Embolus vs. thrombus

Here are a few very good questions about CNS infarcts. There are two types of CNS infarcts: red (hemorrhagic) and pale (ischemic). (more…)

Here are a few very good questions about CNS infarcts. There are two types of CNS infarcts: red (hemorrhagic) and pale (ischemic). (more…)
Q. I have a question about the coagulation lab tests. I saw that an increased PT would result from Coumadin and Heparin. (more…)
There are some Pathology Student posts that readers seem to turn to over and over.
Q. What’s the whole deal with Gla residues, vitamin K and the Coumadin drugs?
Q. Does medullary expansion mainly happen in alpha thalassemia patients because they cannot make any useful hemoglobin due the the absence of the alpha chain? (more…)
Q. Why is there a microangiopathic hemolytic anemia in thrombotic thrombocytopenic purpura and disseminated intravascular coagulation?
Q. I had some confusion on why the PT, PTT, and TT are prolonged in disseminated intravascular coagulation. Intuitively I thought they might be shorter because everything is already present and turned on due to the constant state of coagulation, but the only way I can think it might be prolonged would be that are the factors being used up which then shows up as a long PT, PTT and TT? If you could just clarify that for me that would be great.
A. Yes! That’s exactly why they are prolonged! In disseminated intravascular coagulation (DIC) there’s a ton of clotting going on – so the platelets and coag factors are getting used up. As the coag factors get used up, the PT (prothrombin time), PTT (partial thromboplastin time) and TT (thrombin time) go up. You also see increased FDPs (fibrin degradation products) – but that’s an incredibly sensitive test, best used for other purposes.
By the way, Ed’s Pathology Notes has a way to remember the seriousness of DIC – he calls it “Death is Coming.”
Q. How come the PT and PTT are not increased in TTP and HUS? You have clots all over, so why don’t the coag tests go up like they do in DIC? (more…)
Q. I understand that hemophilia is caused by factor VIII or IX deficiency and both factors work in the intrinsic pathway. (more…)
Here’s how you make a clot:
If you think back to the basics of the coagulation cascade, you might recall that there are two arms – an extrinsic arm and an intrinsic arm – which come together in the final common pathway, which ends up turning fibrinogen into fibrin. When somebody is bleeding, and you think it’s due to a coagulation problem (as opposed to a platelet problem), it’s helpful to know what part of the cascade is screwed up. That helps you figure out what’s wrong with the patient (is it hemophilia? or liver disease? or coumadin overdose?).
There are two main tests for evaluating the cascade: one for the extrinsic arm (the PT/INR) and one for the intrinsic arm (the PTT). There are other tests too – but those will have to be for another post.
1. The PT/INR
The prothrombin time (PT) is performed by adding thromboplastin to the patient’s plasma, and seeing how long it takes to make fibrin (as soon as you see the first strands of fibrin form, the test is over, and you measure the result in seconds.
Thromboplastin contains a tissue-factor-like substance, and therefore it just measures the extrinsic pathway. The annoying thing about thromboplastin is that its strength varies considerably from manufacturer to manufacturer. So the PT done at one hospital (using manufacturer A’s thromboplastin) will be significantly different than the PT done at another hospital (using manufacturer B’s thromboplastin). Dumb.
To deal with this annoying issue, someone figured out how to make some mathematical calculations that take into account each manufacturer’s thromboplastin strength. Now, you just do your PT assay, add on those mathematical calculations, and you wind up with something called the International Normalized Ratio (INR). This means that you can do the PT with anybody’s thromboplastin, and you’ll wind up with a result (the INR) that removes that variability. Super important.
2. The PTT
The PTT, or partial thromboplastin time, is performed by adding just some phospholipid to the patient’s plasma and waiting to see how long it takes to form fibrin. You have to add in a little “contact factor” like kaolin to activate XI to XIa – but other than that, that’s it!
It’s called the “partial thromboplastin” time because initially, it was found that by adding a part of thromboplastin to a test tube, you could activate fibrin formation. It turns out that the part of thromboplastin people were adding was just phospholipid, and that thromboplastin consists of both phospholipid and tissue factor. This test measures the intrinsic pathway, which is that arm of the cascade involving factors XI, IX, VIII and the final common pathway.
Recent Comments