Working with Gen X: How Other Generations Can Adapt

Generation X is sandwiched between the two largest generations alive today: Baby Boomers and Generation Y/Millennials. This means that Generation X will never be the largest generation at the workplace, but even so, their impact is significant. Gen Xers are in a unique position as they started their careers relatively recently and can understand the challenges Millennials face, while also starting to enter leadership positions and can therefore relate to Baby Boomers.

One of the things that make Generation X stand out from other generations is that many of them have young children and aging parents. This means that having a work-life balance is important to them as they often have responsibilities to take care of their family members. They typically also prefer a divide between their personal and work lives. This is not to say that they do not make friends at work or not hang out with colleagues after work, but they tend to have a “business first” approach to their work relations.

When working with Generation X, note that they appreciate it if you use their time efficiently. When presenting an idea of have a meeting with them, make it as productive as possible and focus on what is in it for them. Gen Xers value brevity, fast turnarounds, and efficiency. This is a stark contrast with Baby Boomers, who focus on interpersonal relationships before getting a task done. Making your communication, whether it is in-person, over the phone, or via Gen X’s preferred mode of communication (email), as concise and to the point as possible will increase your effective collaboration with this generation.

As leaders, Gen Xers dislike micromanagement, both as a leader and as a follower. Their leadership style revolves around trusting others to get the job done and they expect the same courtesy in return. They value people doing what they say they are going to do, so do not promise Gen Xers that you will do something if you know you cannot. Their leadership style is therefore quite informal as they expect people to follow deadlines and get the job done, while giving their workers a high degree of freedom.

Generation X is an efficient generation who hate wasting time with empty words, promises, and incompetence. They appreciate immediate actions, a focus and straightforward approach to work without long social interactions. They respect child-friendly environments, such as being able to have a flexible schedule that allows them to accomplish their professional tasks while also taking care of their family members. They can brief and blunt, but they have an authentic and results-orientated approach to work. If you work with a Gen Xers, give them freedom to do their work and explore and only make promises you can keep. Keep your emails and interactions to the point and follow up quickly after a meeting. Having an efficient but friendly approach will take you far with this generation.

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-Lotte Mulder earned her Master’s of Education from the Harvard Graduate School of Education in 2013, where she focused on Leadership and Group Development. She’s currently working toward a PhD in Organizational Leadership. At ASCP, Lotte designs and facilitates the ASCP Leadership Institute, an online leadership certificate program. She has also built ASCP’s first patient ambassador program, called Patient Champions, which leverages patient stories as they relate to the value of the lab.


So what does working with a Gen Xer really mean? Does it only apply to the laboratory, or do we work with people outside of the laboratory? Hmmm. How about our family, friends, social and community relationships? That said, I took this question to the streets as well as the laboratory and asked these questions.

Boomers, what’s it like working with a Gen Xer?

Gen Xers have a good work ethic; however, their family often ranks higher than their job. Boomers pride themselves in their work ethic. The Gen Xers are still so busy taking care of their aging parents, as well as, their kids, even when they’re off at college. They are the “Sandwich Generation.”

Millennials, what’s it like working with a Gen Xer?

I took this question to the classroom where I teach. My students are all working on their Masters Degree, and by the way, I have three Gen Z students in my class. Both the Millennials and Gen Z students found that the communication with a Gen Xer is different. The stated that the Gen Xers use email, messaging and Slack. As a Boomer, I didn’t know what Slack was! The Generation Y and Z students felt that the Gen Xers were resistant to change and to some technology.

One Millennial by the name of Erika shared that she found Gen Xers relatable and at ease. I found her most profound statement to be that she said the Gen Xers seemed like they were in-between and strike a balance between the Boomers and the Millennials. Hmmm…. They are known as the “Sandwich Generation” because they are often taking care of their parents and their children, but it’s interesting Erika saw them “sandwiched” in a different way.

Time to hear from our Gen Xers and how they feel about working with the Boomers and Millennials.

Gen Xers, what’s it like working with the Boomers and Millennials?

My first Gen X interview came from a regional director of a Beverage Company. As a Gen Xer, he felt that he was more effective working with the Boomers when the communication was face to face, or on the telephone. Emails worked, but he definitely noticed the Boomer preference. On the other side of the coin, this Gen Xer found that the Millennials who worked for him or with him preferred the technology communication.

The Gen X laboratory professional I interviewed found the Boomers resistant to change. This was interesting because this is how the Millennials felt about the Gen Xers! Again, is this the “Sandwich Effect!” Overall, this Gen Xer appreciated the depth and vast knowledge of the Boomer and how they wore that hard work as a badge of pride.

Lastly, on a high note, the Gen X laboratory professional really appreciated the Millennial’s enthusiasm. The grass doesn’t grow under their feet in the work place. If they perceive there’s no place to climb the ladder, they’re off and running. The Gen Xers let go of the “Boomer Job Loyalty Program,” however, they are more stable than the Millennials in the work place.  Again, they possess the gifts from the Boomers and Millennials. They are “The In-betweeners!”

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-Catherine Stakenas, MA, is the Senior Director of Organizational Leadership and Development and Performance Management at ASCP. She is certified in the use and interpretation of 28 self-assessment instruments and has designed and taught masters and doctoral level students.  

Just Say Know! From Mentoring to High Performance: A Resident Perspective

As pathologists, we are responsible for increasingly intricate anatomic pathology and clinical laboratory services in a continually changing healthcare landscape that requires us to integrate emerging technologies for improved quality of medical care while also being hypervigilant to cost control and efficiency. Hospital systems working under managed care business models seek to expand their coverage networks and boost the number of patients served, and as such, it is going to be very critical for the next generation of pathologists to develop and implement the management skills and techniques necessary to effectively advocate for investment in their departments and meet such goals.

The problem, however, is that we are largely shielded from these issues during our undergraduate and even graduate medical education experiences. We focus, of course, on the basic sciences and clinical skills, which are undeniably important; however, we get significantly less instruction or discussion on functioning within our health care system, addressing quality issues, or general leadership training that is indispensable and highly valuable for practicing physicians.

Earlier in the summer, I saw a number of pathology folks on Twitter promoting and strongly encouraging residents to apply for the two-day “Just Say Know! From Mentoring to High Performance” program, formed through collaboration between ASCP and USCAP, on an approach to leadership, management, and business for pathology. I was highly intrigued and had a feeling this program was the sort of experience for which I had been looking. Traveling to Palm Springs in the middle of the Chicago winter was not a bad deal either!

Drs. Blair Holladay and David Kaminsky assembled an impressive collection of speakers for the weekend, which was divided into four focus areas: leadership, management, business and policy, and change. After an engaging introduction by Drs. Holladay and Kaminsky, current trainees Drs. Kabeer Shah and Melissa Hogan set the stage by highlighting the increasing importance of “management” and “leadership” as reflected in the ACGME milestones as well as recent literature suggesting expectations for newly-trained pathologists include these very skills (Post et al. Arch Pathol Lab Med 2017;141: 193-202).Above all, they encouraged all of the thirty residents and fellows in attendance to “be honest, be open, and be vulnerable,” and ask the tough questions of themselves to gain the most from the weekend.

Lotte Mulder from ASCP led an enlightening discussion on the differences between emotional intelligence (EI) and conventional IQ, as well as the critical need to be self-aware of how our emotions can affect our performance and to understand the extent of our own abilities, strengths, and weaknesses. Dr. Karen Kaul followed with a very timely overview of strategies for identifying mentors. She discussed how our mentorship needs will evolve over the course of our careers and that fulfilling the mentor role for another junior individual while having your own mentors is key to the professional development necessary in leadership positions.

 After lunch, Dr. Dan Milner from ASCP took us through some very interesting global health case studies that forced our group to think critically about the role of pathology and the clinical laboratory in underserved settings as well as the major obstacles and economic disparities that must be considered. There were a number of important teaching points from Dr. Milner’s international cases that will be equally helpful for understanding the disparities we encounter right here in our backyard.

Dr .Yael Heher led off the afternoon management focus series with a really comprehensive look into how she has championed quality improvement and patient safety reviews at her institution to address root causes for laboratory errors, followed by a well-timed interactive session in which we divided into groups to use the six sigma methodology to work in concrete steps through a real-life laboratory error. It was a great opportunity to see people from different institutions and backgrounds bring unique perspectives to a common problem. The first day of the program concluded with a very unique session on art and leadership in which Dr. Kaminsky led us into Downtown Palm Springs to view the Palm Springs Babies art installation set up by David Cerny. Our powers of observation as pathologists were put to the test as we were asked to describe and interpret the meanings behind the exhibit in the same way that we often use visual evidence in our day-to-day work.

The second day of the program focused on business and policy with talks by Dr. Gary Procop on how pathologists can help integrate interventions into the laboratory to improve system-level metrics and by Khosrow Shotorbani on how laboratory data can be used to optimize laboratory services in the model of the rideshare service, Uber. The morning also included an interactive session on negotiation skills, in which each of us assumed the roles of departmental chair and owner of a private practice group negotiating with newly-hired pathologists. The weekend concluded with Dr. Nathan Johnson’s 18 steps to make change a part of an organizational culture, which was based on his experiences in academic research, military operational theory, and real-life lab experiences.

The weekend provided an incredibly impactful and high-yield array of discussions, so much so that I am already finding myself applying many of the strategies and techniques described over the weekend in my role as chief resident as well as to some of the changes and initiatives that I am hoping to bring to our department. Most important, though, were the opportunities to interact with my peers from around the country. We all face similar challenges as residents, and the opportunity to learn each other’s perspectives and approaches to similar issues was just as illuminating as the structured portions of the program. I hope that the ASCP and USCAP continue to offer the Just Say Know! Program and enthusiastically join all those pathology folks on social media promoting the program last summer with my own strong recommendation to challenge yourself and be open to new ways of learning by considering participating in this event!

From Twitter, @Blair_Holladay, December 12, 2018
Photo by Imran Uraizee

-Imran Uraizee, MD, is currently chief resident and a third-year anatomic and clinical pathology resident at the University of Chicago. He also manages the Department of Pathology Twitter account, @UChicagoPath. He majored in Biology at Duke University before earning his MD at the University of Rochester School of Medicine and Dentistry. Dr. Uraizee can be followed on Twitter at @IUraizee3MD.

Hematopathology Case Study: A 43 Year Old Man with Difficulty Breathing

Case History

43 year old man presented with symptoms of superior vena cava syndrome including swelling of the head and neck and difficulty breathing. He was found to have a 9 cm anterior mediastinal mass on imaging.

Excisional Biopsy

Top: H&E morphology of diffuse large cells infiltrating through fibrotic tissue.
Bottom: Small lymphocytes with scattered large multinucleated Hodgkin and Reed-Sternberg (HRS) cells.
Left: CD30 showing dim/variable staining in the diffuse large cell component.
Right: CD30 highlighting Hodgkin and Reed-Sternberg cells with a golgi and membranous staining pattern.
Left: CD15 showing golgi staining in the diffuse large cell component.
Right: CD15 highlighting Hodgkin and Reed-Sternberg cells with a golgi and membranous staining pattern.
Left: CD20 diffusely highlighting the large cell infiltrate.
Right: CD20 highlighting small B-cells surrounding a negative HRS cell.
Left: PAX5 diffusely highlighting the large cell infiltrate.
Right: PAX5 showing bright staining in small B-cells surrounding a dimly stained HRS cell.
Left: Ki-67 showing a high proliferation index (90%) in the diffuse large cell component.
Right: Ki-67 showing increased staining in the HRS cells.

Diagnosis

Sections show fragments of fibrotic tissue with crush artifact. Two distinct morphologies are seen in different tissue fragments. Some tissue fragments show infiltration by cords and aggregates of abnormal large lymphoid cells with irregular nuclear contours, somewhat vesicular chromatin, small nucleoli and small to medium amounts of cytoplasm. Frequent apoptotic cells and mitotic figures are seen. In other tissue fragments, the large cell component is absent and there are focally vague nodules. The nodules are composed of small mature appearing lymphocytes, rare eosinophils and scattered medium and large mononuclear and multinucleated cells with prominent nucleoli consistent with Hodgkin cells and Reed-Sternberg cells, respectively. Admixed histiocytes are also seen.

By immunohistochemistry, the areas with different morphologies also show different staining patterns. The areas with the large cell infiltrate are immunoreactive for CD20, BCL6, and MUM1, dimly positive or negative for CD45 and negative for CD10. CD30 is variably positive in the large cell population and CD23 is largely negative. CD15 shows a golgi staining pattern. The Hodgkin and Reed-Sternberg (HRS) cells present in the areas without the large cell infiltrate are brightly immunoreactive for CD30 and CD15 (membranous and golgi pattern), dim positive for PAX5 and are negative for CD20. CD20 and PAX5 highlight small B-cells present in aggregates surrounding the HRS cells. By Ki-67 staining, the proliferation index is high (90%) within the diffuse large cell component and also highlights the HRS component.

Overall, the findings are of a composite lymphoma composed of both a diffuse large B-cell lymphoma (DLBCL) and a classic Hodgkin lymphoma (CHL).  

Discussion

Composite lymphomas occur when two morphologically and immunophenotypically distinct lymphomas occur at the same anatomical site. They are most commonly composed of two Non-Hodgkin B-cell lymphomas (NHL), however rare cases of composite CHL with NHL have been reported. In a review of the literature, Goyal et. al. documented 20 previously reported cases of composite lymphoma with CHL and DLBCL components. The median age at presentation was 51 years with 12 men and 9 women. Fifteen of the cases presented with nodal involvement and of those, three had mediastinal disease. The most common subtype of CHL was nodular sclerosis. Evaluation for IGH gene rearrangements was performed on both components of 6 cases, with either a complete or partial clonal relationship between the components seen in all of the cases tested. This suggests a shared origin from a common B-cell precursor.1

A review of literature by Wang et. al. documented 10 previously described composite lymphomas consisting of DLBCL and CHL. The most common site of occurrence was in lymph nodes, followed by three cases seen in the stomach, one case in the small intestine and one case in the anterior mediastinum. CHL is more commonly associated with EBV infection than NHL In the reviewed cases, 6 showed positivity for EBV infection in both the DLBCL and CHL components. This suggests that the lymphomas shared a common EBV-infected progenitor cell, and are also clonally related as seen in the Goyal review. 2

Composite lymphomas must be distinguished from another WHO defined entity called B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and classic Hodgkin lymphoma. This entity has previously been referred to as “grey-zone lymphoma.” These lymphomas tend to present as mediastinal masses and can cause superior vena cava syndrome. They show a wide spectrum of histologic appearances within a single tumor and often show sheet-like growth of pleomorphic cells. Some areas may resemble CHL while others resemble DLBCL. The neoplastic cells typically do not show the characteristic immunophenotype of either CHL or DLBCL. Areas that may resemble CHL will show preservation of B-cell markers, while areas more characteristic of DLBCL might lose B-cell markers and express CD30 and CD15. These tumors will show clonal rearrangement of the immunoglobulin genes. They tend to have a more aggressive clinical course and worse outcome than either CHL or DLBCL. 3

This case was ultimately diagnosed as a composite lymphoma (CL) because it consisted of separate areas with the morphologic and immunophenotypic features of both classic Hodgkin lymphoma and diffuse large B-cell lymphoma. Patients tend to have a poor prognosis with short survival. There is no standardized treatment for composite lymphomas due to their rare occurrence; however cases with a component of DLBCL are generally treated with aggressive chemotherapy such as R-CHOP.

References

  1. Goyal, G. et al. “Composite Lymphoma with Diffuse Large B-Cell Lymphoma and Classical Hodgkin Lymphoma Components: A Case Report and Review of the Literature.” Pathology – Research and Practice vol. 212,12(2016):1179-1190. http://www.ncbi.nlm.nih.gov/pubmed/27887763.
  2. Wang, Hong-Wei et al. “Composite diffuse large B-cell lymphoma and classical Hodgkin’s lymphoma of the stomach: case report and literature review” World journal of gastroenterology vol. 19,37(2013):6304-9.
  3. Swerdlow SH, Campo E, Harris NL, et al. WHO Classification of Tumours of Haematopoetic and Lymphoid Tissues (Revised 4th edition). IARC: Lyon 2017.

Chelsea Marcus, MD is a Hematopathology Fellow at Beth Israel Deaconess Medical Center in Boston, MA. She has a particular interest in High-grade B-Cell lymphomas and the genetic alterations of these lymphomas.

Dead Wrong About Forensic Pathology

(•_•)         ( •_•)>⌐■-■       (⌐■_■)

[Puts my sunglasses on dramatically]

[Won’t Get Fooled Again by The Who plays]

Image 1. Looks like this medical lab science blogger made quite the … shady… joke. CSI: Miami’s Lt. Horatio Caine (played by David Caruso) donned his shades at pivotal plot times. (Source: CBS)

Okay-okay, I couldn’t resist that. How many times have you just wanted a CSI-style joke on here? No? Just me? That’s fine…

Hello again everybody! Welcome back! Last month I talked a bit about “Just Culture,” a sort of bridge between the values we tout as clinical leaders in our laboratories and the medical culture’s evolving and value-informed paradigm shift. There was a little in there about the lessons paralleled in LMU and the benefits of interdisciplinary teamwork. This month, on the subject of interdisciplinary collaboration, I’d like to talk about our colleagues who often are secluded or in more remote areas in our hospitals, offices, and academic centers. Not here to stereotype; I’m talking about our friends in forensic pathology!

Before I get there, let me go back a bit. I’ve already written several times about the stereotypes that surround our field of lab medicine and there are two times when that is glaringly present: when you’re a medical student or when you’re in forensics. I got the chance to meet someone who falls into both categories.

I’ve just finished up my OB/GYN rotation. But before my last day, I went to the lab at our hospital and followed up on some pending biopsy results. Okay, I can’t lie to you guys: they wanted me to see if I could rush “my lab friends” to expedite the process of fixing, setting, cutting, staining, and reading/reporting—because that’s possible. So, I went to the lab and had a pleasant chat with the staff explaining the situation and they were happy to help. While I was there, however, I happened to see another short white coat (ironically from my same school) who was helping some lab personnel with some grossing. Turns out she wants to match into a pathology residency—just like me—and specifically was interested in forensic path, a field which I don’t know much about. After talking more, I asked if she’d like to share some information. Here’s my conversation with Kyla Jorgenson, a 3rd year medical student at AUC-SOM from Toronto, Canada:

I get lots of hassle when I say I want to become a pathologist. People often ask me, “what’s your back up choice” or “don’t you like patients?” It can be a challenge. What’s your experience been like?

You want to do autopsies, so you want to be a mortician, right? Not quite. Many times, I’ve been faced with blank stares when I say I want to be a forensic pathologist. Other times I get the other end of the spectrum, that’s so cool! Clearly, they’ve seen a few crime-shows and think that I’ll get to go to crime scenes in stiletto high heeled shoes with a song by The Who playing in the background as I arrive. Even today when talking with a dermatopathologist I got a, “well when you realize that hanging out with dead bodies every day isn’t the greatest, you might consider surg path.” Then after hearing my experience as an autopsy assistant and that I’m sure this is what I want to do it was the resigned sigh signalling that I was a lost cause already.

A “lost cause,” that’s frustrating. A lot of specialities rag on other ones, it seems to be part of the culture of medicine—hopefully not forever, but still can’t we all just get along?

So, my background leading to pathology involved me working for several years between college, graduate school, and medical school; in hospitals of various sizes. I have personal experiences in these fields and sort of feel “at home” when I’m dealing with hematopathology, transfusion medicine, cell therapy—that sort of thing. What piqued your interest in forensics?

I started my undergraduate degree in forensic biology at the University of Toronto in the fall of 2008 just as a major review of pediatric forensic pathology in Ontario was being released. After numerous issues came to light, the inquiry looked at policies, procedures, practices, accountability and oversight mechanisms, quality control measures and institutional arrangements within the field in Ontario from 1981 to 2001. Ontario Court of Appeal’s Honourable Justice Stephen T. Goudge developed 169 recommendations on how pediatric forensic pathology in Ontario needed to address and correct its systemic failings to restore public confidence.

(Read more about these inquiries here: https://www.attorneygeneral.jus.gov.on.ca/inquiries/goudge/index.html)

After studying the cases that prompted the inquiry and its recommendations in class, what left the greatest impression was the importance of having medicolegal autopsies performed by those trained in not just pathology, but specifically, forensic pathology. What I took away from the cases of accidental deaths falsely attributed as homicides due to lack of experience on behalf of the pathologist and other such issues, is that forensic pathology isn’t something to be dabbled in. While our patients are no longer alive, there are lives that can be affected by the work we do. In Ontario, false convictions not only stemmed from “junk science” but also from inadequacies in the training of pathologists working in a forensic capacity and also a general shortage of forensic pathologists.

Seems like a lot of us (of the few of us) who enter medical school knowing we want to go into pathology have to sort of wait their turn, as it were, collecting experiences which help make us competitive for residency matching—what keeps your “commitment algorithm” going?

Since discovering that forensic medicine is a career path as a high school student, I’ve geared my education towards training in forensics. First my undergraduate degree and then a side trip for my master’s degree in Forensic Death Scene Investigation and a job as a pathology technician at the Medical Examiner’s office on my way to medical school. I have in each step along the way, confirmed that both medicine and forensics fascinate me. Scroll through my Netflix account and you’ll find crime dramas (with the British shows being my favourite) or my podcast app filled with true crime shows; I am enraptured using science to figure out what happened.

Sidebar: at this point Kyla showed me a first-author published piece in the Journal of Forensic Sciences from 2017 that talked about law enforcement-involved firearm related deaths in Oklahoma, where she worked at the time. Basically, it showed through metadata analysis that gun-related deaths were on the rise. Not just over time, but number of times being shot. Remember when we talked about pathology’s role in the #StayInYourLane/#ThisIsOurLane discussion? Well which pathology speciality do you think works with this stuff directly? Chemistry? Cytology? Last time I checked GSWs don’t get screened for lead poisoning and you can’t FNA a bullet. Forensic pathology has often been tasked with seeing trends in morbidity and mortality and translating that to effective social and public health change: think seatbelts, stents, and maybe someday gun-related legislation changes.

Image 2a. Monthly aggregates of gun-related deaths over a 16-year period in OK. (Source: Jorgenson, K et al (2017) Trends in Officer-Involved Firearm Deaths in Oklahoma from 2000-2015, Journal of Forensic Sciences, doi: 10.1111/1556-4029.13499)
Image 2b. Number of gun shot wounds per victim over time. (Source: Jorgenson, K et al (2017) Trends in Officer-Involved Firearm Deaths in Oklahoma from 2000-2015, Journal of Forensic Sciences, doi: 10.1111/1556-4029.13499)

I was interested when I shadowed at the Cook County ME’s office a few years ago—I saw some cool things. I also remember learning a lot from the first real autopsy I saw in a hospital, ultimately it seems like a totally different field that maybe gets underappreciated even within the pathology umbrella. AP/CP residents have to do a certain number of autopsies to graduate, but the attitude I’ve noticed around the topic is a “necessary evil” and most are working towards not having to do that. So let me ask you definitively, why forensic pathology?

Medicine is science being applied to find out what happened in the body and how we can change or manipulate those variables to diagnose, prevent, treat and manage disease. Each diagnosis is solving a crime occurring within the cells in the body, if you will. In forensic medicine, not only do you get to do all that but add in the crime solving element and you get to be “Dr. Nancy Drew.” While medicolegal systems are different all over the US and Canada, chances are that as a forensic pathologist you won’t only be working on your stereotypical “forensics” cases, the gunshot wounds, stab wounds and other nefarious causes of deaths many associate with that term. You could get the generic, “cause of death atherosclerotic cardiovascular disease, manner of death natural,” for a large proportion of cases.

It’s not glamorous, you could spend your day with a two-week-old decomposing decedent that has a pulsating maggot mass devouring its torso or documenting 51 stab wounds or signing out your cases after reviewing your histology and toxicology reports or testifying on a homicide case you worked on. But for me, those all sound like pretty interesting ways to spend the day, sign me up. As a pathology technician assisting with the autopsies and external exams, I was never required to think about what was happening in the body, but I wanted to understand it all. Now as I progress through medical school and look towards residency and fellowship, I eagerly await the chance to perform my first autopsy as a physician, to put all the knowledge and experience I’ve gained towards helping move Ontario and forensic pathology forward.

Image 3. Kyla M. Jorgenson is a 3rd year medical student at the American University of the Caribbean School of Medicine with prior undergraduate and graduate studies in the field of forensic pathology, professional experience as an autopsy technician, as well as a vested interest in pursuing a career in the field moving forward in residency and fellowship. (Source: Kyla M. Jorgenson)

I’d like to thank Kyla for her time in talking with me and her willingness to share her insights with all of you. I wish her all the best of luck as she continues through her training with electives and core rotations both in the UK and state-side. If you have any questions to relay to her, please feel free to comment below and I will forward appropriately. And as always, don’t forget to share with your colleagues across every discipline!

Thanks for reading, I’ll see you next time where I’ll be writing from the Mayo Clinic Hospital in Rochester, Minnesota, conducting a formal rotation in Anatomic and Clinical Pathology! Don’t miss it, I’ll have lots to share while learning at one of the nation’s top institutions!

Until next time!

–Constantine E. Kanakis MSc, MLS (ASCP)CM graduated from Loyola University Chicago with a BS in Molecular Biology and Bioethics and then Rush University with an MS in Medical Laboratory Science. He is currently a medical student actively involved in public health and laboratory medicine, conducting clinicals at Bronx-Care Hospital Center in New York City.

Surgical Pathology Case Study: A 64 Year Old Man with History of Loose Stools and Abdominal Pain

Case History

A 64 year old male presented with a one year history of loose stools, lower abdominal crampy/gassy pain that improved with defection, and an unclear history of melena. A colonoscopy revealed a circumferential, villous, carpet-like lesion extending from 15 cm to the anal verge, with biopsies demonstrating fragments of a villous adenoma. A follow-up CT scan was negative for metastatic disease. The decision was then made to proceed with a low anterior resection with hand-sewn colo-anal anastomosis and diverting loop ileostomy.

Diagnosis

Upon opening the rectum, a 13.8 cm long circumferential, carpet-like lesion is identified, extending to the distal margin (Image 1). Sectioning demonstrated a lesion with a maximum thickness of 1.0 cm, which grossly appears to be confined to the mucosa. Due to the prior biopsy history of a villous adenoma, the entire lesion was completely submitted. This required 116 blocks to be submitted, which were then mapped out to show where each block would have been taken from (Image 2). Although there were many foci of intramucosal carcinoma present, clear cut submucosal invasion was not identified, and the specimen was signed out as a villous adenoma (Image 3).

Image 1. Opened rectum demonstrating the 13.8 cm-long carpet-like lesion.
Image 2. Mapping the lesion to show from where each block is taken.
Image 3. Photomicrograph showing the transition from normal mucosa (black arrow) to villous adenomatous tissue (red arrow).

Discussion

Polyps are an abnormal tissue growth that is a common occurrence within the colon, although they can also be found throughout the small intestine, stomach and esophagus. Polyps can be further classified as being neoplastic or non-neoplastic based on the histological pattern of the cells. The most common types of neoplastic polyps found within the GI tract are colonic adenomas, which are benign polyps that serve as precursors to the majority of colorectal cancers. Nearly half of adults in the Western world will develop adenomas by the age of 50, and there is no gender predilection. It is because of this that it is recommended that all adults get a colonoscopy by the age of 50 (even earlier when there is a family history of developing colorectal cancer).

Most polyps are small, measuring 0.5 cm or less, but can grow to be over 10 cm in size (as seen in this case). When a colonoscopy is performed, these polyps can appear as sessile, meaning flat, or pedunculated, meaning on a stalk. Due to the abnormal epithelial growth of the mucosa, the surface of an adenoma can have a velvety appearance, resembling that of a raspberry. Most patients will not demonstrate any symptoms from their polyps, with the exception of occult bleeding and anemia which are associated with larger polyps.

Dysplasia, which literally means “disordered growth”, occurs when the individual cells lose their uniformity and architecture, often resulting in cells with a hyperchromatic nuclei and a high nuclear to cytoplasmic ratio. The presence of dysplasia contained within the epithelium of a polyp is what classifies the polyp as an adenoma (Image 4). Based on their epithelial growth pattern, adenomas can be classified as either tubular adenomas or villous adenomas. Tubular adenomas tend to be smaller polyps, with a smoother surface and rounded glands on histologic examination. Villous adenomas, in contrast, tend to be larger polyps with long, slender villi noted on histology (Image 5). If an adenoma contains a mixture of tubular and villous elements, they are classified as tubulovillous adenomas. When a dysplastic cell is no longer contained within the epithelium, and instead breaches the basement membrane which separates the epithelium from the underlying tissue, it is termed invasive.

Image 4. Photomicrograph of the villous adenoma, demonstrating the dysplasia that is confined to the mucosa and not extending to the deeper tissue.
Image 5. Photomicrograph of the long, slender villi that are commonly seen in villous adenomas.

What makes this case so interesting is that there is a direct correlation between the size of an adenoma, and the risk of developing colorectal cancer. This is not true with most other cancers, however, as size plays no part in determining whether the tumor is cancerous or not. With colon polyps, the larger the polyp, the greater the chance of developing invasive carcinoma (i.e. cancer). This is why screening colonoscopies are so important. Studies have shown that regular colonoscopies, combined with the removal of the polyps found on the exam, reduce the incidence of colorectal cancer. Why this case is so interesting is that you could assume based on the size of this polypoid lesion, you would find some invasive component. However, after reviewing 116 blocks, not a single focus of invasion could be identified.

It should be stated that although there is a correlation between an adenomas size and the risk of developing cancer, the majority of adenomas will not progress to cancer, and in fact, there are no tools currently available that help to determine why one patient’s adenoma will progress to cancer, while another patient’s adenoma will not.

References

  1. Association of Directors of Anatomic and Surgical Pathology, adapted with permission by the American Cancer Society. Understanding Your Pathology Report: Colon Polyps (Sessile or Traditional Serrated Adenomas). cancer.org. https://www.cancer.org/treatment/understanding-your-diagnosis/tests/understanding-your-pathology-report/colon-pathology/colon-polyps-sessile-or-traditional-serrated-adenomas.html. Accessed February 14, 2019.
  2. Colon Polyps. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/colon-polyps/symptoms-causes/syc-20352875. Accessed February 14, 2019.
  3. Turner JR. Polyps. In: Kumar V, Abbas AK, Fausto N, Aster JC. Robbins and Cotran Pathologic Basis of Disease, 8th edition. Philadelphia, PA: Elsevier, Inc; 2010: 815-820

-Cory Nash is a board certified Pathologists’ Assistant, specializing in surgical and gross pathology. He currently works as a Pathologists’ Assistant at the University of Chicago Medical Center. His job involves the macroscopic examination, dissection and tissue submission of surgical specimens, ranging from biopsies to multi-organ resections. Cory has a special interest in head and neck pathology, as well as bone and soft tissue pathology. Cory can be followed on twitter at @iplaywithorgans.


Hematology Case Study: Symptomatic Anemia in Myelodysplastic Syndrome with Progression to Acute Myelogenous Leukemia

The patient is a 77 year old woman who presented in late Jan 2019 with severe anemia. In Feb 2017 she was diagnosed with myelodysplastic syndrome with no evidence of transformation to acute myelogenous leukemia. A bone marrow biopsy at the time showed 5-7% blasts in the bone marrow. She went through 5 rounds of chemotherapy with Vidaza (azacytidine) over the course of 9 months, with no significant response. She received one unit of RBCs with her 4th round of chemo and was given Aranesp (darbepoetin alfa) injections for anemia support. Aranesp is a man-made erythropoiesis stimulating protein which can be used to treat symptomatic anemia associated with myelodysplastic syndromes (MDS). After the 5th cycle of chemo, because of the lack of response, Vidaza was discontinued. Since then she has received several RBC transfusions to treat anemia and the Aranesp injections have continued.

In Oct 2018, the patient’s CBC showed leukocytosis, anemia, thrombocytopenia and neutrophilia.  See results below:

Patient results 10/2018       reference ranges

WBC  31.6                         4.5-10.5 x 103/μL

RBC  3.0                           3.7-5.3 x 106/μL

Hgb  7.0                            12.0-15.5 g/dl

Hct  23.6                            36.0-46.0 %

MCV  78.4                         80-100 fl

Plt  82                                150-450 x 103/μL

The CBC with automated differential performed at this visit flagged for a smear review. The technologist suspected blasts and the slide was sent for a pathologist’s review. The pathologist’s interpretation was that the differential showed “an aberrant myeloblast population, representing 6% of leukocytes along with an immature appearing monocytic population with phenotypic aberrancies representing 21% of leukocytes.” A leukemia/lymphoma flow cytometry was ordered. Results of the flow cytometry commented that an acute myeloid leukemia could not be excluded, however the differential diagnosis could also include chronic myelomonocytic leukemia. 

By Jan 2018, the patient was receiving blood transfusions every 6-8 weeks. CBC results from this visit shown below:

Patient results 1/2019         reference ranges

WBC  36.5                         4.5-10.5 x 103/μL

RBC  2.7                           3.7-5.3 x 106/μL

Hgb  6.2                            12.0-15.5 g/dL

Plt  65                                150-450 x 103/μL

Unfortunately the differential on this visit showed over 25% myeloblasts, confirmed by pathologist’s review. This sample was sent out for a second leukemia/lymphoma panel. A myeloblast phenotype was detected representing 27% of the leukocytes.

Diagnosis: Acute monoblastic/monocytic leukemia, no remission.

Image 1. Blasts, RBC morphology consistent with severe anemia
Image 2. Blasts seen on slide.

Myelodysplastic syndrome is a disorder of hematopoietic cell production involving clonal proliferation of an abnormal hematopoietic stem cell. It is most commonly diagnosed in patients in their 70s. Failure of the bone marrow to produce mature healthy cells is a gradual process, and therefore MDS is not necessarily a terminal disease. However, pancytopenia is a hallmark of MDS, and when pancytopenia is accompanied by the loss of the body’s ability to fight infections and control bleeding, MDS can be fatal. In addition, patients with MDS have a high risk of conversion to AML. About 30% of patients diagnosed with MDS will progress to acute myeloid leukemia (AML).

This patient was exhibiting pancytopenia, with accompanying anemia and infections, until her WBC began climbing several months ago. This was accompanied by the left shift and blasts seen on the peripheral smear, and prompted the flow cytometry studies.

Acute monoblastic/monocytic leukemia is considered a type of acute myeloid leukemia. In order to fulfill World Health Organization (WHO) criteria for AML-M5, a patient must have greater than 20% blasts in the bone marrow, and of these, greater than 80% must be of the monocytic lineage. AML-M5 can further be classified as M5a or M5b depending on whether the monocytic cells are predominantly monoblasts (>80%) or a mixture of monoblasts and promonocytes (<80% blasts).

The patient’s situation was discussed with the patient and her family. The patient chose more conservative and palliative treatment options over further chemotherapy.

References

https://www.merckmanuals.com/professional/hematology-and-oncology/leukemias/myelodysplastic-syndrome-mds

http://wiki.clinicalflow.com/amol-acute-monoblasticmonocytic-leukemia-m5

-Becky Socha, MS, MLS(ASCP)CM BB CM graduated from Merrimack College in N. Andover, Massachusetts with a BS in Medical Technology and completed her MS in Clinical Laboratory Sciences at the University of Massachusetts, Lowell. She has worked as a Medical Technologist for over 30 years. She’s worked in all areas of the clinical laboratory, but has a special interest in Hematology and Blood Banking. When she’s not busy being a mad scientist, she can be found outside riding her bicycle.

Hematopathology Case Study: A 33 Year Old Man with a Mass Behind the Ear

Case History

A 33 year old man of Japanese ethnicity presents with a 2 month history of a mass behind the right ear. Examination reveals a non-tender local with no other local or generalized adenopathy or hepatosplenomegaly. Laboratory investigations reveal an elevated ESR, serum IgE and peripheral blood eosinophilia. The lesion is excised.

Biopsy Findings

H&E stained sections demonstrate a follicular hyperplasia. The germinal centers demonstrate polarity and tingible body macrophages (A). Focally, follicular centers reveal eosinophilic microabscesses (B, C). Immunohistochemical analysis with an IgE stain reveals deposition in germinal centers (D). A diagnosis of Kimura disease is rendered.

Discussion

Kimura disease, also known as eosinophilic lymphoid follicular hyperplasia is a rare, chronic inflammatory disorder of unknown etiology. While an infectious etiology has been suggested, no pathogen has been identified to be causal, to date. Historically, Kimura disease was considered to be the same as Angiolymphoid Hyperplasia with Eosinophilia (ALHE); however, these entities are not the same.

Generally occurring in Asian males, Kimura disease is most common in the 3rd decade of life and in a head/neck site. It presents as painless, slow-growing adenopathy. An association with nephrotic syndrome has been reported. Peripheral blood eosinophilia, elevated ESR, and serum IgE are common findings. Histologically, nodes reveal hyperplastic follicles with well-formed germinal centers and mantle zones with deposition of IgE and eosinophilic microabscesses, as seen in this case. Perinodal soft tissue may be involved. Necrosis may be present, but is not extensive. Cytologically, FNA material may reveal polymorphous cell population with many eosinophils.

Prognosis is indolent; however, most cases recur after excision and radiation therapy usually yields best outcome.

References:

  1. Zhou P. et al. Kimura disease. Dermatol Online J. 2017 Oct 15;23(10).
  2. García Carretero R et al. Eosinophilia and multiple lymphadenopathy: Kimura disease, a rare, but benign condition. BMJ Case Rep. 2016 Aug 31;2016. pii: bcr2015214211. doi: 10.1136/bcr-2015-214211.
  3. Sun QF et al. Kimura disease: review of the literature. Intern Med J 2008;38:668–72.  

Kamran M. Mirza, MD, PhD, MLS(ASCP)CM is an Assistant Professor of Pathology and Medical Education at Loyola University Health System. A past top 5 honoree in ASCP’s Forty Under 40, Dr. Mirza was named to The Pathologist’s Power List of 2018. Follow him on twitter @kmirza