The Thrombocyte Reference Materials

‭The thrombocyte‬ ‭ These circulating elements are well represented: 150 to 400 giga/L. They intervene mainly in‬ ✪ ‭primary hemostasis. These are anucleate particles of 2 to 4 micrometers in diameter. After MGG we‬ ‭distinguish 2 zones: a central zone = the granulomere which are purplish red dots and a lighter‬ ‭peripheral zone called the hyalomere.‬ ‭ The platelet membrane has a classic structure: phospholipid bilayer nevertheless on the external‬ ✪ ‭side there is an environment called the periplatelet atmosphere and it is this zone which is capable‬ ‭of absorbing coagulation factors so the platelets are involved not only in primary hemostasis but‬ ‭also in the coagulation. Under the phospholipid layer we can highlight microfilaments made up of‬ ‭contractile proteins such as trombostenin. This during the contraction of the platelet will allow the‬ ‭emission of pseudopodia, the creation of canaliculi and this will allow the expulsion of‬ ‭granulations. There are 2 types of granules:‬ ‭ ‬ ➔ ‭alpha granules‬‭:Contain fibrinogen, coagulation factor‬‭8 antigen, beta‬ ‭thromboglobulin, platelet factor 4, fibronectin.‬ ‭➔‬ ‭dense granules‬‭:contain calcium, serotonin, ATP, ADP.‬ ‭ hese platelets are well represented at the circulating level, there is also a hen stored at the level of‬ T ‭the spleen and which corresponds to 1/3 of all platelets. The shelf life is 8 to 10 days and their‬ ‭volume is 8 to 11 fenton liters.‬‭Noticed‬‭:Following‬‭trauma, patients can be splenectomized so they‬ ‭will no longer be able to store platelets in the spleen and these are patients who will have figures‬ ‭systematically higher than 450 giga/L without however that there is a particular risk of thrombosis.‬ ‭ Unlike people who present a hypersplenism (large spleen): for example a former alcoholic who‬ ✪ ‭has developed hepatic cirrhosis, the consequence is portal hypertension therefore put into action‬ ‭charge of all the ships of mount and therefore there is consequently a spleen which increases by‬ ‭volume. The consequence of this increase in volume is that the storage of platelets is increased and‬ ‭these are people who will systematically have thrombocytopenia, that is to say, the number of‬ ‭circulating aquettes slightly decreased. Often at the same time there is storage of polynuclear‬ ‭neutrophils in the spleen and therefore also neutropenia.‬ ‭ ‬ ➔ ‭Properties :‬‭They are involved in primary hemostasis‬‭and in the coagulation thati can arrive‬ ‭after primary hemostasis. This primary hemostasis will occur, for example, during lesions of small‬ ‭vessels and this will lead to the formation of a platelet thrombus which will close the vessels and‬ ‭then there will be tissue repair. Chronologically :‬ ‭ -‬ 1 ‭Vascular lesion‬‭:When there is vascular injury there‬‭will be loss of endothelial cells, the‬ ‭endothelium is torn and we will have exposure of the subendothelium, collagen fibers in the‬ ‭circulatory stream.‬ ‭2-‬ ‭Vascular reaction:‬‭It is a vasoconstriction and therefore‬‭there is a drop in pressure locally‬ ‭and a drop in the scrolling speed of the elements and in particular of the platelets. This will make it‬ ‭possible to achieve the 3th stage which is the phase from:‬ ‭3-‬ ‭Membership:‬‭In fact, if the platelets pass very quickly‬‭at the level of the lesion, they‬ ‭do not cannot adhere to the subendothelial so during the adhesion phase we will have platelets‬ ‭which will adhere to the subendothelium viaVim Brant factor which recognizes platelet‬ ‭glycoprotein 1B (GP1B). Once the platelet is bridged to the subendothelium, there is:‬ ‭4-‬ ‭Activation of platelets‬‭there is initially a morphological change of the platelet, it will‬ b‭ ecome spherical, it will emit pseudopodia, there will be invaginations and there is the reaction of‬ ‭release of granular content:the ADP will be important to activate these platelets even more, calcium‬ ‭will allow the bridging between the platelets as well as fibrinogen.‬ I‭ n platelets there is a synthesis of prostaglandins:from arachidonic acid there is constitution of‬ ‭endoperoxide thanks to an enzyme cyclooxygenase and in platelets these endoperoxides are‬ ‭transformed into thromboxane A2 and this molecule is a powerful vasoconstrictor and it is an‬ ‭inducer of aggregation.‬ ‭At the level of the endothelial cell there is synthesis of endoperoxide from the acid arachidonic but‬ ‭we will not have TXA2 but there is synthesis of PGI2 (prostaglandin) which is a vasodilator and‬ ‭anti-aggregant agent.‬ ‭From a physiological point of view, when there is no vascular lesion, the endothelial cell produces a‬ ‭vasodilator factor and an anti-aggregant factor. When it is affected by the endothelium, locally there‬ ‭is a decrease in the concentration of this anti-aggregating factor. Due to the activation of platelets‬ ‭which have been bridged to the subendothelium via Von Vimbrant factor, an increased release of‬ ‭TXA2 promotes platelet aggregation. On the other hand, the plate is also the support of a‬ ‭procoagulant activity and platelet factor 3 is expressed on the surface of these platelets and it will‬ ‭support endogenous coagulation.‬ ‭5-‬ ‭Platelet aggregation phase:‬‭It is carried out by fibrinogen‬‭which will bridge the platelets‬ ‭and recognizes a glycoprotein heterodimer: the 2B3A glycoprotein and this bridge can only be‬ ‭carried out in the presence of calcium. This hasPlatelet aggregate is produced quickly in 2 to 3‬ ‭minutes and it will be consolidated by the formation of fibrin which is the purpose of coagulation.‬ ‭Coagulation occurs synergistically with primary hemostasis. On the other hand‬ ‭These Platelets have receptors on their surface for the FC fragment of immunoglobulins G, E and‬ ‭they can induce degradation, so platelets must be considered as elements involved in immunity.‬