Hemostasis I Flashcards Preview

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Flashcards in Hemostasis I Deck (48):
1

Hemostasis components

-vascular system
-platelet system
-coagulation system
-fibrinolytic system
-coagulation inhibition system

2

Mechanism of hemostasis

1. vascular constriction
2. formation of platelet plug
3. formation of blood clot
4. Fibrinolysis

3

Causes of vascular constriction in hemostasis

1. Platelet-released thromboxane A2
2. nervous system reflex to pain

4

Formation of platelet plug (primary hemostasis)

Injury--> Collagen + VWF + PLTs + fibrinogen

5

How are platelets activated

1. Binding of VWF to GPIb
2. Thrombin, adrenalin, ADP, collagen

6

Activated platelets release?

ADP, thromboxane, Calcium

7

Activation of plts by ADP exposes what receptor?

GPIIb/IIIa

8

Other than ADP, what else leads to GPIIb/IIIa exposure?

thromboxane A2

9

Function of GPIIb/IIIa

Receptor that binds to fibrinogen, linking platelets together

10

Secondary hemostasis

Clot formation

11

Function of thrombin in hemostasis?

Fibrin conversion, platelet activation

12

Name for Factor I

Fibrinogen

13

Name for Factor 2

Prothrombin

14

Name for Factor 3

Tissue factor or thromboplastin

15

Name for Factor 4

Calcium

16

Name for factor 13

Fibrin-stabilizing factor

17

Prothrombin is converted to thrombin by the action of what?

Prothrombin activator

18

fibrinogen is converted to fibrin monomer and eventually fibrin fibers by

Thrombin

19

Fibrin fibers are converted to cross-linked fibrin fibers by the action of what factor?

Factor 13. Fibrin-stabilizing factor

20

Aspirin works on what pathways (site of action) to inhibit the production of?

COXs pathways to inhibit the production of thromboxane A2

21

Extrinsic pathway is activated by?

Tissue factor, which is released into the blood as a result of vascular injury.

22

Primary factor in the extrinsic pathway

Factor 7

23

TF:FVII activates what factor?

Factor ten, and is considered a TENase

24

Intrinsic pathway is activated by?

Trauma to the blood, or exposure to collagen

25

Factors specific to the intrinsic pathway

12, 11, 9, 8

26

Factors of the common pathway

10, 5, 2, 1

27

Final common pathway

where the intrinsic and extrinsic pathway converge, resulting in fibrin formation

28

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

29

3 Phases of coagulation activation in the contemporary view of hemostasis?

1. Initial phase
2. Amplification phase
3. Propagation phase

30

Initiation phase

Tissue factor exposed--> TF:FVIIa complex --> Activation of FX and FIX--> Generation of small amounts of thrombin FIIa

31

Is the amount of thrombin generated in the initial phase large or small?

small

32

Amplification phase

-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

33

Factors thrombin acts on in the positive feedback loop

11-->11a, 8-->8a, 5-->5a

**Thrombin also leads to further PLT activation and aggregation

34

Propagation phase

Thrombin burst -->plt aggregation and the formation of fibrin fibers, which stabilized by FXIIIa into cross-linked fibrin strands, to form a stable network

35

Fibrinolysis

Dissolution of thrombi and maintaining patency of vascular system

36

Fibrinolysis pathway

Plasminogen activated to plasmin which cleaves fibrin

37

Factors that activate plasminogen

Physiologic- tPA, Urokinase
Exogenous- Streptokinase

38

Medications that block plasmin from cleaving thrombin

Amicar
Tranexamic acid

39

Hemophilia A is a deficiency in what factor?

Factor VIII

40

Severe hemophilia

<1% of normal factors

41

Mild hemophilia

>5% but <40% normal factors

42

Hemophilia B

Factor IX deficiency

43

Treatment for hemophilia

-Replacement of factor
-DDAVP
-sometimes antifibrinolytics

44

because of frequent factor replacement, 30% of patients with hemophilia A develop?

antifactor antibodies

45

Disseminated intravascular coagulation

Thrombohemorragic d/o involving the generation of intravascular thrombin and consumption of procoagulants and platelets

46

Common conditions that cause DIC

Sepsis, obstetric complications, trauma, shock, massive hemolysis, hepatic failure

47

Management of DIC primarily focuses on treating?

the underlying disorder

48

DIC diagnosis

plts 10-20k
-Symptoms of thrombosis
-Bleeding from three unrelated sites
-Lab findings- prolonged clotting times, decreased clotting factors