By Prof. Dr. med. Fritz Reinhard Matthias (auth.)
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Extra info for Blood Coagulation Disorders: Hemorrhagic Diatheses and Thromboembolic Diseases
16. Mechanisms of hemostasis A mild hemostatic disorder with moderate lowering of one or some coagulation factors can be compensated without manifest hemorrhagic diathesis occurring. Hemorrhages from capillaries stop mainly by compression and agglutination of the endothelial cells. With in juries of the arterial and venous vessels the hemostatic process progresses in several phases (Fig. 16): 1. Vascular lesion or endothelial damage with reflex vascular constriction. 2. Adhesion of thrombocytes to exposed subendothelial tissue, collagen and pervascular structures.
It is possible to quantify the fibrinogen/fibrin split products by: 1. tanned red cell hemagglutination inhibition immunoassay (TRCHII test, Wellcome) 2. latex agglutination test (Wellcome) 3. staphylococcal clumping test (Behringwerke, Boehringer) 4. Laurell electrophoresis 5. immune precipitation. To avoid interference with fibrinogen, the test must be carried out in the serum. There are possibilities of error in that some of the split products, particularly the macromolecular ones, are incorporated into the clot during production of the serum, and minimal amounts of fibrinogen or fibrin persist as complexes with split products dissolved in the serum.
The use of the Thrombotest and Normotest makes it possible to distinguish whether a reduction in the prothrombin complex factors is due to liver cell damage, vitamin K deficiency, or vitamin K antagonism due to coumarins. If the two tests are equally reduced, there is little or no PIVKA. Then probably one has liver cell damage. It should be mentioned that in hepatic cirrhosis also it is possible for the inactive precursors of the prothrombin complex (PIVKA) to be produced for various reasons. If the value in the Thrombotest is decidedly less than that in the Normotest, then a disorder of vitamin K metabolism is present.