The<unk>  is characterized by large amounts of uPA in platelets. Consequently, stored platelet plasminogen is converted to plasmin, which is thought to play a role in degrading a number of proteins stored in platelet α-granules. These proteins include platelet factor V, von Willebrand factor, fibrinogen, thrombospondin-1, and osteonectin. There is also a quantitative deficiency in the platelet protein multimerin 1 (MMRN1). Furthermore, upon QPD platelet activation, uPA can be released into forming clots and accelerate clot lysis, resulting in delayed-onset bleeding (12-24hrs after injury). In 2010, the genetic cause of QPD was determined as a mutation involving an extra copy of the gene encoding uPA. The mutation causes overproduction of uPA, an enzyme that accelerates blood clot breakdown.
Quebec platelet disorder
Harris platelet syndrome
Gray platelet syndrome
Sticky platelet syndrome
Glanzmann's thrombasthenia
Bernard–Soulier syndrome
Pseudo gray platelet syndrome
Von Willebrand disease