hyperfibrinolysis

hy·per·fi·bri·nol·y·sis

(hī'pĕr-fī'brin-ol'i-sis), Avoid the mispronunciation hyperfibrinoly'sis.
Markedly increased fibrinolysis, as in subdural hematomas.
Farlex Partner Medical Dictionary © Farlex 2012

hy·per·fi·bri·nol·y·sis

(hī'pĕr-fī-brin-ol'i-sis)
Markedly increased fibrinolysis, as in subdural hematomas.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012
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References in periodicals archive ?
Sympathoadrenal activation and endotheliopathy are drivers of hypocoagulability and hyperfibrinolysis in trauma: A prospective observational study of 404 severely injured patients.
Vascular endothelial growth factor and uPA/suPAR system in early and advanced chronic kidney disease patients: a new link between angiogenesis and hyperfibrinolysis? Transl Res 2012; 160: 346-354.
Tranexamic acid for treatment and prophylaxis of bleeding and hyperfibrinolysis. Wien Klin Wochenschr 2017; 129(9): 303-16.
In addition, Apo B and Lp(a) are involved in the synthesis and assembly of VLDL, LDL, and IDL, and different levels of Apo B and Lp(a) can bind to fibrin binding sites, inhibit the activity of plasmin, and lead to the formation of thrombus, with compensatory secondary hyperfibrinolysis, and cause a significant increase in D-dimer levels.14 Different levels of VLDL have a certain impact on the body's fibrinolytic function, and can promote the formation of thrombosis.15 Serious thrombosis can lead to severe secondary hyperfibrinolysis.
Recombinant tissue-type plasminogen activator-evoked hyperfibrinolysis is enhanced by acidosis and inhibited by hypothermia but still can be blocked by tranexamic acid.
T Ganter et al., "Acute coagulopathy of trauma: hypoperfusion induces systemic anticoagulation and hyperfibrinolysis," Journal of Trauma-Injury, Infection and Critical Care, vol.
Current opinions suggest that the pathogenesis is multifactorial and mechanisms like activation of the protein C pathway, endothelial injury, coagulation factor deficiency, hyperfibrinolysis, and platelet dysfunction participate in the development of TIC [6-8].
AF has been associated with hypofibrinolysis due to increased levels of plasminogen activator inhibitor type 1 (PAI-1) [17], although in other studies hyperfibrinolysis with elevated tissue plasminogen activator (t-PA) [18-22] and plasmin-[[alpha].sub.2]-antiplasmin (PAP) complex levels were found [23].
The ability of thromboelastometry to predict bleeding and risk of thrombosis and confirm hyperfibrinolysis and the need for activating a massive transfusion protocol (MTP) allows for faster intervention.
The most common causes of coagulation disorders in the patients with massive bleeding or massive transfusions are: coagulopathy due to loss of blood type, dilutional coagulopathy, consumptive coagulopathy, hyperfibrinolysis, acidosis, hypothermia, anemia and electrolyte imbalance [26].