Overview of Working with Different Generations: Composite of Current Workforce

There are currently five different generations at work today: Traditionalists, Baby Boomers, Gen Xers, Millennials, and Generation Z. This means that in any work environment, you can have a group of people between the ages of 15-80. This is an exciting time to be working because we can all learn from many different generational experiences, values, and communication styles.

The two largest generations in the work place are the Baby Boomers and the Millennials. This is because these are both the largest generations in terms of population. However, with the Baby Boomers slowly moving into retirement, the Millennials are about to take over.

Traditionalists are still present in the workforce for a few reasons. First, they have tremendous experience and organizational knowledge and many organizations are trying to keep them around so that they do not lose that information. This means that Traditionalists are often Presidents of organizations or members of their Board of Directors. Secondly, Traditionalists are loyal to their organizations and they generally keep working as long as they can because of their values of security and getting the job done.

Generation X and Z are also in the workplace, but neither is very large. However, Gen Xers serve an important purpose because they are flexible and adaptable and because they value work-life balance and constructive feedback. They understand both the world without technology, so that can relate to Baby Boomers, and the world of the internet and social media, so they learn technology fast, which is appreciated by Millennials. Generation Z is only now starting to enter the workforce, so little is known about their work styles. However, they are expected to be independent, entrepreneurial, determined, and loyal.

The key to working with multiple generations is respect. Everyone wants to be respected and appreciated for what they bring to an organization. Being open and flexible to learning about different generational values and communication styles, will set any leader and employee up for success. Provide everyone with positive and constructive feedback and create a work environment that allows for more flexibility in terms of work hours, work location, and dress code whenever possible. Finally, realize that what motivates you personally is not necessarily what motivates other, especially if they are from different generations. Working with a diverse group of generational workers is a great benefit, to both the organization and to individuals.



-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.

Microbiology Case Study: A 37 Year Old Man with Endocarditis

Case History 

A 37 year old African American male was transferred from an outside hospital due to mitral valve endocarditis. His past medical history was significant for diabetes mellitus type II and end stage renal disease requiring long-term dialysis. Four months prior, he was bacteremic with methicillin resistant Staphylococcus aureus and received IV vancomycin therapy. At admission, his temperature was 102.1°F and labs revealed a white blood cell count of 25.3 TH/cm2 with 95% neutrophils and a left shift, a normocytic anemia, and a creatinine of 5.39 mg/dL. Physical exam revealed a severe mitral valve regurgitation. Various imaging modalities showed vegetations on the mitral valve, complete occlusion of the distal infrarenal abdominal aorta, several subacute infarcts in the brain, multiple sites of osteomyelitis of the spine, and a pelvic bone abscess. After collecting initial blood cultures, vancomycin and cefepime were started.

Laboratory Identification

Image 1. Large, whitish-yellow colonies grew from a positive blood culture bottle that showed gram positive cocci in clusters. These features are consistent with Staphylococcus aureus
Image 2. Susceptibility testing of the isolate revealed a vancomycin Etest minimum inhibitory concentration (MIC) of 3 µg/ml.

Multiple blood cultures were positive and Staphylococcus aureus was identified by MALDI-TOF mass spectrometry (Image 1). Susceptibility testing of the isolate showed resistance to cefoxitin and oxacillin, consistent with methicillin resistant S. aureus (MRSA). Due to a vancomycin MIC of 2 ug/ml by broth microdilution, an Etest was set up and results showed an MIC of 3 ug/ml (Image 2). Rounded up to next doubling dilution, this resulted in a MIC of 4 ug/dl, which was concerning for a vancomycin intermediate S. aureus (VISA). Repeat identification and susceptibility testing confirmed these findings. For this reason, the isolate was sent to the department of health for confirmatory testing.


 Vancomycin is the first line agent for treating infections caused by methicillin resistant S. aureus (MRSA). When MRSA isolates show reduced susceptibility results to vancomycin, they are classified as vancomycin intermediate S. aureus (VISA) or vancomycin resistant S. aureus (VRSA). This phenomenon is concerning, as it leaves clinicians with relatively few therapeutic options. Broad spectrum antibiotics such as daptomycin, linezolid, or 5th generation cephalosporins (ceftaroline & ceftobiprobe) are potential treatment selections in these cases.

The Clinical and Laboratory Standards Institute (CLSI) has set the following MIC breakpoints for vancomycin in relation to S. aureus: ≤2 ug/ml susceptible, 4-8 ug/ml intermediate, and ≥16 resistant. If elevated vancomycin MICs are encountered in the laboratory, the isolate should be checked for purity, the organism identification should be confirmed, and susceptibility testing repeated. The laboratory should notify the state health department and hospital infection prevention team if a VISA or VRSA is suspected. Further testing of the isolate by the health department and/or CDC is required. Appropriate infection control measures, such as wearing gowns & gloves and adherence to hand hygiene, should be taken to decrease the spread of VISA/VRSA, as treatment options are limited.

While not fully understood, the reduced vancomycin susceptibility in VISA isolates is thought to be due to an abnormally thickened peptidoglycan cell wall that makes it more difficult for vancomycin to reach the cell membrane and inhibit cell growth. On the other hand, VRSA isolates most commonly acquire the vanA vancomycin resistance gene from Enterococcus faecium, which confers high-level vancomycin resistance. Usually those with VRSA infections previously have been infected with both VRE and MRSA. This co-infection allows for the vanA gene to be transferred by a plasmid or transposon from the VRE to the MRSA isolate, resulting in a S. aureus isolate that is now resistant to vancomycin.

In the case of our patient, further testing by the health department showed his MRSA isolate had a vancomycin MIC of 2 ug/ml by broth microdilution (susceptible) and an MIC 3 ug/ml by Etest. It was noted these results were within a single doubling dilution. As broth micro dilution is the reference method, his isolate was considered susceptible to vancomycin. However, the elevated MICs by both methods suggest the isolate is developing reduced susceptibility to vancomycin. Due to septic emboli in various organs, he was not a surgical candidate and was managed medically with ceftaroline and linezolid.


-Jaswinder Kaur, MD, is a fourth year Anatomic and Clinical Pathology chief resident at the University of Mississippi Medical Center. 


-Lisa Stempak, MD, is an Assistant Professor of Pathology at the University of Mississippi Medical Center in Jackson, MS. She is certified by the American Board of Pathology in Anatomic and Clinical Pathology as well as Medical Microbiology. She is the Director of Clinical Pathology as well as the Microbiology and Serology Laboratories.  Her interests include infectious disease histology, process and quality improvement, and resident education.

Hematopathology Case Study: A Newborn Infant with a High White Blood Cell Count

Case History

The patient is a 1 day old baby boy born at 39 weeks to a 44 year old woman. On physical examination, the baby had a mildly flattened occiput with thickened nuchal skin, downward slant of palpebral fissures with epichanthal folds and slightly low set ears. On imaging, he had a ventricular septal defect. A CBC was performed which revealed a white count of 34.2 K/uL with a differential that included 37 blasts.

Peripheral Blood Smear 







The peripheral blood showed an increased white count, many nucleated red blood cells as well as a population of blasts. The cytogenetic analysis confirmed the suspicion of trisomy 21. Flow cytometry showed that the population of blasts expressed myeloid as well as erythroid and megakaryocytic lineage specific antigens. The patient was found to have a GATA1 mutation. Approximately one month after birth, the patient’s white count normalized to 7.2 K/uL with only 4 circulating blasts counted.


In a patient with trisomy 21, this presentation is consistent with a diagnosis of transient abnormal myelopoiesis associated with Down syndrome (TAM). TAM occurs in 10% of newborns with Down syndrome. Patients typically present with cytopenias, leukocytosis, an increase in blasts and hepatosplenomegaly. Less commonly, patients can have respiratory distress, bleeding, skin rash or jaundice. The blasts are morphologically and immunophenotypically similar to those seen in acute myeloid leukemia. They often have basophilic cytoplasm, coarse basophilic granules and cytoplasmic blebbing, which suggests a megakaryocytic lineage. The immunophenotype generally includes expression of myeloid markers such as CD117, CD13 and CD33 plus erythroid and megakaryocytic markers like CD41, CD42b and CD61.1

In addition to trisomy 21, mutations in GATA1 are almost always seen in the blast cells of patients with TAM. GATA1 is a hematopoetic transcription factor. Bhatnagar, et al. (see diagram below) describe a three step model to explain the evolution of TAM. The initial event is abnormal hematopoesis in the fetal liver caused by trisomy 21. This causes an increase in megakaryocyte-erythroid progenitors in the hematopoetic stem cell compartment.  The second step is the acquisition of an N-terminal truncating GATA1 mutation before birth. GATA1 is a regulator of normal megakaryocyte and erythroid differentiation. The truncated mutation causes marked expansion of megakaryoblastic progenitors.

TAM5TAM has a high rate of spontaneous remission and typically resolves spontaneously in 90% of patients over several weeks to 6 months. This coincides with extinction of the GATA1 clone. However, in around 10% of these patients, myeloid leukemia of Down syndrome (ML-DS) develops within 5 years of the initial presentation. Additional mutations in cohesion component genes and epigenetic regulators occur in these patients that result in clonal expansion and non-transient leukemia. 2 Children who develop ML-DS generally have a good response to chemotherapy and a have a better prognosis than children without Down syndrome who develop AML.


  1. Swerdlow SH, Campo E, Harris NL, et al. WHO Classification of Tumours of Haematopoetic and Lymphoid Tissues (Revised 4th edition). IARC: Lyon 2017.
  2. Bhatnagar, Neha et al. “Transient Abnormal Myelopoiesis and AML in Down Syndrome: An Update.” Current Hematologic Malignancy Reports5 (2016): 333–341. PMC. Web. 21 Oct. 2018.


Marcus, Chelsea_099-Edit

Chelsea Marcus, MD is a third year resident in anatomic and clinical pathology at Beth Israel Deaconess Medical Center in Boston, MA and will be starting her fellowship in Hematopathology at BIDMC in July. She has a particular interest in High-grade B-Cell lymphomas and the genetic alterations of these lymphomas.



Investing in the Best Testing

“Damn that q-tip goes in deep!

But it lit up negative so d/c to street

But it was flu, cuz he bounced back again

And now my Press Gayney’s a minus ten…”

Video 1. Another classic excerpt from a favorite: ZDoggMD, singing about this year’s flu season and available testing options on the horizon—because, let’s face it—rapid flu tests aren’t quite cutting it anymore.

Hello again everyone! Back again to talk about a new set of recommendations from last month’s post. This time it’s about influenza. Recommendation: get vaccinated. Thank you. See you next time…

Seriously, as the 2018-2019 flu season dawns upon us, it’s time to talk about vaccines, tests, prevention, and health literacy. I’m sure many of your social media pages are filled with various debates, articles, and fake news stories on one side or another pitting science, pseudo-science, and non-science all against each other for public spectacle. In the lens of laboratory science and medicine at large, I think most if not all of us agree that preventable diseases should be prevented, and if not, at the very least detected accurately, sensitively, and early. Influenza A/B is a prime example of a consistent threat to our health and safety that has wavered responses in various socio-medical circles.

Official communication and guidance from the Centers for Disease Control and Prevention (CDC) clearly tells those of us in health-care to embrace a multi-tiered approach to protecting public health regarding the flu. That approach includes vaccination, testing, infection control, anti-viral treatment, and anti-viral prophylaxis. And why such a fuss over the flu? It’s a big deal! Last year, the CDC reported approximately 80,000 deaths associated with influenza as a primary cause. 80,000 deaths! That’s almost 7 times as many that died from H1N1/Swine Flu complications back in 2009, where only 12,000 patients were killed by the virus. And even more so, in the terrifying Ebola epidemic of 2016—in which there was a staggering 1 recorded death in the US—nearly 29,000 people were infected globally and only 11,300 died (despite under-reporting). I’m being dramatic, I know. But it’s important for us to recognize true epidemics when they happen, and even more important for societies like ours to be at the forefront of preventing them from developing any further.

Image 1. The CDC recommends you get your flu shot every year, because obviously.


Image 2. I’m not here to talk about the anti-vax elephant in the room. That’s not fair to elephants. But imagine if the CDC reported 44% of flu vaccine misconceptions were addressed!

As an aside, I’ll probably recommend that you get your annual flu shot a hundred times in this post alone. But just to have a clear reference, please look at the following table. It’s critical to be able to both distinguish common cold versus influenza symptoms for yourself, as well as educate your patients and peers about the differences between the two. This information can change the way people perceive treatments (i.e. why the doctor only recommended rest/Tylenol and didn’t give out antibiotics for their symptoms) and why it’s absolutely crucial to protect vulnerable populations from an otherwise fatal virus. So, micro-rant aside, it should be clear that by now we should be working on a way to both improve our prophylaxis with vaccines and medications as they always leave room for improvement—I’m looking at you Tamiflu and Relenza! Notwithstanding any analysis of efficacy for the flu vaccine, the CDC reports a variable and transparent success rate of vaccines. It can be difficult to predict and assess epidemiologic trends and mutations as the influenza virus continues to change annually.

Table 1. Distinguishing the common cold, and “flu-like symptoms” from a proper influenza viral infection.
Image 3. CDC Report on seasonal flu vaccine effectiveness since 2004.

So, what was the deal with ZDoggMD plugging some PCR testing in the opening credits here? That’s a good question and one that inspired this article in the first place. Obviously, if you follow my posts you know I follow his, and at the end of this latest video he discusses new available options for influenza point-of-care testing (POCT) for clinics and emergency rooms. This was a partnership with the company Cepheid and linked with their promoting their POCT PCR-based FluA-B testing. Here’s a quick paraphrasing of the CDC recommendations on influenza testing: because of the numerous false negative tests every season, the bests tests in order of preference are RT-PCR, immunofluorescence, and rapid antigen testing. Did you catch that? Rapid Flu swabs are bottom of the barrel stuff here. UpToDate, the clinical resource for current practices and standards discusses rapid influenza tests as sacrificing turn-around-time (TAT) for accuracy: “commercially available rapid antigen tests for influenza virus yield results in approximately 15 minutes or less but have much lower sensitivity than RT-PCR, rapid molecular assays, and viral culture.” (I didn’t bold those words, they did). Most of the places I’ve worked run through boxes of rapid flu swab kits ALL DAY LONG. But what are we missing? Clinically, this is supposed to be an important “no miss” diagnosis—it’s dangerous, it’s contagious, it’s mutatable…

Who remembers learning biostatistics in school? Remember SPIN and SNOUT? “Specificity is used to rule IN, Sensitivity is used to rule OUT” So why are we relying on the LOWEST sensitivity available to us for ruling out influenza? Probably because of technological/practical limitations up to this point in time, and of course the most glaring limiting reagent of all: funding, also known as “administrative buy-in.” Have I hit enough lab management buzz words in this post? Not yet.

Table 2. Per UpToDate, these are the quick and dirty details on our favorite available flu tests currently on lab benches across the country. I’d say there’s got to be a better way, but there already is.

Sweet. So, it’s a little expensive but ultimately better for our patients, right? Done and done, whip up a cost-benefit-ratio report for the suits upstairs and let’s start a validation project! Well, yes and no. I’m a big proponent of utilizing MALDI-TOF—the mass spectrometry based system to replace traditional bacterial identifications. A 2015 study published in the Journal of Clinical Microbiology stated, “The use of MALDI-TOF MS equated to a net savings of 87.8%, in reagent costs annually compared to traditional methods. …The initial cost of the instrument at our usage level would be offset in about 3 years. MALDI-TOF MS not only represents an innovative technology for the rapid and accurate identification of bacterial and fungal isolates, it also provides a significant cost savings for the laboratory.” What promise! Cepheid’s ED POCT PCR Flu test promises 18% fewer tests needed, 17% fewer antibiotics prescribed, and overall savings per patient visit of up to $700. But this sounds like another, too familiar, recent promise from another voice in our profession. Something about quick, easy, and accurate testing on chips with micro-laboratories available commercially and only using microliters of whole blood for analysis. “Unfortunately, none of those leads has materialized into a transaction. We are now out of time,” read the goodbye letter to the company’s stockholders—Theranos, that’s the one. The moral of the story here: it’s good to remain fiscally prudent when deciding what your clinic or hospital should invest in with regard to testing. However, when something has been a proven and successful replacement which ultimately is recommended by multiple societies within the field then something’s got to give.

Image 4. MALDI-TOF saves money! You spend a little upfront, but then your hospital can write articles about how your bacteriology department has a swab-to-sensitivity TAT of a few hours. Less errors, less antibiotics, more likes on social media!

What do you see in your practice or laboratory as far as influenza testing? Are there issues I missed? What is your experience with rapid tests, or PCR testing? Is anyone else as big a fan of MALDI-TOF as I am? Did you get your flu shots yet? Leave your comments and questions below! Share with a colleague today!

See you next time!

I have absolutely no affiliation with Cepheid, financial or otherwise, but as an educational/professional resource read more information about Cepheid’s molecular rapid flu tests, read their literature at www.GetTheRightTest.com



  1. Carreyrou J. (2018) Blood Testing Firm Theranos to Dissolve. Wall Street Journal. Health: Theranos Co. Letter to Shareholders. Accessed at: http://online.wsj.com/public/resources/documents/Theranos_Stockholders_Letter_2018.pdf?mod=article_inline
  2. Cephid (2018) Is it really flu? Cutting emergency department costs with bedside rapid molecular tests. Accessed at: http://www.cepheid.com/images/Cepheid-WP-ED-Cost-FINAL.pdf
  3. CDC (2017) Interim guidance for influenza outbreak—management in long-term care faciltites. e Recommendations of the Advisory Committee on Immunization Practices – United States, 2016-17 Season. Accessed at: http://cepheid.com/images/CDC-interim-guidance-outbreak-management.pdf
  4. CDC (2018) Seasonal Influenza Vaccine Effectiveness, 2004-2008. Accessed at: https://www.cdc.gov/flu/professionals/vaccination/effectiveness-studies.htm
  5. CDC (2018) Flu Symptoms and Complications. https://www.cdc.gov/flu/consumer/symptoms.htm
  6. Dayhoff-Brannigan, M (2018) To Tamiflu or Not to Tamilflu? National Center for Health Research. Accessed at: http://www.center4research.org/tamiflu-not-tamiflu/
  7. Dolin, R. (2018) Diagnosis of Seasonal Influenza in Adults. UpToDate. https://www.uptodate.com/contents/diagnosis-of-seasonal-influenza-in-adults?search=influenza&source=search_result&selectedTitle=6~150&usage_type=default&display_rank=6#H1289544319
  8. McNeil, D. (2015). “Over 80,000 Americans Died of Flu Last Winter, Highest Toll in Years” The New York Times.
  9. McNeil, D. (2015). “Fewer Ebola cases go unreported than thought, study finds”. The New York Times
  10. ZDoggMD (2018) This Flu Test https://www.youtube.com/watch?v=YKTYw-7ikJQ#action=share
  11. Tran A, et al. (2015) Cost Savings Realized by Implementation of Routine Microbiological Identification by Matrix-Assisted Laser Desorption Ionization–Time of Flight Mass Spectrometry. Journal of Clinical Microbiology. DOI:1128/JCM.00833-15


–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.

Hematopathology Case Study: A 63 Year Old Man with Fatigue

Case history

A 63 year old male presented with extreme fatigue and weakness of unknown duration. Physical examination revealed scattered petechiae and mildly decreased muscle strength. His past medical history included a one year history of cough that had recently improved. Laboratory investigation demonstrated severe anemia and thrombocytopenia with a mild leukopenia.

Review of the peripheral blood smear showed smudge cells, circulating neutrophils with Döhle bodies and toxic granulation. CT scan of the chest showed upper/anterior mediastinal lymphadenopathy without hilar lymphadenopathy.

A biopsy of the bone marrow was performed.

Microscopic Findings



hod 2.jpg

The bone core biopsy revealed a hypercellular marrow for the patient’s age with a pronounced lymphohistiocytic infiltrate involving 30-40% of the biopsied marrow space. Interspersed along the infiltrate were large, atypical lymphoid cells with pleomorphic nuclei and prominent nucleoli. The marrow aspirate smear reveals progressive trilineage hematopoiesis with scattered hemophagocytic histiocytes.



The large atypical lymphoid cells were positive for CD30 and EBER, while being dimly positive for PAX5 and negative for CD20.


The detection of mononuclear Hodgkin cells staining for CD30 along with a characteristic reactive infiltrate, together with dim PAX-5 staining, positive EBER, and negative CD20 is sufficient to diagnose involvement of a secondary site by Hodgkin lymphoma. The lymphoma was associated with a secondary hemophagocytic lymphohistiocytosis.


Hodgkin lymphoma (HL) is a B-cell derived monoclonal lymphoid neoplasm. HL has a bimodal age distribution, with teenagers or patients in their early 20s and patients older than 55 years having the highest incidence. Although the typical presentation is with peripheral lymph node involvement, extranodal sites may be involved by either direct invasion or hematogenous dissemination. These sites include the spleen, liver, lung and bone marrow. About one third of patients have constitutional symptoms such as high fevers, night sweats, and weight loss.

Two broader forms of Hodgkin lymphoma exist: Classic Hodgkin lymphoma (CHL) and the less common nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL). NLPHL tends to preserve the entire B-cell transcriptional phenotype, while the neoplastic cells in CHL fail to do so.

CHL is composed of mononuclear Hodgkin cells and multinucleated Reed-Sternberg cells surrounded by an infiltrate of non-neoplastic reactive cells that might encompass small lymphocytes, plasma cells, eosinophils, neutrophils, and histiocytes. Fibrosis may also be present in the form of bands or may be more diffusely spread. The four histological subtypes: nodular sclerosis CHL, lymphocyte-rich CHL, mixed cellularity CHL, and lymphocyte-depleted CHL are based on the composition and characteristic of the reactive infiltrate, and the cytological features of the neoplastic cells.

The classic Reed-Sternberg cell is binucleated, with prominent eosinophilic nucleoli, often referred to as having an “owl’s eye” appearance. However many neoplastic cells are not of the typical Reed-Sternberg variant, and can be mononuclear, termed Hodgkin cells, or cells with more condensed cytoplasm and pyknotic reddish nuclei known as mummified cells.

Hodgkin/Reed-Sternberg cells (HRS) in Classic Hodgkin Lymphoma fail to preserve their B-cell traits, and this is reflected by their immunophenotype. The majority of cases are negative for CD45, and although CD20 may be expressed, it is usually present only on a minority of the neoplastic cells and stain with varied intensity. The HRS cells stain with PAX5 with a lower intensity than the surrounding reactive cells, making them easily detectable. The HRS cell stains positive for CD30 and CD15 in nearly all cases. Both of them stain the membrane with accentuation around the Golgi apparatus. EBV associated Hodgkin Lymphoma will stain positive with EBER, detecting EBV-encoding small RNA.

Bone marrow involvement is rare, ~5-10% of cases, and suggest vascular dissemination of the disease. Bone marrow trephine biopsies are commonly performed in the staging of patients with newly diagnosed CHL which guides the further treatment and gives us information about prognosis. Involvement of the bone marrow represents stage IV disease (advanced stage) in the Ann Arbor staging classification and patients with advanced stage disease typically receive a more prolonged course of chemotherapy. The 5-year survival rate of stage IV Hodgkin lymphoma is ~65%,  a much worse prognosis when compared with stage I, stage II, and stage III with ~90%, ~90%, and ~80% 5-year survival rates respectively.


  1. Stein H, Pileri SA, Weiss LM, et al. Hodgkin Lymphomas. In Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, editors: WHO classification of tumours of haematopoietic and lymphoid tissues, revised ed 4, Lyon, France, 2017, IARC Press, pp 423-464
  2. Ansell SM. Hodgkin Lymphoma: Diagnosis and Treatment. Mayo Clin Proc. 2015 Nov;90(11):1574-83.
  3. Howell SJ, Grey M, Chang J, Morgenstern GR, Cowan RA, Deakin DP, Radford JA. The value of bone marrow examination in the staging of Hodgkin’s lymphoma: a review of 955 cases seen in a regional cancer centre. Br J Haematol. 2002 Nov;119(2):408-11.
  4. Clarke C, O’Malley C, Glaser S. Hodgkin lymphoma. In: Ries LAG, Young JL, Keel GE, Eisner MP, Lin YD, Horner M-J, eds. SEER Survival Monograph: Cancer Survival Among Adults: U.S. SEER Program, 1988-2001, Patient and Tumor Characteristics. National Cancer Institute, SEER Program, NIH Pub. No. 07-6215, Bethesda, MD, 2007.



-Hans Magne is a 6th- year medical student at Poznan University of Medical Sciences. Follow Hans on Twitter @HHamnvag


-Kamran M. Mirza, MD PhD is an Assistant Professor of Pathology and Medical Director of Molecular Pathology at Loyola University Medical Center. He was a top 5 honoree in ASCP’s Forty Under 40 2017. Follow Dr. Mirza on twitter @kmirza.

Reflective Judgment

Reflective judgment—the ability to evaluate and process information in order to draw plausible conclusions—is one of the most critical leadership skills. People move through three different phases (pre-reflective judgment, quasi-reflective judgment, and reflective thinking) as they learn to develop their judgment skills.

During the pre-reflective thinking period, people acquire knowledge through experience, observations, evaluation, and authority figures. All information collected is seen as absolute and the truthfulness of the data is not questioned. Problems and challenges views through this lens are resolved with well-structured assumptions and people are certain about the effect of their solutions. This phase has three stages itself. People in the first stage see knowledge as absolute and concrete. Different beliefs are not seen and/or believed. The second stage is exemplified by a similar view, namely that knowledge is certain and absolute, but it is understood that knowledge is not always immediately available. People in this stage also heavily rely on authority figures to get their knowledge from and there is no critical thinking. The third stage embodies knowledge that is either certain or uncertain for a short period of time. If knowledge is uncertain, people in this stage rely on personal beliefs. Authority figures still play an essential role in providing information and all their information is seen as absolute.

The second developmental phase for reflective judgment is the quasi-reflective thinking phase. During this period, people start to recognize and understand that not all information is completely accurate or absolute. Additionally, people acknowledge that claims from authority figures also contain some uncertainty. This uncertainty can be caused by missing or incomplete information or by the methods that were used to gather information. People in this phase use evidence to draw conclusions, but they do not yet understand to process of how to get to a sound conclusion. In this phase, there are two different stages. During the first stage, people understand that knowledge is not absolute or certain. People also acknowledge that there is always a sense of ambiguity in knowledge. In the next stage, context starts playing a significant role. People start to understand that knowledge is bound by a certain context and that it is therefore more subjective than initially assumed. Conclusions are sometimes delayed, because knowledge is created through individual perceptions of reality. During both these stages, information from authority figures are thus not seen and absolute, but as more subjective and uncertain.

The third developmental period of reflective judgment is reflective thinking. In this phase, people understand that knowledge is never certain or absolute. However, instead of becoming stuck because of this understanding, people in this phase work to make conclusions that are reasonable. Knowledge and knowledge claims are actively evaluated based on their context. Critical thinking is an important part of this phase, as knowledge is judged and reflected upon prior to making conclusions. This phase also has two different stages: in the first stage, people understand that knowledge is not absolute and certain. However, information is evaluated and judged by comparing evidence and different opinions about the information. During this stage, the solutions people create are based on certain criteria, for example if the solution is pragmatic. During the final stage of reflective judgment, knowledge is created and accepted through a reasonable inquiry process that promotes critical thinking. The solutions are evaluated based on their probability and reasonableness.



-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.

Hematopathology Case Study: The Case of Lymphocytosis

Case History

53 year old female was found to have leukocytosis upon a wellness examination. A CBC was performed and found a WBC of 34.0, HgB 13.2, and Plt of 263,000. The WBC differential consisted of 80% Lymphocytes and 12% neutrophils. The patient states that she is feeling well, no fever, chills, or night sweats. She denies any adenopathy. Flow Cytometry was recommended as well as morphologic review along with Cytogenetics and FISH (fluorescence in-situ hybridization).

Lab Identification


WBC               33.68  [103/uL] NEUT             4.17 [103/uL]      12.3 [%]
RBC                4.54  [106/uL] LYMPH          26.91 [103/uL]    79.9 [%]
HGB               13.2   [g/dL] MONO           2.04 [103/uL]      6.1  [%]
HCT               40.0   [%] EO                  0.39 [103/uL]      1.2  [%]
MCV               88.1   [fL] BASO             0.11 [103/uL]      0.2  [%]
MCH               29.1   [pg] IG                    0.06 [103/uL]      0.2  [%]
MCHC            33.0   [g/dL] NRBC             0.00 [103/uL]      0.0  [%]
RDW-CV         14.3   [%]
PLT                263   [103/uL]
MPV                9.4   [fL]

Morphologic Review

Image 1. 40x magnification showing lymphocytosis.
Image 2. 60x magnification showing lymphocytosis with occasional smudge cells.

Flow Cytometry: Population of Interest – Abnormal Lymphocytes




Cytogenetics: 46,XX[20] Normal Female Karyotype

It is not unusual to observe a normal karyotype in CLL due to the limited number of abnormal cells and/or low spontaneous proliferative activity of the malignant cells. Fluorescence in situ hybridization studies may identify cytogenetic abnormalities of prognostic significance in interphase nuclei not observed in the metaphase cells analyzed. In cases of CLL molecular profiling may be performed to aid in predicting course of the disease. If clinically indicated these studies may be considered. Standard cytogenetic analysis may not detect subtle submicroscopic rearrangements and may not include metaphases from abnormal cell populations with low mitotic rates or present in low levels.

Metaphases Counted: 20 Metaphases Analyzed: 20
Metaphases Karyotyped: 2 Culture Type: 48EB, 72IL2/DSP30
Banding Technique: GTG Banding Resolution: 400

Fluorescence in-situ Hybridization: Abnormal – 13q14 deletion present

Fluorescence in situ hybridization (FISH) analysis was performed using a specific set of probes for Chronic Lymphocytic Leukemia (CLL). This study revealed a 13q14 deletion. Counts for all other probes were within the normal reference range. This finding represents an ABNORMAL result. Deletion of 13q14 is the most common deletion in CLL being reported in 10-20% of cases by conventional cytogenetics and up to 64% of cases by FISH analysis. When present as a sole abnormality this deletion is associated with a good prognosis and a median survival longer than CLL patients with a normal karyotype.

Del(6q) Not Detected
Del(11q)(ATM) Not Detected
Trisomy 12 Not Detected
Del(13q)/-13 DETECTED
t(11;14) Not Detected
Del(17p)(TP53) Not Detected


Chronic Lymphocytic Leukemia is a neoplasm of about 5 cases per 100,000 people with a median age of around 70 years old. The neoplasm is composed of monotypic mature B-cells that typical express CD5. Other immunophenotypic characteristics of the leukemic B-cells include CD19, CD20, CD22, and CD79b with dim surface expression of one of the immunoglobulin light chains, Kappa or Lambda. These cells typically express CD200 which helps differentiate the leukemia from Mantle Cell Lymphoma/Leukemia. Patients found to have a mutated IGHV genes typically have a better prognosis than those with an unmutated genes. Expression of ZAP70, CD38, or CD49d is also associated with an adverse prognosis. Complex karyotypes also trend towards a poor outcome. Adverse predictive factors include rapid lymphocyte proliferations in the blood, typically doubling in < 12 months.

Monoclonal B-cell Lymphocytosis is typically characterized as a monoclonal
BCell count of <5 X109/L in the peripheral blood. Monoclonal B-cell Lymphocytosis with a Chronic Lymphocytic Leukemia-type phenotype is the most common which accounts for about 75% of all cases. It has been reported that virtually all Chronic Lymphocytic Leukemias are preceded by Monoclonal B-cell Lymphocytosis, although not all MBLs progress to CLL.


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Troy G. Krieger, MS, MLS(ASCP)CMSCYMCMQLSCMCLS(MT) graduated from Montana State University Billings with a BS in Biology, Medical Laboratory Science option. He received a NAACLS Certificate and clinical training from the University of North Dakota in Grand Forks, ND, where he also received his Master’s degree. He is a Medical Laboratory Scientist / Flow Cytometrist at Yellowstone Pathology Institute, Inc in Billings, MT and his interests include Hematology, Immunopathology, and Flow Cytometry.