After a bleeding injury, platelet aggregation initiates recovery as an important step in wound care. It ensures that platelets accumulate within a few minutes, agglutinating the damaged area and thus causing blood flow to cease.
What is platelet aggregation?
Platelet aggregationIt causes platelets (shown in white in the figure) to accumulate in a wound within a few minutes, sticking to the damaged area and thus causing blood flow to ebb. Platelet aggregation is the name for an essential sub-process during blood clotting. In the first phase of blood clotting (primary hemostasis), the platelets (Greek: thrombos, clumps) ensure primary wound closure by clumping and aggregating (Latin: aggregare, to accumulate). The process is accompanied by constriction of the affected blood vessels and those in the surrounding area. The blood platelets (thrombocytes) change their appearance and the properties on the cell surface during clumping. The change in shape of the platelet exposes receptors acting on the surface, which now become active. Through them, the activated platelet can attach to the vessel wall. In addition, other processes take place that support hemostasis. For example, factors released at the damaged vessel wall direct the platelets to this site. In addition, substances are released that prevent inflammation and initiate the next steps in blood clotting. They ensure permanent wound closure and, ultimately, healing.
Function and task
Platelet aggregation prevents major blood loss after an injury. This process is part of the blood clotting system. This system functions as a complex and finely tuned interaction of various cells (platelets), clotting factors, and several messengers. It runs much like a chain reaction. Clotting factors are predominantly proteins that are activated under certain conditions and in turn themselves initiate or accelerate reactions within the clotting process. The clotting factors have been given Roman numbers (from 1 to 13) in medical usage. Platelets initiate the clotting reaction when damage occurs on the surface. The process behind this occurs in three phases. Adhesion (Latin: to adhere) as well as the aggregation of the platelets and the formation of a plug that closes the wound. The cell walls of the injured vessels or tissue release a coagulation-active factor, the so-called Von Willebrand factor. This is a protein molecule synthesized by the cells in the inner vessel wall (endothelial cells) and the precursor cells of the platelets. It is stored in the platelet and released upon activation. This factor is responsible for the adhesion of platelets (adherence to the vessel wall) so that they cover the wound thinly. At the same time, platelet aggregation is initiated in this way. This occurs because after platelet activation, genes are also activated that initiate the synthesis of a receptor necessary for aggregation. With the cooperation of the structural protein collagen, thrombin, an important enzyme in blood clotting, the nucleotide adenosine diphosphate (ADP), hormones such as adrenaline and other endogenous substances, the platelets change their shape. In the process, other components are released and the affected area is prepared for the next steps of blood clotting. A cascade of different factors is activated. While platelet aggregation is initially reversible, a level is eventually reached at which platelets cross-link with the participation of a specific protein (fibrinogen, factor I) and an irreversible thrombus (blood clot) is formed.
Diseases and medical conditions
Platelet aggregation disorders may present as an increased or decreased response. They may occur in patients with a hereditary predisposition or after taking certain medications. The congenital disorders are rare and involve platelet aggregation itself or various processes accompanying the process. Affected individuals are conspicuous by spontaneously occurring mucosal and nasal hemorrhages and by their tendency to develop hematomas (bruises). Female patients suffer from heavy menstrual and obstetric bleeding.One of these congenital disorders was named after the Swiss pediatrician E. Glanzmann: Glanzmann-Naegeli disease (also Glanzmann thrombasthenia). It is inherited in an autosomal recessive manner. Affected is a receptor in the platelet membrane, which is not provided in sufficient quantity due to a genetic change (mutation). Patients with this defect are at high risk from taking antiplatelet drugs such as aspirin. In Willebrand-Jürgens syndrome, the factor that is important for platelet adhesion and aggregation is not present in sufficient quantity or with qualitative limitations. Thus, it is not fully functional and platelet adhesion as a preparatory step of aggregation is impaired. Two French hematologists are the namesakes of another inherited, very rare platelet disorder: Bernard-Soulier syndrome. It primarily affects platelet adhesion. It is reduced and in this way also reduces platelet aggregation. Patients with storage pool disease show impaired secretion after platelet activation. The culprits are the missing granules. These are cellular deposits (vesicles) from which the various factors are released during platelet activation. Gray platelet syndrome (gray platelet syndrome) is a special form. More frequently, acquired or drug-induced platelet aggregation disorders are also diagnosed. So-called exhausted platelets, which are no longer capable of aggregation, can occur in dialysis patients, due to heart–lung machines, in severe kidney disease or after burns. The situation in these cases is similar to that seen in storage pool disease. Increased platelet aggregation is found in coronary artery disease, after strokes, in vascular disease and acute thrombosis. Drugs that inhibit platelet function are commonly used for thromboprophylaxis. Acetylsalicylic acid (e.g., in aspirin) is one of them. In addition, there are some chemotherapeutic agents that decrease platelet aggregation.
