dilute russell’s viper venom test (drvvt) which coagulation factor is activated by the venom
Dilute Russell's viper venom time This in vitro diagnostic test is based on the ability of the venom of the Russell's viper to induce thrombosis. The venom contains some substances (RVV-V and RVV-X) which directly activate factor V and factor X,[3] which turns prothrombin into thrombin in the presence of phospholipid and calcium.[4] In the dRVVT assay, low, rate-limiting concentrations of both Russell's viper venom and phospholipid are used to give a standard clotting time of 23 to 27 seconds.[citation needed] This makes the test sensitive to the presence of lupus anticoagulants, because these antibodies interfere with the clot-promoting role of phospholipid in vitro, and their presence results in a prolonged clotting time.[5] A mixing study is then performed, which consists of adding an equal volume of the patient's plasma to normal plasma; in this study, one would expect the clotting time to return to the normal range if there was only a deficiency of coagulation factors alone. A prolonged clotting time of 30 seconds or greater that does not correct despite the mixing study suggests the presence of a lupus anticoagulant.[5] An abnormal result for the initial dRVVT assay should be followed by a dRVVT confirmatory test.[6] In this test, the inhibitory effect of lupus anticoagulants on phospholipids in the dRVVT can be overcome by adding an excess of phospholipid to the assay. The clotting times of both the initial dRVVT assay and confirmatory test are normalized and then used to determine a ratio of time without phospholipid excess to time with phospholipid excess. In general, a ratio of greater than 1.3 is considered a positive result and implies that the patient may have antiphospholipid antibodies.[7] The dRVVT test has a higher specificity than the aPTT test for the detection of lupus anticoagulant, because it is not influenced by deficiencies or inhibitors of clotting factors VIII, IX or XI as the venom only activates factors V and X.[3][4]
Coagulation Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium lining the vessel. Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial tissue factor to plasma Factor VII, which ultimately leads to fibrin formation. Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: Additional coagulation factors or clotting factors beyond Factor VII (listed below) respond in a complex cascade to form fibrin strands, which strengthen the platelet plug.[2]
Denial-of-service attack A wide array of programs are used to launch DoS-attacks.
Pulse Pressure waves generated by the heart in systole move the arterial walls. Forward movement of blood occurs when the boundaries are pliable and compliant. These properties form enough to create a palpable pressure wave.