Disseminated intravascular coagulation (DIC) results in a paradoxical combination of thrombosis and bleeding. The primary driver of coagulopathy in acute DIC is:

• A Massive platelet production causing thrombocytosis and clotting
• B Autoantibody-mediated destruction of von Willebrand factor
• C Lupus anticoagulant causing hypercoagulability without fibrinogen consumption
• D Widespread thrombin activation consuming coagulation factors and platelets, with secondary fibrinolysis generating FDPs that further inhibit clotting ✓

Explanation

In DIC, widespread endothelial injury and tissue factor release trigger massive thrombin generation throughout the microvasculature. This consumes fibrinogen, factors V, VIII, X, and platelets ('consumptive coagulopathy'), while secondary fibrinolysis generates fibrin degradation products (FDPs/D-dimers) that act as anticoagulants. The result is paradoxical simultaneous microvascular thrombosis (organ damage) and severe bleeding from the consumption of clotting factors and platelets.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.