5.1....coagulation anticoagulation balance
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Transcript of 5.1....coagulation anticoagulation balance
Coagulation-anticoagulation balance & imbalance of haemostatic system
Hemostasis and Blood Coagulation
( DIC )
The term hemostasis means prevention of blood loss.
Whenever a vessel is ruptured, hemostasis is achieved by several mechanisms:
(1)vascular constriction,
(2) formation of a platelet plug,
(3) formation of a blood clot as a result of blood coagulation, and
(4) eventual growth of fibrous tissue into the blood clot to close the hole in the vessel permanently.
Coagulation cascade
The coagulation cascade is classically divided into three pathways.
The tissue factor and contact activation pathways both activate the "final common pathway" of factor X, thrombin and fibrin.
The coagulation cascade
Disseminated Intravascular Coagulation ( DIC )
Concept of DIC Acquired blood coagulation disorder= Thrombosis + / or Bleeding
• Coagulation is always the initial event
Etiology
Acute ~ : infection ( G- & G+ )
obstetric accident
serious trauma
malignant tumor
Pathology of DIC
Fibrin deposition, thrombosis
Bleeding
Edema
Organ failure
Pathogenesis of DIC
Over activation of TF.
Over activation of factor XII
Decrease Fibrinolytic activity.
Decrease anticoagulative property ( Protein C etc.)
Mechanism
1.TF release into blood and hyperexpression.
Septicemia
Injury
Obstetric accident
2. VEC lesion
TFTF Expression
TFPI↓: Degradation of Protein C and Antithrombin-III system
Fibrinolysis inhibited: Tissue Plasminogen Activator (t-PA)↓, PAI-1↑
Platelet adherence and aggregation: Collagen exposure , though NO,PGI2 and ADP enzyme ↑
XII activation.
3. Entrance of procoagulant to blood
① Snake venom② Metastatic tumor③ Pathogenic microorganism④ Foreign particles: amniotic fluid
Tumors and traumatized or necrotic tissue release Tissue factor into the circulation.
Endotoxin from gram-negative bacteria activates several steps in the coagulation cascade.
In addition to a direct effect on the activation of Hageman factor (factor XII), endotoxin induces the expression of tissue factor on the surface of monocytes and endothelial cells.
These activated cell surfaces then accelerate coagulation reactions.
4. Blood cell damage
RBC: Haemolysis usually a result of incompatible transfusion trigger the coagulation activation.
WBC: leukemia, endotoxin, IL-1, TNFa
Platelet: Endotoxin, immune complex, directly damage platelet promote their adhesion, release, as well as aggregation.
Platelet adhere to exposed ECM via vWF and are activated, release ADP , TXA2 lead to further platelet aggregation, which form platelet plug.
Aggregated platelets (white) surrounded by red blood cells
Predisposing factors for DIC
(1) Mononuclear phagocyte system dysfunction :
MPS plays a important role in protection from DIC.
The phagocyte can remove Endotoxin, Thrombin, Fibrinogen and FDP.
Thus, their function of clearance will be blocked while the cells are dysfunctional.
(2) Liver dysfunction.
(3)Microcirculation dysfunction:*Blood stagnation *Plt aggregation *Acidosis: VEC damage
(4)Hypercoagulable state :
Pregnancy : clotting factors ↑, plt ↑, but t-PA, AT-III, PC ↓; TF rich in placenta.
Typical clinical manifestation of DIC
Bleeding
Shock
MOF(MODS)
HEMOLYTIC ANAEMIAA
1. Bleeding
(1)Consumption of coagulant and platelet.
(2)Activation of fibrinolytic system.
Patient with DIC bleed
2.Organ dysfunction
Thromboembolism ischemia Thromboembolism ischemia
Ischemia-reperfusion injuryIschemia-reperfusion injury
3.shock
Bleeding
Coronary thrombosis
Vascular dilation
Microcirculatory thrombosis
Pathophysiological Basis of DIC diagnosis & Treatment
Diagnosis
1.Disease history 2.Clinic manifestation 3.Lab test 3+1
Diagnosis of DIC
Presence of disease associated with DIC
Appropriate clinical setting Clinical evidence of thrombosis, hemorrhage or
both.
Laboratory studies
no single test is accurate
Lab test
Screen test (3 items)
Platelet: <100 000/mm3 ( 100 000 ~ 300 000)
plasma fibrinogen count: <150 mg% (200~400)
PT: prolonged 3 sec (13~15 sec )
Confirm test ?? ??3P test
1. D-dimer or “3P ” positive
Principles of prevention and treatment for DIC
1.Management of the underlying disorder
2.Improving the microcirculation
3.Reconstructing the balance of coagulation and fibrinolysis
The End