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Antiplatelet therapy with one or more of these drugs decreases the ability of blood clots to form by interfering with the platelet activation process in primary hemostasis. Antiplatelet drugs can reversibly or irreversibly inhibit the process involved in platelet activation resulting in decreased tendency of platelets to adhere to one another ...
Platelet function can be decreased by the use of ketorolac. [15]: 279 Though uncommon, potentially fatal adverse effects include stroke, myocardial infarction, GI bleeding, Stevens–Johnson syndrome, toxic epidermal necrolysis and anaphylaxis. In terms of safety, ketorolac has been assessed to be a relatively higher-risk NSAID when compared to ...
One primary function of thromboregulation is the control of primary hemostasis, which is the platelet aggregation process. Some thromboregulators enhance platelet aggregation and some others inhibit the process. Platelet aggregation plays a critical role in the genesis of a resulting thrombus. Adhesion should remain local, but platelet ...
Thromboxane A 2 (TXA 2) is a type of thromboxane that is produced by activated platelets during hemostasis and has prothrombotic properties: it stimulates activation of new platelets as well as increases platelet aggregation.
Multiplate multiple electrode aggregometry (MEA) is a test of platelet function in whole blood. [1] [2] The test can be used to diagnose platelet disorders, [3] [4] [5] monitor antiplatelet therapy, [6] and is also investigated as a potential predictor of transfusion requirements and bleeding risk in cardiac surgery. [7]
Other causes of reactive thrombocythemia include: post surgery, iron deficiency, drugs, and rebound effect after bone marrow suppression. [8] Research suggests that thrombocytosis can also occur after physical exercise, and is triggered by hemoconcentration and the release of platelets from the liver, lungs and spleen. [3] [9]
Platelet donation therapy is frequently needed by cancer patients, because chemotherapy for such patients can render them unable to generate platelets of their own. The basic principles of automatic platelet apheresis are the same as in the manual procedure, but the whole procedure is performed by a computer-controlled machine.
The treatment may mirror that of chemotherapy-induced myelosuppression or may be to change to an alternate drug or to temporarily suspend treatment. Because the bone marrow is the manufacturing center of blood cells, the suppression of bone marrow activity causes a deficiency of blood cells.