We’ve talked already about how you’d differentiate chronic lymphocytic leukemia from a benign lymphocytosis. So how about the same thing for the myeloid series, namely, how do you tell apart chronic myeloid leukemia from a benign neutrophilia? (more…)
Q. If you have a blood smear that shows a lymphocytosis, and all the lymphocytes look pretty mature, how do you know whether it’s chronic lymphocytic leukemia (CLL) or just a plain old benign lymphocytosis? (more…)
Here’s a very good question about the diagnostic use of the bleeding time.
Q. I’m currently studying heme for boards and came across a practice questions that used platelet count, bleeding time, PT and PTT values to differentiate between certain diseases/problems. I was just wondering how in both Vitamin K deficiency and liver disease you can get an increase in PT and PTT but the bleeding time doesn’t change…I guess I figured that bleeding time would have to increase. Can you explain this to me?
A. Yeah, that does sound weird, you’d think the bleeding time would change – but actually, the bleeding time is only a measure of platelet function. It really has nothing to do with coagulation!
I kind of think of it like this: the platelet plug is the first thing to form, and that is enough to stop the bleeding from the incision made at the beginning of the test. The coagulation cascade happens next, and the status of that won’t be apparent in the bleeding time results. The patient might have some more bleeding later if their coagulation system is really screwed up…but the bleeding time assay will be done by then. In reality, it probably happens a little more concurrently than that (platelet plug is followed very closely by fibrin formation – the two probably even overlap a bit), but I think it’s a good way to remember the concept.
The same reasoning fits with the way that people with coagulation factor disorders bleed (as opposed to patients with platelet disorders). People with platelet abnormalities tend to bleed spontaneously into mucous membranes without much provocation (probably because they’re having a hard time forming that initial platelet plug) whereas patients with coagulation factor abnormalities, like hemophilia, tend to have deep, severe bleeds that happen after some time has elapsed (because they form the initial platelet plug okay, but they can’t seal it up with fibrin very well, so they end up bleeding later on).
Before you can really appreciate pathologic changes in red cells, you need to know what normal red cells look like. Â Here is a normal blood smear image, taken at high power. (more…)
Who names this stuff, anyway?!
Coagulation factors, for the most part, have two names: a Roman numeral name and an English wordy name. (more…)
Mapo doufu is an ancient Chinese dish that made me feel dizzy the first time I ate it. (more…)
Rudolf Virchow, a German pathologist in the 1800s, is considered by many to be “the father of pathology.” His famous Omnis cellula e cellula (“every cell originates from another existing cell like it”) theory, published in1858, rejected the then-prevalent belief that organisms could spontaneously arise from non-living matter (e.g., that maggots could spontaneously appear in decaying meat). (more…)
Queen Victoria reigned as British sovereign from 1837 until 1901. Britian enjoyed prosperity and growth under her monarchy, but her genetic legacy was another story. (more…)
The term “left shift” means that a particular population of cells is “shifted” towards more immature precursors (meaning that there are more immature precursors present than you would normally see). (more…)
Sickle cell anemia is one of a larger group of inherited red blood cell disorders called hemoglobinopathies. (more…)
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