disseminated intravascular coagulopathy

Hematology An acquired bleeding diathesis with a generally bad outcome in which the balance between coagulation and fibrinolysis tips toward the former; DIC is characterized by accelerated platelet consumption with coagulation factor depletion–↑ PT, ↑ PTT and stimulation of fibrinolysis–generation of fibrin split products Etiology Severe sepsis–30-65% of DIC is caused by infection, extensive burns, trauma, retained dead fetus, heat stroke, mismatched blood, metastatic CA, leukemia Clinical forms Fast DIC–acute, fulminant, uncompensated consumptive coagulopathy with severe bleeding, and ecchymosis due to abruptio placentae, septic abortion, amniotic fluid embolism, toxemia, malignancy, massive tissue injury–eg burns, surgery, trauma, infections, gram-negative sepsis, meningococcemia, RMSF, incompatible blood; 'fast' DIC requires replacement of deficient or consumed factors Slow DIC Due to chronic compensated illness, with few overt signs of bleeding; clinical picture is painted by thrombosis, microcirculatory ischemia, end-organ infarction, due to acute promyelocytic leukemia, coagulation factor transfusion, CA of pancreas, prostate, lung, stomach, aortic aneurysm, cocaine, IMAOs, giant hemangioma–Kasabach-Merritt syndrome, liver disease, vasculitis, chronic and/or low-grade infections–eg, histoplasmosis, aspergillosis, malaria, obstetrics,–eg, hemolysis, eclampsia, dead fetus, infection, hypoxia, acidosis, respiratory distress; 'slow' DIC may respond to heparinization Lab ↑ PT, aPTT, FDPs, fibrinopeptide A; ↓ fibrinogen, prothrombin, platelets, factor V, factor VIII, antithrombin III, plasminogen, ↓ factors VII, IX, X, XI

单词	disseminated intravascular coagulopathy
释义	disseminated intravascular coagulopathy disseminated intravascular coagulopathy Hematology An acquired bleeding diathesis with a generally bad outcome in which the balance between coagulation and fibrinolysis tips toward the former; DIC is characterized by accelerated platelet consumption with coagulation factor depletion–↑ PT, ↑ PTT and stimulation of fibrinolysis–generation of fibrin split products Etiology Severe sepsis–30-65% of DIC is caused by infection, extensive burns, trauma, retained dead fetus, heat stroke, mismatched blood, metastatic CA, leukemia Clinical forms Fast DIC–acute, fulminant, uncompensated consumptive coagulopathy with severe bleeding, and ecchymosis due to abruptio placentae, septic abortion, amniotic fluid embolism, toxemia, malignancy, massive tissue injury–eg burns, surgery, trauma, infections, gram-negative sepsis, meningococcemia, RMSF, incompatible blood; 'fast' DIC requires replacement of deficient or consumed factors Slow DIC Due to chronic compensated illness, with few overt signs of bleeding; clinical picture is painted by thrombosis, microcirculatory ischemia, end-organ infarction, due to acute promyelocytic leukemia, coagulation factor transfusion, CA of pancreas, prostate, lung, stomach, aortic aneurysm, cocaine, IMAOs, giant hemangioma–Kasabach-Merritt syndrome, liver disease, vasculitis, chronic and/or low-grade infections–eg, histoplasmosis, aspergillosis, malaria, obstetrics,–eg, hemolysis, eclampsia, dead fetus, infection, hypoxia, acidosis, respiratory distress; 'slow' DIC may respond to heparinization Lab ↑ PT, aPTT, FDPs, fibrinopeptide A; ↓ fibrinogen, prothrombin, platelets, factor V, factor VIII, antithrombin III, plasminogen, ↓ factors VII, IX, X, XI
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