plaatjesfunctieonderzoeken

plaatjesfunctie, or platelet function, describes the ability of platelets to participate in hemostasis by forming a temporary plug at sites of vascular injury. Platelets are small, anucleate cells derived from megakaryocytes and circulate in the blood at a typical count of 150 to 450 billion per liter. In normal hemostasis, platelets first adhere to damaged endothelium via von Willebrand factor binding to the platelet GPIb-IX-V receptor. This adhesion triggers platelet activation, prompting shape change, granule secretion (ADP, serotonin, thromboxane A2), and exposure of activated GPIIb/IIIa receptors, which bind fibrinogen and other ligands to promote aggregation and formation of a platelet plug. Endothelial cells release inhibitory factors such as prostacyclin and nitric oxide to limit platelet activation, while thrombin and collagen exposure provide procoagulant signals that amplify the response.

Assessment of platelet function uses laboratory tests that assess adhesion, activation, and aggregation. Common tests include light transmission aggregometry, impedance aggregometry, and platelet function analyzers that measure closure time. Flow cytometry can quantify activation markers; genetic tests identify inherited platelet function disorders such as Glanzmann thrombasthenia (defective GPIIb/IIIa) and Bernard-Soulier syndrome (defective GPIb-IX-V). Platelet function is also influenced by medications; aspirin inhibits thromboxane A2 synthesis, while P2Y12 inhibitors and glycoprotein IIb/IIIa inhibitors reduce aggregation.

Clinical relevance includes risks of excessive platelet activity leading to thrombosis, or impaired function causing mucocutaneous bleeding. Treatments may target platelet function in diseases such as cardiovascular disease or bleeding disorders.