GT in medical terms most commonly refers to Glanzmann Thrombasthenia.
Glanzmann Thrombasthenia Explained
Glanzmann thrombasthenia (GT) is a rare, inherited bleeding disorder. As noted in medical literature, it was first described in 1918. The primary problem in GT is a defect or deficiency in a platelet integrin called alpha IIb beta3. This integrin is vital for proper platelet function because it acts as the receptor for fibrinogen, a protein essential for platelets to clump together (aggregate) and stop bleeding. Without enough functional alpha IIb beta3, platelets can't aggregate effectively, leading to prolonged bleeding.
Key Aspects of Glanzmann Thrombasthenia
- Cause: Genetic defect affecting the alpha IIb beta3 integrin on platelets.
- Function of Alpha IIb Beta3: This integrin is a receptor for fibrinogen, crucial for platelet aggregation.
- Effect: Impaired platelet aggregation and hemostasis (the process of stopping bleeding).
- Symptoms: Patients with GT often experience easy bruising, nosebleeds, gum bleeding, heavy menstrual periods (in females), and prolonged bleeding after injuries or surgeries.
Diagnosis and Treatment
Diagnosis typically involves blood tests to assess platelet function and identify the integrin deficiency. Treatment strategies focus on preventing and managing bleeding episodes and can include:
- Platelet transfusions
- Medications to promote blood clotting
- Local measures to control bleeding
