it’s always from someone’s perspective.
Viswanathan: Abstractly I think it’s almost like a nice PDSA cycle. So it’s a continuing evolution of, “Does this piece of information, does it fit into my narrative?” And if not, should I actually stop and think about my narrative, and then go back and say, “Okay, if this isn’t the narrative that I think is going on with the patient, then how can I tie this piece of information with everything else?”
Cindy: So I’m gonna take this chance to digress again, and talk about framing bias, a term we hear in M&Ms a lot. We often define framing bias as, “The manner in which data is presented can affect decision making.” To an extent, a different story telling perspective can be a kind of framing. Framing as a psychological phenomenon was first described by prospect theory. The prospect theory describes how people’s decision making behavior is affected by their perspective of loss and gain in gambling.
Most of the research in the medical field on framing usually had studies designed in positive or negative terms, like how it was described in the prospect theory (“Glass half full” or “half empty”? Do you present a treatment as having 70% cure rate or 30% failure rate? Then they study the subjects decision making as they perceive how the numeral numbers are presented). When we talk about the framing effect in real life, or in M&M conferences, we typically are extrapolating and talking about the broader meaning – that the manner in which data or the narrative is presented can affect our perception of the case. When used in this abstract term, it is difficult to measure how prevalent and pervasive framing bias is in our everyday clinical practice. If all our cases are being presented to us by someone, and all stories have the potential to be framed, that just makes me so sad. Well, if I just ignore everything my med student and interns and residents tell me, and go straight to the source and only gather data from my patient, then I should be okay, right?
John: I mean, your objective is my subjective, Cindy. You want to take care of the patient yourself, that’s fine.
But I think I have another objection. Let me just ask you this question: Do you think the patient actually came in and volunteered that he had a white streak in his stool? Remember he came in because he was having abdominal pain and fever, those were his chief complaints. Or did that become a prominent feature of the story after he was interviewed by one, two, five, too many times by providers, who all knew he had that eosinophilia of 17,000?
Cindy: You know, as I did wonder that when I put together the case Like you said, the patient is the original story teller. And in the past episodes we talked about reasons why you should not always take the patients words at face value: language barriers, cultural differences, health literacy, etc. ext. It may be difficult for some patients to distinguish between chest pain versus pressure.
John: And don’t forget the factor of repeat interviews. As patients get interviewed over and over again, as they get re-exposed to us, to the healthcare setting, their stories change. They start to incorporate our vocabulary. A patient with prolonged chest pain that comes in every month for ACS rule out? On the first visit they probably did not start out calling their pain “substernal, crushing, exertional, and 9/10”. But as I meet someone who’s been in the chest pain unit 14 times, I’m cognizant that what I’m hearing now is no longer their original experience, their original perception — it’s not their words. I’m starting to hear the words of the doctors who have taken care of this patient before.
Cindy: Psychologists have done a lot of studies on the topic of memory recall, mainly in legal settings in terms of accuracy of eyewitness testimony. You know that question your patients always ask you when you meet them for the first time the morning after they are admitted?
John: …The first question they ask me? “You’re a doctor???” Or, “I feel great, can I go home now?”
Cindy: No, it’s “I answered these same questions FIVE times already, don’t you doctors talk to each other”? Well, it turned out the system is set up this way for a reason. Psychologists who study memory recall learned that repeat interviews aid memory retention and retrieval, and some factual details only surface after repeat interviews. But at the same time there are many factors embedded in repeat interviews can also distort accuracy of memory recall: duration of interviews, form of questions used in the interview, the number of people being interviewed together, their age, their confidence level, and so many other elements. It’s not uncommon that information can be distorted, or even created, without the interviewees knowing that.
John: So when you were reviewing that literature, Cindy, did they talk about solutions? Repeat interviews are just a fact of modern medicine, right? Is there some way to maximize the benefits while minimizing the distortions introduced by this practice?
Cindy: We know we probably need to standardize our questions and conduct objective interviews to keep the “side effects” of repeat interviews to a minimum. But how do we counter these side effects? I don’t know if I found an answer in my literature search, especially not in the medical field. For now, we’ll say it exists, be aware of it, and be aware that being aware may or may not help you avoid the problems.
John: Alright, so back to the case. So what do we have at this point? You’re saying the patient has a giant mass in the kidney, probably a solid tumor, and this is what’s causing the pain and irritation, the fever, and the eosinophilia. …Everything kind of fits, actually. Case solved?
Cindy: Not yet for Dr. Viswanathan. After betting money on malignancy and seeing a giant mass on the CT scan, he turned around and asked for a thorough infectious work up, including a full parasitic panel and an ID consult.
Viswanathan: I don’t think I’m satisfied. Why is this guy having fevers? Is there an infectious source that I haven’t thought about? I think we try to aim to tie everything to one process. However, in reality, we often see patients with simultaneous processes, parallel processes that just intersect in time. And we actually see this all the time. We see patients coming to the hospital and they have incidentally-diagnosed malignancy because they came in for pneumonia and
So I think looking at him initially, with that leukemoid reaction sort of white count, with the high white count, fever, tachycardia — It’s not something where I want to just say, “Oh, it’s definitely this large mass that doesn’t look infectious at all, looks like it may just be this nice mass that’s not bothering anyone.”
I don’t think we’ve really had a satisfying answer about what this fever is. I wouldn’t feel comfortable about initiating any treatment until a thorough infectious workup was done.
John: So Cindy, for this patient — what happened in the end?
Cindy: In real life, GU oncology was consulted, and he thought this could be renal cell carcinoma. He requested a thorough ID work up, for the same reason Dr. V suggested — this patient fulfilled sepsis criteria, and the oncologist would love to rule out all other causes before he commits the patient to possible post-op chemotherapy. HIV, blood parasite, O&P, schistosomiasis, and a lot of parasites I cannot even pronounce were tested. Like the rest of the infectious work up, they all came back negative.
Ultimately the mass was surgically resected. The path returned as a benign sarcoma. Stains for fungal and AFB were all negative. By post-op day five, the patient was completely afebrile. The eosinophilia resolved. The cough also resolved, so it was thought to be from diaphragmatic irritation. He was discharged home good as new.
John: Hang on. I would’ve bet money it was RCC. Benign sarcoma…?
Cindy: It’s rare, it’s case reportable, but it can cause a high eosinophilia like this.
John: Wow. Case reportable.
Cindy: I’m sorry… I try to find Hoofbeats cases, not zebra cases. So this one doesn’t fit our segment’s name here.
John: And the eosinophilia was gone by day 5?
Cindy: It really plummeted post-op. By the sixth day it was down to about 600.
John: And the mechanism? Do we know anything about that?
Cindy: I tried my best to read up on it. There are theories about tumor-mediated inflammatory cytokines ..
John: …Never mind.
John: Alright listeners, that should do it for this episode. As always, let us know what you think.
Cindy: And remember, if you have a case you’d like to submit for discussion, or someone you’d like to come on and hear as a discussant, or if you’re interested in developing and hosting an episode, please, get in touch with us! Visit our website at www.coreimpodcast.com or send us an email at email@example.com. We are also on Facebook and Twitter, at @CoreIMpodcast.
John: Thank you to Dr. Anand Viswanathan as our discussant, Dr. Pawan Punjabi for submitting the case, as well as Drs. Amy Ou, Shreya Trivedi, and Marty Fried. Special thanks to our audio editor for this episode Harit Shah & Solon Kelleher, along with our other CoreIM colleagues.
Cindy: … And an honorable mention, as always, to Dr. Steven Liu.
John: Dr. Fang and I are general internists and faculty with the NYU School of Medicine.
Cindy: Opinions expressed in this podcast are our own, and do not represent the opinions of other affiliated institutions, nor should they be construed as medical advice.
John: Thank you for joining us. With CoreIM, I’m John Hwang.
Cindy: And I’m Cindy Fang.. See you next time.
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Tags: eosinophilia, framing bias, mnemonics