This thesis deals with the processes of primary haemostasis and how they can be analyzed. Very important components are platelets, therefore their cell biology is summarized, especially those parts, which are involved in the clot forming process. Furthermore the physiological procedure and congenital and acquired dysfunctions of primary haemostasis are explained. Among others the Bernard-Soulier syndrome, where a congenital defect of adhesion is the reason of bleeding disorder, the Glanzmann’s thrombasthenia with a dysfunction of the GPIIb-IIIa complex and acquired disorders, e. g. uraemia, chronic liver diseases, acute leukaemia and chronic myeloproliferative disorders. The subsequent part deals with the aggregation in diagnosis, especially with conventional methods and quick tests. At almost every test agonists are added to whole blood or platelet rich plasma. The clot forming is measured either optically or with resistance change or the recording of the hole closing time. Although most of the time conventional methods are one step ahead of quick tests, the latter has one big benefit: the response time is much shorter. More benefits and disadvantages are explained.