UPDATES IN HAEMOSTASIS IN LIVER DISEASE
Asmaa Mohamed Hyder;
Abstract
Haemostasis describes the physiology relating to cessation of
bleeding following vessel injury. Upon a breach in vascular integrity,a complex reaction ensues leading to rapid transformation ofblood fromits fluid state into localized thrombus at the site of tissuedamage. Haemostasis is therefore designed to minimize blood loss,restore vascular integrity and ultimately preserve life.
Damage to the blood vesselwall leads to the intricate interplay of four key components: thevascular endothelium, platelets, the coagulation pathway andfinally fibrinolysis. When the endothelium is physically disrupted, it switches toa prothrombotic and proinflammatorystate .This state is characterized by vasoconstriction, platelet andleucocyte activation and adhesion, promotion of thrombinformation in addition to coagulation and fibrin deposition at thevascular wall.The thrombin formation and proinflammatorystate also form the initial steps towards vascular repair. Platelet plug formation if often referred to as primary haemostasis,while secondary haemostasis involves the complex interactionof plasma coagulation factors, which form fibrin strandsused to strengthen the platelet plug.
Antithrombotic mechanismsrestrict the permanent plug to the site of vessel injury,ensuring that the permanent plug does not inappropriatelyextend to occlude the vascular tree.
The physiology of the hemostatic system isclosely linked to liver function because the liver parenchymalcells produce most of the factors of clotting andof the fibrinolytic systems and because the liver regulatesthe activation or inhibition of both systems. A disturbed liverparenchymal cell function adversely impacts the hemostasissystem, the extent of which correlates with thedegree of disease. These changes may be modest inpatients with mild liver disease but are severe in patientswith grossly compromised liver function.
Patients who have liver disease can present with substantial alterations in the primaryhemostatic system. Abnormal platelet numbers and function are commonand traditionally have been thought to contribute to impaired hemostasis in bothacute and chronic liver disease.
Multiple factors can cause or contribute to the development of thrombocytopenia in patients with chronic liver disease. These include portalhypertension with resulting hypersplenism, cirrhosis, hepatocellular carcinoma and chemotherapy, anti-platelet antibodies, decreased levels or activity of the platelet growth factor thrombopoietin.
A number of coagulation proteins aresynthesized by the liver and their synthesis is variably impaired inliver disease .Factor VII,Factors II, V and X are also reduced in acute liver injury, with additional deficiencies of factors IX and XI in chronic liver injury.Conversely, plasma factor VIII levels are elevated in liver disease,This is likely secondary to enhanced vWF synthesis,These procoagulant protein
deficiencies are counter balanced by a deficit in anticoagulant proteins. These proteins are also synthesized within the liver, and their diminished circulating levels swing the coagulopathy pendulum in favor of clotting. Plasma levels of antithrombinIII, protein C (PC) and protein S (PS) are decreased in those with chronic liver disease.
bleeding following vessel injury. Upon a breach in vascular integrity,a complex reaction ensues leading to rapid transformation ofblood fromits fluid state into localized thrombus at the site of tissuedamage. Haemostasis is therefore designed to minimize blood loss,restore vascular integrity and ultimately preserve life.
Damage to the blood vesselwall leads to the intricate interplay of four key components: thevascular endothelium, platelets, the coagulation pathway andfinally fibrinolysis. When the endothelium is physically disrupted, it switches toa prothrombotic and proinflammatorystate .This state is characterized by vasoconstriction, platelet andleucocyte activation and adhesion, promotion of thrombinformation in addition to coagulation and fibrin deposition at thevascular wall.The thrombin formation and proinflammatorystate also form the initial steps towards vascular repair. Platelet plug formation if often referred to as primary haemostasis,while secondary haemostasis involves the complex interactionof plasma coagulation factors, which form fibrin strandsused to strengthen the platelet plug.
Antithrombotic mechanismsrestrict the permanent plug to the site of vessel injury,ensuring that the permanent plug does not inappropriatelyextend to occlude the vascular tree.
The physiology of the hemostatic system isclosely linked to liver function because the liver parenchymalcells produce most of the factors of clotting andof the fibrinolytic systems and because the liver regulatesthe activation or inhibition of both systems. A disturbed liverparenchymal cell function adversely impacts the hemostasissystem, the extent of which correlates with thedegree of disease. These changes may be modest inpatients with mild liver disease but are severe in patientswith grossly compromised liver function.
Patients who have liver disease can present with substantial alterations in the primaryhemostatic system. Abnormal platelet numbers and function are commonand traditionally have been thought to contribute to impaired hemostasis in bothacute and chronic liver disease.
Multiple factors can cause or contribute to the development of thrombocytopenia in patients with chronic liver disease. These include portalhypertension with resulting hypersplenism, cirrhosis, hepatocellular carcinoma and chemotherapy, anti-platelet antibodies, decreased levels or activity of the platelet growth factor thrombopoietin.
A number of coagulation proteins aresynthesized by the liver and their synthesis is variably impaired inliver disease .Factor VII,Factors II, V and X are also reduced in acute liver injury, with additional deficiencies of factors IX and XI in chronic liver injury.Conversely, plasma factor VIII levels are elevated in liver disease,This is likely secondary to enhanced vWF synthesis,These procoagulant protein
deficiencies are counter balanced by a deficit in anticoagulant proteins. These proteins are also synthesized within the liver, and their diminished circulating levels swing the coagulopathy pendulum in favor of clotting. Plasma levels of antithrombinIII, protein C (PC) and protein S (PS) are decreased in those with chronic liver disease.
Other data
| Title | UPDATES IN HAEMOSTASIS IN LIVER DISEASE | Other Titles | الجديد فى الإرقاء وعلاقته بأمراض الكبد | Authors | Asmaa Mohamed Hyder | Issue Date | 2014 |
Recommend this item
Similar Items from Core Recommender Database
Items in Ain Shams Scholar are protected by copyright, with all rights reserved, unless otherwise indicated.