In disseminated intravascular coagulation (DIC), why does the patient paradoxically develop both thrombosis and hemorrhage simultaneously?

• A DIC consumes coagulation factors and platelets while simultaneously generating excessive thrombin, causing widespread microvascular thrombosis and consumption coagulopathy ✓
• B Massive platelet aggregation causes vessel occlusion while simultaneously releasing heparin-like substances that anticoagulate the blood
• C DIC activates the fibrinolytic system alone, which degrades clotting factors and causes bleeding while platelet aggregates form independently
• D The paradox results from alternating release of tissue factor and thrombomodulin from damaged endothelium

Explanation

DIC is initiated by massive tissue factor (TF) exposure (from obstetric catastrophes, sepsis, tumor lysis, trauma), generating a thrombin burst that consumes fibrinogen, platelets, and factors V and VIII in widespread microvascular thrombi throughout organs, causing ischemia. The same thrombin burst and fibrin clot formation secondarily activates the fibrinolytic system (plasmin), generating fibrin/fibrinogen degradation products (FDPs/D-dimers) that act as anticoagulants by inhibiting fibrin polymerization and platelet function. Thus, the patient simultaneously has thrombotic organ failure and hemorrhagic diathesis from consumed coagulation factors — the 'consumption coagulopathy' paradox.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.