PA20.1-2 | Platelet & Vascular Bleeding Disorders — Summary & Reflection

REFLECT

Think about a patient presenting with spontaneous bruising. What two questions — one about the location of bleeding, one about the timing after injury — would most efficiently direct you toward either a platelet/vascular cause or a coagulation factor cause?

Also reflect: why is the spleen uniquely positioned to be both the organ producing anti-platelet antibodies (in ITP) AND the organ destroying antibody-coated platelets? What does this mean for the treatment strategy of splenectomy?

KEY TAKEAWAYS

Core take-homes from this module:

• Primary haemostasis (platelet/vascular) bleeding = mucocutaneous, immediate; secondary = deep/delayed. Normal PT + aPTT confirms a primary defect.
• Thrombocytopenia is classified as: ↓ production (marrow failure, megaloblastic, infiltration) vs ↑ destruction (ITP, TTP, DIC, hypersplenism) vs dilutional.
• ITP: anti-GPIIb/IIIa IgG → splenic phagocytosis; marrow megakaryocytes increased; diagnosis of exclusion; acute form in children (post-viral, self-limiting) vs chronic form in adults (autoimmune).
• TTP: ADAMTS13 deficiency → UL-vWF–mediated platelet microthrombi → pentad (MAHA + schistocytes, thrombocytopenia, neuro, renal, fever); PT/aPTT relatively normal (unlike DIC).
• Qualitative defects: Glanzmann (GPIIb/IIIa, ↓ aggregation), Bernard-Soulier (GPIb, ↓ adhesion + giant platelets), aspirin (COX-1 inhibition), uraemia (metabolite inhibition).
• Vascular purpuras: HSP (IgA vasculitis, palpable), scurvy (collagen deficiency), senile (connective tissue atrophy), HHT (autosomal dominant AVM).
• Lab cornerstone: platelet count + film + BT/PFA + PT/aPTT + marrow megakaryocyte assessment.