pathology – Page 30 – Lablogatory

Pancytopenia in a 67-Year-Old Female

A 67-year-old female presents with pancytopenia, a markedly enlarged spleen, and extramedullary hematopoiesis. Her blood smear is shown here. She is found to have a JAK-2 mutation. What is the diagnosis?

Chronic myelofibrosis
Chronic myeloid leukemia
Hairy cell leukemia
Metastatic breast carcinoma
Renal cell carcinoma

The diagnosis in this case is chronic myelofibrosis. Chronic myelofibrosis is one of the four main chronic myeloproliferative disorders (the others are chronic myeloid leukemia, essential thrombocythemia, and polycythemia vera). In this disorder, the bone marrow is initially hypercellular, with proliferation of all of the myeloid cell lines (neutrophils, red cells, and megakaryoblasts). Over time, however, the marrow becomes progressively fibrotic. Eventually, there is not enough room for normal hematopoiesis, and the body starts making hematopoietic cells elsewhere (most notably in the spleen, which becomes markedly enlarged).

In these later stages of chronic myelofibrosis, the blood is characterized by pancytopenia (a decrease in white cells, red cells and platelets). Teardrop-shaped red cells (dacryocytes) may also be seen as a result of the red cells wending their way through a fibrotic marrow. Red cell precursors, such as the normoblast present in this image, are also commonly present, as there is less and less room for red cells to mature fully before leaving the marrow.

These blood smear findings are not specific for chronic myelofibrosis. Teardrop-shaped red cells may be seen when the marrow is fibrotic for other reasons, such as metastatic cancer, and pancytopenia and normoblasts may be seen in many other conditions. The JAK-2 mutation, however, is seen most frequently in three of the four chronic myeloproliferative disorders: polycythemia vera, essential thrombocythemia, and chronic myelofibrosis.

-Kristine Krafts, MD, is an Assistant Professor of Pathology at the University of Minnesota School of Medicine and School of Dentistry and the founder of the educational website Pathology Student.

New Study Suggests No Difference in Mortality Rate in Two Different Transfusion Ratios

From the study published in the Journal of the American Medicine Association: “Among patients with severe trauma and major bleeding, early administration of plasma, platelets, and red blood cells in a 1:1:1 ratio compared with a 1:1:2 ratio did not result in significant differences in mortality at 24 hours or at 30 days. However, more patients in the 1:1:1 group achieved hemostasis and fewer experienced death due to exsanguination by 24 hours.”

You can read the NIH press release here.

You can read the abstract for the study here.

Final Thoughts from the Fellowship Application Process

And with the dawning of a new year, I’m another year closer to becoming a full-fledged pathologist. Exciting and yet daunting at the same time as I have only 1.5 years and my AP/CP boards left before I start my fellowships! So, I thought I’d leave some final words on what I learned during the fellowship application process for those who have yet to go through it.

The earlier you decide on your choice of fellowship(s), the better you can prepare by presenting and publishing research in your area of interest, spending extra rotation time and study in areas related to your interest, and networking within your academic subspecialty organizations. I would say for the first half of first year, concentrate on your rotations especially surgical pathology and grossing technique. But at the latest by the second half of your first year, start honing in on what you think you’d eventually like to do and working toward that goal. Most residency programs are amenable if you ask them to adjust your schedule so you can rotate early through subspecialties of possible interest during your second or early third year. Don’t forget to ask for lighter rotation months and less/no call duties during peak interview season (Oct-Jan).

If you can, do an elective during your second or early third year in your subspecialty of interest at your dream program(s) before fellowship decisions are made and fund it through grants such as the one offered by ASCP (1/16/14 deadline; application here). I found that often, positions were already promised or eventually went to internal candidates or external candidates who had done an elective prior to their interview. Scheduling for elective rotations takes foresight, time and effort (eg – state medical license can take months), and an available rotation spot during your desired month, so start the process early!

Research early to create your application list. Only you will know the number you feel comfortable applying to which depends on your personal situation (eg – subspecialty competitiveness). I found that attending conferences and listening to speakers in my content area of interest helped me to decide which programs I may like. I’m also very active in CAP and ASCP and the physicians I work with in these roles, pointed me toward programs where the culture might be a good fit for me as they were role models of the type of people that I would like to work with. Of course, I also applied to top programs that I knew or that my attendings advised me were good.

Then check with programs about the opening date for application submissions if it is not posted on their website. I found that frequently, these were not hard deadlines. Since we don’t have a match, decisions are rolling (eg – I got promised an offer during my interview day and have friends who also had similar experiences). Once again, the early bird may catch the worm, and not because they are necessarily the best bird, but the first bird that a program likes. While some programs have a schedule for decisions, I found that just as many made offers as soon as they found someone they liked.

Make sure that personal statements are no longer than one page, shorter is better. You can follow this format: 1) how and why you fell in love with that subspecialty, 2) what you bring to the table especially for the program, and 3) what you want out of your fellowship and why that program is the best to accomplish those goals. Ask multiple people in your subspecialty or more senior residents to give you feedback on your personal statement/CV and for letters of recommendations very early – give a deadline earlier than you need so that you can have them ready by the time you want to submit.

I applied mostly to programs that had both hematopathology and molecular pathology fellowships and stated in my cover letter that I wanted to do both consecutively at the same place (but that it wasn’t a deal breaker). I received invites at almost all but decided to interview at a select number. For the ones where I interviewed for both fellowships (ARUP, Hopkins, MD Anderson, UPMC, Houston Methodist), it was usually the program looking for the fellow first who made the arrangements with the other fellowship. ARUP had interviews over 2 days (paid expenses except airfare) but the others all worked it out so that half a day was interviewing for hematopathology and the other MGP. Receiving an offer from one did not necessarily mean that I would automatically get one from the other. Scheduling both on the same day, also made things a little more difficult.

Respond to invitations quickly because this process is truly rolling. I was often given a limited choice of date(s). One place gave me only one date for an interview that I couldn’t make. Rescheduling can result in losing an interview because programs interview less people over fewer dates than they did for residency and will schedule someone else if you can’t make it. Some programs told me they were interviewing 2-3 per position while others said 5-10.

Be courteous and prompt, send your “thank you” email/note early and no later than by the next day. You can have a basic “thank you” email template ready to go that you can personalize so that you can send it even while waiting at the airport to go to your next interview. And be honest. I found that being upfront made it easier for programs to extend me a counteroffer when I mentioned that I had to make a decision soon on another offer. Once you’ve accepted a position, keep in touch with your program to hit fellowship running! I hope to do a PGY4 research elective in order to submit abstracts for conferences that occur soon after I start my fellowship and to familiarize myself with the EMR and clinical workflow in both fellowship areas.

And finally, be true to yourself about your goals, realistic possibilities, and most importantly, the program characteristics that will make you most happy. When I was applying to college, academic prestige and idealism were important, and for medical school, proximity to my aging parents. But now, what I find most important is the fit of the program. I want to be happy and feel like it is my home. I want to be at a place that hires their alumni and goes out of their way to help them find jobs. I want to be around role models working in areas that I want to as an attending: advocacy, medical education, and research…and of course, foremost, clinical diagnostic excellence…and who I feel will continue to support me as colleagues in the future. For me, fellowship isn’t just the time to merely refine my clinical expertise or learn things that I didn’t get to during my residency. It was more like interviewing for a job rather than for school admissions, making decisions with a more immediate goal of what I want to accomplish after and no longer “down the road”, and most importantly, building toward my future.

And I’m happy to say that I did get multiple offers from great programs and accepted at the place I felt the best fit. It was my last interview in mid-December, so you never know. I can say that having served in positions with CAP actually helped me because I already felt at home with 2 of my interviewers with whom I serve on a CAP Council (we just had a meeting 4 days prior) and one of the current fellows who I also met through being involved with CAP. So, networking, even when it isn’t deliberate or conscious as it was in this case, can help. In case you’re wondering, I’ll be completing hematopathology (2016-2018) and molecular genetic pathology (2018-2019) fellowships at Houston Methodist and also hope to participate in research at the Houston Methodist Research Institute.

-Betty Chung, DO, MPH, MA is a third year resident physician at Rutgers – Robert Wood Johnson University Hospital in New Brunswick, NJ.

Microbiology Case Study

Patient History:

81 year old man with a history of systemic vasculitis (present for the past 10 years ANCA negative, ANA negative, Rheumatoid factor <20) on immunosuppression (plaquenil with prednisone 40mg for flares about every 6 months), type 2 diabetes, and hypertension presented to an outside hospital with weakness and dyspnea. He was found to have a widespread purpura, ulcerative lesions, acute kidney injury (creatinine 4.7), and 3 days of hematochezia. He was started on 7 days of levoquin and zosyn for a presumed pneumonia and with no improvement was transferred to our institution. On admission, a CT scan of the chest demonstrated bilateral multifocal pneumonia and multiple cavitary nodules within the lungs. A thoracentesis was performed and was transudative (wbc 1883, N 63%, protein 2.6).

Laboratory findings:

WBC 7000/cmm
Hemoglobin 9 g/dL
Platelet count 104 K/cmm
Bacterial culture blood, no growth
Cryptococcal antigen negative
Pleural fluid bacterial culture and smear negative
Pleural fluid AFB culture and smear – no acid fast bacilli, modified acid fast bacilli seen from bottle
Pleural fluid fungal culture and smear – no fungi seen, rare modified acid fast bacilli growing
Histoplasma urinary antigen positive
Histoplasma antibodies negative
Blastomyces urinary antigen negative

Gram stain of growth from the AFB bottle showing beaded, branch Gram positive bacilli.

Modified acid fast stain of growth from the AFB bottle showing modified acid fast bacilli.

Discussion:

Based on Gram stain and modified acid fast stain, modified acid fast bacilli suggestive of Nocardia species was reported. Nocardia are strict aerobic, gram positive, filamentous rods that stain partially acid fast. This is due to the mycolic acids in the cell wall which are shorter than those of mycobacteria. Nocardia species produce many virulence factors including Cord factor (prevents intracellular killing), catalase and superoxide dismutase (which inactivate reactive oxygen species that would otherwise prove toxic to the bacteria).

Nocardia grow well on buffered charcoal yeast extract agar and at 30^oC. They produce aerial hyphae and can have a chalky colony appearance. Species level identification is best done with molecular methods. This isolate was identified as Nocardia farcinica at a reference laboratory.

Nocardia species are ubiquitous in the soil. They can cause infections in immunocompromised hosts usually after inhalation or direct inoculation. Infections include bronchopulmonary disease and cutaneous infections. With bronchopulmonary disease, cavitation and spread to the pleura is common, which fits with our patient. Dissemination is also seen with common sites being brain and subcutaneous tissue.

Our patient had a positive Histoplasma urinary antigen, but negative Histoplasma antibodies. The working diagnosis was disseminated Histoplasmosis and he was being treated with amphotericin B. He expired and no postmortem exam was performed. Fungal cultures from the pleural fluid were not growing fungus at the time of this post. Fungal cultures were not obtained from sputum and a BAL was not performed.

-Dan Olsen, MD is a 4^th year anatomic and clinical pathology resident at the University of Vermont Medical Center.

-Christi Wojewoda, MD, is the Director of Clinical Microbiology at the University of Vermont Medical Center and an Assistant Professor at the University of Vermont.

There’s a Fungus Among Us

A 53 year old man with history of stroke, alcoholism, heart failure, hypertension, and atrophic right kidney presented to the ED with acute urinary retention and complained of dysuria and frequency. He was afebrile, denied nausea/vomiting or headaches. His labs at admission are listed below:

WBC: 21 k
Na: 122
Cr: 3 (baseline 1.2)

Urinalysis showed innumerable white blood cells, leukocyte esterase 3+ and negative nitrite.

A catheter was placed and drained 1 L of yellow cloudy urine. The patient refused admission and he was prescribed ciprofloxacin 500 mg BID empirically and was sent home with a foley catheter in place with plans to follow up with Urology. He returned to the ED the following day because his foley catheter was not draining urine and he noted leaking around his catheter. CT scan was obtained and showed ill-defined areas of increased and decreased attenuation within the urinary bladder lumen and left hydroureteronephrosis.

Urine cultures obtained during his initial presentation grew >100,000 yeast and he was treated with fluconazole. The patient was taken to the operating room 11 days after first presentation to diagnose and treat the mass in the bladder. A tan-brown mass was removed and send to surgical pathology. Representative section (H&E stain) of the specimen is shown below:

Which of the following statements regarding Candiduria is true?

Most patients with candiduria are asymptomatic and the yeasts merely represent colonization
The presence of pseudohyphae in the urine or the number of colonies growing in culture help to distinguish colonization from infection
The most commonly involved organ in disseminated candidiasis is the heart
There is a higher propensity for fungal ball formation in adults than children

The correct answer is 1. Most patients with candiduria are asymptomatic and the yeast merely represent colonization. Infected patients may have symptoms (dysuria, frequency, suprapubic discomfort) while others might not. Pyuria is so common in patients with a chronic indwelling bladder catheter that it cannot be used to indicate infection.

Neither the presence of pseudohyphae in the urine nor the number of colonies growing in culture (unlike bacterial cultures) help to distinguish colonization from infection. Ascending infections are rare but usually subacute or chronic, unilateral and can cause perinephric abscesses.

Fungus balls in adults are uncommon with less than 10 adult cases reported in the literature. Risk factors include uncontrolled diabetes, prolonged use of antibiotics or steroids and immune compromise. Classic laboratory findings include marked leukocytosis, pyuria, hematuria and a concomitant bacterial urinary tract infection. Most cases are caused by Candida species although Aspergillus has been implicated in a few cases.

The kidneys are the most commonly involved organ in disseminated candidiasis and there is a higher propensity of fungus ball formation in neonates.

-Agnes Balla, MD is a 1^st year anatomic and clinical pathology resident at the University of Vermont Medical Center.

-Christi Wojewoda, MD, is the Director of Clinical Microbiology at the University of Vermont Medical Center and an Assistant Professor at the University of Vermont.

A Rare Myeloproliferative Disorder

A 59-year-old male presents with skin lesions, hepatosplenomegaly and cardiomyopathy. A representative field of his blood smear is shown here. Of the following, what is the most likely diagnosis?

A. Chronic myeloid leukemia
B. Multiple myeloma
C. Metastatic prostate carcinoma
D. Hypereosinophilic syndrome
E. Bacterial sepsis

The diagnosis in this case is hypereosinophilic syndrome, a rare myeloproliferative disorder characterized by a marked and persistent elevation in the eosinophil count. Although this disease is primarily a hematopoietic disorder, it usually affects many other organ systems, such as the cardiovascular, nervous, respiratory, and gastrointestinal systems. Typical presenting symptoms include cardiomyopathy, skin lesions, thromboembolic disease, neuropathy, hepatosplenomegaly, and pulmonary disease. The pathophysiology behind the damage in these organs isn’t well understood, but it probably has something to do with the release of eosinophil granules in those tissues.

You need to have three things in order to make the diagnosis:
1. Persistent eosinophilia (absolute eosinophil count >1500/μL)
2. No other cause for the eosinophilia
3. Signs and symptoms of organ involvement

Other more common causes of eosinophilia, such as drug reactions, allergic reactions and autoimmune disease, must be ruled out before making the diagnosis.

Usually, patients aren’t treated unless or until they have symptoms (because the treatment itself has its risks). These patients are monitored closely with serum troponin levels (to monitor for MI), echocardiograms and pulmonary function tests.

Some patients with hypereosinophilic syndrome have a tiny deletion in 4q12, which ends up producing a fusion transcript called FIP1LI-PDGFRA (which is also present in some cases of systemic mastocytosis). Imatinib works very well in the majority of these patients.

Patients who have symptoms (but not FIP1LI-PDGFRA) are generally treated with steroids first. If those don’t work, interferon alpha and hydroxyurea are used. If those don’t work either, then imatinib is the treatment of choice (it doesn’t work as well as it does in patients withFIP1LI-PDGFRA, but it does seem to work in at least some of these patients).

Here are the reasons the other answers are incorrect.

Myeloma is a monoclonal disease of plasma cells which manifests mainly in the bone marrow. In the blood, the main thing you see is rouleaux (red cells stacking up on top of each other). This blood smear just has a lot of eosinophils – so it’s not consistent at all with myeloma. The clinical history also doesn’t fit. In myeloma, patients usually have bone pain, signs of anemia (fatigue, palpitations), and maybe signs of renal failure. Hepatosplenomegaly, skin lesions, and cardiomyopathy aren’t generally seen in myeloma.
In CML, you see a massive leukocytosis which is composed of neutrophils and precursors. There is a big left shift and a basophilia. This smear just has a ton of eosinophils, which is not consistent with CML. The patient’s hepatosplenomegaly would be consistent with CML (especially the splenomegaly part) – but the skin lesions and cardiomyopathy don’t go along with that diagnosis.
In metastatic prostate cancer, it’s possible that you might see a rare tumor cell in the blood; you might also see a monocytosis (you occasionally can see that with solid tumors). Eosinophilia, however, is not consistent with prostate cancer. The history is also unsupportive. Patients with advanced prostate cancer may have urinary symptoms (trouble urinating, blood in the urine), abdominal or pelvic pain, or signs of metastasis (bone pain, particularly in the spine).
The characteristic blood finding in bacterial sepsis is a neutrophilia, with or without a left shift. You may also see toxic changes in the neutrophils: toxic granulation, Döhle bodies, and/or cytoplasmic vacuolization. Bacterial infections generally don’t produce an eosinophilia – but some parasitic infections can.

-Kristine Krafts, MD, is an Assistant Professor of Pathology at the University of Minnesota School of Medicine and School of Dentistry and the founder of the educational website Pathology Student.

The Future Cost of Antimicrobial Resistance

Over on Superbug, Maryn McKenna (are you following her yet? No? If you’re into infectious disease, you should) discusses a recent report on the global ramifications of antimicrobial resistance. In it, the authors project by 2050, 10 million deaths a year will be attributed to infections caused by six resistant organisms. (Those are: Klebsiella pneumoniae, E. coli, MRSA; HIV, TB and malaria.) These deaths will cause an estimated loss of 100 trillion dollars of lost gross national product.

So what can laboratory professionals and pathologists do to help stop these predictions from coming true? For starters:

Advocate for and implement antibiotic stewardship programs.
Educate the public about proper antibiotic use.
Practice good laboratory safety practices.

What else can labs, microbiologists, and pathologists do to stem the tide of antibiotic resistance?

–Kelly Swails, MT(ASCP), is a laboratory professional, recovering microbiologist, and web editor for Lab Medicine.

Next Generation Sequencing and Personalized Genomic Patient Care

I’m sure that everyone has heard about next generation sequencing (NGS). But why exactly is it a big deal? Even though I have spent a significant amount of time at the bench performing “wet lab” basic science research and was acquainted with the term, I did not have practical hands-on experience with NGS prior to residency. It was not a readily accessible technology during my biomedical research days prior to medical school and so I did not entirely grasp the full power of this then disruptive technology until I was a pathology resident, and even more so, as an applicant for molecular genetic pathology (MGP) fellowships.

All of us should have previously learned about the “gold standard,” Sanger sequencing. This method combined irreversible dideoxynucleotide chain termination with a detection method such as gel electrophoresis, or on a larger, automated level, capillary electrophoresis. It was powerful because it allowed us to read the genomic map that directs cellular life, albeit only one sequence at a time. It served as the mainstay for more than a quarter of a century and still is employed for smaller scale sequencing or for long (>500 bp) stretches of DNA.

In the 1990’s, initial methods of massively parallel signature sequencing (MPSS) and pyrosequencing began to appear which would lay the groundwork for today’s massively parallel sequencing (MPS), also known as second generation sequencing, or more popularly as NGS. The two most commonly utilized NGS platforms to date are based on semi-conductor technology for the Ion Torrent (now Life Technologies) and reversible dye-terminator, sequencing based synthesis (SBS) technology for the Illumina platforms.

The power of NGS comes from its ability to simultaneously sequence 1 million to 43 billion short reads (400-500 bp each). The Human Genome Project took over a decade to complete and cost nearly $3 billion whereas NGS can sequence the same genome for a cost on the order of $1000’s, a cost that is further decreasing as the technology is refined. When I was working in research (eons ago), we had nitrocellulose based dot arrays where each “dot” represented multiple copies of a specific cDNA sequence and which helped us to build expression profiles for our particular area of study. This would be analogous to analog technology and NGS would now be considered a digital version.

With conventional PCR, we could only amplify one target sequence per sample reaction. The results were also only qualitative. The results only measurable after multiple cycles of denaturation, annealing, and extension as amplified product of the expected size or no amplified product. Then came along real-time or quantitative PCR (qPCR) which some people refer to also as RT-PCR (although this is a confusing term for people like me who were around before qPCR and think of RT-PCR as meaning reverse transcription PCR). The power of qPCR was that within the linear range of detection, we could now quantitate the amount of product present in real time. NGS also provides the resolution of qPCR in terms of quantitation.

So, as a technology, NGS nicely combines and refines some (but not all) characteristics of multiple technologies with large scale profiling. But for a non-molecular person, what is the relevance? Obviously, it has taken us some time to get to this point, even though the Human Genome Project was completed in 2003 (it started in 1990). We needed time for biomedical and translational research to provide us with clinical significance to the mutations and genetic aberrations NGS could identify. We also needed to develop tools to distinguish true mutations with clinical significance from benign polymorphisms present in our population and to build our bioinformatics support.

But here we are, stepping into the new frontier of personalized genomic medicine. Sure, there is a lot of hype surrounding it and these promises will take time to keep. But these are exciting times for someone like me who fell in love with the molecular dance that plays out within our cells. One of the reasons that I want to complete an MGP fellowship is to get more hands-on practical knowledge of the nuances of NGS from a technical standpoint but also to collaborate with other physicians in directing patients to the correct clinical trials and targeted treatment – and therein, is where the power of NGS really lies. For someone who may never get to meet the patient, at least for me, there’s probably no greater satisfaction than knowing you had a pivotal part in helping a patient more effectively combat their disease. Personalized genomic medicine is another step in that direction.

[12/12/2014: edited to fix a few inaccuracies. We apologize for the error.]

-Betty Chung, DO, MPH, MA is a third year resident physician at Rutgers – Robert Wood Johnson University Hospital in New Brunswick, NJ.

The Importance of Relationships and Elective Rotations for the Fellowship Application Process

I know that I’ve said this before, but it is important to cultivate relationships, especially in a small professional community such as pathology. In medical school, it was fine to focus on learning from our lectures, doing well on boards, and performing competently on the wards. This triad was enough then to secure us good letters of recommendation for our residency applications. And most programs invited candidates supposedly based on a magic number calculated from these aspects of our applications. Additionally, most programs, since we have a match and so as not to have to scramble via the SOAP, would invite about 10 candidates per position available.

However, for the fellowship application process, it’s a different ball game. We do not have grades for rotations and most of us have not taken our boards before we apply. So it is no longer as heavily numbers-oriented. Most of our personal statements will not be that different from each other, I would guess. So, the two things that stand out in my mind as having the most impact on receiving an interview invite (at least in my experience), are our letters of recommendation and our CV’s. I know that at every interview, aspects from one or both of these were discussed. Since I was a non-traditional medical student, most often what was brought up from my CV was my extensive research background (I was originally going to be a PhD molecular neuroscientist), long path to residency (I have 4 degrees), and reasons for getting an MPH (two of my main foci were molecular and infectious disease epi because I thought that I’d be interviewing for MGP and clinical microbiology fellowships right now). I also had to explain any gaps in my training.

As far as the CV goes, I think it’s most important to show a consistent commitment to your area of interest through publications, abstracts/poster or platform presentations, and leadership positions with advocacy organizations in your desired subspecialty area. But remember to do things that you are passionate about and not just to put on your CV! Attending national/state/local meetings provides an outlet to meet the experts in your future field who not surprisingly, you may end up interviewing with during the fellowship application process. More weight is now placed on relationships. If you have great letters (or better yet, a phone call or personal email sent on your behalf) from a colleague that the fellowship director knows, you are more likely to be chosen for an interview. Also, if you are a well-liked internal candidate or external candidate who spent time rotating at your dream program, then you also have increased chances of being chosen for their fellowship. Some programs (or subspecialties like some forensics programs that I’ve heard of) either require an “audition” rotation or heavily favor candidates who did rotate with them. So I STRONGLY recommend figuring out what fellowship you want as early as possible and to do an elective rotation (if it is not your own program) at your dream program during your PGY-2.

I cannot emphasize enough that showing what you can bring to your future fellowship by doing an elective rotation before the application period (early PGY-3) and interacting with your future interviewers can only help you. I wish someone had told me this when I was a junior resident. If the program chooses to interview you after you’ve rotated there, it generally means that you’re more competitive than others who they may interview because they know and like you and feel that you meet their competency requirements. I have not had any elective rotations yet so I was surprised at one of my interviews to learn that all the current fellows had completed a 2-month rotation there before they had applied. I had been told just before I left for my interview that this program heavily prefers those who have rotated there but it wasn’t as obvious as when I was told this during the lunch with the fellows. Even though they interviewed only a few candidates, it will be difficult to tease out how much an elective rotation factors into the final decision. I will always wonder if I do not receive an offer.

At this point, the competition is much fiercer than it was for residency, often with only 2-3 candidates invited to interview for each available spot from what I was told at some of my interviews. But I’m not sure how this number varies based on the competitiveness or popularity of each program. I can tell you that the programs I interviewed at would fall under the ‘very competitive’ category so other programs may interview more. But you could always ask the program coordinator how many they plan to interview and how many positions are truly available. They often will let you know if a future position is already filled by an internal candidate. Sometimes, I was given only one day or a few days to choose for scheduling an interview and if I couldn’t on those days, the program moved on down their list. So make sure to ask for lighter rotations and no call during your anticipated interview months (Sept-Jan). This is especially important with small residency programs or those with multiple hospitals to cover where it may be difficult to find someone to switch call coverage with you.

Since applications are accepted and interviews are conducted earlier than in the past and positions may have already been (un)officially promised to internal candidates, research programs and apply early! I do so dislike the word ‘networking’ because to me, it sounds insincere and calculated, but whatever you do, make opportunities for yourself to build relationships with and show your interest to your future colleagues before you have to apply. If you need some financial help to do an external elective, apply for ASCP’s subspecialty grant by clicking here and applying before January 16, 2015!

-Betty Chung, DO, MPH, MA is a third year resident physician at Rutgers – Robert Wood Johnson University Hospital in New Brunswick, NJ.

The Importance of Continuing Medical Education, at Least in Theory…

Hello again residents. It’s the wee hours of the morning and I am in Chicago O’Hare International Airport waiting for my connecting flight to Columbus, Ohio, where I will serve as an ACCME/AMA monitor for the College of American Pathologists (CAP) at the Ohio Society of Pathologists (OSP) meeting. I wasn’t allowed on my flight because I was just beyond the cutoff time even though I had rushed out of the hospital, still in my scrubs. And so I got re-routed through Chicago and spent a couple hours at a hotel in order to sleep before catching an early flight the next day.

As the junior (trainee) member on CAP’s Council on Education (COE), I was given this opportunity to monitor this CME meeting for compliance to ACCME/AMA standards and CAP representation as a joint CME partner. I’ve served on the COE since January 2014. We have four meetings a year with two of them in Chicago. I was just approved for a second term that runs until December 2015. We oversee and approve proposed projects from all the educational committees of the CAP: publications, GME, CP education, and the curriculum committee as well as some of the educational aspects of the Annual Meeting.

Despite the airport snafus (which I’m pretty good at getting myself into), it was interesting to serve as a monitor. I met an attending from the Cleveland Clinic who I remembered from my residency interviews. I also met other residents and fellow who were in attendance. The OSP had taken great care to preclude commercial bias from their meeting. They did have a few exhibitors but they were in a separate room from the lecture sessions. I heard a very informative talk on the clinical oncology applications of next generation sequencing (NGS) as well as an engaging case-based session on dermatopathology cases.

The meeting was held in a hotel in Dublin, OH, which I strongly suspect must have Irish and German roots from the names of the town, streets, and types of restaurants (Irish pubs and German-Austrian) that are common here. The hotel restaurant which had an Irish name served a buffet of Irish food (no surprise) for the participants at a discounted rate. Overall, it was a good meeting with a good balance of germane topics covered. Having been a co-chair of a national medical conference when I was in medical school, I totally can appreciate all the pre-planning that goes on behind the scenes to organize meetings such as this. I was also able to have dinner with and catch up with a friend who is a non-pathology resident at the local Ohio State University.

I know that we, as doctors, would like to believe that once we’ve passed through the gauntlet of medical school and graduate medical education training, that we know everything that we need to know and shouldn’t necessarily have to be retested or do CME, but I believe that it only makes us better doctors if do. We should be life-long learners, especially in a technology-driven specialty such as pathology (that is, if we want to remain in control of lab testing). As a scientist in my life prior to medical school, I intimately understand how even dogmas can change (at one time, people thought that protein was the genetic material of the cell!). We can always learn something new and new disruptive technologies like NGS will always arise that will transform how we diagnose, prosnosticate, and treat our patients. We may not always see patients physically but must remain present within the process and that requires us to continue to test our knowledge base. Since I haven’t graduated yet, I don’t really have the experience to say whether the current mix of CME, SAM, and MOC requirements is the way to do it but in some form, we need regulations to help push us as a profession (not necessarily as an individual if we are self-directed and pro-active) in the right direction to be the best physicians for our patients.

-Betty Chung, DO, MPH, MA is a third year resident physician at Rutgers – Robert Wood Johnson University Hospital in New Brunswick, NJ.