Glanzmann's<unk>  is mainly divided into hereditary GT, variant GT, and acquired GT. Glanzmann<unk>  (GT) is an autosomal recessive inherited qualitative platelet disorder characterized by absence or reduction of platelet glycoprotein GPIIb or GPIIIa or CD61. Hereditary Glanzmann<unk>  is classified into three types  The subtypes vary based on ethnicity. For example, Type I is more common in Arabs and Iraqi-Jews living in Israel, whilst type II is relatively frequent in the Japanese population. Variant type includes patients with platelets expression of αIIbβ3 more than 20% in which mainly the platelets are able to aggregate but they present the clinical phenotype of GT. The reason being that the stimulated platelets can not bind to soluble Fg or antibodies recognizing activation-dependent determinants on αIIbβ3. It is due to a single amino acid substitution. Acquired GT is defined by inhibition of platelet αIIbβ3 actual function due to the attack of autoantibodies. These antibodies can be produced in numerous disorders such as hematologic malignancy, transfusion, drugs and autoimmune diseases.
Glanzmann's thrombasthenia classification
Hemophilia A classification
IMPROVE bleeding risk score
Thrombophilia classification
TIMI bleeding criteria
International Society on Thrombosis and Haemostasis bleeding scale
Glanzmann's thrombasthenia epidemiology and demographics
Glanzmann's thrombasthenia physical examination