In storage pool disease, platelets are primarily deficient in

• A. ADP
• B. Platelet factor 3
• C. Thrombasthenin
• D. Thromboxane A2

Answer: (A)

In storage pool disease, the problem lies with the dense granules inside platelets. These granules store several important signaling molecules, with ADP being the primary one that is released when platelets are activated. Releasing ADP amplifies platelet activation and aggregation by recruiting and stimulating more platelets through ADP receptors. When these dense granules are deficient or their contents aren’t released properly, ADP availability drops, so the amplification of aggregation is markedly reduced. That’s why ADP is the most affected and best answer.

Platelet factor 3 is a phospholipid surface component involved in the coagulation cascade, not a stored dense-granule content. Thrombasthenin isn’t a defined, reliable descriptor for a dense-granule constituent. Thromboxane A2 is produced after activation rather than stored for release, so its deficiency isn’t the hallmark feature of this disorder.