RT Book, Section
A1 Lichtman, Marshall A.
A1 Kaushansky, Kenneth
A1 Prchal, Josef T.
A1 Levi, Marcel M.
A1 Burns, Linda J.
A1 Linch, David C.
SR Print(0)
ID 1189336597
T1 Hemostatic Dysfunction Related to Liver Diseases
T2 Williams Manual of Hematology, 10e
YR 2022
FD 2022
PB McGraw-Hill Education
PP New York, NY
SN 9781264269204
LK hemonc.mhmedical.com/content.aspx?aid=1189336597
RD 2024/04/20
AB Loss  of  hepatic  parenchymal  cells  leads  to  decreased  plasma  levels  of  all  plasma  coagulation  factors  except  factor  VIII  and  von  Willebrand  factor,  which  are  produced  primarily  by  endothelial  cells.Thrombocytopenia  occurs  frequently  and  is  usually  a  result  of  splenic  sequestration  (see  Chaps.  26  and  74)  but  may  also  be  caused  by  an  autoimmune  mechanism,  disseminated  intravascular  coagulation  (DIC)  (see  Chap.  86),  folic  acid  deficiency,  and  decreased  platelet  production  due  to  thrombopoietin  (TPO)  deficiency.  Platelet  dysfunction  also  contributes  to  the  hemostatic  abnormalities.Enhanced  fibrinolysis  is  common  and  appears  to  be  caused  by  complex  pathogenetic  mechanisms,  including  release  and  impaired  clearance  of  plasminogen  activators.Dysfibrinogenemia  is  relatively  frequently  found  in  patients  with  chronic  liver  disease.Patients  with  chronic  liver  disease  may  develop  a  consumption  coagulopathy—in  its  most  extreme  form,  DIC  (see  Chap  86).Studies  employing  sophisticated  coagulation  tests  have  shown  that  due  to  a  rebalancing  of  the  coagulation  system  in  patients  with  chronic  liver  failure,  thrombin  generation  is  basically  normal  in  the  majority  of  patients,  whereas  some  patients  may  have  a  prothrombotic  phenotype.