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Haematological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
If formation of the platelet plug is delayed, abnormal bleeding tends to be immediately obvious from cuts, surgical incisions or mucous membranes (e.g. epistaxis). Careful history-taking is needed to exclude a drug effect mimicking a platelet function disorder (e.g. aspirin use).
Anatomy, physiology, and histology of the skin
Published in Michael Parker, Charlie James, Fundamentals for Cosmetic Practice, 2022
The first step in platelet plug formation is platelet adhesion, whereby platelets stick to parts of a damaged blood vessel, such as exposed collagen fibres of connective tissue on the inside of the damaged endothelial cells. Once platelets have stuck to the wall of a damaged blood vessel, the platelets become active and release their vesicular contents during the platelet release reaction. ADP is secreted to act as an energy source for activating nearby platelets, as well as thromboxane A2 and serotonin, which themselves are important in causing and maintaining vasoconstriction, decreasing the flow of blood to the damaged area and limiting further bleeding.
Cellular Components of Blood
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
After platelet activation by thrombin and collagen, procoagulant activity increases. This procoagulant action requires Ca++ influx across the plasma membrane, and reorientation of phosphatidyl serine from the inner layer to the outer layer of the platelet membrane with the expression of binding sites for specific coagulation processes. Platelet factor 3, an exposed membrane phospholipid, is available for coagulation and protein complex formation. The first reaction involves factors IXa, VIII and X in the formation of factor Xa. The second (or prothrombinase) reaction results in the formation of thrombin from the interaction of factors Xa, V and II. The irreversible fusion of platelets aggregated at the site of endothelial injury is enhanced by ADP and other enzymes released during the platelet release reaction. Thrombin also promotes platelet plug formation.
Platelet calcium signaling by G-protein coupled and ITAM-linked receptors regulating anoctamin-6 and procoagulant activity
Published in Platelets, 2021
Delia I. Fernández, Marijke J. E. Kuijpers, Johan W. M. Heemskerk
Overall, it appears that the magnitude and duration of the Ca2+ signal in platelets is a function of their exposure to agonists, in which GPCR and ILR agonists together evoke the platelet procoagulant response. A differential exposure to agonists can also explain, on top of differences between platelets, why the platelets in a thrombus are heterogeneous in activation stages [70,71]. Herein, the population of most strongly activated platelets is the one showing PS exposure [41,56]. Taken together, the physiological consequences of procoagulant platelet formation can be summarized as: (i) limiting the thrombus growth by reducing the adhesive function of platelets, (ii) enhancing the coagulation by thrombin and fibrin formation, and (iii) a thrombin-induced stabilization and contraction of the platelet plug.
Platelet aggregation measured by single-platelet counting and using PFA-100 devices
Published in Platelets, 2018
Natalia Dovlatova, Stan Heptinstall
Platelets perform their main function in haemostasis through adhering to the vessel wall at the site of damage and forming a platelet plug via recruiting further platelets. One of the first and the most common methods to assess platelet function in vitro has been the measurement of platelet aggregation; the light transmission method was developed by (1). The methodology is still used in the essentially the same way as originally described and is considered to be the “gold standard” method for measuring platelet aggregation. The problem with this approach is that it requires specialised equipment and is time- and labour-intensive. Additionally, it requires a significant volume of blood to prepare the platelet-rich plasma that is used to monitor the changes in light transmission that occur as the platelets aggregate together.
The impact of rivaroxaban on primary hemostasis in patients with venous thrombosis
Published in Platelets, 2020
Nina Haagenrud Schultz, Pål Andre Holme, Stine Bjørnsen, Carola Elisabeth Henriksson, Per Morten Sandset, Eva-Marie Jacobsen
Primary hemostasis is the formation of the platelet plug as the first response to a vessel injury. Platelets bind to von Willebrand factor (vWF) at the site of injury, and the glycoprotein IIb/IIIa receptor (GPIIb/IIIa) on the platelets binds fibrinogen, which leads to aggregation of platelets. In this process platelets become activated, change shape, and release content from their granules, including P-selectin [19]. The activation of platelets results in a primary platelet plug. Simultaneously, the coagulation cascade is initiated by tissue factor released from subendothelial cells beneath the damaged endothelium.