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Specific Management of PPH
Published in Gowri Dorairajan, Management of Normal and High Risk Labour During Childbirth, 2022
The profile in suspected cases includes prothrombin time, activated partial thromboplastin, and platelet count. In the obstetric setting of bleeding, especially in abruption and severe preeclampsia, bedside point of care clot retraction time helps in knowing the capacity to clot and the ability of clot to retract to leave clear serum within 30 minutes of clotting. When the blood does not clot well or does not leave behind clear serum, one should suspect that there is ongoing fibrinolysis where the clot retraction does not leave behind clear serum. Fibrin production can be indirectly measured by assessing the levels of fibrin degradation product D-Dimer. Fibrinogen level assay also reflects DIC, though it is less specific. Fibrinogen levels give clinical guidance to the component transfusion. Thromboelastography (TEG) is an objective method of studying coagulation, but the experience of its use in obstetrics haemorrhage is limited in the literature.
Haemostasis and Thrombosis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
AggregationThe activation of platelets causes GPIIbIIIa to change into an active configuration which binds fibrinogen.Fibrinogen binding to IIbIIIa results in platelet aggregation and signalling, which further reinforces activation.Other adhesion molecules — including VWF and fibronectin — also bind to IIbIIIa and contribute to aggregation.Platelets change configuration to mediate clot retraction which strengthens the clot.
Congenital Platelet Dysfunction and von Willebrand Disease
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
In Glanzmann thrombasthenia, the platelet count is normal, and platelets are normal in appearance on the peripheral blood film. Clumping of platelets may not be observed even in a blood film prepared from nonanticoagulated blood. There is little or no aggregation or dense granule secretion in response to most platelet stimuli, including ADP, epinephrine, thrombin, or collagen. Clot retraction is typically decreased also. Ristocetin, in contrast, does stimulate an initial agglutination response and a normal degree of dense granule secretion.
Investigating the ultrastructural and viscoelastic characteristics of whole blood after exposure to the heavy metals cadmium, lead and chromium, alone and in combination
Published in Ultrastructural Pathology, 2022
L Pretorius, H Taute, M Van Rooy, HM Oberholzer
An increase in potential clot formation was observed in the current study. The presence of sticky thick fibers (green arrows) that are haphazardly organized may be an indication of inadequate clot retraction. This can potentially influence the clot lysis time and increase the risk of thrombosis. The group with the least toxic effect appeared to be the Cd group, while the Cd + Cr combination appeared to be the most toxic group with the fibers being bent and less taut (pink arrows) and forming sticky masses (blue arrows) at the lowest concentration. At the higher concentrations, fibrin fibers fused together (yellow arrows) and formed net-like coverings (red arrows) that can have detrimental effects on coagulation. At higher concentrations, the fibrin network became less organized and appeared mesh-like. This caused the erythrocytes to become trapped in the fibrin network and contributed to their altered erythrocyte morphology. The results are similar to what was observed by Venter et al.24 in an ex vivo study after Cd and Cr exposure in whole blood. Based on Yaprak and Yolcubal10 Cr (224 µg/L) accumulates at a much higher concentration in PRF than the other two metals (Cd: 0.21 µg/L and Pb: 4.4 µg/L) and might explain the general tendency for Cr to have a much larger effect.
Mind the gap: connexins and pannexins in platelet function
Published in Platelets, 2021
Kirk a Taylor, Gemma Little, Jonathan M. Gibbins
Of the 16 connexins screened from blood cells and megakaryocytes, notable levels of Cx37, Cx40 and Cx62 mRNA were detected from cultured megakaryocytes [18]. Expression of Cx37 and Cx40 has been confirmed by Western blotting, immunocytochemistry and flow cytometry [5,6,18]. More recently, Cx62 was identified in human platelets, where it was shown to reside intracellularly before translocating to the plasma membrane upon stimulation by the thromboxane A2 mimetic U46619 [7]. People carrying a single nucleotide polymorphism P319S in the Cx37 gene display modestly enhanced platelet activation, suggesting a role for Cx37 in regulating platelet activation [5]. To date, platelet connexins have been shown to function both as hemichannels and gap junctions [5–7,18]. Of the platelet connexins, evidence suggests that whilst Cx37 and Cx40 cannot form heteromeric structures, they are able to assemble in a heterotypic manner between apposite cells [23]. Clot retraction is a coordinated process whereby microtubules contract to facilitate wound healing [24]. Interestingly, selective peptide inhibitors of either Cx37, Cx40 or Cx62 inhibit clot retraction, suggesting that there may be a role for gap junctions in the coordination of this process [6,7,18]. Connexin intermixing has not been studied in platelets but this could serve to regulate platelet interactions within a thrombus or with other cell types.
Marginal band microtubules are acetylated by αTAT1
Published in Platelets, 2021
Anne-Sophie Ribba, Morgane Batzenschlager, Clotilde Rabat, Thierry Buchou, Sylvie Moog, Saadi Khochbin, Ekaterina Bourova-Flin, Laurence Lafanechère, François Lanza, Karin Sadoul
We have previously reported that the higher acetylation level of HDAC6−/− platelets correlates with faster activation/spreading kinetics. Accordingly, we wondered whether αTAT1−/− platelets would show a retardation of their spreading capacity. We decided to use again a spreading assay to compare the speed of activation and spreading between the different genotypes. HDAC6 deficient platelets spread faster than WT platelets confirming our previously published observations, while αTAT1 deficient platelets behave similar to WT platelets under these conditions (Figure 1C). We also used a clot retraction assay to compare the functional efficiency of the three different platelet populations. Clot retraction reflects the capacity of platelets to activate and to perform a “three-dimensional spreading” within the fibrin network as well as their ability to subsequently reorganize their cytoskeleton to contract the fibrin network. While HDAC6 deficient platelets behave similar to WT platelets, we observe a slight retardation of clot retraction by αTAT1KO platelets (Figure 1D, see also supplementary Figure 1B for a typical example of clot retraction kinetics).