Practical Hemostasis and Thrombosis by Nigel S. Key, Michael Makris, Denise O'Shaughnessy, David

By Nigel S. Key, Michael Makris, Denise O'Shaughnessy, David Lillicrap

This useful consultant presents the entire details essential to comprehend the clotting mechanisms, in addition to the right way to hinder, diagnose, and deal with bleeding and clotting issues. Practical Hemostasis and Thrombosis has been up-to-date to mirror the entire very important advances made because the first version. It contains an in-depth description of platelet abnormalities and disseminated intravascular coagulation, in addition to overlaying the laboratory and molecular organic checks wanted for the analysis of bleeding and clotting issues.

Clinicians will locate valuable recommendation for daily questions in each one strong point region because the publication describes hemorrhagic and thrombotic difficulties in cardiology, neurology, hepatology, nephrology, oncology, obstetrics, pediatrics, extensive care and transfusion medicine.

An beneficial source for all hematologists, trainee hematologists getting ready for examinations and clinicians this e-book can be saved shut handy for common consultation

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Extra resources for Practical Hemostasis and Thrombosis

Sample text

A number of studies suggest that the PFA-100® is a potential in vitro replacement of the bleeding time. The disadvantages are that, like the in vivo bleeding time, the test is sensitive to both the platelet count and hematocrit and it is therefore crucial that a full blood count is performed to help interpret abnormal results. The test is insensitive to coagulation protein defects including afibrinogenemia, hemophilia A and B and other clotting factors. False-negative results are sometimes obtained; for example, in patients with storage pool disease, primary secretion defects, Hermansky–Pudlak syndrome, type 1 von Willebrand disease (VWD) and the Quebec platelet disorder.

Standard morphology, platelet aggregation studies and an evaluation of platelet receptor density will usually establish or exclude a diagnosis of Bernard– Soulier syndrome or Glanzmann thrombasthenia, the two most frequently encountered, but nevertheless rare, recessive inherited platelet disorders. In unusual instances, knowledge of the causative mutation in these patients could be useful, perhaps for prenatal testing. In the Bernard–Soulier syndrome, a heterogeneous mutational pattern has been documented, with both homozygous and compound heterozygous mutations identified in the genes encoding Gp Ibα, Ibβ and IX.

There are no commercially available quality control kits for platelet function testing. Aggregometers can be checked by using the PRP and PPP to check percentage aggregation settings and dilutions (mixes of PRP and PPP) can be performed to check linearity. Glanzmann thrombasthenia There is complete absence of aggregation to agonists such as ADP, but a normal agglutination response to ristocetin. Bernard–Soulier syndrome Platelets aggregate to all of the physiologic agonists, but do not agglutinate to ristocetin.

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