ABC of Clinical Haematology, 3rd Edition (ABC Series) by Drew Provan

By Drew Provan

This ABC has validated itself as a well-liked advent to scientific Haematology, suitable either for postgraduate scholars and first care practitioners. Now in its 3rd variation, the ABC of scientific Haematology has been completely revised, that includes the newest remedies for leukemia, antithrombotics and medicine for lymphoma and protecting the newest advances in hematology and bone marrow transplantation. With each one bankruptcy written by way of experts of their respective fields, this can be a terrific easy textual content for normal perform and medical institution employees with sufferers who've blood similar difficulties, specifically GPs, hematology nurses, junior medical professionals, hematologists, and trainees in hematology.

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Extra resources for ABC of Clinical Haematology, 3rd Edition (ABC Series)

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Platelets play a key role in securing primary haemostasis. 1 Normal platelet function. 33 34 ABC of Clinical Haematology calcium and serotonin, and α granules containing fibrinogen, VWF, platelet-derived growth factor and many other clotting factors. Following adhesion, the platelets are stimulated to release the contents of their granules, essential for platelet aggregation. The platelets also provide an extensive phospholipid surface for the interaction and activation of clotting factors in the coagulation pathway.

Heparin-induced thrombocytopenia Heparin-induced thrombocytopenia occurs during unfractionated heparin therapy in up to 5% of patients, but is less frequently associated with low molecular weight heparins. It may become manifest when arterial or venous thrombosis occurs during a fall in the platelet count and is thought to be due to the formation of antibodies to heparin that are bound to platelet factor 4, a platelet granule protein. The immune complexes activate platelets and endothelial cells, resulting in thrombocytopenia.

Dasatinib This second generation tyrosine kinase inhibitor is active against both Abl and Src oncogenes and in vitro studies show it to be about 300 times more active than imatinib. It has demonstrated considera- Chronic Myeloid Leukaemia ble efficacy in patients resistant to imatinib and patients who respond well should probably be continued on the drug indefinitely. The recommended dose is currently 100 mg daily. Nilotinib This agent, also a second generation tyrosine kinase inhibitor, is also active in patients whose leukemia appears resistant to imatinib.

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