Q. I’m will be starting my pathology residency in about a year. Any suggestions for getting prepared for residency? I have been reviewing www.enjoypath.com and others, but wanted to get your opinion.
A. Good for you! When many people think of pathology (do many people think of pathology?), they think of surgical pathology – stuff that comes out of the operating room, biopsies, etc. But there are many other parts to a pathology residency, such as hematopathology, microbiology, forensic pathology, and blood banking. I’ll run through some of the books used in these areas, then I’ll tell you what I would have done if I knew then what I know now.
Surgical pathology: Rosai’s Surgical Pathology is probably the most commonly-used book; another good source is the set of AFIP Fascicles (there’s a fascicle on pretty much every organ system). These sources are too in-depth for you now (with one exception that I’ll mention in a minute), and probably too expensive. They’re more for reference than for reading through on a Sunday night. You’ll use them until you’re nauseated when you’re a resident though.
Hematopathology: The best source for this is the AFIP Fascicle on the subject: Tumors of the Bone Marrow. This is the exception to what I said above about reading the fascicles before residency – this one would be great to go through ahead of time. There’s a lot to learn, and if you go through it once, it will make a lot more sense when you get to it in your residency. It’s small enough that you can certainly get through it in a few months.
Microbiology: We used Koneman in our residency program, and I think it is a good textbook. It’s more than you’d want to go through ahead of time though; I’d use something like Clinical Microbiology Made Ridiculously Simple. It has nice drawings and mnemonics, which is something you need in microbiology.
Forensic pathology: A couple good ones for this are put out by DiMaio: a textbook (long) and a handbook (short).
Blood banking: We used McCullough’s Transfusion Medicine text in residency. Nice and short and readable. Here’s a fun game that you might want to try too.
I think if I had it to do over again, I would do three things:
1. Read Robbins. All of it. Maybe twice. I know, I know, it is a “med-school” textbook, but we used it all the time in residency. So did the attendings at times, by the way. It’s no small feat, but should be possible in a year, and it would prepare you well. You might even take notes on the histologic appearance of different tumors and diseases; you would have those to refer to during residency. You can look at websites too (like Webpath and Ed’s Pathology Notes) – and you should – but Robbins will give you a systematic and thorough review.
2. Read the AFIP bone marrow fascicle. I actually did this before my med school rotation in hematopathology, and I was so glad I did. It will make you shine when you get to your rotation.
3. Not worry about the other stuff. The other rotations will be easy enough to go through without advance preparation.
Good luck!
Q. Currently I am in a residency course to finish up my training as a medical laboratory technician; for the next two weeks I’ll be doing nothing but cell differentials in the hematology lab. Today as I was skimming the abnormal slides I found that I was having some difficulty distinguishing lymphocytes (particularly plasmacytic lymphs) from plasma cells found in the peripheral blood. Any pointers? In addition, I’m having a similar issue making the distinction from activated lymphocytes and monocytes. Pesky lymphs…
A. Those are very legitimate questions and ones that trouble even people with lots of experience from time to time. The key to both of these problems (and most problems where you’re trying to distinguish one cell from another) is to look at the chromatin.
1. Lymphocytes vs. plasma cells vs. plasmacytoid lymphocytes
Lymphocyte chromatin has a unique look in that it is clumpy and smudgy at the same time. Check out the top photo of normal lymphs – there are light and dark areas (clumping) within the chromatin, but the distinction between the two is not sharp (it’s smudgy). It’s like you licked your thumb and smudged the chromatin. Okay, that’s a weird analogy, but whatever. Plasma cell chromatin is blocky and discrete; it is sometimes arranged in a “clock-face” pattern around the edge of the nucleus. Not smudgy. Plasmacytoid lymphs have the chromatin of a lymphocyte (clumpy and smudgy) but the cytoplasm of a plasma cell (eccentric nucleus with a clearing where the golgi apparatus is).
2. Reactive (activated) lymphocytes vs. monocytes
Reactive lymphocytes – particularly big ones – can look a lot like monocytes. Again, the key is to look at the chromatin. Large reactive lymphocytes are usually immunoblasts, and as such, they have a big nucleolus (or two). In the bottom photo, there is a big reactive lymphocyte (called a Downey 3 cell) on the right. These cells also have fine chromatin (it has to be fine, or you wouldn’t be seeing the nucleolus). Monocyte chromatin is more dense (no nucleoli) and has a “raked” appearance. It is like you dragged a tiny garden rake across the nucleus. Also, the nucleus is often kidney-bean or horse-shoe shaped, or at least has a nice indentation or two. In addition to the chromatin differences, there are cytoplasmic differences (though these are less consistent): monocyte cytoplasm is typically dishwater grey with tiny dust-like granules, whereas reactive lymphocyte cytoplasm is usually light blue (either pale light blue or a relatively bright light blue) and if granules are present, they tend to be larger.
It just takes time and practice. Show everything you’re wondering about to someone who’s been in the lab a while – that’s the best way to learn. Most techs – as you no doubt know – are really nice and very knowledgeable!
Q. I would be highly obliged if you can help me out on one thing. Being an average student, I refer to a textbook by a local author. He writes, “in gastric ulcer the value of basal acid output (BAO) and maximal acid output (MAO) are usually normal or slightly below normal” and “higher values are found in duodenal ulcer.” I am confused on both statements. Shouldn’t the level be higher in gastric ulcers? And if it’s low in gastric ulcer why is it higher in duodenal ulcer? (more…)
Q. If the chronic leukemias have lots of mature cells, and the acute leukemias have immature cells, then how come chronic myeloid leukemia has lots of immature cells? Seems like it belongs in the acute leukemia category! (more…)
Q. I was wondering what the difference was between labeling something as a “leukemia” vs labeling it as a “chronic myeloproliferative disorder.” (more…)
Q. I’ve never been clear on the way iron is handled and was hoping you could clarify. Basically, I don’t understand the difference between serum iron and serum ferritin. (more…)
Q. I’m currently doing a research report on acute lymphoblastic leukaemia and I was wondering, are cytomorphology and cytochemistry important in the diagnosis of ALL? (more…)
Q. Can you write a post about antiphospholipid syndrome? I could not find good source which explains its pathophysiology and laboratory results
A. First, before we get into the antiphospholipid syndrome, we need to talk about antiphospholipid antibodies. As you might expect from their name, antiphospholipid antibodies are autoantibodies in the patient’s plasma that are directed against various phospholipids (there are lots of phospholipid surfaces in the body – including the phospholipid surface upon which the coagulation factors interact). There are a bunch of different types of antiphospholipid antibodies, including anticardiolipin antibodies, anti-glycoprotein antibodies, and the so-called lupus anticoagulants (which were discovered in patients with lupus).
In addition to binding to various phospholipid surfaces in the body, these autoantibodies also just happen to bind to the phospholipid part of the PTT reagent (and sometimes, the PT reagent). Then there’s not enough usable reagent in the test tube, and the patient’s specimen doesn’t clot! The coagulation tests are therefore falsely prolonged.
Antiphospholipid antibodies are sometimes called “inhibitors” because they appear to inhibit coagulation in the test tube. But here’s a weird thing: in the body, they can be associated with thrombosis!
You may be asking yourself: how do you get these antiphospholipid antibodies? And are they dangerous?
It turns out there are different answers for different patients. Children, for example, sometimes develop antiphospholipid antibodies after an infection. In this setting, the risk of thrombosis is only slightly increased; it’s usually not a big deal clinically. Adults sometimes develop antiphospholipid antibodies as part of an autoimmune disorder like lupus (in fact, antiphospholipid antibodies – in whatever clinical setting – are often called “lupus inhibitors” because of this association). In these patients, the risk of thrombosis is moderately increased. Finally, elderly adults may develop antiphospholipid antibodies in association with drugs. This is virtually always a harmless event with no increased risk of thrombosis.
Okay, so here’s where we get to the antiphospholipid antibody syndrome part. This term is used when a patient with an antiphospholipid antibody has thromboses or pregnancy-related complications (like recurrent miscarriage, pre-term labor, or pre-eclampsia). This syndrome is a serious thing. In a small number of patients, the thromboses can be widespread, leading to multi-organ system damage and death. The term is reserved for patients who are symptomatic; you wouldn’t use the term in patients who have an antiphospholipid antibody but no symptoms.
So what would you do if you think your patient might have an antiphospholipid antibody? Well, you’d need to confirm this suspicion with laboratory tests. First, order a PTT (in fact, that’s how a lot of these patients get picked up – they present with an abnormally prolonged PTT in the face of clinical evidence of thrombosis).
Then, order up a mixing study. Remember what a mixing study is? You do this test when you have a patient with a prolonged PTT and you want to know why. It’s performed by taking the patient’s (probably abnormal) plasma and mixing it with some pooled (normal) plasma – then running the PTT on this new mixed sample.
If the new PTT value is within the normal range (if it “corrects”), then you know the pooled human plasma must have supplied something to the patient’s plasma to make it clot normally. The “something” is usually a coagulation factor that the patient is missing.
If the new PTT value is still abnormal (if it’s still prolonged, and doesn’t “correct”), then you know that even though you added a bunch of normal plasma to the mix, the patient’s plasma still couldn’t clot normally. There must be some other problem with the patient’s plasma. The “other problem” is usually an inhibitor.
One caveat: some antiphospholipid antibodies do not prolong the PTT. It all depends on the particular PTT reagent your lab is using (some reagents are just more easily swayed by the antiphospholipid antibodies). So if you really feel your patient may have an antiphospholipid antibody, you shouldn’t stop investigating that possibility just because the PTT comes back normal! There are plenty of fancy lab tests that can be done to detect antiphospholipid antibodies. Just call your friendly neighborhood pathologist and see what he/she has to offer.
Q. In liver cirrhosis, why is the PTT not elevated? In all of my review books, it says the PT is used as one of the ways to evaluate liver function. (more…)
Okay, so this post is more about being a student than it is about the study of pathology. Bear with me: there is important information here! (more…)
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