platelets

So I guess today's snippet is about viscoelastic assays that we use in ICU for testing the coagulation pathways.

So Maddy, the question is with regards to viscoelastic assays, can you please describe the expected alterations and underlying mechanisms resulting from the following? A, platelet dysfunction.

B, therapeutic heparin use.

C, hyperfibrinolysis.

This is particularly important, say, if it's a patient who is on bypass or post-bypass where they have quite a big effect of heparin, which

might be impacting on their coagulation status.

So we'll first talk about platelet dysfunction and the different rotam parameters that are affected and not affected and what change you'd expect and thinking about the underlying mechanism because this was the main feedback in the exam question that you needed to think about what the change was and what the mechanism for that was.

So the clotting time in platelet dysfunction is the time from the start of the test to when the waveform reaches two millimeters above the baseline.

In fact, Talapro-1, in that study, over a third of the patients received transfusion support.

Thrombocytopenia is particularly relevant for norepirib, Platelets decreases occur during the cycle one and stabilize by cycle two or three with dose modifications as the primary management strategy.

Nausea, vomiting are generally grade one to two and manageable with standard antiemetics.

I find that nausea typically peaks early with these PARPs.