Flashcards in Hemostasis I Deck (48):
-coagulation inhibition system
Mechanism of hemostasis
1. vascular constriction
2. formation of platelet plug
3. formation of blood clot
Causes of vascular constriction in hemostasis
1. Platelet-released thromboxane A2
2. nervous system reflex to pain
Formation of platelet plug (primary hemostasis)
Injury--> Collagen + VWF + PLTs + fibrinogen
How are platelets activated
1. Binding of VWF to GPIb
2. Thrombin, adrenalin, ADP, collagen
Activated platelets release?
ADP, thromboxane, Calcium
Activation of plts by ADP exposes what receptor?
Other than ADP, what else leads to GPIIb/IIIa exposure?
Function of GPIIb/IIIa
Receptor that binds to fibrinogen, linking platelets together
Function of thrombin in hemostasis?
Fibrin conversion, platelet activation
Name for Factor I
Name for Factor 2
Name for Factor 3
Tissue factor or thromboplastin
Name for Factor 4
Name for factor 13
Prothrombin is converted to thrombin by the action of what?
fibrinogen is converted to fibrin monomer and eventually fibrin fibers by
Fibrin fibers are converted to cross-linked fibrin fibers by the action of what factor?
Factor 13. Fibrin-stabilizing factor
Aspirin works on what pathways (site of action) to inhibit the production of?
COXs pathways to inhibit the production of thromboxane A2
Extrinsic pathway is activated by?
Tissue factor, which is released into the blood as a result of vascular injury.
Primary factor in the extrinsic pathway
TF:FVII activates what factor?
Factor ten, and is considered a TENase
Intrinsic pathway is activated by?
Trauma to the blood, or exposure to collagen
Factors specific to the intrinsic pathway
12, 11, 9, 8
Factors of the common pathway
10, 5, 2, 1
Final common pathway
where the intrinsic and extrinsic pathway converge, resulting in fibrin formation
In the contemporary view of hemostasis coagulation begins with the activation of factors X and IX by?
TF:FVII complex, thus, linking the intrinsic and extrinsic pathway
3 Phases of coagulation activation in the contemporary view of hemostasis?
1. Initial phase
2. Amplification phase
3. Propagation phase
Tissue factor exposed--> TF:FVIIa complex --> Activation of FX and FIX--> Generation of small amounts of thrombin FIIa
Is the amount of thrombin generated in the initial phase large or small?
-conversion from extrinsic to intrinsic thrombin formation by generation of another tenase (FIXa:FVIIIa)
FIXa:FVIIIa increased production of FXa by 50-100x hence amplification, and increased thrombin production
Thrombin creates a positive feedback group
Factors thrombin acts on in the positive feedback loop
11-->11a, 8-->8a, 5-->5a
**Thrombin also leads to further PLT activation and aggregation
Thrombin burst -->plt aggregation and the formation of fibrin fibers, which stabilized by FXIIIa into cross-linked fibrin strands, to form a stable network
Dissolution of thrombi and maintaining patency of vascular system
Plasminogen activated to plasmin which cleaves fibrin
Factors that activate plasminogen
Physiologic- tPA, Urokinase
Medications that block plasmin from cleaving thrombin
Hemophilia A is a deficiency in what factor?
<1% of normal factors
>5% but <40% normal factors
Factor IX deficiency
Treatment for hemophilia
-Replacement of factor
because of frequent factor replacement, 30% of patients with hemophilia A develop?
Disseminated intravascular coagulation
Thrombohemorragic d/o involving the generation of intravascular thrombin and consumption of procoagulants and platelets
Common conditions that cause DIC
Sepsis, obstetric complications, trauma, shock, massive hemolysis, hepatic failure
Management of DIC primarily focuses on treating?
the underlying disorder