# Hemostasis help **URL:** \ **Category:** Factual Questions\ **Created:** [October 27, 2004, 11:37pm UTC](https://boards.straightdope.com/t/hemostasis-help/271566 "2004-10-27T23:37:24Z")\ **Posts on this page:** 4\ **Page:** 1
**Author:** ![Antigen](https://avatars.discourse-cdn.com/v4/letter/a/848f3c/32.png) [@Antigen](https://boards.straightdope.com/u/Antigen)\ **Post date:** [October 27, 2004, 11:37pm UTC](https://boards.straightdope.com/t/hemostasis-help/271566/1 "2004-10-27T23:37:24Z")
I have a test tomorrow in Hematology & Hemostasis, and I’m stuck on a couple of concepts. These aren’t extremely important, but I’d like to understand what’s going on, so if anyone with the brains cares to share some with me, it would help a whole lot for my stress level. Part 1: My class notes say that patients with Lupus-like inhibitors in their blood will generally not have a tendency to bleed, but will rather have thrombosis as a complication. In other words, they are in a hypercoagulable state. However, the notes also say that the inhibitors are antibodies against phospholipids in the prothrombin complex… but isn’t a functional prothrombin complex required for clotting? How can you get thrombosis when your complex is inhibited? And their APTT is supposed to be elevated as well, which confuses me even more. Part 2: My notes say > [@](#): > > Factor VIII inhibitor presents a prolonged APTT which does not correct with normal plasma. > Factor VIII antibody is a time-dependent inhibitor detected by incubating the normal pool/patient plasma mixture at 37C for 30 minutes. What does this mean? I figure that “time dependent” means that it will appear to correct at first, but given incubation time, it will eventually inhibit the factor VIII of the pooled plasma and APTT will remain high. Am I anywhere close? ---
**Author:** ![KarlGauss](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/karlgauss/32/3713_2.png) [@KarlGauss](https://boards.straightdope.com/u/KarlGauss)\ **Post date:** [October 28, 2004, 12:17am UTC](https://boards.straightdope.com/t/hemostasis-help/271566/2 "2004-10-28T00:17:36Z")
I may be able to help with the first question. The inhibitors (antibodies) are indeed directed at phospholipids. In fact, that is why the aPTT is often elevated in people who have them. In other words, the antibodies tie up the phosholipid needed as substrate for the aPTT test (an _in vitro_ assay). At first glance, this could suggest that these people are actually **anti** coagulated. However, platelets also have phospholipids in their membranes. When the antibodies bind to the platelet phospholipids, it **activates** platelet clumping. Thrombosis results. This is a real, _in vivo_ phenomenon. I don’t think I ever knew the answer to the second question. ---
**Author:** ![KarlGauss](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/karlgauss/32/3713_2.png) [@KarlGauss](https://boards.straightdope.com/u/KarlGauss)\ **Post date:** [October 28, 2004, 12:24am UTC](https://boards.straightdope.com/t/hemostasis-help/271566/3 "2004-10-28T00:24:12Z")
Just to clarify, when you do an aPTT test, you mix patient serum with a mish-mash of stuff including phospholipids. If there’s an antibody in the patient’s serum that binds to phospholipids, it’s as if you didn’t provide the PL’s in the “test tube” in the 1st place, i.e. all the PL’s are used up, or bound, by the antibodies. The result is an elevated aPTT. ---
**Author:** ![Antigen](https://avatars.discourse-cdn.com/v4/letter/a/848f3c/32.png) [@Antigen](https://boards.straightdope.com/u/Antigen)\ **Post date:** [October 28, 2004, 12:56am UTC](https://boards.straightdope.com/t/hemostasis-help/271566/4 "2004-10-28T00:56:59Z")
So the elevated aPTT is an artefact of the test, and not necessarily representative of the patient’s state. That makes a whole lot more sense! Thanks - I never considered that the phospholipids on the platelets would be attacked too, and that it would activate clumping.