The genes of both of these proteins are on chromosome 17. Around 50% of activity of each protein is enough for creating platelet aggregation. Defects in the glycoprotein IIb/IIIa can lead to defected protein aggregation and ensuing bleeding.

Glanzmann Thrombasthenia is inherited in an autosomal recessive pattern. The glycoprotein IIb/IIIa are essential because they have the ability to bind the fibrinogen, vitronectin and fibronectin, whereas, glycoprotein Ib has ability to contact with collagen complex that is exposed when the blood vessel line is damaged and it can also aggregate with thrombocytes.

Glycoprotein IIb/IIIa is an adhesion receptor which can be expressed by thrombocytes, where thrombocytes are cells that play key role in blood clotting. The symptoms for Glanzmann Thrombasthenia are reduced platelet count, excessive bleeding, bleeding gums, easy bruising, excessive bleeding even from injuries, nosebleeds in children and prolonged bleeding time. As the causes of Glanzmann Thrombasthenia, you can consider these following diseases which are all similar to it.

•  Blood diseases

•  Platelet abnormality

•  Coagulation

•  Rare blood disorder

•  Fibronectin

•  Fibrinogen

•  Epistaxis

•  Menorrhagia

It can also be causing due to autoimmune disorder. For diagnosing, doctors usually recommend Anemia tests or thyroid/adrenal glands function tests. The tendency for the bleeding can be variable but severe and Glanzmann Thrombasthenia can be life threatening. Platelets can fail to form plug at injury portion. Women may experience heavy bleeding at menstrual cycles and prolonged bleeding at child birth. The symptoms can suggest one to follow checkups and tests through a doctor's recommendation in order to be assured of safe health and life.