Step 1: Frame the disease by its key step in haemostasis. Glanzmann thrombasthenia breaks the aggregation phase of platelets, not adhesion.
Step 2: Aggregation needs fibrinogen bridges anchored to the $GpIIb/IIIa$ integrin. In this autosomal recessive disorder that integrin is deficient or non-functional.
Step 3: So platelets cannot clump even when stimulated by ADP or collagen, and the bleeding time is long while the count stays normal.
Step 4: Contrast: $GpIb$ loss is Bernard-Soulier (adhesion defect), ADAMTS-13 loss is TTP, and acquired antibodies drive ITP. Only decreased $GpIIb/IIIa$ fits.
\[\boxed{\text{Decreased GpIIb/IIIa}}\]