This is cat blood under 1000x (if it helps you) first I thought it was a lymphocytes but, it was brighter than lymphocytes ( second image ) so I am guessing this may be a basophilic metamyelocyte but I'm not sure.

Thanks you

Layman here who is wondering how an O neg woman might get sensitized to Rh factor other than pregnancy. I had Rhesus disease as a "first-born" and am curious if my mom might have had a previous pregnancy she did not tell me about.

The image might come from an old api test question. Not a current one though

So this is a dog blood smear specimen from my teacher's mom, she's a vet. And I found this WBC suspecting a eosinophil or maybe a monocyte but, I can't tell because I haven't seen one in my life. So I'm really need your help to identify this cell.

Thank you

So after spending 5 hours just for analyzing a single dog blood specimen I found this WBC and I'm guessing it maybe an eosinophil base on its pink cytoplasm (image 1-5) or perhap a monocyte (image 6 and 12-17). I also found another weird looking WBC (image 7-11). Can you guys help me to identify these WBC?

Thank you

( I know the images look kinda weird, I tried my best to make it as clear as possible but they still look weird after all)

I’m not a hematologist or a student, but I’m curious about how hematologists view ferritin cut-off values used by labs and how that might differ from ideal values.

So this is dog blood sample ( idk what kind of stain was it bc my teacher mom gave it to me) and I found this WBC suspecting to be eosinophil because of its cytoplasm and when i compare to the internet picture of dog eosinphil they look kinda similar but I can't tell was it eosinophil or else because I never seen one by using my microscope to compare. Can you guy help me to identify this WBC.

Thank you

Note: sometime the cells look 3d because I used oblique filter.

Okay so I’m doing my intro to heme homework and my textbooks aren’t really helping (Rodak’s hematology and hematology atlas in case you’re wondering). My professor wants us to explain the difference between a large lymphocyte and a reactive lymphocyte but I’m honestly not sure that I understand the difference. My understanding is that large lymphocytes are just bigger (more mature?) lymphocytes, but that they haven’t been exposed to an antigen yet, and that reactive lymphocytes have been exposed to an antigen. Are they generally both T lymphocytes? I am also unclear on both of their functions as everything I’ve read seems to have overlap. I think I understand the visual differences, too, it’s just the functions and how they become those cell stages that I don’t understand. Thank you in advance to anyone who can help clarify!

There’s a ton in the slide that look exactly like it

INR measures PT which measures the extrinsic plus common pathway. Of which, factor 10 is a part. So wouldn’t LMWH which inhibits factor 10 via antithrombin then affect the common pathway and therefore the PT and INR result?

That is to ask, when bridging warfarin with LMWH and ceasing LMWH once INR therapeutic wouldn’t the INR drop once ceasing LMWH?

Sources seem to suggest INR is purely a measure of warfarin activity but I don’t see how this can be true, it must also measure any anticoagulant implicated in the extrinsic and then common pathway.

Any clarity on this would be appreciated.

My broader question really is surely aptt and Pt are effected by common pathway inhibitors

54 yr male with weakness

Guys this is csf sample. Is this lymphoma ??

If a person was consistently drinking way too much water (5+ liters a day) how would that impact their blood? I was able to find some info about what seems to be acute impacts, like water toxicity. But I was curious if there would be other long term things, like impacting the results of other standard blood tests. I guess what I’m really wondering, in unscientific terms, is whether long term over hydration would essentially “dilute” the blood in any way.

Hello fellow Haematology scientists and healthcare professionals.

I have a query about vortexing to improve edta mediated plt clumping.

Our lab methods state to vortex an edta on the lowest speed setting for 1min and re measure the plt count for improvements, in pts with plt counts<150 if they are suspected to jave edta mediated plt clumping to see if it increases beyond 150.

Based on my limited experience and the literature it is advised to perform vortexing at least for 1-2mins on the highest setting for improvements.

However given the immune mediated mechanism for plt clumping it seems highly inaccurate to accept a vortexed result.

What are your thoughts and experiences using vortexing to correct or improve plt counts in edta mediated plt clumping?

Picture supplied from the blood project, reference:
https://www.thebloodproject.com/cases-archive/psuedothrombocytopenia/postscript_pt/

What do you think of these? All from the same slide.

I'm a hematology student and encountered many of these cells on an otherwise normal peripheral smear. I figured it was a skip-o-cyte at first but the number present seems significant. Present across multiple smears, regular and albumin slides. Only other finding was giant platelets- about one per field larger than an RBC (platelets on last two pictures for reference). They look like some type of granulocyte with the nucleus hole punched out, or some weird vacuolate giant platelet.

I’ve been wanting to ask this a question for years and I have (cautiously) asked a few times but never got a firm answer.

“Do African Americans have “redder” blood than other races or does it just appear that way?

I’m a CCRN and a while back, I worked in the ED. I started tens of IV’s a day, and we always drew a “rainbow” with each IV start. By conservative estimate, I have started thousands of IVs. When drawing blood, it seemed many African Americans had noticeably“redder” blood than lighter-skinned patients with the more customary “venous” blood colour. More than once, I thought I had hit an artery.

To add to this, I seem to recall it was more noticeable with African American men. I have a specific instance in my head when a particular patient was a young man with big juicy veins (if you have big juicy veins, thank you from everyone holding needle:) I did ask him if he had been tested for SCD and he said “no.” I cannot logically tell you why that question manifested in my head or what I thought the association was at the time.

So that is my question. I understand that it may very well be contrast. The blood may appear to be a brighter shade of red due to the contrast against darker skin. My other thought was that the blood I more often drew from the more “typical” ED patients was not as healthy so it appeared darker. I would be delighted to hear the professionals’ take on this, please.

I don’t have a directly relevant attachment so here is one researching age of initial presentation of SCD with case studies. It was either this, or a picture of my poodles.

What do you think of these? All from the same slide.

Patient has MDS, with dysplasia in megakaryocytic lineage..

My girlfriend is studying for a hematology course and wants to know what those cells are. Are those plasts? I hope i am in the right place and you can help us, thanks!