Which laboratory pattern is most consistent with primary fibrinogenolysis rather than DIC in a patient with bleeding and the given results?

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Multiple Choice

Which laboratory pattern is most consistent with primary fibrinogenolysis rather than DIC in a patient with bleeding and the given results?

Explanation:
Primary fibrinogenolysis is suggested when the bleeding is driven by rapid destruction of fibrinogen by plasmin without widespread activation of the coagulation sequence. The hallmark lab pattern is very low fibrinogen with elevated fibrin degradation products, while platelet count and coagulation times (PT and aPTT) remain normal or near normal. This indicates fibrinogen is being consumed directly by fibrinolysis, not by consumption from a systemic clotting process. In contrast, DIC involves widespread coagulation with consumption of platelets and clotting factors, so you’d expect prolonged PT and aPTT, low platelets, and elevated D-dimer or FDPs due to crosslinked fibrin degradation. Factor II deficiency mainly affects thrombin generation and would typically prolong PT and aPTT due to decreased factor II, but it wouldn’t cause marked fibrinogen depletion or high FDPs. Coumadin therapy prolongs PT (and INR) by impairing vitamin K–dependent factors, not by primary fibrinogen breakdown, and again wouldn’t match the pattern of hypofibrinogenemia with fibrinolytic product elevation from plasmin acting on fibrinogen.

Primary fibrinogenolysis is suggested when the bleeding is driven by rapid destruction of fibrinogen by plasmin without widespread activation of the coagulation sequence. The hallmark lab pattern is very low fibrinogen with elevated fibrin degradation products, while platelet count and coagulation times (PT and aPTT) remain normal or near normal. This indicates fibrinogen is being consumed directly by fibrinolysis, not by consumption from a systemic clotting process.

In contrast, DIC involves widespread coagulation with consumption of platelets and clotting factors, so you’d expect prolonged PT and aPTT, low platelets, and elevated D-dimer or FDPs due to crosslinked fibrin degradation. Factor II deficiency mainly affects thrombin generation and would typically prolong PT and aPTT due to decreased factor II, but it wouldn’t cause marked fibrinogen depletion or high FDPs. Coumadin therapy prolongs PT (and INR) by impairing vitamin K–dependent factors, not by primary fibrinogen breakdown, and again wouldn’t match the pattern of hypofibrinogenemia with fibrinolytic product elevation from plasmin acting on fibrinogen.

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